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AZIMAT NUCLEAR MEDICINE

BY

DR ZOOL HILMI2012

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SIMPLE PHYSIC

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Radionuclide Decay mode Half time Energy (keV) Production

method

Thallium-201 Electron capture 73.1 hr 69-83(94%) ,

135(3%) 167(10%)

Cyclotron

Gallium-67 Electron capture 78.3 hr 93(37%),185(20%),3

00(17%),395(5%)

Cyclotron

Indium-111 Electron capture 2.8 d 171(90%),245(94%) Cyclotron

Iodine-123 Electron capture 13.2 hr 159 Cyclotron

Iodine-131 Beta minus 8 d 364 Reactor

Technetium-99m Isomeric

transition

6 hr 140 Generator

Cobalt-57 Electron capture 272 d 122 Cyclotron

Fluorine-18 Positron emitting 110 min 0.653 MeV Cyclotron

Gallium-68 Positron emitting 68 min 1.9 MeV Generator

Carbon-11 Positron emitting 20 min 0.96 MeV Cyclotron

Nitrogen-13 Positron emitting 10 min 1.19 MeV Cyclotron

Oxygen-15 Positron emitting 2 min 1.70 MeV Cyclotron

Rubidium-82 Positron emitting 1.3 min 3.15 MeV Generator

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ɤ/xrayinteraction with

matter

Coherent/Rayleigh/

classical scatter

Pair production

Photodisintegration

Photo electric

Compton scatter

-Low energy photon excites atom but then

passes through without energy transfer

-High energy photon interact with nucleus

& converted to electron and photon-Positron and electron annihilation with

two 511 keV 180 degree

-High energy photon absorbed by nucleus

resulting disintegration of nucleus

-Energy threshold 15 MeV

-Photon interact with inner shell electron

-Photon energy totally absorbed by inner

shell electron

-Electron is ejected (photoelectron)

-Outer shell electron fill the inner shell-

characteristic radiation or Auger electron

-Energy of emitted photoelectron =

difference of incident photon energy and

electron binding energy-Low energy dominant

-PE∝ 3/³ 

-Photon interact with outer shell electron

-Loosely bound electron

-High energy photon – more straight scatter

-Compton ∝ electron density/ E

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Decay

Alpha

Beta

Gamma

-Consist 2 neutrons and 2 protons = Helium

-Atomic no > 82

-In decay, atomic no decreases by 2 and mass

no decreases by 4

-Travel from 1 – 10 cm in air

-Travel < 0.1 cm in tissue

-High risk if ingested or injected

Electron

Positron

Electron

capture

Isomeric

transition

Internal

conversion

-Neutron rich

-n/p high

-n= p + ßˉ + v 

-High proton-n/p low

-n= n +ßᶧ + v

-High proton

-n/p low

-p + e = n + v

-Tc-99m = ɤ + Tc99

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eˉ 

eˉ 

Q = EXPOSURE

AMOUNT OF ELECTRICAL CHARGE

PRODUCED BY IONIZING

ELECTROMEGNETIC RADIATION PER

MASS OF AIR

UNIT = C/Kg = Roentgen

1 R = 2.58 x 10 ˉ⁴ C/Kg

.SKIN DOSERADIATION EXPOSURE INCIDENT TO

PATIENT DUE TO RADIOLOGICAL

EXAMINATION

CHEST X RAY = 0.1 – 0.2 mGy

SKULL = 1.5 mGy

ABDOMEN = 3 mGy

LUMBAR = 10 mGy

K = KERMA

ENERGY CARRIED BY PHOTON (OR

OTHER INDIRECT IONIZING

RADIATION) TRANSFER ENERGY TO

CHARGE PARTICLE (

PE/COMPTON/PAIR PRODUCTION

UNIT = J/Kg OR Gray

D = ABSORB DOSE

DIRECTLY IONIZATION CHARGE

PARTICLE DEPOSIT ENERGY BY

(EXCITATION/IONIZING) PER UNIT

MASS

UNIT = J/Kg

1 Gray = 1 J/ Kg100 rad = 1 Gray

Rad = RADIATION ABSORB DOSE

E = EFFECTIVE DOSE

ICRP 1990

MEASURE OF RADIATION AND

ORGAN SYSTEM SPECIFIC DAMAGE

IN HUMAN

UNIT = Sievert

100 rem = 1 Sv = J/Kg

WT = TISSUE WEIGHTING FACTOR

GONAD = 0.2

BONE

MARROW/LUNG/STOMACH/COLON

= 0.12

BLADDER/BREAST/LIVER/THYROID

= 0.05

SKIN/BONE = 0.01

H = EQUIVALENT DOSE

ICRP 1990

MEASURE OF RADIATION SPECIFIC

BIOLOGIC DAMAGE IN HUMAN

UNIT = Sievert

100 rem = 1 Sv = J/Kg

WR = RADIATION WEIGHTING

FACTOR

XRAY/ɤ/ß/e  = 1

PROTON > 2 MeV = 5

NEUTRON = 5 – 20

ΑLPHA = 20

SOURCE

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 PARATHYROID SCINTIGRAPHY

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Pearls & Pitfalls

Parathyroid

imaging

• The most common indication for

parathyroid imaging is to localize thehyperfunctioning gland (adenoma) either

in the thyroid bed or in the ectopic

location (lower neck or mediastinum)

• Parathyroid adenomas are usually single

• Parathyroid imaging is usually performed

by using Tc-99m sestamibi withsequential images after 2 hours, whereas

parathyroid adenomas usually

hyperconcentrate Tc-99m sestamibi and

persist over time

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PARATHYROID SCINTIGRAPHY

ANATOMY AND EMBRYOLOGY

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ANATOMY

• 4 parathyroid glands

• Measuring 6mm x 3mm

• Weighing 35 – 40 gram

• Rarely, may be only 2 glands or as many as 8

glands

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EMBRYOLOGY

• Inferior parathyroid glands arise from 3rd 

branchial pouch and migrate caudally with the

thymus

• Superior glands arise from 4th branchial pouch

and migrate with the thyroid

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Type of cells in parathyroid

1. Chief cell  –  produces parathyroid hormone

(PTH) and it has little mitochondria orcytoplasma

1. Oxyphil cell – high number of mitochondria.

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Pathophysiology

• Hyperpathyroidism :

1. Primary hyperpathyroidism

2. Secondary hyperpathyroidism

3. Tertiary hyperpathyroidism

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Hyperparathyroidism

• Chief cells (single or multiple glands)synthesis

more and release more PTH

• PTH synthesize, stored and secreted by

parathyroid glands

• PTH responsible for calcium and phosphorus

homeostasis by its action on bone, small

intestine and kidneys

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+

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Scan of Tc-99m MIBI

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Tc-99m MIBIHeart

GIKidney

Bladder 

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Normal uptake for Tc-99m MIBI

Salivary gland

Parotid gland

Renal

Bladder

Heart

Intestine

Thyroid

Parathyroid

Concerning imaging of parathyroid

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Concerning imaging of parathyroid

glands

A. Approximately 50% of cases of primaryhyperparathyroidism are due to a single functioningadenoma

B. The sensitivity of parathyroid scintigraphy in the

detection of adenomas within the gland approaches75%

C. In secondary hyperparathyroidism approximately 80%of hyperplastic glands will be visualized

D. The majority are parathyroid adenomas are

functioningE. False positive scans may occur in the presence of

coexisting thyroid disease

Concerning imaging of parathyroid

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Concerning imaging of parathyroid

glands

A. F

B. T

C. F

D. T

E. T

Tc 99m sestamibi uptake may be found

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Tc-99m sestamibi uptake may be found

in

A. Parathyroid hyperplasia

B. Parathyroid adenoma

C. Thyroid adenoma

Tc 99m sestamibi uptake may be found

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Tc-99m sestamibi uptake may be found

in

A. T

B. T

C. T

In performing Tl 201/Tc 99m

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In performing Tl-201/Tc-99m

pertechnitate parathyroid studies, it is

best perform the pertechnitate studyfirst

In performing Tl 201/Tc 99m

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In performing Tl-201/Tc-99m

pertechnitate parathyroid studies, it is

best perform the pertechnitate studyfirst

• FALSE

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What is the typical finding of

parathyroid adenomas on parathyroidimaging with Tc-99m sestamibi?

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What is the typical finding of

parathyroid adenomas on parathyroidimaging with Tc-99m sestamibi?

• Parathyroid adenomas show delayed washout

compared with normal thyroid tissue

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Hyperparathyroidism

1. Tc-99m sestamibi is taken up by thyroid and

parathyroid tissue, but wash out more rapidly

from the thyroid.

2. Parathyroid adenoma in the region of the leftlower lobe of the thyroid.

3. > 90% predictive value for preoperative

localization of parathyroid adenoma, lower testaccuracy for hyperplasia and small tumors.

4. Thyroid follicular adenoma.

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Parathyroid adenoma

1. Dual isotope imaging with subtraction, in the past usingTl-201 and Tc-99m pertechnitate and recently using I-123and Tc-99m sestamibi

2. I-123 by mouth. After a delay of 2 to 3 hours, an anterior I-123 thyroid scan is obtained. Without moving the patient,

an image is obtained after IV injection of Tc-99m MIBI. TheI-123 image is computer subtracted from the Tc-99m MIBIimage.

3. The I-123 thyroid scan appears normal, although the leftlobe extends more inferiorly. The MIBI image shows an

asymmetrical bulbous configuration in the region of theright lower pole of the thyroid. Subtraction demonstratesfocal radiotracer compatible with parathyroid adenoma atthe lower pole of the right thyroid.

4. Parathyroid, thyroid adenoma, thyroid carcinoma and

metastatic carcinoma.

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Mediastinal parathyroid adenoma

1. Parathyroid scan with Tc-99m sestamibi or Tc-

99m tetrofosmin.

2. Focal persistent uptake in the mediastinum,

normal salivary, liver, cardiac uptake. Axillaryuptake resolves with arm elevated, thus is

caused by skin folds.

3. Various benign and malignant neoplasm.

4. Mediastinal parathyroid adenoma.

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ADRENAL SCINTIGRAPHY

Pearls & Pitfalls

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Pearls & Pitfalls

Adrenocorticalimaging

• NP-59 is an adrenal cortical

imaging agent with imaging

performed at 4-5 days.

Unilateral adrenal uptake isusually an adenoma and

bilateral uptake is usually due

to adrenal hyperplasia

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ADRENAL SCINTIGRAPHY

• Common indication is hypercortisolism

(Cushing’s syndrome)

• Less common :

a) Hyperaldosterolism (Conn’s syndrome)

b) Adrenal virilizing tumors

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ADRENAL

CORTEX MEDULLA

ZONA

GLOMERULOSA

ZONA

FASCICULATAZONA

RETICULARIS

ALDOSTERONE CORTISOL ANDROGENS

CUSHING’S CONN’S 

EPINEPHRINE

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Drugs that interfere with NP – 59

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Drugs that interfere with NP   59

uptake

Drug MechanismSpironolactone Aldosterone receptor blocker

Ketoconazole Suppression of cortical biosynthesis

Diuretic/oral contraception Stimulate renin/angiotensin

Glucocorticoids Suppression of ACTH

Cholesterol lowering agents Decrease cholesterol

Hypercholesterolemia Decrease LDL receptor activity

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HYPERALDOSTERONISM NP-59

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HYPERALDOSTERONISM NP 59

PATTERN

SYMMETRICAL

BILATERALLY EARLY

IMAGING (BEFORE DAY 5)

SYMMETRICAL LATE

IMAGING (ON OR

AFTER DAY 5)

UNILATERAL EARLY

IMAGING (BEFORE

DAY 5)

-Bilateral autonomous

hyperplasia-Secondary

aldosteronism

-Conn’s tumor -aldosterone

secreting tumor

Normal adrenal

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CUSHING’S SYNDROME NP-59

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CUSHING S SYNDROME NP 59

PATTERN

ADRENALSCINTIGRAM

BILATERAL

VISUALIZATION

UNILATERALVISUALIZATION

BILATERAL NON

VISUALIZATION

SYMMETRIC

ASYMMETRIC

ADENOMA

CARCINOID

DRUG THERAPY

BILATERAL HYPERPLASIA

BILATERAL HYPERPLASIA

(SOME ASYMMETRY IS

COMMON)

BILATERAL HYPERPLASIA

ASSOSIATED WITH

UNILATERAL ADENOMA

ADRENAL REMNANTAFTER

ADRENALECTOMY

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C i i ti h f th d l

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Concerning scintigraphy of the adrenal

A. Asymmetrical uptake of NP 59 may be seen in twothirds in normal subject

B. Bilateral symmetrical uptake of NP 59 in the presenceof glucocorticoid excess is usually due to adrenalhyperplasia

C. Unilateral increased uptake following NP 59 is mostcommonly due to functioning adenoma

D. Bilateral non visualization of the adrenals in thepresence of endogenous glucocorticoid excess is most

likely to be due to adrenal carcinomaE. Unilateral non visualization exclude an adrenal

carcinoma

C i i ti h f th d l

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Concerning scintigraphy of the adrenal

• TTTTF

In the scintigraphy assessment of

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g p y

adrenal hypertension

A. Pretreatment with dexamethasone in patients withprimary hyperaldosteronism significantly improvesthe diagnostic accuracy of NP 59 scanning

B. Following dexamethasone suppression, a Conn’s adenoma will usually be seen before day five

C. NP 59 scintigraphy can distinguish ACTH dependentfrom ACTH independent Cushing’s syndrome

D. False negative results may be seen during MIBGscanning in patients with pheochromocytoma on

steroid therapyE. Activity in the normal gland is usually suppressed in

the presence of a unilateral pheochromocytoma

In the scintigraphy assessment of

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g p y

adrenal hypertension

• TTTFF

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Adrenocortical scintigraphy

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Adrenocortical scintigraphy

1. A, Unilateral NP-59 uptake consistent with leftadrenal adenoma, concordant with the CT. B,Bilateral adrenal hyperplasia, discordant with CT.

2. Uptake in the right adrenal bed region indicating

adrenal remnant. Discordant with the negativeCT.

3. Transport and receptors system for serumcholesterol account for adrenal uptake.

Cholesterol is required for the production ofadrenal hormones.

4. Hyperaldosteronism (adrenal adenoma orhyperplasia) and hyperandrogenism.

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ADRENOMEDULLARY

SCINTIGRAPHY

Pearls & Pitfalls

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Adrenomedullary

imaging

• MIBG is a medullary adrenalimaging agent which effectivelylocalizes in pheochromocytoma

and neuroblastoma. It may alsolocalize in carcinoid, medullarythyroid carcinoma andparaganglioma.

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Heart

Liver

Kidney

Bladder

MIBG scan

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MIBG scan

Heart

Liver

Kidney

Bladder

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Thyroid blockade

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Thyroid blockade

• Potassium perchlorate for emergency andallergic to iodine= 400 mg

Compound Daily dose

Capsules

Potassium iodate 170 mg

Potassium iodide 130 mg

Solution

Lugol 1% 1 drop/kg max 40 (20 drops bd)

Oncology Committee of the EANM 

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In-111 pentetreotide (octreoscan)

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normal uptake at kidney, spleen, liver ,

thyroid and intestinal activity

Somatostatin analog limitations

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Somatostatin analog limitations

False negative

Small &Few somatostatin receptors

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Multiple endocrine neoplasia (MEN)

t 1

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type 1• Dominantly inherited

• Mutation of MEN 1 gene on chromosomal region11q13

• Include :Parathyroid = hyperplasia or adenoma (90%)

Pancreatic islet = adenoma, carcinoma or

hyperplasia (80%)Anterior pituitary = adenoma (65%)

Adrenal cortex = hyperplasia or adenoma (40%)

Carcinoid tumors and lipomata

Multiple endocrine neoplasia (MEN)

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type 2

Parafollicular cells of thyroid = Medullarycarcinoma (> 95%)

• Adrenal adrenal = pheochromocytoma (50%)

•Parathyroid = hyperplasia or adenoma (<25%)

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The following tissues may show

d k f

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increased uptake of MIBG

• TTFTT

The following are true concerning

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MIBG scanning

A. Focal bone marrow activity in the presence of aknown neuroblastoma may be normal

B. The sensitivity of MIBG scanning in the detection ofneuroblastoma is approximately 90%

C. MIBG scanning is more accurate than CT or MRI in thedetection of primary adrenal pheochromocytoma

D. Increased adrenal uptake of MIBG in the MENsyndrome confirm the presence of

pheochromocytomaE. MIBG scanning accurately reflects the extent of bony

involvement in metastatic neuroblastoma

The following are true concerning

I G i

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MIBG scanning

• FTFFF

A. I-131 NP 59

B In 111 Octreoscan

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B. In-111-Octreoscan

C. I-131 MIBG1. Adrenal cortical adenoma

2. Pituitary adenoma

3. Medullary thyroid carcinoma

4. Pheochromocytoma

5. Carcinoid tumor

A. I-131 NP 59

B In 111 Octreoscan

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B. In-111-Octreoscan

C. I-131 MIBG1. Adrenal cortical adenoma = A

2. Pituitary adenoma = B

3. Medullary thyroid carcinoma =B

4. Pheochromocytoma = C

5. Carcinoid tumor = B

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Neuroblastoma

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1. Bone scan shows uptake symmetrically in the distal

femurs, cranial and facial bones. I-131 MIBG shows a largearea of midline abdominal uptake. Inspection of the bonescan in the same area suggests a soft tissue left perirenaldensity, best seen in the anterior view. In addition, diffusemarrow/bone uptake is seen on the MIBG study.

2. The prominent mid line uptake on the MIBG is consistentwith neuroblastoma. Subtle bone uptake is seen in theregion. The symmetrical bone uptake in the distal femurs,cranial and facial bone is very suggestive of tumor. TheMIBG confirms metastatic disease with extensive tumor inthe marrow/ bone from skull to feet.

3. First, primary neuroblastoma. Osteosarcoma metastatic tothe lung is another. Metastases of various tumorsoccasionally are seen on bone scans, lung, colon andbreast.

4. Combination of Tc-99m bone scan and I-131 MIBG.

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Octreoscan

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1. In-111 octreoscan (octreotide), I-131 MIBG.2. Prominent liver, spleen and kidney uptake is

seen with In-111 octreoscan.

3. Focal abnormal uptake in the right temporalbone that correlates with CT.

4. Paraganglioma considering the patient’s 

history, also meningioma or NET metastasis.

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Pheochromocytoma

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y

1. I-131 MIBG2. Localization occurs through the norepinephrine

reuptake mechanism. It localizes incatecholamine storage vesicles in presynaptic

adrenergic nerve ending and cells of the adrenalmedulla.

3. Sensitivity: 90%, specificity, 95% for detection of

pheochromocytoma.4. Neuroblastoma (90%), carcinoid (50%) andmedullary thyroid carcinoma (25%).

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NET

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1. Peptide analogue of somatostatin and

octreotide. Binds to tumors with somatostatinreceptors.

2. NET

3. A, multiple metastases to both lobe of the liver.Two large foci and one small focus of uptakeconsistent with paraaortic tumor adenopathy.Possible small tumor in right hilum. B,

prominent irregular uptake in the anteriormediastinum and focal uptake in the lower lungposteriorly.

4. Kidney and spleen.

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Infection and inflammation

Pearls & Pitfalls

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Infection and

inflammation

• Gallium-67 citrate and In-111

leukocyte scans are usuallyphoton poor and the imagesare coarse or grainy.

• Tc-99m leukocyte scan have

more counts and the imagesappear less grainy andsmoother.

•Gallium-67 photon energiesare 90, 190, 290 and 390 keV.

• In-111 photon energies are 173keV and 247 keV.

Pearls & Pitfalls

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Infection and

inflammation

• Gallium-67 activity is normally

seen in the skeleton, lacrimalglands, nasopharynx and liver.Liver activity is usually greaterthan spleen. Colon activity is

normal on delayed images.• Indium-111 leukocyte activity is

normally seen in the bonemarrow, liver and spleen with

spleen more intense than liver.• Patchy lung activity may be due

to leukocyte damaged duringlabeling.

Pearls & Pitfalls

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Infection and

inflammation

• Colonic activity is normal on

Ga-67 and Tc-99m leukocytescans but not on In-111

leukocyte scans.

•Renal activity may be seennormally on Ga-67 images

during the 1st  24 hours and on

Tc-99m leukocyte images but

not on In-111 leukocyte scans.

Pearls & Pitfallsl f k

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Infection and

inflammation

• Focal areas of uptake on Ga-67 scanare nonspecific and can represent

either tumor or inflammation.Indium-111 leukocytes have beenreported to localized in someneoplasms although this isuncommon occurrence.

• On Ga-67 imaging, sarcoidosis andlymphoma may have similarappearance. Both may showmediastinal and lymph node

involvement. Sarcoidosis issuggested by the presence of thelambda sign and the panda sign.Abdominal involvement is morecommon in lymphoma.

Pearls & Pitfalls

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Infection and

inflammation

• Diffuse lung uptake on Ga-67

scan is often due to PCP inpatients with AIDS.

• Focal uptake in the abdomen on

leukocyte scan may be due to an

abscess or inflammatory bowel

disease (Crohn’s disease). Activity

in the colon can be seen in

ulcerative colitis or CMV.• Ga-67 is preferred to labeled

leukocyte in the setting of

suspected spinal osteomyelitis

Infection & inflammation

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Gallium 67

citrate

Radiolabeled

leukocytes

Indium-111

oxine

leukocyte

Tc-99mHMPAO Tc-99m

Fenulesomab

F18 -

FDG

Tc-99mSulesomab

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Radiopharmaceutical Gallium-67 Indium-111 Thalium-201

Half life 78 hours 67 hours 72 hours

Photo peak (KeV) 93, 185, 288, 394 173, 247 69-83, 135, 167

Normal Gallium-67 citrate Scan

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Liver

SpleenMarrow

Bone

Gastrointestinal 

• liver/spleen/GI

marrow

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Liver

Spleen

Marrow

Lung

*spleen intense than

liver/ marrow

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(lungs)

• liver/spleen/ bladder

• marrow

Gallium-67 citrate imaging protocol

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Patient preparation No recent barium contrast study

Radiopharmaceutical -Gallium-67 citrate

-5 mCi

-IV

Instrumentation Photopeak :20% window, 93, 285 and 300

KeV

Collimator: medium energy

Imaging procedure 24 hr images (optional):site of suspected

infection if early intervention considered.

48 hrs images : whole body imagingDelayed 72 – 96 hr images : differentiate

intraabdominal infection or normal bowel

clearance

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Tc-99m HMPAO leukocyte protocol

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Patient preparation Wound dressing should be changed priorimaging

Draw 50 ml blood and radiolabeled in

vitro

Radiopharmaceutical Tc-99m HMPAO labeled leukocyte in vitro

10 mCi

Given IV

Instrumentation Photopeak :20% window, 140 KeV

Collimator: low energy GP

Imaging procedure 1 - 2 hr images (mandatory):intra

abdominal imaging

4 hrs images : peripheral skeletal imaging:

osteomyelitis of feet

Whole body imaging

IndicationsGallium-67 In-111 oxine leukocytes Tc-99m HMPAO leukocytes

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Gallium 67 In 111 oxine leukocytes Tc 99m HMPAO leukocytes

Severe leucopenia Intra abdominal infection Pediatric patients

Sarcoidosis Cardiovascular infection Inflammatory bowel disease

Idiopathic pulmonary fibrosis Diabetic mid foot and hind

foot osteomyelitis

Osteomyelitis of extremities

including feet in non diabetic

Pulmonary drug reactions(amiodarone, bleomycin)

Inflammatory bowel disease Diabetic forefoot osteomyelitis

Pneumocytic carinii Hip and knee prosthesis

FUO Orthopedic hardware, prior

fracture or infection

Immunosuppressed patient

with lung infections

Suspected low grade chronic

infections (fungal/protozoa)

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Osteomyelitis

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Type of study Sensitivity

%

Specificity

%

Three phase bone scan

(normal x ray)

94 95

Three phase bone scan

(underlying disease)

95 33

Gallium 67 81 69

Indium-111 oxine

leukocytes

88 85

Tc-99m HMPAO leukocytes 87 81

MRI 95 87

InfectionsRegions Scans

i b i f Di t l f t T 99 HMPAO l k t

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Diabetic foot Distal foot – Tc-99m HMPAO leukocytes

Mid/hind foot – In-111 leukocytes

Vertebral osteomyelitis Ga-67/bone scanF18-FDG

Tc-99m infecton

Infected joint prosthesis In-111 leukocytes/ Tc-99m SC accuracy 90%

Intra abdominal infections In-111 leukocytes sensitivity 90% @ 24 Hr imaging

Tc-99m HMPAO leukocytes @ 2 Hr imaging

Tc-99m Fanolesomab for acute appendicitis

Inflammatory bowel disease Tc-99m HMPAO : Crohn’s small bowel involvement 

Ulcerative colitis = colonic involvement without small bowel

Cardiovascular Prosthetic graft – In-111 leukocytes d/t no blood pool

RenalGa-67 * increased uptake may due to renal/hepatic failure

and iron overload

Intra cerebral Tl-201 : increased uptake = malignant, no uptake = infection

FUO Ga-67

Post op fever=In-111 leukocytes

Malignant external otitisGa-67

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Gallium-67 Thallium-201

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- ve + ve Kaposi’ssarcoma

+ ve - ve Infection

+ ve + ve Lymphoma

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Abnormal CXR

& NormalGallium-67

Kaposi’s sarcoma 

Pulmonary fibrosis

Treated

sarcoidosis

Inactive TB

  PCP

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Normal CXR &

Abnormal

Gallium-67

CMVSarcoidosis

Pulmonary drugtoxicity

Lymphocytis

interstitialpneumonitis

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Gallium scan

100% sensitivity

Burkitt’s

lymphoma

Pyogenic acute

osteomyelitisPyogenic acute

arthritis

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Gallium-67 lung

uptake

associated with

drugs

Bleomycin

Amiodarone

Busulfan

Nitrofurantoin

Cyclophosphamide

Methotrexate

Ga-67 is taken up by the lungs due to

drug toxicity. Which drugs are the

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g y g

culprits?

Ga-67 is taken up by the lungs due to

drug toxicity. Which drugs are the

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g y g

culprits?• Bleomycin is the most common. Uptake can

be seen with cytoxin, nitrofurontoin and

amiodarone.

What is the role of Ga-67 in

sarcoidosis?

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What is the role of Ga-67 in

sarcoidosis?

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•Ga-67 lung uptake is a sensitive test for thediagnosis of active alveolitis of sarcoidosis. Ga-

67 may be markedly increased in the setting of

a normal CXR in early disease and may benegative in the setting of an abnormal CXR in

inactive disease.

Which leukocytes are labeled with In-

111 oxine and Tc-99m HMPAO?

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Which leukocytes are labeled with In-

111 oxine and Tc-99m HMPAO?

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•In-111 binds to neutrophils, lymphocytes,monocytes, erythrocytes and platelets.

• Tc-99m HMPAO binds to neutrophils.

Which of the following statements is

true regarding In-111 oxine

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leukocytes?

A. It is diagnostically useful for evaluating

inflammatory lung disease.

B. It has a high sensitivity for detecting

osteomyelitis in the spine.

C. It should be used when the peripheralleukocyte count is less than 3000/mm³.

D. It is the radiopharmaceutical of choice for

intraabdominal infection.

Which of the following statements is

true regarding In-111 oxine

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leukocytes?

• FFTT

What is the optimal imaging time for

In-111 leukocytes and Tc-99m HMPAO

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leukocytes?

What is the optimal imaging time for

In-111 leukocytes and Tc-99m HMPAO

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leukocytes?• In-111 labeled leukocytes are routinely imaged at 24

hours. Imaging at 4  –  6 hours is less sensitive fordetection of infection. The one exception is

inflammatory bowel disease in which imaging shouldbe done at 4 hours because intraluminal shedding ofinflammed cells may result in inaccurate localization at24 hours.

Tc-99m HMPAO leukocytes should be imaged at 1 -2hours for intraabdominal infection because of biliaryand renal clearance seen by 2 hours. Extra abdominalinfection can be imaged later, usually 4 hours allowingmore time for background clearance.

Regarding osteomyelitis, which of

these statements are true?

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A. The three phase bone scan is sensitive testfor diagnosis.

B. The three phase positive scan is specific for

osteomyelitis.C. A negative flow phase study almost always

rules it out.

D. In patients with prostheses, a bone marrowscan can be useful to rule out a false positive

In-111 leukocyte study.

Regarding osteomyelitis, which of

these statements are true?

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•TTTF

Which of the following statement are

true?

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A. A negative three phase bone scan excludeosteomyelitis with high degree of certainty.

B. The specificity of bone scan is poor in patientswith underlying bone disease such as fractures,orthopedic hardware and neuropathic joints.

C. In-111 oxine and Tc-99m HMPAO leukocyteshave poor specificity for the diagnosis ofosteomyelitis in a patient with a hip prosthesis.

D. Because the three phase bone scan may bepositive in a patient with a Charcot’s  joint, aradiolabeled leukocyte study should beperformed.

Which of the following statement are

true?

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A. TTTF

In the imaging of the lung infection

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A. Gallium uptake is highly sensitive for PCPB. Localized uptake of Gallium is common in PCP

C. Uptake of Indium-111 labeled white cells in the

lungs is relatively non specific for infectionD. Unmatched defects of perfusion are the most

common abnormality seen on V/Q scan in

patients with bacterial infection

E. In patients with TB, only sites of active infection

are Gallium avid

In the imaging of the lung infection

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•TFTFT

Concerning In-111 white cell scans

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A. The white cells must be autologousB. Lung activity is pathological between 1 and 4

hours after injection

C. If a focus of increased uptake is seen on the

early images, the 24 hour images do not need tobe performed

D. In-111 white cell are more useful in chronic PUO

E. If the patient is on appropriate antibiotics, thewhite cell study is unlikely to be positive

Concerning In-111 white cell scans

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•FTFFF

Concerning Tc-99m HMPAO and In-111

labeled white cell scans

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A. Diffuse bowel activity on a Tc-99m HMPAO study at 24hrs indicates severe colitis

B. On a Tc-99m HMPAO labeled white scan, the typicalappearances of IBD is intense activity at 1 hour whichfades with time

C. Rectal disease can be distinguished from bladderactivity on a Tc-99m HMPAO

D. Activity is seen in the bowel in IBD because the

labeled WBC’s fix in the inflammatory bowel wallE. An abscess that communicates with the bowel can bedistinguish from one that does not

Concerning Tc-99m HMPAO and In-111labeled white cell scans

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FFTFT

Concerning the imaging of theimmunosuppressed patient

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A. In-111 labeled WBCs are sensitive as Galliumat detecting PCP

B. Tc-99m DTPA clearance is more useful thanGallium scanning in the following up of PCP

C. Gallium uptake in the colon is highlysuspicious for acute colitis

D. Kaposi’s lesions take up Tl-201

E. Active MAI infection in HIV positive patientshas specific appearance on Gallium scan

Concerning the imaging of theimmunosuppressed patient

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FTFTF

The source of lectoferrin

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A. LymphocytesB. Leucocytes

C. Bacteria

D. Fungus

E. Tissue macrophage

The source of lectoferrin

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FTFFF

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Lactoferrin is physiologically producedby certain organs that localize gallium

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A. Lacrimal glandsB. Salivary glands

C. Lactating breast

D. Bone

E. Liver

Lactoferrin is physiologically producedby certain organs that localize gallium

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TTTFF

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Sarcoidosis

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1. Patient A: lambda sign (hilar and paratrachealnodal uptake). patient B: diffuse pulmonaryuptake.

2. Classic panda sign.

3. Either A or B. The panda sign can be seen atany stage of the disease.

4. Sarcoidosis. Ga-67 scan is used to confirm the

clinical diagnosis and differentiate activealveolitis from inactive fibrosis.

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Tc-99m HMPAO and osteomyelitis

1 A i b l li i i h

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1. A negative bone scan rules out osteomyelitis with ahigh degree of certainty.

2. A bone marrow can improve the specificity of aleukocyte study if there is displaced normal marrow.This is most helpful in the hips and knees.

3. In-111 leukocytes can make same diagnosis. Thesuperior imaging resolution of Tc-99m HMPAO oftenbetter differentiates soft tissue and bone infection.Ga-67 is less specific because increased uptake occurswith bone remodeling from any cause.

4. Patient A: soft tissue uptake. No bone uptake rulesout osteomyelitis, consistent cellulitis. Patient B: softtissue and bone localization consistent withosteomyelitis.

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Tc-99m HMPAO leukocytes free Tc-99m pertechnetate

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1. Activity in the salivary glands, thyroid, stomach,bowel and bladder.

2. Free Tc-99m pertechnetate.

3. Gastrointestinal bleeding, swallowed leukocytes

from oropharyngeal, esophageal or lunginflammation/ infection, accessory spleen,uninfected postoperative surgical wounds,intestinal stomas.

4. Ga-67 = 48 hours, In-111 oxine leukocytes = 24hours, Tc-99m HMPAO = 1 to 4 hours.

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Intraabdominal abscess

1 T 99 HMPAO bi d l t t hil I 111 i

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1. Tc-99m HMPAO binds only to neutrophils. In-111 oxine

binds to mixed leukocytes.2. Normal bone marrow distribution of the radiolabeled

leukocytes.

3. Abdominal imaging: Tc-99m HMPAO images are acquiredat 1 to 2 hours because hepatobiliary, intestinal and renalclearance occurs subsequently, complicatinginterpretation. Extremity imaging: 2 to 6 hours. In-111leukocytes: 24 hours. Four hour imaging for inflammatorybowel disease because sloughing of intestinal mucosaleukocytes may occur and 24 hour may be misleading.

4. Infection in the right lower quadrant overlying thesacroiliac joint in the anterior view and lateral right of thespine. The patient had a perforated appendix.

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Pericarditis – Ga-67

1 Ab l t k i di i di b th

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1. Abnormal uptake in myocardium, pericardium or bothconsistent with pericarditis or myocarditis. Thepatient developed a pericardial fraction rub the dayafter the Ga-67 scan. Incidental note of normal liveruptake and transverse and left colon clearance.

2. Ga-67 shows uptake not only with inflammation andinfection, but also in tumors that can sometimes bethe cause of persistent fever e.g.. lymphoma.

3. Large bowel = 4.5 rads.

4. Most pulmonary inflammatory and infectiousdiseases. Uptake is nonspecific, although the patternof uptake and the clinical setting, e.g. AIDS may behelpful in determine the differential diagnosis.

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Right ileum osteomyelitis

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1. In-111 oxine or Tc-99m HMPAO leukocytes,Ga-67 could also be used. The intense spleenuptake is consistent with a radiolabeledleukocyte study. In-111 oxine leukocytes

were used. The image resolution is poorcompared with Tc-99m leukocytes.

2. Spleen, 15 – 20 rads.

3. Abnormal focal uptake in right groin and rightileum, indicating osteomyelitis.

4. 173, 247 keV. Physical half life is 77 hours.

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Osteomyelitis of spine

1 Bone scan shows increased uptake of the T11

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1. Bone scan shows increased uptake of the T11vertebrae. In-111 oxine leukocyte showsdecreased uptake in the same region. Ga-67shows increased uptake that matches the bonescan in relative intensity.

2. Osteomyelitis fracture, infarction, metastasis,orthopedic hardware, surgical defect, Paget’s disease, radiation therapy.

3. Osteomyelitis in this clinical setting. Many of the

diseases listed can be excluded by history andradiographs.

4. As high as 40%.

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FDG PET paraspinal infection

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1. Intense uptake involving the retroperitoneumanterior to the recent lumbar fusion surgery.

2. Consistent with postoperative infection.

3. Yes. Leukocytes and macrophages utilizeglucose.

4. All positron emitters have 511 keV

photopeak. F-18, C-11, N-13 , O15.

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Knee athroplasty TRO infection

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1. Increased blood flow in the right knee.2. Increased uptake in the proximal tibia on

both.

3. Serves as a template for normal marrowdistribution.

4. Negative for infected prosthesis.

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Skeletal imaging

Pearls & Pitfalls• Common indications for bone

scans include evaluation of

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Skeletal imaging

scans include evaluation ofprimary osseous or metastaticneoplasm, avascular necrosis,trauma, infection and less

commonly, arthritis or RSD.• When bone scans are

performed with Tc-99mdiphosphonate agents, normal

skeletal activity should bereasonably symmetric left andright sites.

Pearls & Pitfalls

• Look at the kidney activity for

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Skeletal imaging

potential abnormalities. Alarge amount of activity of

diffuse soft tissue activity

remaining at 4 hours is

frequently due to renal

insufficiency.

• Activity in the lower cervical

region is frequently due tobenign causes such as

degenerative changes.

Pearls & Pitfalls

• A lesion that is hot all three

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Skeletal imaging

phases of a bone scan can beosteomyelitis bit also may be

an acute fracture,

hypervascular tumor,

neuropathic joint or RSD.

• A flare phenomenon is most

likely seen within 1 to 3

months therapy completion.

Pearls & Pitfalls• Paget’s  disease is commonly

seen as intense activity in the

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Skeletal imaging

seen as intense activity in theskull, femur, vertebral body orhalf of the pelvis. It is usuallypolyostotic but may be

monostotic and may causebowing of a femur.

• Good visualization of thebones and not the kidneys may

indicate a superscan due todiffuse metastases orhyperparathyroidism.

Pearls & Pitfalls• Focal hot lesions in multiple

adjacent ribs are essentially

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Skeletal imaging

j y

always due to fracture.• Long lesions running along the

length of a rib are not usuallyfractures.

• Multiple sequential coldvertebral bodies are almost dueto radiation therapy.

• Tumors that commonly causecold (photopenic) metastaticlesions including kidney, lung,thyroid and breast tumors.

Pearls & Pitfalls

• Stress fractures usually occur

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Skeletal imaging

in the pelvis and below theknees, they can be seen as

focal or fusiform primary

cortical activity.

• Bilaterally increased activity

along the cortex of the tibias

may be due to shin splints,

hypertrophic osteoarthropathyor periosteal reaction.

Pearls & Pitfalls• A loose hip prosthesis is

suggested by activity at the tip

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Skeletal imaging

suggested by activity at the tip

and near the lesser trochanter.

•  An infected prosthesis usually

has activity all along the length of

the shaft.

• Postoperative activity around a

cemented prosthesis can

normally persist for 6 months to1 year and activity around a

noncemented prosthesis can

normally persist for 2 to 3 years.

Pearls & Pitfalls• Diffuse liver activity on a bone

scan is probably due to hepatic

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Skeletal imaging

sca s p obab y due to epat cnecrosis orradiopharmaceutical problem.

• Focal liver activity is often due

to metastasis from colon,breast, ovary or lung.

• Diffused splenic activity due tosplenic infarction.

• Diffused renal parenchymalactivity is probably due tochemotherapy.

Pearls & Pitfalls• Increased activity in two

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Skeletal imaging

adjacent vertebral bodies inthe absence of compression

fractures suggests diskitis

especially in a child.

• Osteomyelitis, acute fractures,

vascular tumors such as

Ewing’s  sarcoma and RSD are

hot on angiographic, bloodpool and delayed bone scan

images.

Pearls & Pitfalls• Cellulitis is hot on the 1st  two

phases but fades on delayed

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Skeletal imaging

p y

images.• Shin splints have normal

angiographic and blood poolimages but are hot on delayedviews in the posteromedialaspect of the tibias.

• Osteomyelitis usually does not

cross joints.• Increased activity seen on both

sides of a joint is more likely dueto septic arthritis.

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Bone pain for bone scan

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Metastatic tumorsBenign bone tumor : osteoid osteoma

Trauma

Avascular necrosisInfection

Osteomalacia

Paget’s 

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  Reduced hydrolyzed

technetium

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Tc-99mpertechnitate

preparation,

there are 3 form

of technetium

Free pertechnetate

Chelated technetium

  Reduced hydrolyzed

technetium

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Liver uptake in

bone scan

Excess amount of

aluminum in Tc-99m

MDP preparation

Excess amount ofstannous ion in Tc-

99m MDP

preparation

Excess amount of

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aluminum in Tc-99m SCpreparation Lungs uptake

Tc-99m pertechnetate

Thyroid

Gastric mucosa

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Metastatic bone disease

Bone tumors

Benign Malignant

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Osteoid osteoma Osteosarcoma

Giant cell tumor Ewing’s sarcoma 

Fibrous dysplasia Chondrosarcoma

 

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Bil t l

Urinary tract

obstruction

Acute tubular

i

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Bilateralincreased

uptake of renal

in bone scan

necrosis

Chemotherapy

Radiation nephritis

Thalassemia

Hypercalcemia

NephrocalcinosisNephrotoxic

antibiotic

 

Bil t l

Tumors Non tumor

Prostate Renal failure

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Bilateraldecreased

uptake of

renal inbone scan

“superscan” 

Lungs

carcinoma

Nephrectomy

Breast

carcinoma

Hyperparathyroidism

Bladder

carcinoma

Osteomalacia

Lymphoma

Fibrous dysplasia

Paget’s disease Renal osteodystrophy

  Breast carcinoma

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Tumors that

metastasize to

bone

Lungs carcinoma

Prostate carcinoma

LymphomaThyroid carcinoma

Renal carcinoma

Neuroblastoma

  Multiple myeloma

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Tumors falsely

normal in bone

scan

Severe anaplastic

tumors

Lytic lesions

 

Diff ti l

Metal artifact

Radiation changes

B i i b l

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Differentialdiagnosis of

cold defect in

bone scan

Barium in bowelEarly avascular necrosis

Multiple myeloma

Benign tumorCysts

Osseous metastasis

Tumor marrow

involvement

Soft tissue calcification

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Dystrophic

calcification

Metastatic

calcification

Heterotrophic

Bone

formation

Calcinosis

cutis

Calcification of

dying or dead

tissue

Normal tissue

with

hypercalcemia

-infection

-osteomyelitis

-cellulitis

-thrombophlebitis

-DVT

-osteosarcoma-osteochondroma

-calcinosis

cutis universalis

-calcinosis

cutis circumcripta

-calciphylaxis-rabdhomyolysis

Soft tissue accumulation ofdiphosphonate

Infarct

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InfarctAmyloid

Muscle: myositis ossificans

FibroidsTumors: meningioma/neuroblastoma

Systemic sclerosis

Histocytosis X

• Disease in which there are focal accumulation

f h l d

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of macrophages in various organs including

bones

• Triad:

1. Letterer-Siwe disease

2. Hand-Schuller-Cristian disease3. Eosinophilic granuloma of bone

  Fibrous dysplasia

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Bone dysplasia's

a/w skeletal

tracer uptake

Osteogenic imperfecta

Albers-Schöenberg

Disease (Marble Bones)Englemann’s disease

Malorheosthosis

Ribbing’s disease 

Fibrous dysplasia

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Osteogenic imperfecta

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Osteopetrosis

• Albers-Schöenberg Disease (Marble Bones)

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Englemann’s disease 

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Ribbing’s disease (multiple diaphyseal sclerosis)

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Melorheostosis

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  Paget’s disease 

(osteitis deformans)

O i

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Metabolic bone

disease

Osteoporosis

osteomalacia &

Rickets

Hyperparathyroidism

Renal osteodystrophy

Hypertrophicosteoathroplathy

DiseaseRenal

osteodystrophy

Primary

hyperparathyroidism

Osteomalacia Aluminum

induced

osteomalacia

Osteoporosis

Metabolic bone disease

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Cause of +ve

bone scan Hyperparathyroid Hyperparathyroid Hyperparathyroid - Fracture

Differentiating

features

Metabolic features:

No tracer in bladder

Metabolic features:

Uncommon: brown

tumor & ectopic

calcification

Metabolic features:

pseudofractures

Long bone

uptake

High

background

activity

Intense linear

uptake at site of

vertebral

fracture

May be

low/patchy

uptake at axial

skeletal

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Increased flow and

intense uptake around

the prosthesis’ stem

Focal skeletal phase uptake

At the tip of the hardware

Loosening Infection

Hip joint prosthesis

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Blood pool image is

normal

Blood pool image is

increased vascularity

Discrete focus oftracer increased

uptake at the tip of

femoral prosthesis in

delayed image

Markedly increasedtracer uptake  in

delayed image

 

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Stress fracture

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Fatigue fracture Insufficient fracture

Cause by repeated

abnormal fractureon normal bone

Resulting from

normal stress onabnormal bone

 

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L C l P th

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FORM OF OSTEOCHONDRITIS DISEASES

CAUSED BY AN INFARCT IN THE CAPITALFEMORAL EPIPHYSIS

Legg-Calve-Perthes

 

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4. Bone scan

• TTFTT

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7. Indication for bone scan

• TTTTT

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8. Bone scan

• TFFTT

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15. Abnormal bone scan uptake inkidneys

• TTTTT

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20. Cause of superscan

• FFFTT

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Malignancy

A. In multiple myeloma the MDP bone scan is usuallyabnormal

B. Increased MDP bone scan uptake into metastaticdeposits 2 months after chemotherapy indicatesfailure of response and progression of disease

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failure of response and progression of disease

C. A solitary rib hot spot in a cancer patient usually

represent benign diseaseD. A rib hot spot which is present over a year is likely to

represent a simple healing fracture

E. A solitary area of abnormal uptake is a patient with a

known primary cancer with normal plain filmappearances is likely to be benign

Malignancy

• TFFFT

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Bone scanning in malignancy

A. A malignant superscan requires more time to

acquire the imageB. It is possible to distinguish a malignantsuperscan from one of metabolic bone disease

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C. A superscan characteristically shows increased

bone and renal uptake of MDPD. Uptake of MDP into malignant bone diseaserelies solely on osteoblastic activity

E. It is not possible to distinguish benign from

malignant vertebral collapse

Bone scanning in malignancy

• FTFFT

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Bone scan in Paget’s disease 

A. A bone scan may be normal in Paget’s disease

B. A bone scan is a method of choice to detectsarcomatous change in Paget’s disease

C Paget’s very rarely only involves a single bone

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C. Paget s very rarely only involves a single bone

D. The appearance of new lesions in a patient withestablished Paget’s  disease is a commonrecognized finding

E. A bone scan is the method of choice in assessing

response to therapy in Paget’s disease

Bone scan in Paget’s disease 

• TFFFF

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Bone scan in malignant disease

A. Patients with a known primary cancer and singleskeletal hot spot have a roughly equal chance that it isbenign or malignant

B. Patients with a known primary cancer and a singlevertebral hot spot are unlikely to have malignant

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vertebral hot spot are unlikely to have malignantdisease

C. A bone scan is a useful routine staging procedure ofprostate carcinoma

D. A bone scan is a useful routine staging procedure forall patients with carcinoma of the cervix

E. A bone scan is a useful routine staging procedure forpatients with stage III and IV breast carcinoma

Bone scan in malignant disease

• TFTFT

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Bone scan in trauma

A. Tibial stress fractures are indistinguishable fromshin splint on bone scan

B. Compartmental syndromes are indistinguishablefrom shin splint on bone scan

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C. Reflex sympathetic dystrophy syndrome may

show reduced uptake of MDPD. 50% of non pathological rib fractures heal byone year

E. In talar coalition increased activity is usually at

the site of coalition

Bone scan in trauma

• FFTFF

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Bone scan in avascular necrosis

A. Septic arthritis of the hip in children may cause absentuptake of MDP into the femoral head

B. Osteomyelitis and bone infarction are easilydistinguishable in sickle cell disease

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C. Decreased MDP accumulation lasts for about 6 weeks

following bone infarction in sickle cell diseaseD. In chronic Perthes disease bone scan has a sensitivity

and specificity of over 90%

E. Bone scan a few weeks following femora; neck

fracture that is associated with higher uptake in thefemoral neck indicates a favorable prognosis

Bone scan in avascular necrosis

• TFFFT

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Bone scan in infection

A. Labeled WBC scanning is the method of choice indiagnosing osteomyelitis in HIV patients

B. Tc-99m HMPAO labeled WBC are preferable to In-111labeled in detection of acute osteomyelitis ofextremities

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extremities

C. Tc-99m HMPAO labeled are the method of choice in

diagnosing infection in childrenD. It is not possible to carry out WBC scanning in

severely neutropenic patients

E. WBC scanning is the method of choice indifferentiating acute infarct from osteomyelitis insickle cell disease

Bone scan in infection

• FTTFF

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Increased uptake of MDP is seen in

A. Bone island

B. Osteopoikilosis

C. Fibrous dysplasia

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D. Melorheostosis

E. Eosinophilic granuloma

Increased uptake of MDP is seen in

• FFTTT

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Primary bone tumors

A. Vertebral hemangiomata may cause reduced orincreased uptake of MDP into a vertebral body

B. It is possible to differentiate benign from malignantbone tumors from the degree of uptake of MDP

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C. Bone scan is a good method for assessing the extent

of involvement of a bone in osteogenic sarcomaD. Bone scan is a reliable method of detecting soft tissuemetastasis e.g.. lung in osteogenic sarcoma

E. Bone scan is a useful preliminary staging procedure in

Ewing's sarcoma

Primary bone tumors

• TFFFT

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Metabolic bone disease

A. The tie sign is a recognized feature

B. Reduced uptake of MDP into the diaphyses oflong bones is a recognized feature

C. Osteomalacia causes a reduction in uptake ofMDP h i d i f b

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MDP as there is reduction of bone mass

D. Aluminum osteomalacia in hemodialysispatients causes a metabolic superscan inadvanced disease

E. Treatment with biphosphonates may cause a

reduction in MDP uptake into the skeleton

Metabolic bone disease

• TFFFT

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Infection

A. Both infection and loosening of a hip prosthesis will show

both increased vascularity and uptake on delayed images

B. Increased activity in relation to a knee prosthesis one year

after surgery nearly always signifies infection or loosening

C C ll li i i h li b i d k i b

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C. Cellulitis in the limb may cause increased uptake into bone

on a bone scan

D. Uptake of Gallium into a bone at the site of increased uptake

on a bone scan nearly always signifies infection

E. Bone scan are less sensitive in detecting osteomyelitis in

neonates because of their small size

Infection

• FFTFF

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Photon deficient bone scan lesionsmay be found in

A. Metastatic disease

B. Legg-Calve-Perthes disease

C. Infarct of sickle cell disease

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Photon deficient bone scan lesionsmay be found in

• TTT

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Pulmonary, gastric, and enhancedkidney activity on a bone scan is often

seen in patients with

A. Myelosclerosis

B. Histocytosis

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y

C. Metastases from osteogenic sarcomaD. Hyperparathyroidism

E. Hyperthyroidism

 Pulmonary, gastric, and enhancedkidney activity on a bone scan is often

seen in patients with

• FFFTF

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Spleenic uptake in bone scan is mostoften seen in

A. Cirrhosis with portal hypertension

B. Hypersplenism

C. Sickle cell disease

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D. Lymphoma

E. Splenic abscess

Spleenic uptake in bone scan is mostoften seen in

• FFTFF

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The following neoplasm does notfrequently metastasize to bone

A. Ovary

B. Prostate

C. Lung

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D. Lymphoma

E. Breast

The following neoplasm does notfrequently metastasize to bone

• TFFFF

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Which of the following commonly

cause photopenic lesions on a bonescan

A. Malignant melanomaB. Ewing’s sarcoma

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C. Multiple myeloma

D. Hypernephroma

E. Colon carcinoma

Which of the following commonlycause photopenic lesions on a bone

scan

• FFTTF

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What are the potential impurities in

Tc-99m labeled diphosphonatecompounds, based on their

biodistribution.

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What are the potential impurities in

Tc-99m labeled diphosphonatecompounds, based on their

biodistribution.• Activity in the oropharynx, thyroid gland and

stomach suggestive of free pertechnetate.

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gg p

Activity in the liver suggests of colloidalimpurity.

• Rarely, activity is seen in the gut, the result of

excretion of activity through the biliarysystem.

What is the distribution of metastatic

deposit from epithelial primary

malignancies in the skeleton?

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What is the distribution of metastatic

deposit from epithelial primary

malignancies in the skeleton?•

80% at axial skeleton (spine, ribs, pelvis andsternum)

• 10% at skull

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%

10% at long bones

What factors distinguish a superscan

resulting from metastatic disease or

from metabolic disease?

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What factors distinguish a superscan

resulting from metastatic disease or

from metabolic disease?

• Metastatic disease: uptake seen at axial

skeleton and proximal parts of the femur and

humeri

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humeri.

• Metabolic disease: entire skeleton is typicallyeffected with increased uptake seen at

extremities as well as in the axial skeleton.

What is the mechanism of the flare

phenomenon?

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What is the mechanism of the flare

phenomenon?

• In some patients treated with chemotherapy

for metastatic disease, regression of thetumor burden is associated with increased

osteoblastic activity, presumably caused by

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y, p y y

skeletal healing in response to chemotherapy.This can appear on bone scan as a paradoxical

increased “worsening” tracer uptake which up

to 6 months after therapy.

What factors contribute to prolonged

fracture positivity on bone scan?

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What factors contribute to prolonged

fracture positivity on bone scan?

• Displaced or comminuted fractures and

fractures involving joints tend to haveprolonged tracer uptake. Elderly patients have

delayed healing.

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y g

What is the scintigraphy pattern of

osteomyelitis in children

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What is the scintigraphy pattern of

osteomyelitis in children

• Hot focus in metaphyseal region

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What is scintigraphy finding in RSD

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What is scintigraphy finding in RSD

• Increased blood flow and diffusely increased

periarticular activity in delayed images

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What is the explanation for the

abnormal bone scan in RSD

• Loss of sympathetic stimulation

• Results in vasodilatation

• Increased blood flow and bone turnover

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Synovitis contributing diffusely increasedperiarticular activity

What is shin splint

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What is shin splint

• Periostitis along posteromedial angle of tibia

• Tear of tibialis posterior muscle or soleusmuscle tendon complex

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What is scintigraphic appearance in

shin splint

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What is scintigraphic appearance in

shin splint

• Longitudinal wavy irregular uptake in the

periosteal aspect of the posteromedial tibia

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What is the three phase bone scan

finding in the acute phase of AVN

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What is the three phase bone scan

finding in the acute phase of AVN

Diminish flow and cold defect in delayed view

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What is the finding in the chronic

phase of AVN

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What is the finding in the chronic

phase of AVN

• Increased or normal flow with increased

uptake

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How is the bone marrow scan used in

AVN

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How is the bone marrow scan used in

AVN

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How is the bone marrow scan used in

AVN

• A cold defect in the region of increased uptake

in bone scan indicates the bone scanabnormality is due to infarct

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What are the scintigraphic finding of

cellulitis

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What are the scintigraphic finding of

cellulitis

• Increased flow and blood pool images in the

first and second phase• Delayed phase normal uptake

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What are the scintigraphic finding of

osteomyelitis

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Name four primary tumors causing

photopenic metastases

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Name four primary tumors causing

photopenic metastases

• Renal

• Thyroid• Multiple myeloma

• Lung

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Lung

Describe the scintigraphic pattern in

Paget’s 

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Describe the scintigraphic pattern in

Paget’s 

• Expansile or thickening of the bone with sharpdemarcation of normal area

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How does Paget’s affect the bone 

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How does Paget’s affect the bone 

• Increased bone resorption accompanied by

bone formation

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What is the scintigraphic finding of

radiation osteitis in bone scan

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What is the scintigraphic finding of

radiation osteitis in bone scan

• Increased activity in the first few weeks,

followed by defect

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What is the scintigraphic pattern of

early fracture in bone scan

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What is the scintigraphic pattern of

early fracture in bone scan

• Cold defect in the first few hours

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What are the reasons of cold defect in

first few hours of fracture in bone scan

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What are the reasons of cold defect in

first few hours of fracture in bone scan

• Rupture of vascular supply from fracture andtoo early for reactive bone formation

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How soon will fracture become

positive and what is the time course in

bone scan

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How soon will fracture become

positive and what is the time course in

bone scan

• Cold defect in the first few hours

• Increasing activity up to few weeks or months

• Then tapering off until resolved

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Then tapering off until resolved

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Stress fractures

1. Increased activity in a linear pattern along theposterior and medial aspect of both mid tibias.

2. Shin splints

3. B , focal ovoid activity posteromedial right tibiaat the junction of the proximal 2/3 and distal

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1/3. C, focal fusiform activity posteromedially inthe right proximal tibia and linear activity alongthe posteromedial left tibia proximally and moreprominently distally.

4. B, stress fracture. C, stress fracture and shinsplints

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Paget’s disease 1. Abnormal increased uptake in the entire left femur,

which appears bowed and widened and the distal

third of the left tibia, which tapers proximally.2. A sharp leading edge, referred to as “flame  shaped” 

or :blade of grass”, may be demonstrated on the lyticphase on radiograph and bone scan.

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3. Paget’s  disease, fibrous dysplasia, chronicosteomyelitis, primary bone tumors.

4. High output congestive heart failure may occur. Oncebelieved to be the result of arteriovenous shunting

within the bone lesion, now hyperemia and increasedblood flow through the lesion and not shunting arelikely the causes.

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Rib fractures1. Patient A; focal increased uptake in multiple ribs

posterolaterally and the costovertebral

 junctions. Patient B; increased vertical linearuptake in the sternum from the manubrium tothe xiphoid.

2. The uptake in adjacent (patient A) and the

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vertical uptake in the sternum both have ageometric and characteristic pattern.

3. Trauma or surgery

4. Patient A; multiple rib fracture. Patient B;

median sternnotomy for coronary artery bypassgrafting (CABG)

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Osteomyelitis1. First phase; arterial blood flow to the bone.

Second phase; blood pool. Third phase; delayed

phase or bone uptake at 3 hours after injection.All three phases are typically focally increasedwith osteomyelitis. With cellulitis only twophases are positive.

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2. Increased flow, blood pool and delayed uptaketo the left first digit distal phalanx.

3. Consistent with osteomyelitis of the digit.

4. Sensitivity and specificity 95% if the radiograph

is normal or has only suggestive changes ofosteomyelitis.

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Abnormal breast uptake

1. Nonuniform abnormal soft tissue uptake

exists in the soft tissue overlying the chest,likely the right breast.

2. Breast ca, aseptic mastitis or radiation

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therapy.3. Breast examination, mammography and

possible biopsy.

4. To determine whether breast cancer bonemetastases are present.

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Extra renal pelvis

1. Solitary right kidney with prominent renalpelvis. Incidental uptake at antecubitalinjection site

2. Ureteropelvic junction obstruction orobstruction secondary to other processes,

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extrarenal pelvis.3. The renal pelvis has drained and the kidney is

now seen inferomedial to its prior location

4. Image B was taken with the patient erect,leading to gravity drainage of an extra renalpelvis. The kidney is mobile (ptotic)

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Lymphedema

1. The soft tissues of the left arm enlarged and

show abnormal increased soft tissue activity,the left anterior ribs are uniformly more

intense than the right.

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2. Venous or lymphatic obstruction, soft tissueneoplasm, soft tissue injury.

3. Breast cancer.

4. Lymphedema secondary to axillary lymphnode dissection and left mastectomy

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Renal position1. The right kidney is not in the renal fossa.

Nonuniform activity is noted in the rightsacroiliac region, which extends beyond theexpected superior margin of the bone.

2. Congenital renal anomaly, pelvic kidney.

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3. Anomalies of number (supernumerarykidney), position (malrotation) and fusion(horseshoe)

4. Yes. Ureteropelvic junction obstruction,vesicoureteral reflux, decrease function andincrease risk of trauma.

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Metastatic prostate cancer1. Abnormal focal uptake throughout the axial

and appendicular skeleton stronglysuggestive of metastatic disease.

2. Greater than 20 ng/ml. the prevalence ofbone scan – evidence od metastases is < 1%.

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3. Multiple myeloma, thyroid ca,, renal cell caand lymphoma

4. CT and MRI have poor sensitivity for

detection of prostate cancer soft tissue/nodalmetastases.

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Fibrous dysplasia

1. A , shows increased uptake in the entire

mandible. B, shows intense increased uptakein the mandible and maxilla which appear

deformed and overgrown.

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2. Check the rest of the bone scan for othersites

3. Fibrous dysplasia, cherubism.

4. Fibrous dysplasia.

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Sacral insufficiency fracture

1. Patient A has increased blood pooling and

delayed uptake bilaterally in the region of thesacroiliac joints and across the sacrum (H

pattern). The bone scan for patient B.

2 Both of these are diagnostic of sacral

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2. Both of these are diagnostic of sacral

insufficiency fractures.

3. Proximal femur, wrist and proximal humerus

4. Osteoporosis

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Heterotopic ossification1. Intense activity is seen overlying the right

acetabulum with a separate area of uptake

overlying the proximal right femur.

2. Urinary contamination; fracture with exuberantcallus; heterotopic ossifican or myositis

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ossificans; soft tissue injury (contusion).3. If urinary contamination is suspected; removeclothing and overlying bed sheets; wash thepatient’s  skin in the area of suspected

contamination.4. Heterotopic ossification.

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Superscan

1. Increased tracer in the large majority of the

visualized bones, with nonuniforminvolvement in both femurs, both humeri and

skull.

2. Soft tissue and GI tract.

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2. Soft tissue and GI tract.

3. The kidneys are not visualized, but faint

activity is seen in the urinary bladder. Little

soft tissue activity is seen.

4. Superscan.

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hyperparathyroidism1. Abnormal diffuse uptake in the lungs and stomach.

Poor visualization of small kidneys and bladder,

increased uptake in the shoulders, hips, knees andankle.

2. Hyperparathyroidism, metastatic calcification causedby hypercalcemia, renal failure or metabolic bone

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disease.3. This particular pattern of metastatic calcification is

characteristic of long standing hyperparathyroidism.

4. Free Tc-99m pertechnetate has gastric, thyroid and

salivary gland uptake. The latter two are not seen inthis patient, who also shows large uptake.

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Reflex sympathetic dystrophy1. Three phase study demonstrate abnormal increased

blood flow and blood pool of the distal right upper

extremity. The delayed bone phase shows increasedactivity in the bones in the same distribution with astriking increased in periarticular activity causing the joints to stand out.

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2. RSD. Disuse of a limb of new onset e.g.. recent strokeor immobilization by orthopedic cast or splint.

3. Shoulder hand syndrome, a frequently encounteredform of RSD

4. Neurogenic origin with loss of sympathetic autonomictone is the generally accepted explanation, althoughnot firmly establish.

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Myocardial uptake1. Horseshoe pattern of uptake in the anterior

chest that does not correspond to normalbony anatomy and therefore is most likelyabnormal soft tissue uptake.

2. Cardiac uptake either the myocardium or

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pericardium.3. Tc-99m pyrophosphate

4. Idiopathic or secondary cardiomyopathy e.g..

due to cardiotoxic drugs, myocarditis orpericarditis.

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Avascular necrosis of femoral heads

1. Nonvisualization of the left ilium, leg lengthdiscrepancy as a result of high riding left hipand increased uptake both femoral heads,left worse than right.

2. The ilium has been surgically resected.

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Femoral heads; avascular necrosis, fracture,osteotomies, slipped capital femoralepiphyses in the appropriate group.

3. Trauma, steroid, sickle cell disease, chronicrenal disease, alcoholism.

4. Humeral head and tarsal navicular.

Cardiac

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Pearls & Pitfalls

Myocardialperfusion imaging

• The common indication for

MPI is to determine whether

there is normal perfusion,

ischemia or infarction.

• Tl-201 photon energy (69  – 81

keV)

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• Myocardial uptake of Tl-201

chloride and Tc-99m

sestamibi/tetrofosmin is

proportional to regional blood

flow and requires cell viability.

Pearls & Pitfalls

Myocardialperfusion imaging

• Thallium is actively taken up by

Na/K pump in the cells.

Tc-99m sestamibi/tetrofosminpassively diffuse across the

membrane and localize in

cytoplasmic mitochondria.

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• Thallium redistributes over

time, so post stress images

must be obtained immediately

after injection.

Pearls & Pitfalls

Myocardialperfusion imaging

• Tc-99m sestamibi/tetrofosmin

do not redistribute and best

images are made 30 to 90

minutes after injection to allow

clearance of interfering

background activity from the

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liver but before the activityreaches the transverse colon.

• Infarcts and hibernating

myocardium produce perfusiondefects on the rest images.

Pearls & Pitfalls

Myocardialperfusion imaging

• Stress images are needed toelucidate ischemia with lesserdegree of stenosis (50 – 90%).

Stenosis less than 50% in diameterare not detected at rest and arevariably diagnosed with exerciseimaging.

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Stress may be physical orpharmacologic.

• Physical stress should bediscontinued with patientexhaustion, claudication, severeangina or hypotension, arrhythmiaor severe ECG changes.

Pearls & Pitfalls

Myocardialperfusion imaging

• Dipyridamole and adenosine

are used instead of physical

stress to dilate normal

coronary arteries.

• Vessels in ischemic areas are

already maximally dilated and

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do not dilate further.

• The adverse effect of the

dipyridamole are reversed with

100 to 200 mg IV

aminophylline.

Pearls & Pitfalls

Myocardialperfusion imaging

• Dipyridamole and adenosineshould not be used in patientswith asthma.

Dobutamine is inotropic andchronotropic and is used forpharmacologic stress.

• Adverse effects may be reversed

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by using short acting betablocker.

• The most common cause of falsenegative is submaximal stress.

The most common cause of falsepositive is artifact.

Pearls & Pitfalls

Myocardialperfusion imaging

• The myocardium normally thins

at the apex, membranous

septum and base of inferior wall.

• A high degree of lung activity on

exercise Thallium images (>50%

of peak myocardial activity) is

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related to poor prognosis, moreextensive disease and LV

dysfunction on exercise.

On Tc-99m sestamibi scans, lungactivity is uncommon.

Pearls & Pitfalls

Myocardialperfusion imaging

• Transient LV dilatation withexercise may be related tosubendocardial ischemia and less

often to real LV dilatation. It issign of poor prognosis.

• With adequate exercise, thesensitivity and specificity of MPI

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are about 85%.• An occluded coronary artery with

adequate collaterals or balancedthree vessels disease canproduce an apparently normalscan

Pearls & Pitfalls

Myocardialperfusion imaging

• Real defects on MPI should be

seen on at least 2 views (e.g..,

short and vertical or horizontal

long axes)

• LBBB may produce myocardial

perfusion findings

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indistinguishable from stressinduced reversible septal

ischemia.

A defect seen at the base of theheart is frequently artifactual

unless it extends to the apex.

Pearls & Pitfalls

Myocardialperfusion imaging

• Not all fixed defects are infarcts.They may also be soft tissueattenuation artifacts, hibernating

or repetitive stunnedmyocardium.

• Hybernating myocardium is achronically hypoperfused area

h h d d ll l

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that has reduced cellularmetabolism.

• This area has decreasedcontractility andrevascularization is usuallyneeded.

Pearls & Pitfalls

Myocardialperfusion imaging

• Stunned myocardium is due to

an acute occlusion with

relatively rapid perfusion.

• These area have normal or

near normal perfusion and

decreased contractility and

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revascularization is not usually

needed.

• LV walls that diverged towards

the apex should raisesuspicious of a LV aneurysm.

Pearls & Pitfalls

Myocardialperfusion imaging

• Diaphragmatic attenuation looks

like an inferior wall defect but it

goes away on prone images.

• Relatively intense GI activity

adjacent to the inferior wall can

cause an apparent inferior

di l d f S C

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myocardial defect on SPECTstudies as a result of a

reconstruction artifact.

Breast attenuation usually causesan apparent defect in the

anterior or lateral LV wall.

Pearls & Pitfalls

Myocardialperfusion imaging

• Bull’s  eye plot underestimate

apical defect and overestimate

basal defects.

• The normal LVEF is 50 - 65%.

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Cardiac Muscle Layers

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parasympathetic sympathetic

SA NODES ↓ heart rate ↑ heart rate ( β receptor )

ATRIUM ↓ contractility  ↑ contractility and conduction

velocity ( β receptor )

AV NODES AND CONDUCTION

SYSTEM

↓ conduction velocity and 

block conduction

↑ conduction velocity ( β 

receptor )

VENTRICLE - ↑ contractility and conduction

l it ( β t )

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velocity ( β receptor )

CORONARY ARTERY - Constriction (α receptor )

Dilatation ( β receptor )

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Coronary artery

Right coronary artery (RCA) Left main artery (LMA)

Left circumflex (LCX) Left anterior

Descending (LAD)

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AV node

branch

Acute marginal

Branch (AM)

Posterior

descending

Artery (PDA)

Descending (LAD)

Marginal

branches

Obtuse M1& M2 

Diagonal

branches

D1 & D

Septal

branches

CORONARY CIRCULATIONCORONARY ARTERY VASCULAR DISTRIBUTIONS

Left anterior descending ( LAD ) Septum

Anterior wallApex

Left circumflex ( LCX ) Lateral wall

Posterior wall

Posterior inferior wall

Apex

Right coronary ( RCA ) Inferior wall

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Right coronary ( RCA ) Inferior wall

Posterior inferior wall

Right ventricular wall

Left main coronary Anterior wall

Septum

Posterolateral wall

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Planes used for SPECT MPI

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CONDUCTION SYSTEMSA ( sinoatrium node )• Pacemaker of heart

• Posterior wall of right atrium

• Depolarize spontaneously 70-80 time/ min

• Contraction of atrium

(interatrium septum)  AV ( atrioventricular node )

(interventricular septum) ( AV bundle )

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( p ) ( AV bundle )

PURKINJE FIBRES

INNERVATIONparasympathetic sympathetic

SA NODES ↓ heart rate ↑ heart rate ( β receptor )

ATRIUM ↓ contractility  ↑ contractility and conductionvelocity ( β receptor )

AV NODES AND CONDUCTION

SYSTEM

↓ conduction velocity and 

block conduction

↑ conduction velocity ( β 

receptor )

VENTRICLE ↑ t tilit d d ti

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VENTRICLE - ↑ contractility and conduction

velocity ( β receptor )

CORONARY ARTERY - Constriction (α receptor )

Dilatation ( β receptor )

STROKE VOLUME•  volume of blood pumped by left ventricle in 1

minute

• SV ( STROKE VOLUME ) x HR ( HEART RATE )

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VENTRICLE CONTRACTILITYEF = EDV – ESV X 100

EDV

• Stroke volume = EDV – ESV

• EF = ejection fraction ( % )

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EF = ejection fraction ( % )• EDV = End diastolic volume ( ml )

• ESV = End systolic volume ( ml )

ECG STAT

DR ZOOL HILMI

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DR ZOOL HILMI

• ECG paper 25 mm/s

• Large square = 5mm = 0.2 s

• Each large square = 5 small square = 1 mm =

0.04 s

• 1 mV = 1 cm vertically

0 1 V 1 1 ll

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• 0.1 mV = 1 mm = 1 small square

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• 6 chest leads = V1 to V6

6 limb leads = I, II, III, aVR, aVL, aVF

- II, III, aVF = inferior

- V1 to V4 = anterior

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- V1 to V4 = anterior- I, aVL, V5 to V6 = lateral

- V1 and aVR = right atrium and cavity of left ventricle

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INTERPRETATION OF ECG• RATE

RHYTHM• AXIS

• P WAVE

• PR INTERVAL

• ST SEGMENT

T WAVE• QT INTERVAL

• U WAVE

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PR INTERVAL• QRS COMPLEX

• Q WAVE

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IMPORTANT• PR = 3 – 5 SMALL SQUARE / 0.12 – 0.2 SECONDS

• QRS ≤ 3 SMALL SQUARE / ≤ 0.12 SECONDS 

• BBB > 3 SMALL SQUARE

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• QT < 11 SMALL SQUARE OR < 0.44 SECONDS OR

< 0.5 RR INTERVAL

CORRECTED QT = QT/√RR 

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RHYTHM• Lead II

• Sinus rhythm = originates in the sinus node and

conduct to the ventricle

CARDINAL FEATURES OF SINUS RHYTHM

P wave is upright in leads I and II

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P wave is upright in leads I and II

Each P wave is usually followed by QRS complex

Heart rate between 60 to 99

CARDIAC AXISNORMAL

AXIS

RIGHT AXIS

DEVIATION

LEFT AXIS

DEVIATION

LEAD I

+ - +LEAD II

+ +/

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+ +/- -LEAD III

+/- + -

CARDIAC AXISLEAD I AVF

NORMAL + +

LEFT AXIS + & (LEAD II -) -

RIGHT AXIS - +

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RIGHT AXIS +

INDETERMINATE - -

CARDIAC AXIS CAUSESLEFT AXIS RIGHT AXIS

LVH RVH

INFERIOR MI LATERAL MI

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INFERIOR MI LATERAL MI

LEFT ANTERIOR

FASCICULAR BLOCK

LEFT POSTERIOR

FASCICULAR BLOCK

NORMAL FINDINGS ECG• Tall R waves

• Prominent U waves

• Exaggerated sinus arrhythmia• Sinus bradycardia

• Wandering atrial pacemaker

Wenckebach phenomenon• Junctional rhythm

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Wenckebach phenomenon• Junctional rhythm

• 1st degree heart block

• ST segment elevation(high take off, benign early

repolarization)

P WAVE• Atrial depolarization

Characteristic of the P wave: positive in leads I and II

Best seen in lead II and V1

Commonly biphasic in lead V1

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Commonly biphasic in lead V1< 3 small square (0.12s)in duration

< 2.5 small square (0.25mV) in amplitude

NORMAL ECG

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P WAVE• Bifid P, in lead II , notch with peak to peak interval

of > 1 mm = mitral stenosis

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P WAVE

• Large negativedeflection = left atrial

enlargement

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PR INTERVAL• Electrical impulse conducted through the AV

node, the bundle of His and bundle branches

and the Purkinje fibers

• Beginning of the P wave to the 1st deflections

of QRS complex whether it is Q or R wave

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of QRS complex, whether it is Q or R wave

3 to 5 small square (0.12 – 0.20 s)

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QRS COMPLEX• Ventricular depolarization

• Not > 2 ½ small square (0.10 s)

• BBB > (0.12 s) wide QRS

Q wave : any initial negative deflection

R wave : any positive deflection

S wave : any negative deflection after R wave

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S wave : any negative deflection after R wave

• Non pathological Q wave seen at: leads I, III,aVL, V5 and V6

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ST SEGMENT• QRS complex terminates at the J point or ST

 junction

• ST segment lies between the J point and the

beginning of the T wave

• Period between the end of ventricular

depolarization and the beginning of the

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depolarization and the beginning of the

repolarization

ST SEGMENT• Leads V1 to V3, rapidly S wave merges directly

with the T wave, making the J point indistinct

and the ST segment difficult to identify

• This produces elevation of the ST segment,

and this is known as high take off

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and this is known as high take off

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EARLY REPOLARISATION

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T WAVE• Ventricular repolarization

• Normal T is ASYMMETRICAL

• SYMMETRICAL, Inverted T = myocardial

ischemia

Tall T wave = MI and hyperkalemia• T a e < 2/3 amplit de of R

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yp• T wave < 2/3 amplitude of R

• T wave amplitude < 10 mm

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QT INTERVAL• Total time for depolarization and

repolarization of the ventricle

• Beginning of the QRS complex to the end of

the T wave

• 0.35 – 0.45 s

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PROMINENT U WAVE

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CONDITIONS AFFECTINGTHE LEFT SIDE OF THE

HEART

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CONDITIONING AFFECTING LEFT SIDE

OF THE HEART

1. Left atrial dilatation and

hypertrophy

2. LVH

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LEFT ATRIAL ABNORMALITY• Atrial hypertrophy or dilatation or both

• P wave in lead V1 is often biphasic

• Early right atrial forces giving rise to an initial

positive deflection

These are followed by left atrial forcestravelling posteriorly, producing a later

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travelling posteriorly, producing a later

negative deflection

LEFT ATRIAL ABNORMALITY

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• Biphasic P wave in V1

LEFT ATRIAL ABNORMALITY• A large deflection (>1 small square) suggests a

left atrial abnormality

• Prolongation of P wave duration to greater

than 0.12 s is often found in association with

the left atrial abnormality

• Normal P wave may be bifid

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LEFT ATRIAL ABNORMALITY• Any condition causing left ventricular

hypertrophy may produce left atrial

enlargement as a secondary phenomenon

• Causes of Left atrial enlargement :

Hypertension

Aortic stenosis

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Mitral incompetence

Hypertrophic cardiomyopathy

LEFT ATRIAL ABNORMALITY

• P mitrale in lead II• Commonly seen in

mitral stenosis

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LEFT VENTRICULAR HYPERTHROPHY

• Difficult to diagnose < 40 with ECG

• Causes:

1. Hypertension

2. Aortic stenosis

3. Co-arctation of aorta

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LEFT VENTRICULAR HYPERTHROPHY

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LEFT VENTRICULAR HYPERTHROPHY

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LEFT VENTRICULAR HYPERTHROPHY

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LEFT VENTRICULAR HYPERTHROPHY

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TAHCYCARDIA

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• HR > 100 bpm

TAHCYCARDIA

• Divided into 2:

1. Supraventricular

tachycardia

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2. Ventricular

tachycardia

SUPRAVENTRICULAR TACHYCARDIA

(SVT)• From atria or sinoatrial node

1. Sinus tachycardia

2. Atrial fibrillation

3. Atrial flutter

• From atrioventricular node

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1. Atrioventricular re-entrant tachycardia

2. Atrioventricular nodal re-entrant tachycardia

SUPRAVENTRICULAR TACHYCARDIA

(SVT)

• At the atrium

• Above bundle of

His

• Narrow complext h di

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tachycardia

SUPRAVENTRICULAR TACHYCARDIA

(SVT)

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SUPRAVENTRICULAR TACHYCARDIA

(SVT)

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• SINUS TACHYCARDIA

SUPRAVENTRICULAR TACHYCARDIA

(SVT)

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• SINUS TACHYCARDIA

SUPRAVENTRICULAR TACHYCARDIA

(SVT)• Normal P wave in

inferior lead II,III

and aVF• Atrial rate 100-200

bpm

• Regular ventricularrhythm

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• SINUS TACHYCARDIA

rhythm

• Ventricular rate 100-

200 bpm

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ATRIAL FIBRILATION

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ATRIAL FIBRILATION

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• NO P WAVES IN AF

ATRIAL FIBRILATION

• Mapping R waves

against a piece of paper

usually confirmdiagnosis

• May be paroxysmal,

persistent or

permanent

T Di i

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• Treatment : Digoxin

ATRIAL FIBRILATION

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ATRIAL FLUTTER

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ATRIAL FLUTTER

• Re-entry circuit in the

right atrium with

secondary activation ofleft atrium

• Atrial contraction 300

bpm

• Broad and appear

t th b t t

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sawtooth best seen at

inferior leads and V1

ATRIAL FLUTTER

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JUNCTIONAL TACHYCARDIA

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1. Atrioventricular re-entrant tachycardia

2. Atrioventricular nodal re-entrant tachycardia

JUNCTIONAL TACHYCARDIA

• Negative P waves in

inferior leads

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JUNCTIONAL TACHYCARDIA

• PR interval < 3 ss

• P wave negative

deflection in lead II

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ECTOPIC ATRIAL TAHYCARDIA

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SUPRAVENTRICULAR TACHYCARDIA

(SVT)

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JUNCTIONAL TACHYCARDIA

• WOLF PARKINSON

WHITE SYNDROM

• Atrioventricular re-

entrant tachycardia

• Electrical signal re-

enters the atria over

b l

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an abnormal extra

pathway

JUNCTIONAL TACHYCARDIA

• WOLF PARKINSONWHITE SYNDROM

This extra pathwayallows electrical signalsto pass between theventricles and atria

Signals on this extrapathways causing theatria and ventricles to

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atria and ventricles tobeat too fast

JUNCTIONAL TACHYCARDIA

• WOLF PARKINSONWHITE SYNDROM

• Short PR interval < 3small square

• Slurred upstroke to

the QRS indicatingpre-excitation (delta)

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wave)

• Broad QRS

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VENTRICULAR TACHYCARDIA

• At the ventricle

• Below bifurcation

bundle of His

• Broad QRS

complex

tachycardia

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tachycardia

VENTRICULAR TACHYCARDIA

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VENTRICULAR TACHYCARDIA

• Define as 3 or more ventricular extrasystoles insuccession at rate > 120 bpm

• Causes :

1. IHD

2. Cardiomyopathy

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y p y

3. Myocarditis

4. Drugs: quanidine

ATRIOVENTRICULAR CONDUCTION

BLOCK• Delayed 1st degree block

• Intermittently blocked – 2nd degree block

Completely blocked – 3rd

 degree block

• Causes:

1. MI

2. Degeneration of His Purkinje system

3 Lyme disease diphtheria

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3. Lyme disease, diphtheria

4. Surgery

5. Congenital disorder

1st DEGREE BLOCK

• A delay conduction of atrial impulse to ventricle

At level of atrioventricular node• Prolonged PR interval > 2.0 s

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• A QRS complex follows each P wave, and PR

interval remains constant

1st DEGREE BLOCK

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• Prolonged PR

2nd DEGREE BLOCK

•MOBITZ TYPE I BLOCK (WENCKEBACH

PHENOMENON)

• MOBITZ TYPE II BLOCK

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2nd DEGREE BLOCK• At the level of

atrioventricular node

• Intermittent failure of

transmission of the atrial

impulse to the ventricles

• Initial PR interval is normal

but progressively lengthens

with each successive beat

until AV transmission is

blocked completely and the

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P wave is not followed by

QRS complex

• PR interval then return tonormal and cycle repeats

MOBITZ TYPE I (WENCKEBACH)

i l i f i l

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• Progressive prolongation of PR interval

within group

2nd DEGREE BLOCK

• Less common but is more likely to produce

symptoms

• Intermittent failure of conduction of P wave• PR interval is constant, though it may normal or

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prolonged

Block is often at the level of the bundle brunches andis therefore associated with wide QRS complexes

MOBITZ TYPE II

• Constant PR interval in a group

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3rd  DEGREE BLOCK

• Complete failure of conduction between atria

and ventricles

• Complete independence of atria and

ventricular contractions

b l i i h Q S l

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• P waves bear no relation with QRS complexes

Usually proceed with faster rate

AV BLOCK SUMMURY

• 1st  DEGREE AV BLOCK

All P waves conducted with prolonged PR

• 2nd DEGREE AV BLOCK

Some P waves not conducted

Mobitz type I : Progressive PR prolongation

Mobitz type II : Constant PR interval

3rd DEGREE AV BLOCK

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• 3rd DEGREE AV BLOCK

No P waves conducted

BUNDLE BRANCH BLOCK

• Right bundle branch block

• Left bundle branch block

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Left bundle branch block

COMPLETE RBBB

• QRS prolongation (≥ 

0.12s)

• Slurred S  wave in

lead V6  and/or rSR

pattern in lead V1

• Overall positive QRScomplex in lead V1 

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p

(a must)

RBBB

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COMPLETE LBBB

• QRS prolongation (≥ 

0.12s)

• Broad R  waves in

lead I  and V6  with

no Q waves

• Broad S waves in theseptal leads

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p

LBBB

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HYPERKALAEMIA

• Potassium

concentration rises

above 5.5-6.5mmol/L

• Classic tall,

symmetricallynarrow and peaked T

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waves

HYPOKALEMIA

• Serum potassium <

2.7 mmol/L

• Broad, flat T waves

• ST depression

• QT interval

prolongation

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ACUTE CORONARY SYNDROME

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STEMI

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STEMI

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STEMI

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STEMI

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STEMI

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• Normal Q wave

STEMI

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STEMI

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• Viable myocardium

STEMI

ECG ONSET RESOLUTION

HYPERACUTE T WAVE

CHANGES

< 5 MINUTES HOURS

ST ELEVATION < 20 MINUTES HOURS TO 3 DAYS

TERMINAL PORTION QRS

CHANGES

HOURS HOURS

Q WAVE FORMATION 9 HOURS TO 2 DAYS PERMANENT

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T WAVE INVERSION VARIABLE WEEKS

STEMI LOCALISATION

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NSTEMI/UNSTABLE ANGINA

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NSTEMI/UNSTABLE ANGINA

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• T INVERSION

NSTEMI/UNSTABLE ANGINA

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• ST SEGMENT DEPRESSION AND T INVERSION

NSTEMI/UNSTABLE ANGINA

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SUMMARY

COMPLETE OCCLUSION

(STEMI)

PARTIAL OCCLUSION

(NSTEMI)ST ELEVATION ST DEPRESSION

Q WAVES T INVERSION

NO Q WAVES

FULL THICKNESS MI NON Q WAVE MI

Q WAVE MI PARTIAL THICKNESS MI

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TRANSMURAL MI SUBENDOCARDIAL MI

Cardiac scan

Radionuclideventriculography

Myocardial perfusion

imaging (MPI)Infarct avid

Metabolic 

Neuronal

Single photon

PET

PET

Tetrofosmin 

Sestamibi

Thallium 

Teboroxime

NOET

Planar

O15

Rb82 

N13 

Pyrophosphate Antimyosin  Glucarate

FDG

Fatty acid

C11epinephrine

Tc-99m labeled

Tc-99m DTPA

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MUGA First pass

Planar

MIBGC11phenylephrine

C11hydroxyephdrine

Tc-99m

pertechnitate

Tc-99m RBCTc-99m serum

Human albumin

Chemical, physical &

pharmacokinetic

Thalium-201 Tc-99m Sestamibi

( Cardiolite )

Tc-99m Tetrofosmin

( Myoview )

Chemical Element cation Isonitrile cation Diphosphine cation

Preparation cyclotron Generator/kit Generator/kit

Mode of decay Electron capture Isomeric transition Isomeric transition

Half life 73 H 6 H 6 H

Principle emissions Mercury x rays 69-

83KeV

Gamma rays 140KeV Gamma rays 140KeV

Mechanism of uptake Active transport Passive diffusion Passive diffusion

Myocyte localization Cytosol Mitochondria Mitochondria

Redistribution Yes No No

Extraction fraction 85% 60% 50%

Percent cardiac uptake 3% 1.5% 1.2%

Body clearance Renal Hepatic Hepatic

Highest radiation Kidney Colon Gallbladder

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Highest radiation

absorbed dose

Kidney

( rads/3mCi )

Colon

( rads/30mCi )

Gallbladder

( rads/30mCi )

Imaging timeStress

Rest

10 min

3-4 hrs

15-30 min

30-90 min

5-15 min

30 min

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WHAT IS REDISTRIBUTION?

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REDISTRIBUTION

• Only occurs with Tl 201

• Is misnomer

• Tl 201 exits the myocardium more slowly from

ischemic segments

• In delayed imaging, more rapid exit of Tl 201

from normal segments result in equilibrium

among normal and ischemic segment

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STUNNED MYOCARDIUM

• Myocardium with persistent contractile

dysfunction despite restoration of perfusion

after ischemia• Improves with time

• Normal by perfusion imaging

• Absence of ventricular contraction on wallmotion studies

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• Increased uptake by FDG

WHAT IS HIBERNATING

MYOCARDIUM?

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HIBERNATING MYOCARDIUM

• Chronically ischemic myocardium that is still

viable

• Appears cold on immediate Tl 201 imaging

• Absence of ventricular contraction on wall

motion studies

• Increased uptake of FDG compared toperfusion imaging

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• Improved perfusion on reinjection of Tl 201

Normal scan

Stress (top) and rest (bottom) MPI images from normal male subject

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ISCHEMIC MYOCARDIUM IMAGES?

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ISCHEMIC MYOCARDIUM

• Reduced Tl 201 myocardial uptake on post

stress images

• Improves uptake on the rest images

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Apical ischemia

Stress (top) and rest (bottom) MPI images from a subject with apical

ischemia

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ischemia.

SCAR IMAGES ?

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SCAR

• Reduced Tl 201 myocardial uptake post stress

images

• Reduced uptake on the rest images

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Antero-apical infarct

Stress (top) and rest (bottom) MPI images from a patient with prior

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extensive antero-apical MI and no residual ischemia.

MYOCARDIAL IMAGINGRADIOPHARMACEUTICAL DOSE ( mCi ) IMAGING TECHNIQUE TYPE OF STUDY

²⁰¹Tl Cl 2-3 Planar or SPECT Perfusion

Tc 99m sestaMIBI 10-30 Planar or SPECT Perfusion

Tc 99m teboroxime 15-30 Planar or SPECT Perfusion

Tc 99m PYP 10-15 Planar Infarct

¹¹¹In labeled antimyosin

antibody

2-3 Planar Infarct

⁸²RbCl  60 PET Perfusion

¹³NH₃  15-20 PET Perfusion

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¹⁸F-FDG 5-10 PET Metabolism

Sensitivi ty & Specif ici ty  

Sensitivity Specificity

Myocardial

Perfusion Scan 93% 88%

Stress

Echocardiography 81% 82%

Exercise StressTest 68% 77%

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INDICATIONS FOR MYOCARDIAL

PERFUSION SCAN• Detection of CAD

• Assessment of severity of myocardial ischemia orinfarction

• Assessment of myocardial viability• Evaluation for candidate of coronary bypass or

angioplasty

• Clinical indication of MI, chest pain and SOB

• ↑ CPK,LDH, +ve troponin and myoglobin• Detection of viable/hibernating myocardial tissue

• Evaluation of angioplasty/bypass surgery

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• Evaluation of prognosis

CONTRAINDICATIONS FOR

MYOCARDIAL PERFUSION• Chest pain

• Ventricular arrhythmia at rest

• Very high BP

• Allergy to pharmacological stress drugs

• Third degree heart block

• Severe valvular disease ( aortic valve stenosis )

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Selection of Stress Technique

Mean hyperemic flowMean resting flow

X 4

X 3

X 2

X 1

Restin blood flow

Treadmill exercise

Dobutamine

D iridamole/ Adenosine

Coronary flow disturbance vs diameter narrowing

Diff. btw.

sternotic

& non-

stenotic

counts.

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% diameter narrowing50 100

STRESS PROTOCOLS

1. PHYSICAL EXERCISE

2. PHARMACOLOGICAL STRESS

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STRESS TESTING INDICATIONS

• Diagnosis of CAD

• Evaluation of CAD, location and extent of ischemia

• Determine the cause for change in symptom pattern inpatients with known CAD

• Evaluate the effectiveness of medical therapy

• Risk stratification post myocardial infarction

Pre operative evaluation for major non cardiac surgeryin patient with known CAD

• Assessment after angioplasty or bypass

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• Guide to rehabilitation therapy

STRESS TESTING CONTRAINDICATIONS

• Acute MI

• Unstable angina

• Severe tachyarrhythmias and bradyarrhythmias

• Uncontrolled symptomatic heart failure

• Critical aortic stenosis

• Acute aortic dissection

• Pulmonary embolism

l ll d

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• Poorly controlled HPT

INDICATIONS FOR TERMINATING A

STRESS TEST• Patient’s request

• Inability to continue due to fatigue, dyspnea, orfaintness

• Moderate to severe chest pain• Dizziness, near syncope

• Pallor

• Ventricular tachycardia

• Atrial fibrillation• Third degree heart block

• ST segment depression > 3 mm

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• Increased SBP > 240 mmHg or DBP > 120 mmHg

Myoview counseling

Stop medications:At the appointment date :

1. Aspirin

2. OHA/insulin

2 days prior :

1. Neulin (theophylline)

2. Beta blockers3. Viagra

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3 days prior : 1. Nitrates/trimetazidine

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CARDIAC STRESS TEST : EXERCISE AND

PHARMACOLOGY• LEG EXERCISE

• Treadmill

• Bicycle ergometer

• PHARMACOLOGIC STRESS

• Dipyridamole• Adenosine

• Dobutamine

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• Dobutamine

STRESS PROTOCOLS

1.PHYSICAL EXERCISE

2. PHARMACOLOGICAL STRESS

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PHYSICAL EXERCISE

• Treadmill or bicycle

• ECG 10-12 lead used

• Run baseline ECG

• Start exercise

• Monitor HR, BP, ECG changes till target HR is

achieved > 85% of ( 220-AGE )• Radiotracer is injected when target HR is reached

• Maintain exercise for 1 minute

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• Maintain exercise for 1 minute

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STRESS PROTOCOLS

1. PHYSICAL EXERCISE

2.PHARMACOLOGICALSTRESS

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PHARMACOLOGICAL STRESS

1. ADENOSINE

2. DOBUTAMINE

3. DIPYRIDAMOLE

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Dobutamine

✔β adrenergic agonist 

✔Synthetic catecholamine

✔β1 affinity

✔Short plasma half life

✔Cause ionotrophic/chronotrophic effect due

to high O2 demand cause by artery stenosis

✔Infusion rate (40-50 υg/kg/min) 

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Dobutamine

✔Can be used in asthma patients

✔Side effect:Supraventricular and ventricular arrhythmia

Palpitation

SOBGI symptom

Chest pain

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p

Dobutamine

✔Contraindications:

ST depression

Ventricular tachycardia

Systolic BP > 220 mmHg

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Adenosine Dypiridamole Dobutamine

Mechanism of

action

Direct Indirect Indirect

Half life < 10 s 30 – 60 min 2 min

Onset of action Seconds 2 min 1 – 2 min

Patients with side

effect requiring

medical

intervention

0.6% 16% NA

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ADVERSE EFFECTS: ADENOSINE AND

DIPYRIDAMOLEADVERSE EFFECT ADENOSINE ( % ) DIPYRIDAMOLE ( % )

Flushing 37 3

Dyspnea 35 3

Chest pain 25 20GI symptoms 15 6

Headache 14 12

Dizziness 9 12

A-V block 8 2

ST wave changes 6 8

Arrhythmia 3 5

Hypotension 2 5

h 0 1 0 1

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Bronchospasm 0.1 0.15

MI 0.0001 0.05

Death 0 0.5

ARTIFACTS FOR MPI

• Patient motion

• Diaphragm in men and breast in female cause

attenuation artifacts• Medallion, necklaces, pacemaker or metallic

button

• Left arm of the patient, lying on the side maycause unwanted attenuation

• Gallbladder with sestaMIBI may causeproblems

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problems

Breast attenuation effect

Stress (top) and rest (bottom) MPI images from a female subject

showing a reduction in counts anteriorly in both stress and rest

images

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images.

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Reporting MPI

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PET Cardiac

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Concerning the blood supply of the

normal heart

1. The right coronary artery supplies the AVnode

2. The anterior intraventricular artery is abranch of RCA

3. Arise from the inferior aspect of the aorticarch

4. The circumflex artery is a branch of the LCA

5. The great cardiac vein drains the territorysupplied by the RCA

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Concerning the blood supply of the

normal heart

1. The right coronary artery supplies the AV node

2. The anterior intraventricular artery is a branch

of RCA3. Arise from the inferior aspect of the aortic arch

4. The circumflex artery is a branch of the LCA

5. The great cardiac vein drains the territorysupplied by the RCA

TFFTF

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FOLLOWING ARE INDICATIONS OF

GATED BLOOD POOL STUDY

1. Measuring right ventricular ejection fraction

2. Quantifying shunts

3. Cardiotoxic drugs4. Extent of infarct

5. Myocardial reserve

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FOLLOWING ARE INDICATIONS OF

GATED BLOOD POOL STUDY

1. Measuring right ventricular ejection fraction

2. Quantifying shunts

3. Cardiotoxic drugs4. Extent of infarct

5. Myocardial reserve

FFTFT

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IMAGING OF INFARCT

1. Tc pyrophosphate is the infarct avid imagingprocedure of choice

2. Pyrophosphate uptake is taken more around the

infarct than in the infarct3. Myosin monoclonal antibody is useful only in

imaged within 2-3 days after administration

4. Pyrophosphate is taken up by bone5. Images are acquired after 48 hours in myosin

antibody

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IMAGING OF INFARCT

1. Tc pyrophosphate is the infarct avid imagingprocedure of choice

2. Pyrophosphate uptake is taken more around the

infarct than in the infarct3. Myosin monoclonal antibody is useful only in

imaged within 2-3 days after administration

4. Pyrophosphate is taken up by bone

5. Images are acquired after 48 hours in myosinantibody

FTFTF

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CONTRAINDICATION FOR

MYOCARDIAL PERFUSION IMAGING (

EXERSICE STRESS )

1. Sinus bradycardia

2. Third degree heart block3. Ventricular arrhythmias

4. Aortic stenosis

5. Unstable angina

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CONTRAINDICATION FOR

MYOCARDIAL PERFUSION IMAGING (

EXERSICE STRESS )

1. Sinus bradycardia

2. Third degree heart block3. Ventricular arrhythmias

4. Aortic stenosis

5. Unstable angina

FTTTT

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MYOCARDIAL PERFUSION IMAGING

1. Bulls eye maps are used to predict theprognosis of infarct

2. Stress images are acquired 30-60 mins afterinjection

3. GTN is administered when acquiring restimages

4. Rest images are acquired far later than stressimages

5. Injection is done at maximum stress

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MYOCARDIAL PERFUSION IMAGING

1. Bulls eye maps are used to predict the prognosisof infarct

2. Stress images are acquired 30-60 mins after

injection3. GTN is administered when acquiring rest images

4. Rest images are acquired far later than stress

images5. Injection is done at maximum stress

TTTTT

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STRESS IN MYOCARDIAL PERFUSION

IMAGING

1. Dipyridamole is the stress agent of choice

2. Systolic pressure less than 100mm is

contraindication for adenosine3. The aim of stress is to decrease the coronary

arterial flow

4. Adrenaline is the antidote to adenosinecomplication

5. Asthma is a contraindication to adenosine

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STRESS IN MYOCARDIAL PERFUSION

IMAGING

1. Dipyridamole is the stress agent of choice

2. Systolic pressure less than 100mm iscontraindication for adenosine

3. The aim of stress is to decrease the coronaryarterial flow

4. Adrenaline is the antidote to adenosine

complication5. Asthma is a contraindication to adenosine

FTFFT

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CARDIAC SCINTIGRAPHY

1. LAO best for left ventricle

2. RAO 30 best for right ventricle

3. For assessing RV ejection fraction, inject thetight bolus

4. For shunt quantification, inject over 3

seconds5. First pass takes 15 seconds

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CARDIAC SCINTIGRAPHY

1. LAO best for left ventricle

2. RAO 30 best for right ventricle

3. For assessing RV ejection fraction, inject thetight bolus

4. For shunt quantification, inject over 3

seconds5. First pass takes 15 seconds

TTFFT

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CARDIAC SCINTIGRAPHY

1. MIBI is more prone for liver uptake

2. Tetrofosmin is easier to prepare than MIBI

3. Stannous pyrophosphate and pertechnateare mixed before administrating in vein

4. MUGA scan are better than LIST studies

5. Acquisition begins with R wave of each cycle

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CARDIAC SCINTIGRAPHY

1. MIBI is more prone for liver uptake

2. Tetrofosmin is easier to prepare than MIBI

3. Stannous pyrophosphate and pertechnateare mixed before administrating in vein

4. MUGA scan are better than LIST studies

5. Acquisition begins with R wave of each cycleTTFTT

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THALLIUM 201

1. Decays by electron capture to Tl 203

2. Mainly produce gamma photon of 135 and

167 keV3. After IV administration 15% is localized in the

myocardium

4. All the thallium ions enter the myocytes bythe sodium potassium ATPase pump

5. Extraction of thallium is reduced in acidosis

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THALLIUM 201

1. Decays by electron capture to Tl 203

2. Mainly produce gamma photon of 135 and 167keV

3. After IV administration 15% is localized in themyocardium

4. All the thallium ions enter the myocytes by the

sodium potassium ATPase pump5. Extraction of thallium is reduced in acidosis

FFFFF

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FEATURES OF HIBERNATING

MYOCARDIUM

1. Reversible

2. FDG PET is the standard for assessing

myocardial viability3. Adverse cardiac events in these patients are

higher if treated with revascularization

4. Decreased uptake in FDG5. Decreased perfusion in thallium scans

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MYOCARDIAL PERFUSION IMAGING

1. 2 separate injection are required for thallium,unlike for MIBI and tetrofosmin

2. ST segment depression more than 3mm is

indicator that dobutamine should be stopped3. Rest images are performed first, followed by

stress images

4. At least 2 days are required for satisfactory

testing using MIBI5. Infarcts will show decreased uptake during

stress and improved in rest images

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MYOCARDIAL PERFUSION IMAGING

1. 2 separate injection are required for thallium, unlikefor MIBI and tetrofosmin

2. ST segment depression more than 3mm is indicatorthat dobutamine should be stopped

3. Rest images are performed first, followed by stressimages

4. At least 2 days are required for satisfactory testingusing MIBI

5. Infarcts will show decreased uptake during stress andimproved in rest images

FTFFF

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THALLIUM 201 IMAGING

1. Taken up by infarcts

2. Left ventricular function can be assessed

using first pass studies3. Can be used to assess a left to right shunt

4. Normal to have a photon deficient area at

the apex5. Left ventricular failure is associated with

increased lung uptake

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THALLIUM 201 IMAGING

1. Taken up by infarcts

2. Left ventricular function can be assessed usingfirst pass studies

3. Can be used to assess a left to right shunt

4. Normal to have a photon deficient area at theapex

5. Left ventricular failure is associated withincreased lung uptake

FTTTT

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THALLIUM SCINTIGRAPHY

1. Involves a lower radiation dose than Tc99m

MIBI scanning

2. Reverse redistribution is commonly due toartifact

3. Injection is performed at peak exercise

4. There is increased uptake in areas ofmyocardial infarction

5. Is more sensitive than cardiac stress testing

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THALLIUM SCINTIGRAPHY

1. Involves a lower radiation dose than Tc99m MIBIscanning

2. Reverse redistribution is commonly due to

artifact3. Injection is performed at peak exercise

4. There is increased uptake in areas of myocardial

infarction5. Is more sensitive than cardiac stress testing

FTTFT

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THALLIUM 201

1. Kidney is the critical organ

2. Distribution is proportional to perfusion

3. Physical half life is 24 hours, making it lowdose

4. Images are of high resolution

5. High signal to noise ratio

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THALLIUM 201

1. Kidney is the critical organ

2. Distribution is proportional to perfusion

3. Physical half life is 24 hours, making it lowdose

4. Images are of high resolution

5. High signal to noise ratioTTFFF

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PET AGENTS USED IN HEART IMAGING

1. Nitrogen 13 ammonia

2. Rubidium 82

3. Potassium 384. Oxygen 15 labeled water

5. Inhaled 15 CO2

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PET AGENTS USED IN HEART IMAGING

1. Nitrogen 13 ammonia

2. Rubidium 82

3. Potassium 384. Oxygen 15 labeled water

5. Inhaled 15 CO2

TTTTT

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UPTAKE OF THALLIUM IS SEEN IN

FOLLOWING STRUCTURES

1. Kidney

2. Lungs

3. Salivary glands4. Skeletal muscle

5. Liver

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UPTAKE OF THALLIUM IS SEEN IN

FOLLOWING STRUCTURES

1. Kidney

2. Lungs

3. Salivary glands4. Skeletal muscle

5. Liver

TTFTF

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STRESS TESTING

1. Adenosine combined with exercise improves

detection of perfusion defects

2. Dobutamine avoided if patient has asthma3. Adenosine should be avoided if patient has

bifascicular block or LBBB

4. Bradyarrhythmia is reduced by exercise5. Dipyridamole has the highest sensitivity and

specificity among pharmacological agents

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STRESS TESTING

1. Adenosine combined with exercise improvesdetection of perfusion defects

2. Dobutamine avoided if patient has asthma

3. Adenosine should be avoided if patient hasbifascicular block or LBBB

4. Bradyarrhythmia is reduced by exercise

5. Dipyridamole has the highest sensitivity andspecificity among pharmacological agents

TFFTF

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MIBI CARDIAC IMAGING

1. Rescan is done at 4 hours as redistributionoccurs

2. 5% of negative studies go on to get MI within

one year

3. Increased uptake is seen in myocardialinfarction

4. Gated studies useful to look at wall motion5. Fatty meal should not be taken as it produces

hepatic uptake

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MIBI CARDIAC IMAGING

1. Rescan is done at 4 hours as redistributionoccurs

2. 5% of negative studies go on to get MI within

one year3. Increased uptake is seen in myocardial infarction

4. Gated studies useful to look at wall motion

5. Fatty meal should not be taken as it produces

hepatic uptakeFFTTF

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INCREASED UPTAKE OF THALLIUM

1. Graves’ disease 

2. Thyroid ca

3. Bronchogenic ca in lung4. Lymphoma of lung

5. Brain in encephalitis

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INCREASED UPTAKE OF THALLIUM

1. Graves’ disease 

2. Thyroid ca

3. Bronchogenic ca in lung4. Lymphoma of lung

5. Brain in encephalitis

TTTTT

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MYOCARDIAL PERFUSION

SCINTIGRAPHY

1. The physical properties of thallium 201 are such thatits use is preferable to that of Tc99m labeledcompounds in myocardial perfusion imaging

2. The effective dose from Tl 201 myocardial perfusionscan is one of the highest in diagnostic imaging androughly equates to 3 barium enemas

3. The uptake of Tl 201 relies solely on regional

myocardial perfusion4. Tl 201 is a Na analogue

5. Tl 201 remains irreversibly fixed to the myocardiumwithin a few minutes of injection

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MYOCARDIAL PERFUSION

SCINTIGRAPHY1. The physical properties of thallium 201 are such that

its use is preferable to that of Tc99m labeledcompounds in myocardial perfusion imaging

2. The effective dose from Tl 201 myocardial perfusion

scan is one of the highest in diagnostic imaging androughly equates to 3 barium enemas

3. The uptake of Tl 201 relies solely on regionalmyocardial perfusion

4. Tl 201 is a Na analogue5. Tl 201 remains irreversibly fixed to the myocardium

within a few minutes of injection

FTFFF

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THE FOLLOWING MAY CAUSE

REDUCTION IN Tl 201 UPTAKE TO THE

MYOCARDIUM

1. Myocardial infarction2. Hibernating myocardium

3. Cardiomyopathy

4. Cardiac sarcoidosis5. Dobutamine

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THE FOLLOWING MAY CAUSE

REDUCTION IN Tl 201 UPTAKE TO THE

MYOCARDIUM

1. Myocardial infarction

2. Hibernating myocardium3. Cardiomyopathy

4. Cardiac sarcoidosis

5. DobutamineTTTTT

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PROGNOSIS IN CORONARY ARTERY

DISEASE1. Increased uptake of Tl 201 into the lungs is a poor

prognostic indicator during myocardial perfusion imaging

2. Myocardial perfusion imaging may identify patients atincreased risk of cardiac events following major vascular

surgery3. Myocardial perfusion imaging has greater prognostic

power than exercise ECG

4. Myocardial perfusion imaging has less prognostic powerthan coronary arteriography

5. In a patient with a strongly positive ECG but a normalmyocardial perfusion scan, the perfusion scan is the mostappropriate for defining prognosis

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PROGNOSIS IN CORONARY ARTERY

DISEASE1. Increased uptake of Tl 201 into the lungs is a poor

prognostic indicator during myocardial perfusion imaging

2. Myocardial perfusion imaging may identify patients atincreased risk of cardiac events following major vascular

surgery3. Myocardial perfusion imaging has greater prognostic

power than exercise ECG

4. Myocardial perfusion imaging has less prognostic powerthan coronary arteriography

5. In a patient with a strongly positive ECG but a normalmyocardial perfusion scan, the perfusion scan is the mostappropriate for defining prognosis

TTTFT

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CONCERNING PHARMACOLOGICAL

STRESSOR AGENTS

1. Dipyridamole reduces uptake of myocardialperfusion agents to myocardial

2. Adenosine may be use as a cardiac stressor

3. Caffeine intake should be restricted before anexercise myocardial perfusion

4. Aminophylline may reverse chest pain caused

by dipyridamole5. Dipyridamole is a potent coronary

vasodilator

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CONCERNING PHARMACOLOGICAL

STRESSOR AGENTS

1. Dipyridamole reduces uptake of myocardialperfusion agents to myocardial

2. Adenosine may be use as a cardiac stressor

3. Caffeine intake should be restricted before anexercise myocardial perfusion

4. Aminophylline may reverse chest pain caused by

dipyridamole5. Dipyridamole is a potent coronary vasodilator

FTTTT

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Tc 99m LABELLED MYOCARDIAL

PERFUSION AGENTS1. Stress and redistribution images of Tc 99m SestaMIBI

accurately identify ischemic myocardium

2. Tc99m SestaMIBI is more suited to SPECT scanningthan Tl 201

3. A fatty meal is required following sestaMIBI injection4. Tc 99m SestaMIBI stress and rest myocardial perfusion

scans cannot be performed on the same day due tothe long redistribution time of this agent in

myocardium5. Tc 99m SestaMIBI imaging should be performed as

soon as possible following injection

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Tc 99m LABELLED MYOCARDIAL

PERFUSION AGENTS1. Stress and redistribution images of Tc 99m SestaMIBI

accurately identify ischemic myocardium

2. Tc99m SestaMIBI is more suited to SPECT scanning than Tl201

3. A fatty meal is required following sestaMIBI injection4. Tc 99m SestaMIBI stress and rest myocardial perfusion

scans cannot be performed on the same day due to thelong redistribution time of this agent in myocardium

5. Tc 99m SestaMIBI imaging should be performed as soon as

possible following injectionFTTFF

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EQUILIBRIUM GATED BLOOD POOL

IMAGING

1. Tc 99m DTPA is preferable to labeled red bloodcells in gated ventriculography asradiopharmaceutical preparation is easier

2. Red cells may be labeled with Tc 99m in vivo3. Concurrent ECG recording is only necessary ifthere is risk of arrhythmia

4. It is possible to assess regional wall motion

abnormalities of the left ventricle5. Background substraction is not usually requiredin measuring LV ejection fractions as activitywithin the adjacent lung is negligible

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EQUILIBRIUM GATED BLOOD POOL

IMAGING1. Tc 99m DTPA is preferable to labeled red blood cells in

gated ventriculography as radiopharmaceuticalpreparation is easier

2. Red cells may be labeled with Tc 99m in vivo

3. Concurrent ECG recording is only necessary if there isrisk of arrhythmia

4. It is possible to assess regional wall motionabnormalities of the left ventricle

5. Background substraction is not usually required inmeasuring LV ejection fractions as activity within theadjacent lung is negligible

FTFTF

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EQUILIBRIUM GATED BLOOD POOL

IMAGING1. Patients with coronary artery disease typically show an

increase in LV ejection fraction of only 5-10% on exercise

2. Regional wall motion abnormalities are more specific forcoronary artery disease than changes in ejection fraction

with exercise3. Patients receiving chemotherapy should be suspected of

having cardiotoxicity if the ejection fraction falls by morethan 10% on sequential scans

4. It is possible to differentiate alcoholic from viral

cardiomyopathy by gated blood pool imaging5. It is possible to differentiate ischemic cardiomyopathy

from dilated idiopathic cardiomyopathy with gated bloodpool imaging

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EQUILIBRIUM GATED BLOOD POOL

IMAGING1. Patients with coronary artery disease typically show an increase in

LV ejection fraction of only 5-10% on exercise

2. Regional wall motion abnormalities are more specific for coronaryartery disease than changes in ejection fraction with exercise

3. Patients receiving chemotherapy should be suspected of havingcardiotoxicity if the ejection fraction falls by more than 10% onsequential scans

4. It is possible to differentiate alcoholic from viral cardiomyopathyby gated blood pool imaging

5. It is possible to differentiate ischemic cardiomyopathy from

dilated idiopathic cardiomyopathy with gated blood pool imagingFTTFT

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RADIONUCLIDE VENTRICULOGRAPHY

1. Radionuclide ventriculography is a more accurate andreproducible method for measuring ejection fraction thanechocardiography

2. Assumptions for the calculation of ejection fraction are

greater for echocardiography than they are forradionuclide ventriculography

3. In severe left ventricular dysfunction the volume ofinjected radiopharmaceutical is reduced to avoid overload

4. Exercise ventriculography is not possible because there is

too much motion of the patient5. It is not possible to measure RV ejection fraction using

gated equilibrium technique

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RADIONUCLIDE VENTRICULOGRAPHY

1. Radionuclide ventriculography is a more accurate andreproducible method for measuring ejection fraction thanechocardiography

2. Assumptions for the calculation of ejection fraction are

greater for echocardiography than they are forradionuclide ventriculography

3. In severe left ventricular dysfunction the volume ofinjected radiopharmaceutical is reduced to avoid overload

4. Exercise ventriculography is not possible because there is

too much motion of the patient5. It is not possible to measure RV ejection fraction using

gated equilibrium technique

TTFFF

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FIRST PASS RADIONUCLIDE

ANGIOGRAPHY

1. It is possible to detect R to L cardiac shunts with thistechnique

2. It is possible to detect L to R cardiac shunts with this

technique3. As large a dilution of radiopharmaceutical as possibleshould be used in this technique

4. It is an accurate technique to quantify cardiac

shunting which coexist with coaortation of the aorta5. It is often not possible to accurately quantitate

cardiac L to R shunts in the presence of tricuspidregurgitation

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FIRST PASS RADIONUCLIDE

ANGIOGRAPHY1. It is possible to detect R to L cardiac shunts with this

technique

2. It is possible to detect L to R cardiac shunts with thistechnique

3. As large a dilution of radiopharmaceutical as possibleshould be used in this technique

4. It is an accurate technique to quantify cardiacshunting which coexist with coaortation of the aorta

5. It is often not possible to accurately quantitatecardiac L to R shunts in the presence of tricuspidregurgitation

TTFFT

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MYOCARDIAL INFARCT SCANNING

1. A myocardial infarction may be seen on an MDPbone scan

2. Tc 99m labeled pyrophosphate imaging may

detect myocardial infarction before cardiacenzyme changes

3. Rib fracture may give false positive results withpyrophosphate scanning

4. Positive antimyosin monoclonal antibodyscanning is specific for myocardial infarction

5. Rejection of heart transplants can be detectedwith antimyosin scanning

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MYOCARDIAL INFARCT SCANNING

1. A myocardial infarction may be seen on an MDP bonescan

2. Tc 99m labeled pyrophosphate imaging may detectmyocardial infarction before cardiac enzyme changes

3. Rib fracture may give false positive results withpyrophosphate scanning

4. Positive antimyosin monoclonal antibody scanning isspecific for myocardial infarction

5. Rejection of heart transplants can be detected withantimyosin scanning

TFTFT

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How does the percent extraction of

thallium-201 passing through the

myocardial capillary bed comparedwith the extraction of c-99m sestamibi

and Tc-99m teboroxime?

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How does the percent extraction of

thallium-201 passing through the

myocardial capillary bed comparedwith the extraction of c-99m sestamibi

and Tc-99m tetrofosmin?• Tl-201 has a myocardial extraction fraction of

0.85 in normal subjects at a normal flow rates.

The myocardial extraction of Tc-99m sestamibiand Tc-99m tetrofosmin is considerably lower

0.5 and 0.6 respectively.

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What percentage of Tl-201, Tc-99m

sestamibi and Tc-99m tetrofosmin

localizes in the heart?

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What percentage of Tl-201, Tc-99m

sestamibi and Tc-99m tetrofosmin

localizes in the heart?

• Tl-201 : 3-4%

Tc-99m sestamibi : 1.5%• Tc-99m tetrofosmin : 1.2%

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What are the advantages and

disadvantages of Tl-201 as perfusion

agent?

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What are the advantages and

disadvantages of Tl-201 as perfusion

agent?Advantages

• Single injection because of

redistribution• Imaging within 10 – 15

minutes

• Can be used to assess

viability

Disadvantages

• High radiation

• Poor imaging characteristicswith a low photopeak of 69

 – 80 keV

• High scatter fraction

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What quality control to detect patient

motion?

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What quality control to detect patient

motion?

• Review raw data in cinematic display and

review of sonogram can confirm the extend of

the problem.

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In what ways can the image

interpreter determine if fixed

decreased activity is due to artifact ordisease?

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In what ways can the image

interpreter determine if fixed

decreased activity is due to artifact ordisease?

• Review the raw data in the cinematic display

to look for soft attenuation.

• Review the gated SPECT can help determine if

there is wall motion and thickening that

would indicate infarct or attenuation.

• Attenuation correction can be helpful.

• Prone can differentiate attenuation from

infarction in inferior wall.

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What is the significant of lung uptake

on Tl-201 exercise study?

• Lung uptake on exercise stress images, but not

the delayed images is consistent with exercise

induced cardiac dysfunction.

• This finding is usually associated with three

vessel disease.

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What other scintigraphic finding

suggest three vessel disease?

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What is the mechanism of action of

dipyridamole?

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What is the mechanism of action of

dipyridamole?

• Dipyridamole inhibits the action of adenosine

deaminase.

• By augmenting the effects of endogenous

adenosine, dipyridamole is a powerful

vasodilator.

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What effect can a cup of coffee have

on dipyridamole or adenosine stress

test?

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What effect can a cup of coffee have

on dipyridamole or adenosine stress

test?• Caffeine in coffee, tea, soft drinks or food such

as chocolate are chemically related to

dipyridamole and adenosine and can block theeffect of dipyridamole pharmacological stress

testing.

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What percentage of stenosis at rest is

necessary in the coronary arteries for

resting blood flow to be effected?

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What percentage of stenosis at rest is

necessary in the coronary arteries for

resting blood flow to be effected?•  > 85 – 90%

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Why is imaging delayed for 30 – 90

minutes after administration of Tc-99m

sestamibi or tetrofosmin?

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Why is imaging delayed for 30 – 90

minutes after administration of Tc-99m

sestamibi or tetrofosmin?• Lung uptake is also significant.

• The lung and liver clear with time and the

target to background ratio improves.

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What pharmaceutical is administered

to allows the Tc-99m to bind to RBC?

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What pharmaceutical is administered

to allows the Tc-99m to bind to RBC?

• Stannous (tin) pyrophosphate and stannous

chloride has been used.

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What part of the RBC does the Tc-99m

label bind?

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What part of the RBC does the Tc-99m

label bind?

• Beta chain of hemoglobin when the patient is

pretreated with stannous ion.

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What do amplitude and phase images

portray?

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What do amplitude and phase images

portray?

• Amplitude and phase images are parametric

or derived images.

• The amplitude images portrays the maximum

count difference at each pixel location during

the cardiac cycle. High EF areas have high

amplitude and background areas have low

amplitude.

• The phase images portrays the timing of

cyclical activity with respect to a reference

standard.

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What is the hallmark of a ventricular

apical aneurysm by phase analysis?

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What is the hallmark of a ventricular

apical aneurysm by phase analysis?

• Aneurysms demonstrate paradoxical motion.

• Activity in the area of the aneurysm is typically

180 degrees out of phase with the rest of the

ventricle.

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LAD ischemia

1. Severe decreased perfusion in the majority of

the anterior wall, apex and septum which

normalizes on the rest image indicating

extensive severe ischemia.

2. LAD territory.

3. Transient cavity dilatation.

4. VT, angina related ST abnormalities,

decreased systolic pressure and level of

exercise achieved.

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Apical infarct

1. Fixed stress and rest severe apical perfusion

defect. Heart and cavity size appear normal.

2. Myocardial infarction, apical thinning and

attenuation.

3. Small apical lateral scar.

4. Technical factors, operator error and

interpretation error

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Breast attenuation

1. Mild fixed anteroseptal hypoperfusion thatdemonstrates uniform brightening on gatedSPECT, indicating normal myocardial wall

thickening on gated images.2. Apparent decreased tracer in the upper

portions of the heart is most obvious on theleft anterior oblique and lateral frames.

3. Normal perfusion study with normal wallthickening and breast attenuation.

4. Assessment of regional wall motion/ wall

thickening and LVEF

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Inferolateral wall infarction

1. If the patient develops severe angina chest pain,a decrease in blood pressure, frequentpremature ventricular contraction or ST

elevation suggestive of acute infarct. Also ifpatient can walk no further on the treadmillbecause of general fatigue, leg pain or dyspnea.

2. Severe stress and rest fixed defect in the

basolateral, inferior and inferolateral walls,sparing the apex.

3. MI or possibly hibernation. Circumflex artery.

4. The exercise stress level.

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Dipyridamole induced reversible

ischemia

1. A perfusion defect involving the entire

inferior wall extending to the apex shows

partial reversibility.

2. RCA

3. Inferior wall ischemia with incomplete

reversibility. The latter may represent scar or

hibernating myocardium.

4. The patient is at risk for further cardiac

event, either infarct or death.

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Adenosine stress

1. A. adenosine is infused IV for 6 minutes (140μg/kg/min)  after 3 min the tracer is injected andadenosine is continued for 3 more minutes. B.adenosine is cleared from circulation <10 sec. return

to baseline blood flow levels occurs in 2 to 3 minutesafter stopping the infusion. C. stop infusion

2. Sinus node disease, 2nd  to 3rd  degree block,bronchospastic lung disease and adenosine allergy

3. Small to moderate severe fixed defect at the apex on

both stress and rest images consistent with infarct.Mildly improved perfusion of the anterior and lateralwalls at rest compared with stress consistent withmild anterolateral ischemia.

4. Whenever adequate exercise stress is not possible.

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Viability

1. Extensive fixed defects involving the anterior

wall, apex, septum extending to the lateral

wall.

2. Myocardial infarction vs. hibernating

myocardium.

3. In hibernating myocardium, blood flow and

function e.g.. contractility are chronically

reduced.

4. Blood flow is normal with reduced function.

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Bull’s eye 

1. A polar plot is constructed by layering short axis slicesone on top of the other with the apex forming thecenter and the base of the heart being the outermostportion.

2. Misregistration use of inappropriate referencedatabase.

3. Stress; hypoperfusion of the anterior, lateral andinferior walls. Rest; normalized perfusion of theanterior and lateral walls and incomplete

normalization of the inferior wall. Most consistentwith ischemia of the LCX and infarct of the right RCA.

4. Include location and extent, severity and reversibilityfor each perfusion abnormality. If gated SPECT is

performed, include LVEF, wall motion with or withoutwall thickening fractions.

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Inadequate stress

1. Severe fixed defect involving the both entire

lateral wall

2. Dilated left ventricular cavity at both stress

and rest.

3. LCX artery

4. False negative studies for ischemia may result

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LBBB

1. Dipyridamole or adenosine

2. Exercise or dobutamine. Methods of stress thatresult in increased heart rate can be associated

with false positive findings of septal reversibilityin patient with LBBB

3. These agents do not result in an increased inheart rate.

4. The mild decreased activity in the anterior wallappears fixed and likely is caused by breastattenuation in light of the reported normal wallmotion.

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Dobutamine stress

1. Dobutamine stress; patients who are not

candidate for either exercise; asthma

2. Angina and inability to tolerate dobutamine

3. Mild fixed anteroseptal perfusion defect with

decreased wall thickening. Severe fixed

inferior defect with absent wall thickening.

Dilate LV. No reversibility. Myocardialthickening and wall motion signify

functioning viable myocardium.

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Patient motion artifact

1. A. the first study shows an abnormal

configuration of the anterior wall; the repeat

study is normal. B, The initial sinogram shows a

discontinuity or break, the second is normal.2. To visually present the raw unprocessed

projection images to evaluate for patient

motion.3. Review SPECT projection, image by image or in

cinematic display.

4. Artifact caused by patient motion.

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Breast attenuation

1. Tc-99m sestamibi, tetrofosmin and not Tl-201

because the GB is seen.

2. Mild fixed defect in the anterior wall.

Projection images; decreased uptake in the

half of the heart at stress and rest

3. Breast attenuation, anterior wall infarction.

4. Assessment of regional wall motion, wall

thickening and EF

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Bowel activity

1. Dipyridamole inhibits the action of adenosinediaminase, increasing endogenous adenosine, apotent coronary artery vasodilatation. Coffee, tea,caffeine containing soft drinks or chocolate,theophylline and aminophylline.

2. Dipyridamole is infused for 4 minutes. Tracer is given3 minutes after completion of dipyridamole infusion.Side effects can be reversed with aminophylline.

3. Mild to moderate fixed defect of the anterior wall.

Severe, mostly fixed defect involving the entireinferior wall but small area of reversibility in theinferioapical region. Dilated LV.

4. Obtained delayed SPECT to allow additional hepaticclearance or movement of bowel activity, have thepatient drink water.

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Brain scintigraphy

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Pearls & Pitfalls

Brain imaging

• The commonest indications for brain imagingare perfusion abnormalities (stroke),dementia (Alzheimer’s  or multi infarct),epilepsy, brain death, and distinguishingrecurrent tumor from radiation necrosis.

• The radiopharmaceutical Tc-99m HAMPAO,

TC-99m ECD, N-13 PET.

• The radiopharmaceutical Tc-99m HAMPAO,TC-99m ECD are lipophilic, extracted on firstpass and reflect perfusion.

• Their uptake is highest in the cortical andsubcortical grey matter.

• On imaging, the central area of decreasedactivity is primarily white matter and shouldnot be mistaken for dilated lateral ventricle

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Pearls & Pitfalls

Brain imaging

• The radiopharmaceuticals Tl-201

and FDG PET are metabolic agentsthat show activity in viablerecurrent and persistent tumors butnot in areas of radiation necrosis.

• Multi infarct dementia presentswith multiple asymmetric corticalperfusion defects.

• Multiple small perfusion defectscan also occur from cocaine abuseor vasculitis

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Pearls & Pitfalls

Brain imaging

• Alzheimer's dementia classically

presents with symmetricallydecreased activity in the posteriorparietal-temporal lobes withpreserved activity in the calcarinecortex and basal ganglia and can be

also seen in Parkinson’s dementia.

• About 30% of Alzheimer's patientshave symmetrically decreased

activity.

• Herpes encephalitis can be seen asincreased activity in the temporal

lobe

l f ll

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Pearls & Pitfalls

Brain imaging

• Epileptic seizure foci show increased

perfusion (Tc-99m HMPAO or Tc-99mECD) and metabolism FDG PET duringseizure activity but decreased or normalactivity interictally

• A normal radionuclide angiographicexamination of the brain presents atrident appearance of intracranial flow inthe anterior cerebral and right and leftmiddle cerebral territories.

• In brain death, there is no obvious arterialphase (the trident is absent) and onlyscalp activity is seen, which is often

accompanied by a hot nose sign.

l & f ll

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Pearls & Pitfalls

Brain imaging

• These studies can also be

performed by Tc-99m HMPAOor Tc-99m ECD.

•A Diamox challenge studyevaluate cerebral vascularreserve.

• In areas of vascular disease,regional perfusion worsensafter Diamox compared with

perfusion without Diamox

l & i f ll

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Pearls & Pitfalls

CSF imaging

• Common indications for CSF

imaging are for evaluation of a CSFleak or for differentiating normal-pressure hydrocephalus from othercauses of hydrocephalus.

• These study are done withintrathecal administration of In-111

DTPA

• Most CSF leaks occur in the ear,paranasal sinuses or nose

P l & Pi f ll

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Pearls & Pitfalls

CSF imaging

• Substantial leaks can be

imaged by noting asymmetricactivity around the region ofthe ears on the frontal view oractivity in the nose on thelateral view.

• Some leaks are detected only

by removing and countingcotton pledgets that wereplaced in the area of concern

P l & Pi f ll

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Pearls & Pitfalls

CSF imaging

• Cysternography images are

usually obtained anteriorly.

• Six hours after injection, these

images normally show a

trident appearance of activityproduced by labeled CSF in the

anterior interhemispheric,

right and left sylvian cisterns• Any abnormal entry into the

lateral ventricles is seen as

heart shape activity

P l & Pi f ll

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Pearls & Pitfalls

CSF imaging

• Early ventricular entry with

stasis, accompanied by lack ofactivity over the superiorsurface of the brain after 24 to48 hours, support thediagnosis of normal pressurehydrocephalus.

• The classical clinical triad ofnormal hydrocephalus includesataxia, incontinence and

dementia

FDG

RADIOPHARMACEUTICALS F-18 FDG

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RADIOPHARMACEUTICALS F-18 FDG

HOW THE STUDY IS

PERFORMED

- IV FDG (10-20 mCi)

- Imaged about 45 min later

- Patient sit in a quiet, darkened room

- EEG monitoring

PATIENT PREPARATION - Fasting except water- Withheld alcohol/caffeine/psychiatric medication

- Differ 4-6 weeks after RT

UNDERSTANDING THE

REPORT

FDG uptake dependent on blood flow & by active cells

Neoplasia

FDG is taken up by higher grade tumors

Most metastasis have increased uptake

Radiation necrosis have little or no uptake

Dementia

Alzheimer’s  dementia= decreased uptake in bilateral posteriortemporoparietal, posterior cingulate gyrus and frontal lobe if more

advanced

Prick’s disease = decreased uptake at frontotemporal

Lewy bodies = temporoparietal and more occipital

Parkinson’s dementia = temporoparietal and visual cortex

Vascular dementia = focal, asymmetric, wedge shape at cortical and

subcortical

AIDS dementia = multifocal cortical at frontal, temporal and parietal

Seizures Ictal = seizure = hyperperfusion

Interictal = after seizure = hypoperfusion

POTENTIAL PROBLEMS

Diaschisis phenomenon which abnormal in one segment will decreased uptake in

uninvolved region

False positive Inflammation / radiation necrosis with gliosis

False negative Steroid/ high glucose/ RT/ small lesion/ low histologic grade

Thyroid disease Hypothyroid may effect FDG uptake at parietal and temporal region

Brain perfusion SPECT imaging

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RADIOPHARMACEUTICALS Tc-99m HMPAO / Tc-99m ECD / Xenon-133

HOW THE STUDY IS

PERFORMED

- IV RPC (15 – 30 mCi)

- Patient went in the dark room for 5 – 15 min

- For seizure, EEG is compulsory

PATIENT PREPARATION- Fasting except water

- Withheld alcohol/caffeine/psychiatric medication

- Differ 4-6 weeks after RT

UNDERSTANDING THE REPORT

Cerebrovascular disease

Brain perfusion highly sensitive to blood flow

Hemorrhagic stroke cannot be differentiated from other infarct

Lacuna strokes may be too small to detect

Dementia

Alzheimer’s  dementia= decreased uptake in bilateral posterior

temporoparietal, posterior cingulate gyrus and frontal lobe if more

advanced

Prick’s disease = decreased uptake at frontotemporal

Lewy bodies = temporoparietal and more occipital

Parkinson’s dementia = temporoparietal and visual cortex

Vascular dementia = focal, asymmetric, wedge shape at cortical and

subcortical

AIDS dementia = multifocal cortical at frontal, temporal and parietal

Seizures Ictal = seizure = hyperperfusion

Interictal = after seizure = hypoperfusion

POTENTIAL PROBLEMS

Diaschisis phenomenon which abnormal in one segment will decreased uptake in

uninvolved region

Age of infarct It is not possible to determine the age of infarct

Luxury perfusion Radiotracer may be deposited at an infarct due to increased flow, even

the brain cells are actually nonfunctioning. It’s seen with Tc-99m HMPAO

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Blood Brain barrier protocol

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SPECT cerebral perfusion imaging protocol

Brain death scan

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RADIOPHARMACEUTICALS Tc-99m HMPAO / Tc-99m ECD / Tc-99m pertechnitate / Tc-99m DTPA

HOW THE STUDY IS

PERFORMED

- Tc-99m pertechnitate / DTPA bolus (20 mCi) for cerebral blood flow

- Tc-99m HMPAO / ECD (15 – 30 mCi), delayed images from 20 min to 2 hours postinjection

PATIENT PREPARATION - No specific preparation

UNDERSTANDING THE

REPORT

Absent of cerebral blood flow

Hot nose sign

POTENTIAL PROBLEMS

Barbiturates or

hypothermia

Barbiturate coma, taking phenobarbital or hypothermia

False negative Scalp blood flow may be increased due to inflammation

Continuum ofbrain death Ineffective blood flow can persist despite true brain death

Diamox Brain stress scan

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Diamox Brain stress scan

RADIOPHARMACEUTICALS Tc-99m HMPAO / Tc-99m ECD

HOW THE STUDY IS

PERFORMED

- 1 g Diamox injected

- Rpc (9 mCi) injected 20 min later- The base line scan can be performed a day before or after

PATIENT PREPARATION - Contraindication for sulfa drug allergy

- Diamox is to be avoided within 3 days of acute stroke

UNDERSTANDING THEREPORT

Carotid arterystenosis

Decreased flow to the affected region onDiamox scan compared to base line

Multiinfarct

dementia or

Alzheimer’s

disease

MID = defect are often pronounced

following Diamox

AD = normal

POTENTIAL PROBLEMS

Side effect of Diamox = vertigo/ tinnitus/nausea/ postural

hypotension

Completely balanced bilateral lesion may give false negative

Thallium-201 or Tc-99m SestaMIBI Brain Scan

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RADIOPHARMACEUTICALS

Tc-99msestamibi = localizes in mitochondria by active diffusion across

an interrupted BBB

Thallium 201 = concentrated like potassium in viable tumor, less in

inflammatory and no in necrotic tissue

HOW THE STUDY ISPERFORMED

- Tl-201 (2  –  4 mCi) IV , image at 10  –  30 min and delayed at 2  –  4hours

- Tc-99m SestaMIBI (10 – 30 mCi) IV an image at 10 min to 4 hours

PATIENT PREPARATION - No special preparation

UNDERSTANDING THE

REPORT

Normal brain Little or no thallium uptake

High grade gliomas

and lymphoma

Increased uptake “hot” 

Infection or radiation

necrosis

No significant increase from background

POTENTIAL PROBLEMS

False positive

There has been reports of thallium uptake with

abscess, certain infections, inflammatory

demyelinating disease and radiation necrosis

SestaMIBI less prone to false positive

False negative

If a lesion is necrotic, partially treated, near an

areas of normal uptake in the skull base or

scalp, or below the resolution of imaging

Radionuclide Cysternogram

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RADIOPHARMACEUTICALS Indium-111 DTPA

3 days half life

Study requires 24 – 72 hours

HOW THE STUDY ISPERFORMED

- LP is performed- In-111 DTPA (9-18 MBq) into intrathecal

- Image at 1-4 hr, 24 hr, up to 48 – 72 hr

PATIENT PREPARATION - Lumbar puncture should be informed to patient before

procedure

- LP and radiotracer administration under fluoroscopic

guidance

UNDERSTANDING THE

REPORT

Normally radiotracer reaches basal cisterns by 1 hr,

frontal poles and Sylvian fissures by 2 – 6 hr

Convexity by 12 hr

Sagittal sinus by 24 hr

POTENTIAL PROBLEMS

Lumbar puncture Extravasation will manifest as persistent

activity at the lumbar puncture site and

slow or no progression to the cranium

Overlapping

patterns

Often there is overlap of finding

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Cysternography protocol

CSF leak

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RADIOPHARMACEUTICALS Indium-111 DTPA

3 days half life

HOW THE STUDY IS

PERFORMED

- Before the exam, labeled cotton pledgets are placed into the nasal

cavity and/or ears by ENT

- In-111 DTPA is introduced into the thecal sac via LP (9 – 18 MBq)

- Patient lies supine or in Trendelenberg

- Image at 1 – 4 hr

- Patient may be asked to Valsalva to increased CSF pressure

- The pledgets usually withdrawn when leak is detected or at 4 – 24 hr

and weighed and counted for radioactivity

- Plasma sample is collected to calculate a pledget to plasmaradioactivity ratio because CSF is absorbed into the blood stream

and will appear in normal nasal secretions

- Further delayed up to 72 hr

PATIENT PREPARATION - Informed for lumbar puncture

UNDERSTANDING THE

REPORT

A corrected pledget to plasma ratio > 2:1 indicates CSF leakage

POTENTIAL PROBLEMS

Lumbar puncture

Pledgets falling out

Nasal secretion radioactivity

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CSF leak protocol

CSF Shunt Patency scan

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RADIOPHARMACEUTICALS Tc-99m DTPA/ MAA

In-111 DTPA

HOW THE STUDY IS

PERFORMED

- Tc-99m DTPA or MAA (0.5  –  1 mCi) 0r In-111 DTPA (0.25  – 0.5 mCi)

injected into the shunt

- Image taken at 30 min to 2 hr

PATIENT PREPARATION - Aware type of shunt

UNDERSTANDING THE

REPORT

Normal flow through the tubing should be seen with significantreservoir clearance by 30 min

Ventriculoperitoneal shunt free distribution within abdominal cavity

If the tip is intra artrial – MAA is trapped in the lungs

Hold up of tracer at shunt tip in peritoneum indicates a loculation

Ventricular chemotherapy shunt – radiotracer appear at convexities by

24 hr if no obstruction

POTENTIAL PROBLEMS

Unfamiliar with shunt

Peri shunt injection  –  injecting not into reservoir will cause false

positive

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Prick’s disease  Generalize cortical hypoperfusiond h t b li f i

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and hypometabolism favoring

prefrontal regions

Multiinfarct dementia Scattered foci of decreased cortical

perfusion and metabolism

Alzheimer’s disease  Hypoperfusion and metabolism in

temporoparietal regions

Huntington’s disease  Decreased glucose metabolism and

perfusion in caudate nucleus and

putamen

Wilson’s disease  Severe depression of lenticularnuclei glucose metabolism

AIDS dementia Diffuse hypometabolism affecting

subcortical more than cortical gray

matter

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Tc-99m HMPAO SPECT for brain in

Alzheimer's disease showing

posterior temporoparietal defects

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Tc-99m HMPAO SPECT of the brain

in dementia of Lewy bodies showing

posterior perfusion defect withinvolvement of occipital cortex

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Tc-99m HMPAO SPECT of the brain

in frontotemporal dementia(Prick’s  disease) of showing

anterior perfusion defect

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Tc-99m HMPAO SPECT of the brain

in vascular dementia showing

multiple perfusion defects, with

generally reduced perfusion in the

right internal carotid territory

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Language activation H215O study in a

patient with a left hemisphere

glioma. Activation during

articulation (red) and verb

generation (blue) is anterior to thetumor

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Coronal a and b 11C methionine PET in

a patient with recurrent glioma in the

left temporal lobe

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Stroke TumorBrain death

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Stroke

Dimentia

Movement disorder

Lewi body

Tumor

TraumaTIA

Brain death

Epilepsy

Cortical cerebral imaging

AIDS

Alzheimer

Attention deficit

PSY

Obsessive compulsive

Schizo

Parkinson

Huntington’schorea

Multi infarct

Prick’s disease 

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Brain

Blood brain barrier Brain perfusion MetabolismBrain tumors Cysternography

Tc-99m

glucoheptonate

Tc-99m DTPA

IMP

I-123 iodoamphetamine

Tc-99m ECD

Ethyl cysteinate dimer

Tc-99m HMPAO

F-18 FDG F-18 FDG Tc-99m DTPA

Tc-99m sestamibi

Thallium-201

Indium-111

DTPA

Indium-111 pentreotide

CNS

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CNS

Blood Brain barrier

Diffusible lipophilic Non diffusible

Tc-99m DTPA

Tc-99m pertechnetate

F-Flurodopa

Tc-99m ECD

FDG

Tc-99m HMPAO

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Tc-99m HMPAO Tc-99m ECD

Accumulation Frontalthalamus

cerebellum

parietaloccipital

Extraction 80% 60-70%

Dose remains in blood 1 hour < 12% 1 hour 5%

Good brain to background

ratio

Imaging time Can image until 24

hours

Superior quality 15-30 min

Suboptimal quality if delayed

Excretion Renal 40% and GI Renal and GI

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Dementia

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Temporoparietalhypoperfusion

Frontotemporalhypoperfusion

Multiplefocal defects

Lewy body

Frontotemporal

degeneration

Prick’s

Parkinson

Progressive

supranuclear palsy

Alzheimer

Pseudodepressive

Schizo

Normo pressure

hydrocephalia

Chronic alcoholism

Multi infarct

Creutzfeldt-Jakob

AIDS

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Concerning Tc-99m HMPAO

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A. Tc-99m HMPAO crosses BBBB. Regional uptake of Tc-99m HMPAO is

proportional to regional cerebral blood flow tothe same area

C. Distribution of Tc-99m HMPAO in the brain siindependent of brain maturation

D. Diffuse lung uptake of Tc-99m HMPAO is seenonly in people with a history of smoking

E. Focal cerebral uptake is seen in herpes simplexencephalitis

Concerning Tc-99m HMPAO

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• TTFTT

Brain SPECT

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A. The distribution of Tc-99m HMPAO reflects regionalglucose metabolism

B. Tc-99m HMPAO has to be used within 30 min of beingprepared

C. It is helpful to create images in the axis of temporallobes when investigating temporal lobe epilepsy

D. Bright light or loud sounds at the time of injectionmay alter the distribution of Tc-99m HMPAO

E. It is possible to accurately assess the size of lateralventricles with brain blood flow tracer

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Concerning dementia

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A. Increased accumulation of cerebral blood flow traceris seen in the frontal lobes in Prick’s disease

B. Abnormalities in Alzheimer’s  disease are oftenbilateral and predominantly effect temporal andparietal lobe

C. AIDS dementia complex usually shows noabnormalities on brain SPECT imaging

D. Typical blood flow changes are seen in the basalganglia in asymptomatic patients with Huntington’s 

choreaE. A characteristic pattern of reduced rCBF is seen inidiopathic Parkinson’s disease

Concerning dementia

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• FTFTF

Concerning brain scintigraphy

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A. In the initial stage of cerebral ischemia, regionalcerebral blood flow increases.

B. In the initial stage of cerebral ischemia, regionaloxygen extraction fraction increases.

C. With cerebral infarction, cerebral metabolic ratefor glucose increases.

D. Following cerebral infarction, local cerebralblood flow increases.

E. In Parkinson’s  disease, PET perfusion studiesdemonstrate decreased perfusion to the basalganglia contralateral to the affected limb.

Concerning brain scintigraphy

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•FFFTF

Concerning brain scintigraphy

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A. In Parkinson’s  disease, there is increased F-18 flourodopauptake by the stratum (caudate and putamen nuclei).

B. Concerning brain tumors, an advantage of PET is that it canimage metabolically active cells versus gadoliniumenhanced MRI and contrast enhanced CT, which imageareas where there is blood brain barrier breakdown.

C. Gadolinium enhanced MRI and F-18 FDG PET imaging areequally capable of distinguishing between recurrent braintumor and radiation necrosis.

D. All malignant brain tumors demonstrate hypermetabolism

over F-18 FDG.E. In differentiating between infectious and neoplastic brain

lesions, the presence of hypermetabolism is not useful.

Concerning brain scintigraphy

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•FTFFF

Concerning brain scintigraphy

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A. F-18 FDG freely crosses the BBB via the same carriermediated transport system as glucose

B. Local cerebral metabolic rates of glucose (specificareas of the thalamus, basal ganglia, lobes) can be

determined through PET studiesC. Approximately 20  –  30 mCi of FDG PET should beadministered for a brain study

D. A routine FDG study can be performed 5 minutes

after radiopharmaceutical administrationE. External stimuli can increased regional glucose

metabolism within particular areas of the brain

Concerning brain scintigraphy

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•TTFFT

Concerning brain scintigraphy

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A. Global glucose metabolism compared with normaldecreases to a greater degree in multiinfarctdementia than in Alzheimer’s dementia

B. Small white matter lacunar infarcts are much moreeasily identified with FDG PET than with CT

C. CT can reliably distinguish Alzheimer’s  disease frommultiinfarct dementia

D. In Huntington’s disease, changes in the caudate nucleican be observed on PET earlier than the CT

E. Persistent ventricular filling on a radionuclidecisternogram is diagnostic of communicatinghydrocephalus

Concerning brain scintigraphy

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•FFFTT

Concerning Tc-99m DTPA in brain

scintigraphy

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A. Does not cross the BBBB. Redistribute over several hours

C. In subacute stroke appears as an area of

increased uptakeD. Is the current agent of choice for

radionuclide cisternography

E. Requires preparation with oral perchlorate toblock the unwanted choroid plexus uptake

Concerning Tc-99m DTPA in brain

scintigraphy

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•TFTFF

Which radiopharmaceuticals havebeen used for blood brain

scintigraphy?

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scintigraphy?

Which radiopharmaceuticals havebeen used for blood brain

scintigraphy?

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scintigraphy?

• Tc-99m pertechnetate, Tc-99m DTPA and Tc-

99m GH. The letter two were preferred

because of their faster background clearance,lack of choroid plexus uptake and lower

radiation dose.

What is the ‘flip-flop’ phenomenonseen in the cerebrovascular

i i h d h i h

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scintigraphy and what is the

significance?

What is the ‘flip-flop’ phenomenonseen in the cerebrovascular

i ti h d h t i th

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scintigraphy and what is the

significance?

• On the flow phase, parenchymal flow is

delayed on the abnormal side compared withthe contralateral normal side. Thus, as thenormal cortex clears, uptake in the abnormal

side peaks. This may be seen with the highgrade carotid artery stenosis with or withoutcerebral infarction. Delayed carotid flow isseen concomitantly.

Pearl

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•A ‘hot  nose’  may be seen on the flow phaseimages and delayed images as a result of

shunting of the blood from the internal to the

external carotid system that supplies the face

and the nose in patients with severe carotid

stenosis, brain death, psychoactive drug use

and use of other drugs that cause nasal

congestion.

What is luxury perfusion?

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What is luxury perfusion?

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•Increased perfusion may be seen in the regionof an infarct after a recent stroke (1 to 10

days) cause by an uncoupling of blood flow

from metabolism and oxygen demand.

How is brain death diagnosed?

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How is brain death diagnosed?

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The diagnosis is primarily by clinical. The patientmust be in deep coma with total absence ofbrainstem reflexes and spontaneous respiration.Reversible causes (drug or hypothermia) must be

excluded; the cause of the dysfunction must bediagnosed (trauma or stroke); and the clinicalfindings of brain death must be present for adefined period of observation (6 to 24 hours).

Confirmatory EEG and radionuclide must be usedto increased diagnostic certainty, but thediagnosis is primarily clinical. The radionuclidestudy is more specific than EEG.

Which radiopharmaceuticals are used

to evaluate brain death and what are

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the advantages of each?

Which radiopharmaceuticals are used

to evaluate brain death and what are

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the advantages of each?• Tc-99m flow agents such as DTPA are inexpensive.

The 60 second flow study can be interpreted at

the bed side. Because Tc-99m HMPAO and Tc-99m ECD fixes in the cortex, delayed static images

can be obtained and interpreted for diagnosis.

The clinician is not dependent on a flow study,which demand a good bolus and good timing

with proper computer acquisition. However it is

more expensive.

What is the difference in mechanism

of uptake between F-18 FDG and Tc-

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99m cerebral perfusion imaging

What is the difference in mechanism

of uptake between F-18 FDG and Tc-

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99m cerebral perfusion imaging

• F-18 FDG is a glucose analog and its uptake

represent regional glucose metabolism. It’s metabolically trapped intracellularly.

• Tc-99m HMPAO and Tc-99m ECD are lipid

soluble cerebral perfusion agents taken up inproportion to regional cerebral blood flow.

They fixed intracellularly.

How can SPECT brain perfusion or PETFDG imaging can be useful in the

differential diagnosis of dementia?

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differential diagnosis of dementia?

How can SPECT brain perfusion or PETFDG imaging can be useful in the

differential diagnosis of dementia?

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differential diagnosis of dementia?

• Multiinfarct dementia is characterized by multipleareas of past infarct, recognized as areas of decreaseduptake that correspond to the vascular distributions.

• Alzheimer’s  disease exhibits characteristic pattern ofbitemporal and parietal hypoperfusion andhypometabolism.

• Pick’s disease is associated with decreased frontal lobeuptake.

• AISS dementia complex is associated with a pattern ofmultifocal or patchy cortical regions of decreaseduptake seen particularly in the frontal, temporal andparietal lobes and the basal ganglia

What is the purpose of cerebralperfusion imaging in patients with

i d h t i th t d PET

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seizure and what is the expected PET

or SPECT pattern?

What is the purpose of cerebralperfusion imaging in patients with

i d h t i th t d PET

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seizure and what is the expected PET

or SPECT pattern?

• PET F-18 FDG and SPECT cerebral perfusionstudies can often localize the seizure focus inpatients requiring surgery (typically temporallobectomy) for seizure control.

• Interictally, a seizure focus shows decreased

metabolism (FDG) on PET and decreasedperfusion on SPECT.

• Ictally there is increased activity is seen during aseizure.

Which radiopharmaceuticals havebeen found useful in imaging brain

tumors and what is their clinical

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tumors and what is their clinical

utility?

What is the purpose of cerebralperfusion imaging in patients with

seizure and what is the expected PET

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seizure and what is the expected PET

or SPECT pattern?

• F-18 FDG imaging demonstrates increased uptakein tumors owing to increased glycolysis. Uptake of

FDG is proportional to the malignant grade ofglioblastomas.

• SPECT with Tl-201 and Tc-99m sestamibi can beused in similar manner. Both Tl-201 and PET can

differentiate lymphoma from infection, mostoften toxoplasmosis in AIDS patients.

• Uptake of Tl-201 or FDG is indicative oflymphoma.

Name the radiopharmaceutical usedfor cysternography and the most

common clinical indication in this

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common clinical indication in this

study

Name the radiopharmaceutical usedfor cysternography and the most

common clinical indication in this

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common clinical indication in this

study

• In-111 DTPA. The most common use of this

radiopharmaceutical in modern practice is toconfirm the diagnosis of normal pressure

hydrocephalus (NPH). The next common use is

for (CSF) leaks.

What is the pattern of NPH oncysternography?

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What is the pattern of NPH oncysternography?

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• Persistent ventricular filling and evidence of

convexity block.

• The symptoms of NPH are incontinence,

dementia and gait disturbance.

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Primary brain tumor

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1. Low grade gliomas typically have poor or nouptake

2. Intense uptake in the large temporoparietalmass

3. Transformation of a low grade to a high gradeglioma

4. No. malignant tumors usually do not have

receptor for binding of RP, which is necessarybefore intracellular incorporation

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Brain death

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1. Flat EEG :hypothermia/ barbiturates/ depressivedrugs

2. Deep coma/ no spontaneous breathing/ no

brain stem reflex

3. Tc-99m DTPA/ Tc-99m pertechnetate or Tc-99m

HMPAO/ Tc-99m ECD

4. Tc-99m DTPA – no blood flow to cerebral cortex,

Tc-99m HMPAO  –  shows salivary gland/ normalbrain perfusion – cerebral cortical activity seen

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Cerebral infarct

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1. F18- FDG is dependent on glucose metabolism2. SPECT Tc-99m HMPAO/ ECD are cerebral

perfusion agents that are lipid soluble, distribute

according to blood flow (gray to white matter

ratio, 3:1 to 4:1) and fix intracellularly

3. Wedge shape severe decreased metabolism in

the left posterior parietal region

4. Cerebral hemorrhage/ infarct/ neoplasm

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Seizure disorder

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1. Decreased metabolism in the left temporal lobe.2. Temporal lobe infarct, benign mass or lower

grade tumor, post RT changes, interictal left

temporal lobe seizure focus.

3. Interictal left temporal lobe seizure focus.

4. Conformation of the location of the seizure

focus in a candidate for temporal lobe

lobectomy. Study is an alternative to surgicaldepth electrode placement.

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Alzheimer’s disease 

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1. Multiinfarct, Alzheimer's disease, AID’s  related,substance abuse, alcoholism, Parkinson’s disease, Prick’s,  Creutzfeldt-Jacob disease,depression, metabolic.

2. Diagnostic pattern using Tc-99m HMPAO, ECD orFDG PET: multiinfarct dementia or Alzheimer’s.

3. Hypometabolism (decreased FDG uptake) of theposterior parietal and temporal lobes bilaterally

and to a lesser extent the frontal lobes.4. Alzheimer’s disease > 80%

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Prick’s disease 

1 Alzheimer’s disease multiinfarct late stage

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1. Alzheimer s  disease, multiinfarct, late stageParkinson’s disease, metabolic, drug related anddepression.

2. The lipophilic Tc-99m HMPAO or ECD, cross theintact BBB and have rapid intracellular uptake inproportion to cerebral blood flow. They are fixedintracellularly. Subsequent imaging provide asnapshot of the blood flow pattern at the timeof injection.

3. Alzheimer’s, multiinfarct or Prick’s disease4. Decreased blood flow in the frontal cortex

bilaterally as a result of frontal lobe dementia.

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Herpes Encephalitis

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1. Increased uptake in the temporal lobe2. Increased blood flow in this region

3. Seizure focus (ictal injection), infection or

tumor4. Herpes encephalitis

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Normal pressure hydrocephalus

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1. In-111 DTPA administered intrathecally bylumbar puncture

2. Ventricular reflux and convexity block with no

flow over the cerebral hemispheres abovethe sylvian fissure

3. Communicating hydrocephalus, in this case is

normal pressure hydrocephalus

4. Triad of dementia, ataxia and incontinence

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Huntington’s disease 

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1. Hypometabolism of the basal ganglion2. Progressive motor abnormalities of

involuntary choreiform movements and

akinetic rigidity with progressive cognitivedeteriotion

3. Neuronal degeneration in the striatum, with

the caudate more involved than the putamen

4. Huntington’s disease

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CSF leak

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1. In-111 or Tc-99m DTPA2. Intrathecal injection

3. Activity in the region of the nose, indicating

CSF leak, probably at the cribriform plate4. Anterior views. With the use of nasal

pledgets placed in the superior, middle and

inferior nasal turbinates

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Thyroid

Pearls & Pitfalls

• A normal 24-hour iodine

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Thyroid

uptake in most lab rangesbetween 10% and 30% to 35%.

• Common indications for

radionuclide thyroid imaging

are to differentiate between

various types of hyperfunction

(Grave’s disease, toxic MNG or

autonomous adenoma) and toassess nodularity (cold or hot)

and ectopic tissue.

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Pearls & Pitfalls• A thyroid gland with an

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Thyroid

organification defect is usuallyseen as a normal gland on a Tc-

99m pertechnetate scan but

manifests no activity on an

iodine scan in a child with ahigh TSH level.

• A large gland with intense

homogenous activity is usuallyGrave’s disease.

Pearls & Pitfalls• A large gland with patchy

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Thyroid

activity is usually a MNG butcould also be chronic

thyroiditis or an infiltrative

process.

• Most hot nodules are benign

hyperfunctioning adenomas.

They can be single or multiple

and can suppress the normalportions of the glands.

Pearls & Pitfalls• Subacute thyroiditis classically

presents with a markedly

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Thyroid

p y

depressed radioiodine uptakeand nonvisualization of thegland in a patient with

thyrotoxicosis and a tender,swollen thyroid.

• Chronic thyroiditis can mimicnumerous thyroid conditions

but on imaging is usuallypatchy and decreased inactivity.

Pearls & Pitfalls• Thyroid cancer is usually a

single focal cold lesion and

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Thyroid

single focal cold lesion and

only rarely is seen to be diffuse

or multifocal on thyroid scan.

• Thyroid cancer can concentrate

Tc-99m sestamibi and persist

on delayed images. They are

typically cold on Tc-99m

pertechnetate scans.

Pearls & Pitfalls• Activity in the bladder,

stomach and bowel and diffuse

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Thyroid

stomach and bowel and diffuse

activity in the liver is usually

normal on a WBS of I-131.

• After successful RAI ablation of

residual thyroid tissue, serum

Tg are sensitive to detect

recurrent thyroid cancer.

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Thyroid

function

Increased

thyroid

uptake

Normal

thyroid

uptake

Decreased thyroid

uptake

Thyrotoxicosis Grave’s disease  Antithyroid drugs

PTU/CBZ

Expended iodide pool

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Thyrotoxic phase ofsubacute thyroiditis

Hashitoxicosis Thyrotoxicosis factitia

Antithyroid drugs

Struma ovarii

Euthyroid Rebound after

antithyroid drug

withdrawal

Recovery from

subacute

thyroiditis

Hypothyroid Hashimoto’sdisease Hashimoto’sdisease after RAI

therapy

Hypothyroidism:primary/secondary

Subacute

thyroiditis

 

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The following may cause a solitary cold nodule

in thyroid sca

  Thyroid adenoma

h d d

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Solitary cold

nodule inthyroid scan

Parathyroid adenomaLymphoma

TB

Colloid cyst

Metastatic carcinoma

Primary thyroidcarcinoma

ld

Percentage to become thyroid carcinoma

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Nodules

Cold 15 – 20%

Indeterminate 15 – 20%

MNG 5%

Hot <1%

20% malignant = trapping but not organified

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Discordantnodule

(thyroid

adenoma)

Hot nodule of Tc-99m

Cold nodule of I-131

Small amount of functioning thyroid tissue

with intact trapping and organified

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Reverse discordant

nodule(thyroid adenoma/

Hashimoto’s

thyroiditis/

thyroglassal duct)

Cold nodule of Tc-99m

Hot nodule of I-131

 

O l’ i

Photopenic area in center of

functioning autonomous thyroid

d l ti d ti ithi

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Owl’s eye sign  nodule = cystic degeneration within

solitary functioning thyroid nodule

Fish eye sign

Central core of functioning tissue

surrounded by a rim of decreased

uptake = functioning adenoma with

cystic degeneration at periphery

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Causes of

hyperthyroidism

Grave’s Disease 

Toxic multinodular Goitre

Toxic adenoma

Antithyroid drugs

Surgery

Radioiodine

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Toxic adenoma

Thyroiditis

• Hashimoto’s 

 Subacute (De Quervain’s) • Silent (post partum)

Factitious

Iodine and iodine-

containing drugs agentsDrugs - amiodarone 

Trophoblastic disease

Radioiodine

Self limiting

Symptomatic

Treatment of causes

Treatment Choices 

Antithyroid drugs (thionamides)

• inhibit thyroxine production

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• inhibit thyroxine production • immunomodulation 

Surgery• reduce thyroid bulk to decrease thyroxineproduction

Radioiodine• same principle as surgery 

Physical Characteristics of 131Iodine

•reactor produced

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reactor produced• T ½ 8.02 days

• ßeta and gamma emitter

•ßeta - 606 keV max, 191 keV mean

• Beta-particle emission tissue range – 0.8mm (local therapeutic effect)

gamma - 364 & 637 keV• Clinical Form : Sodium Iodide

131I concentrated by the cellsAdministration of oral

Sodium iodide

Physiological Basis of Radioiodine Treatment

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Reduce thyroid mass/size

Decreased thyroxine

production

High local radiation (beta

particle emissions)

cytotoxic effect

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Contraindications

• Pregnant women

a cross the placenta – accumulate in the

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a. cross the placenta   accumulate in the

fetal thyroid gland – severe neonatal

hypothyroidism

b. irradiation –  risk of thyroid cancerc. retained activity in maternal bladder – direct

exposure to the fetus

• Lactating mother

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Patient’s Preparation 

• No solid foods or drink dairy products for at least two

hours before and after treatment.

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• Low iodine diets for about 3 - 7 days

• GD patients should be counseled regarding the risks of

ophthalmopathy.

• Render patients euthyroid before treatment with 131I

or thyroidectomy.

- older patients (> 50 –60 years old)

- very thyrotoxic patients (symptomatic)

- patients with cardiac problems.

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Patient’s Preparation 

• Follow drug interactions notes

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• Antithyroid drugs - resumed 3 to 10 daysfollowing

treatment, or earlier, if clinically necessary

• Beta blockers medications - to reduce symptoms

which may occur during treatment:

propranolol, 80 –160 mg/day, oratenolol, 50 –150 mg/day, or

diltiazem 30 – 180mg/day (bronchospasm)

Doses

Two common approaches:

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1. Fixed Dose

2. Calculated Dose - based on the size of the

thyroid & percentage uptake at 24 h.

• Although treatments based on dose calculations

Doses

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 Although treatments based on dose calculations

appear efficacious, they have not proven superior to

the use of empirically selected administered

activities.

• Fixed dose advantages – simple & successful

outcome in an acceptable number of patients.

Initial Therapy

Grave’s

Disease

Subacute

Thyroiditis

Toxic adenoma

(Plummer Disease) 

Hyperfunctioning

Multinodular

Goiter

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Β-block

Antithyroid

Β-block

Steroids until

resolution of

symptoms

Β-block

Antithyroid

Β-block

Antithyroid

Grave’s Disease 

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Β-blockers

Carbimazole or PTU

Modulate therapy

until normalization

of TSH, FT3, FT4

(18 – 24 months)

Withdrawal of Β-blocker

Progressively reduce

Carbimazole or PTU

Check TSH, FT4, FT3

Every 3 month

Grave’s Disease - 1° relapse

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Β-blockers

Carbimazole or PTU

• Inform the pt on alternative

advantages and limitations of13I I therapy and surgery

• Needs of substitutive Tx in

both cases

• Pt’s age and gender • Size of goiter

• Tracheal compression

• Narcosis risks

• Complications of thyroid surgery

Fixed dose

• Vary but are commonly in the range of

185–555 MBq (5–15 mCi)

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185  555 MBq (5  15 mCi)

• Depending on the size of the gland

Calculation of Administered Activities for Treatment of Benign Thyroid

Diseases

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Use the following equation to correct for 24-hour RAI

uptake in target thyroid tissue:

Administered activity = Thyroid tissue mass (g) x Activity per g

tissue/RAI uptake at 24 hours

with RAI uptake expressed as a fraction of 100% uptake.

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Toxic adenoma

(Plummer

Disease) 

Hyperfunctioning

Multinodular

Goiter

Long Term Therapy

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131I THERAPY vs. SURGERY

• Pt’s age and gender 

• Size of goiter

• Tracheal compression

• Narcosis risks

• Complications of thyroid surgery

Toxic Nodular Goitre

• Definitive treatment is more commonly accomplishedwith RAI or surgery

• > RAI resistant than GD

• Large doses

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Large doses

• Standardized administered activities:

740 – 1110 Mbq (20 - 30 mCi)

• Administered less than 370 MBq (10mCi)

 – common Tx failure

(Estour B, Millot L, Vergely N, et al. Efficacy of low doses of radioiodine in the treatment of autonomous

thyroid nodules: importance of dose/area ratio. Thyroid 1997; 7(3):357 –361.)

• Large solitary nodules – percutaneous ethanol injection. (Del Prete S, Caraglia M, Russo D, et al. Percutaneous ethanol injection efficacy in the treatmentof large symptomatic thyroid cystic nodules: ten-year follow-up of a large series. Thyroid 2002;12(9):815 –821.)

Total thyroidectomy for clinically benign disease ofthe thyroid gland

Incidence of:

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Incidence of:

• temporary recurrent laryngeal nerve palsy 2.3%

• temporary hypoparathyroidism 14.4%

• Permanent recurrent laryngeal nerve palsy 1.1%• permanent hypoparathyroidism 2.4%

• Neither the initial clinical diagnosis nor a history of previous

treatment significantly influenced the rate of complications.

Bron LP, O'Brien CJ. Br J Surg. 2004 May;91(5):569-74.

Euthyroid Multinodular Goitre

• Surgery – first-line treatment esp. for enlarged goiter

• Preferable for patients > 65 years old

• > 90% of patients demonstrate a decrease in goiter size

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- Average reduction of 40% at 1 year .(Freitas JE. Therapeutic options in the management of toxic and nontoxicnodular goiter.

Semin Nucl Med 2000; 30(2):88 –97. )

• A small percentage may developed transient

hyperthyroidism

• Approximately 4% developed autoimmune thyroiddisease.(Huysmans AK, Hermus RM, Edelbroek MA, et al. Autoimmune hyperthyroidism occurring late after radioiodinetreatment for volume reduction of large multinodular goiters. Thyroid 1997; 7(4):535 –539.)

• RAI > effective than L-thyroxine suppression for reducingthe size of nontoxic goitre

Goals and outcomes• 80% response rate should be expected.

• Primary goal of treatment is to resolve

hyperthyroidism

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hyperthyroidism

• Hypothyroidism is preferable to persistent

hyperthyroidism - if not optimally treated, may

produce significant morbidity.• Hypothyroidism tends to occur more frequently

in patients with small thyroid glands & lower 24-

hour uptake measurements• Significantly reduce thyroid gland size in patients

with GD - 50% to 80% reduction in gland volume

Outcomes

• Euthyroid

• Hypothyroid

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Hypothyroid

 – transient

 – permanent early

late

• Hyperthyroid

Side Effects

Generally it is mild, infrequent and self-limiting.

GeneralTh id t d

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• Thyroid tenderness

• Salivary gland swelling

• Nausea

• Vocal cord paresis – extremely rare

Hormonal related

• Transient hypothyroidism, permanent hypothyroidism

• Transient hypoparathyroidism

• Exacerbation of hyperthyroidism – Beta blockers

• Thyroid storm is uncommon

NSAIDs

Side EffectsSevere side effects > likely in patient with large goitre – risk of

tracheal compression.

Ophthalmopathy

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p p y• Ophthalmopathy may be particularly severe in 3%

to 5% of patients with GD.

• Progression of ophthalmopathy - approximately

15% of patients especially:

- who smoke

- have pre-existing eye disease

- high levels of TSH-receptor antibody- severe manifestations of thyroid disease

Side Effects

• Prednisone, 0.4 –0.5 mg/kg per day,

beginning immediately after radioiodined f h

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g g ytreatment, continued for one month,and then tapered over three months,has been shown to be effective in arandomized controlled trial.(Bartalena L, Marcocci C, Bogazzi F, et al. Relation between therapy for hyperthyroidism andthe course of Graves’ ophthalmopathy. N Engl J Med 1998; 338(2):73–78. )

• Referral to Ophthalmologist isrecommended.

Side EffectsCancer Risk

• remains controversial

• Ron et al, a study of >35,000 hyperthyroidi f d h h i id f

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, y , yp ypatients found that the incidence ofthyroid cancer in RAI-treated patients overa 27-year period was not significantly

different from its incidence in the generalpopulation.

Genetic Effects to Offspring

• no evidence that exposure to radioiodineaffects the long-term outcomes ofsubsequent pregnancies and offspring.

Patient’s Instruction & Precautions • First 72 hours after treatment:

• Drink plenty of fluids.

Do not spend prolonged periods of time closer than 3 feet to anyadult or within the same room as any child

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adult, or within the same room as any child.

• For the next 4 –7 days:

• Void as often as possible. Flush toilet twice after use.

• Wash hands thoroughly and routinely.• Do not share eating utensils or towels. Wash utensils or clothing

separately.

• Avoid close contact with children and pregnant women (not

closer than 2 feet) for long periods of time.• Sleep in a separate bed.

• Avoid kissing and sexual intercourse.

Follow up

• To assess the need for

- further 131Iodine treatment

- L-thyroxine replacement

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y p

• Symptoms of uncontrolled hyperthyroidism

should be described, and patients should beinformed to seek medical attention if suchsymptoms occur.

4 to 6 weeks and at regular intervalsthereafter.

Children with hyperthyroidism

• Incidence of side effects from antithyroid

medications is higher & less consistent in taking themedications remission rates are lower

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medications remission rates are lower.

• Surgery - may have the highest cure rates butthyroidectomy is technically more difficult in young

children.• Several authorities have promoted the

administration of 131I earlier in the management ofpediatric patients and even as the primarytreatment.

• Children as young as 3 year old can be treated.

 

Chronic Renal Failure and DialysisPatients

• Holst et al. reviewed the medical literature

and concluded that:

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and concluded that:

131

I dose does not need to be adjusted.However, recommended 131I administration

as soon as possible after dialysis and a

delay in subsequent dialysis until the

maximum 131I uptake has occurred in the

thyroid.

 

Temperature

37.2-37.6 5

37.7-38.2 10

38.3-38.7 15

38.8-39.3 20

39.4-39.9 25

>40 30

CNS

Mild agitation 10

Moderate delirium/psychosis 20

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Seizure/coma 30

GI/liver dysfunctionDiarrhea/vomiting/abd pain 10

Unexplained jaundice 20

Cardiovascular dysfunction

99-109 5

110-119 10

120-129 15

130-139 20

>140 25

Heart failure

Pedal edema 5

Bibasilar rates 10

APO 15

AF 20

Precipitant historynegative 0

positive 10

Score >45 suggestive of thyroid storm, 25 – 44 supports the diagnosis and < 25 unlikely thyroid storm

Molecular genetic of thyroid

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Molecular genetic of thyroid

carcinoma

Introduction

• Thyroid cancer- most common malignant

tu of endocrine system & accounts for 1%of all newly diagnosed cancer cases.

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of all newly diagnosed cancer cases.

• Most thyroid cancers originate fromthyroid follicular cells .

• Type of thyroid malignancy :

• papillary ca 80%,

• follicular ca 15% may be of conventionalor oncocytic (Hurthle cell) type.[4] 

• Follicular ca develop either from pre-existing benign follicular adenomas ordirectly, bypassing the stage of adenoma.

2%

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Schematic representation of thyroid ca origin and its putative progression. Oncocytic adenoma

and ca are considered to be variants of follicular adenoma and ca. Papillary ca may be of the

classical type or manifests as one of its variants, including oncocytic variant of papillary ca

3%

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Papillary Ca• Activating mutations of BRAF, RET or RAS genes

seen in 70% papillary ca.

• Genes mutations rarely overlap in the same

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y p

tumor, suggesting that activation MAPK signaling

is essential for tumor initiation

• Alteration of a single effector of the pathway is

sufficient for cell transformation

 

BRAF

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Mol p/way in thyroid papillary ca & typical microscopy & clin feat of tu assoc with specific

mutations

BRAF mutation• Involve nucleotide 1799 and result in a val-to-glut

substitution at residue 600 (V600E).

• Other mech include K601E point mut, small in-

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frame insertions or del surrounding codon 600,[14 –

16] & AKAP9-BRAF rear which is more common in

papillary ca a/w radiation exposure.[17] 

With BRAF mutation…. 

• Extrathyroidal extension , advanced tu stage

@ presentation, tu recurrences & lymph nodedi t t t

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or distant mets.

• BRAF V600E is independent predictor of tu

recurrence even in stage 1-2.• Decreased ability of tu to trap radioiodine &

dysregulation of function of Na iodidesymporter ( NIS) & other genes metabolizing

iodides in follicular cells

BRAF mut as therapeutic target….. 

• BRAF inhibitors like BAY 43-9006, a multikinase

inhibitor with potent activity against RAF & otherprotein kinases.

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protein kinases.

• BAY 43-9006 effectively blocks the wild-typeBRAF and the mutant V600E BRAF kinase

activity.[13,31]

 • Sudies showed that BAY 43-9006 inhibit BRAF

signaling and growth of all thyroid cancer celllines carrying mutant BRAF   and it impair the

growth of the cell line xenografts in nude mice.[32]

 

RET/PTC rear in papillary thyroid ca

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RET/PTC• Fusion between the 3´-portion of the RET  

receptor tyrosine kinase gene and the 5´-portion

of various genes.

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• Two most common rear types, RET/PTC1  and

RET/PTC3, are paracentric inversions, because

both RET  and its respective fusion partner, H4 orNCOA4 (ELE1), reside on the long arm of

chromosome 10.[36 –39] 

 

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RET/PTC 1

Two most common rear types RET/PTC 1 & RET/PTC 2 areparacentric inversions bcoz both RET & its respective fusion

patner, H4 or NCOA4(ELE1), reside on the long arm of chr 10

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RET/PTC 3

 

RET/PTC 3

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RET/PTC

• Most of these rare RET/PTC   seen in papillary

ca fr pts with a h/o environmental or[40

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therapeutic exposure to ionizing radiation,[40 –

46] & in children & young adult.

• In papillary ca assoc/w exposure to ionizingradiation (i.e. post Chernobyl), RET/PTC1 a/w

classic papillary histology, RET/PTC3 more

common in solid variant

RET/PTC 2 t(10;17)(q11.2;q23)

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RET/PTC2 and nine more recently identified types of

RET/PTC  are all interchromosomal translocations

 

RET/PTC 2 t(10;17)(q11.2;q23)

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RET/PTC 5 t(10;14)(q11.2q32)

 

RET/PTC 5 t(10;14)(q11.2q32)

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RET/PTC 6 –

 t(7;10)(q32;q11.2)

 

RET/PTC 6  – t(7;10)(q32;q11.2

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RET/PTC 7 –

 t(1;10)(p13;q11.2)

 

RET/PTC 7  – t(1;10)(p13;q11.2

 

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RET/PTC 8 –

 t(10;14)(q11.2;q22.1)

 

RET/PTC 8 t(10;14)(q11.2q22.1)

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RET/PTC 9 –

 t(10;18)(q11.2;q21)

 

RET/PTC 9  – t(10;18)(q11.2;q21)

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PCM 1/ RET  – t(8;10)(p21;q11.2)

 

PCM 1/ RET  – t(8;10)(p21;q11.2)

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RFP/RET –

 t(6;10)(p21;q11.2)

 

RFP/RET  – t(6;10)(p21;q11.2)

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RET/PTC

• ELKS-RET  and HOOK3-RET  fusions identified in

papillary ca with no apparent h/o of radiationexposure [47 48]

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exposure.[47,48] 

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ELKS/RET - t(10;12)(q11.2;p13.3)

 

ELKS/RET - t(10;12)(q11.2;p13.3

 

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HOOK3/RET –

 t(8;10)(p11.21;q11.2)

 

HOOK3/RET  – t(8;10)(p11.21;q11.2)

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• All fusions leave the tyrosine kinase domain of

the RET receptor intact and enable theRET/PTC oncoprotein to bind SHC and activate[ ]

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the RAS-RAF-MAPK cascade.[49] 

RET/PTC mut as therapeutic target…. • ZD6474, orally active low m.w receptor kinase

inhibits VEGVR-2 & blocks RET tyrosine

kinase.• ZD6474 block phosphorylation and signalling

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p p y g g

from RET/PTC3 in vitro, induce growth arrest

of human papillary ca cell lines carryingRET/PTC1 and prevent growth of RET/PTC3-

transformed fibroblasts in nude mice.[64,65] 

RET/PTC mut as therapeutic target…….. 

• SU 12248 (multikinase inhibitor - sunitinib)

effectively inhibit signalling from RET/PTCkinase in the experimental models and has

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kinase in the experimental models and has

been tested in Phase II clinical trial in

radioiodine-refractory, unresectabledifferentiated thyroid cancer.[66] 

RAS• RAS  genes (HRAS, KRAS  and NRAS) encode G-proteins

important in the intracellular transduction of signals arisingfrom cell membrane receptors.

• In its inactive state, RAS protein is bound to GDP.

• Upon activation it releases GDP and binds GTP activating

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Upon activation, it releases GDP and binds GTP, activatingMAPK and PI3K/AKT.

• Normally, the activated RAS-GTP protein becomesquickly inactive due to its intrinsic GTPase activity andthe action of cytoplasmic GTPase-activating proteins.

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• Point mut in the discrete domains of the RAS 

gene either increase its affinity for GTP (mut incodons 12 and 13) or inactivate its

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autocatalytic GTPase function (mut in codon61).

• As a result, the mutant protein becomespermanently switched in the active positionand continuously activates its downstream

targets

Follicular Ca & Adenoma

• RAS

• PAX8-PPAR

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• PIK3CA

• PTEN

 

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Mol p/way in follicular thyroid ca

Foll Ca & Adenoma - RAS• Mutations found in 40 to 50% conventional

foll ca & in 20 to 40% adenomas.

Hotspots – NRAS codon 61 & HRAS codon 61.• Mutations seen in 15 to 25% oncocytic cell ca.

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y

• Mut correlates with tu dedifferentiation &

metastasis

Foll Ca & Adenoma - PAX8-PPARy• Due to t(2,3)(q13;p25)

• Leads to fusion of PAX8 & PPARy genes.

• 35% of conventional foll ca & lower in hurtlecell ca.

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• A/w younger age, smaller size, solid/nested

growth pattern & vas invasion• If seen in adenoma –  ? Insitu (preinvasive foll

ca, ?invasion overlooked in histo)

Foll Ca & Adenoma – other mut

• P13K/AKT pathway mut seen in 6-13% foll ca

& 0-6% of foll adenoma

In exons 20 & 9 of PIK3CA genes.•  LOH in regions harboring different tu supp

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genes..

Del of 2p, 3p, 9q,10q,11p,15q & 17p.• LOH assoc/w aggressiveness & recurrences

Oncocytic Ca• LOH on chr 3q,18q,1p,2p,8q,14q

• Mut of GRIM-19 in 15% oncocytic ca

• GRIM-19 encodes a protein linked to retinoid-interferon-induced p/way of cell death &

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p y

involved in mitochondrial met.

Poorly diff & Anaplastic Ca

• TP53

• CTNNB1 ( Beta catenin)

RAS

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• RAS

• BRAF

• PIK3Ca

PTEN

Poorly diff Ca & Anaplastic Ca-TP53• Point mut of TP53 are late events

• Most involve exons 5-8 of gene & alter DNA

binding properties

A / l t d ll th & i

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• Assoc/w accelerated cell growth & progressive

This is the neck after removal

of the cancerous lymph nodes

Medullary Thyroid Ca

• RET   is activated by point mutation vs chr rear in

papillary ca.• Germline mutations in specific functional regions of

RET found in almost all pts with familial medullary ca

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RET   found in almost all pts with familial medullary ca.

• MEN 2A & familial medullary ca, mutations are

typically located in the extracellular domain, within thecysteine-rich region.[124] 

• 90% of MEN 2A mutations affect a single codon 634,whereas in familial medullary ca they are more evenly

distributed along the cysteine rich region.[125]

 

In MEN 2B, the majority of germlinemutations occur in codon 918 in the

intracellular tyrosine kinase domain of RET .

This alter the substrate specificity of RETkinase, resulting in phosphorylation of

l i t ll l t i [126]

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unusual intracellular proteins.[126] 

This CT scan shows a thyroid cancer

tu in the throat, encircling,narrowing,

& displacing the windpipe(trachea)

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• RET kinase inhibitors ZD6474 and SU12248

(sunitinib), now in Phase II clinical trials in ptswith familial & sporadic medullary thyroid

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p y y

cancer.[63,66] 

Summary

• FNA dx of thyroid nodules can be improved by

testing for BRAF , RET/PTC  and other mutations.• BRAF , RET/PTC  and RAS mutations correlate with

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, /

specific phenotypical features of papillary ca.

• BRAF   is a reliable diagnostic marker formalignancy and an independent prognostic

marker for tumor recurrence and more

aggressive behaviour of papillary carcinomas.

These are lymph nodes that

received cancer cells fr the

primary ca in the thyroid gld

Summary• PAX8-PPAR γ  & RAS mut correlate with specific

phenotypical feat of follicular ca.

• Limitations…..Papillary ca (~30%),

conventional follicular cas (~20%) & oncocytic

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conventional follicular cas ( 20%) & oncocytic

follicular ca (>50%) do not harbour any of the

known mutations.

Black discoloration of cancerous

lymph nodes.Papillary ca is

sometimes black in color especially

afer having spread to lymph nodes

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In the investigation of hyperthyroidism

A. In Grave’s  disease, uptake of Tc-99m is usuallyuniform

B. If, after 2 years following I-131 treatment for Grave’s disease the patient is still euthyroid, the incidence ofsubsequent development of hypothyroidism is

li ibl

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negligible

C. A normal isotope scan exclude Grave’s diseaseD. Hypothyroidism following I-131 treatment of a

solitary hyperfunctioning nodule is more commonthan in Grave’s disease

E. Low tracer uptake into the thyroid gland may occur inuntreated hyperthyroidism

In the investigation of hyperthyroidism

• TFFFT

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The following are true

A. About 25% of toxic nodules are palpable

B. The scan appearances of Grave’s disease may beconfused with toxic MNG

C. Thallium-201 may be used to demonstratethyroid tissue in which uptake but not metabolic

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thyroid tissue in which uptake but not metabolicactivity has been diminished

D. Almost 10% of patients with Grave’s disease willrelapse following a prolonged course ofantithyroid drugs

E. RAI therapy for thyrotoxicosis is contraindicatedin pregnancy

The following are true

• FTTFT

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Concerning thyroid imaging in

thyroiditis

A. Thyroid uptake usually diffusely decreased inacute(supurative) thyroiditis.

B. Uptake in the early phase of subacute (deQuervian’s)thyroiditis is usually increased

C Scan appearances in Hashimoto’s thyroiditis may

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C. Scan appearances in Hashimoto s thyroiditis maybe difficult to distinguish from Grave’s disease

D. Radiation induced thyroiditis is commonly seenfollowing external radiation therapy

E. RAI uptake in Reidel’s thyroiditis is increased

Concerning thyroid imaging in

thyroiditis

• FFTFF

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In the investigation of solitary thyroid

nodules

A. A single warm nodule is likely to be an adenoma

B. The risk of carcinoma in a hot nodule is 10%C. The risk of carcinoma in a cold nodule is at least

10%

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D. The risk of carcinoma in the dominant nodulewithin MNG is approximately 1%

E. A history of childhood of head and neckirradiation substantially increases the risk of

malignant change in solitary thyroid nodule

In the investigation of solitary thyroid

nodules

• TFTFT

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The following are true

A. The commonest site for ectopic thyroid tissue isthe base of tongue

B. I-123 is superior than Tc-99m in confirming thepresence of a lingual thyroid gland

C Isotopes of Iodine are superior than Tc-99m for

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C. Isotopes of Iodine are superior than Tc 99m forlocalizing retrosternal thyroid tissue

D. Absence of activity below the sternal notchexcludes an intrathoracic goitre

E. Ectopic thyroid tissue may be found in up to 50%

of cases of neonatal hypothyroidism

The following are true

• TTTFT

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Concerning malignancy of the thyroid

gland

A. The majority of tumors are follicular type

B. Most tumors are well differentiatedC. Most thyroid tumors are detected following

demonstration of an area of increased uptake

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prelative to normal thyroid on Tc-99m scan

D. Anaplastic carcinoma never takes up I-131

E. Screening of relatives is mandatory inanaplastic carcinoma

Concerning malignancy of the thyroid

gland

• FTFTF

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The following may cause a solitary cold

nodule in thyroid scan

A. Lymphoma

B. Parathyroid adenomaC. TB

D W ’ l t

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D. Wegner’s granulomatous

E. Metastatic adenocarcinoma

The following may cause a solitary cold

nodule in thyroid scan

• TTTFT

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The following are true

A. The patient with toxic MNG presenting with pressuresymptoms should be treated with RAI first instance

B. Patients receiving I-131 for thyrotoxicosis should takeapproximately 1 week off work following treatment

C. The absolute of thyroid hormones and TSH beforetreatment with RAI is a useful predictor of the

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treatment with RAI is a useful predictor of the

development of hypothyroidism in Grave’s D. A rise of thyroglobulin level following completeablation for thyroid carcinoma is indicative ofrecurrent malignant disease

E. Uptake of RAI into thyroid carcinoma metastases hasprognostic significance

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What is the origin of lingual and

sublingual thyroid tissue?

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What is the origin of lingual and

sublingual thyroid tissue?

• The main thyroid anlage begins as a

downgrowth from the foramen cecum.• Thyroid tissue may be seen anywhere along

the tract of the thyroglassal duct from the

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y g

foramen cecum to the usual location of thegland.

• However with lingual thyroid tissue, there is

usually a failure of normal development andno tissue in the normal location of the thyroid

What is meant by the organification of

iodine?

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What is meant by the organification of

iodine?

• In thyroid metabolism, iodide is oxidized to

iodine and incorporated into tyrosine to formeither monoiodotyrosine or diiodotyrosine.

• A deficiency in peroxidase which catalyzes the

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y p y

reaction, is cause of congenitalhypothyroidism.

What is the difference in mechanism

of thyroid uptake between Tc-99mpertechnetate and radioiodine?

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What is the difference in mechanism

of thyroid uptake between Tc-99mpertechnetate and radioiodine?

Radioiodine is taken up or extracted (trapped)by the thyroid follicular cell and organified,

binding to tyrosine residues on thyroglobulin

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and stored in colloid in the follicle.

• Tc-99m pertechnetate is trapped but not

organified.

Which are common causes of falsely

low thyroid uptake?

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What is the difference between

thyroid scan and thyroid uptake?

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What is the difference between

thyroid scan and thyroid uptake?

• A thyroid uptake is usually a nonimaging study

using gamma detector probe.• Thyroid scan results from gamma camera

imaging.

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How can a thyroid uptake test

differentiate two most common causesof thyrotoxicosis, Grave’s and subacute

thyroiditis?

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How can a thyroid uptake test

differentiate two most common causesof thyrotoxicosis, Grave’s and subacute

thyroiditis?• In the initial phase of subacute thyroiditis, thyroid

hormone are released from the inflamed glandcausing thyrotoxicosis.

D t it it f db k TSH i d

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• Due to pituitary feedback, TSH is suppressed.

• Radioiodine or Tc-99m uptake requires TSHstimulation.

• Thus, the uptake of radioiodine or Tc-99mpertechnetate is low or suppressed.

• With Grave’s  disease, TSH is suppressed,however the gland is autonomous and the uptakeis high.

What is the mechanism of action of

antithyroid drugs PTU and CBZ?

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What is the mechanism of action of

antithyroid drugs PTU and CBZ?

• Both PTU and CBZ are thiourea antithyroid

drugs that block the organification of iodine

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Cold thyroid nodule

1. IV Tc-99m pertechnetate, 140 keV, 6 hours;

oral sodium I-123, 159 keV and 8 hours.2. A single cold nodule has a 15% to 20%

chance of malignancy.

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3. FNA4. Pinhole collimator 4 to 6 mm

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Hyperthyroidism/ thyroiditis1. Grave’s  disease, toxic nodules, thyroiditis,

iatrogenic thyroid hormone ingestion, iodine

induced, trophoblastic tumors, Hashitoxicosisand struma ovarii.

2. Aid in the DD of hyperthyroidism

3 A i i b bt i

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3. A nonimaging gamma probe obtainscounts/time from neck and a phantom countingactivity equal to the orally administered dose toconvert to gamma probe counts µCi % RAIU =neck (µCi) divided by the total administered

dose (µCi) after background correction.4. Subacute thyroiditis based on the history of

neck tenderness, laboratory finding and RAIU.

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Grave’s disease 1. Scan appearance may be similar. With the large goiter the

scan often has a plumper appearance with convex

borders. The pyramidal lobe may be seen as in this case.2. Surgery is seldom performed because of the high risk. PTU

and CBZ sometimes are used initially who require coolingdown most of the patients are treated with RAI after 6 to12 months of antithyroid medication. Many patients are

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12 months of antithyroid medication. Many patients are

treated initially with I-131.3. I-131 uptake (10 µCi), I-123 scan and uptake (300 µCi) andGrave’s disease therapy; I-131 (5-15 mCi)

4. Short term; occasional exacerbation of hyperthyroidismand thyroid storm. Long term; hypothyroidism. There is no

increased incidence of secondary cancers or reduction infertility.

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I-131 star artifact

1. A. Post therapy I-131 WBS shows intense uptake

in the neck with a star effect, diffuse liveractivity and bladder clearance. B, Pinhole image

of the neck with three foci of uptake.

2 Septal penetration of high energy of I 131

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2. Septal penetration of high energy of I-131

gamma rays through the collimator septa.

3. Pinhole collimator centered on the thyroid.

4. Radiolabeled thyroid hormone is metabolized in

the liver. This usually seen only on the posttherapy scan.

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Toxic autonomous thyroid nodule

1. Hot nodule in the mid right of the thyroid

with increasing suppression of the remaininggland at each successive year

2. Toxic autonomous thyroid nodule

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3. Surgery and RAI I-1314. The iodine uptake may be moderately

elevated, but it often is in the normal range.

Normal 24 hour uptake is 10 to 30%

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Lingual thyroid

1. Tc-99m pertechnetate is taken up by thyroid

follicular cells like iodine but not organified. I-123 taken up and organified.

2. Lower radiation exposure to the pediatric

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patient.3. Focal uptake at the base of the tongue.

Normal is submandibular glans and mouth.

No thyroid in the neck.4. Lingual thyroid.

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Left thyroid agenesis1. Uniform uptake in the right lobe. No activity

seen at the left lobe or elsewhere in the neck or

upper chest.2. The uniform activity in the right lobe is more

intense than the salivary glands indirectevidence of an elevated uptake in the absence

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evidence of an elevated uptake in the absence

of intrinsic salivary gland disease.3. Surgical excision, replacement by

hypofunctioning adenoma or carcinoma oragenesis of the left lobe with Grave’s disease of

the solitary right lobe.4. Grave’s disease with agenesis of the left lobe.

Gastrointestinal & Hepatobiliary

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Pearls & Pitfalls

Gastric emptyingstudies

• The study usually are performed

the rate of emptying of solids

from stomach, they are most

commonly performed by Tc-99m

colloid mixed with scramble eggs

before they are cooked.

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• Half of the activity of a solid mealshould be out of the stomach in

about 90 minutes.

•Solids leave the stomach in alinear fashion, liquids

exponentially.

Pearls & Pitfalls

Gastrointestinalbleeding studies

• Usually these are performed byTc-99m labeled RBC, but Tc-99msulfur colloid can also be used.

• A focus of bleeding shouldchange shape and location onsequential images. If the activitydoes not move it may represent

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does not move, it may representa vascular abnormality such asaneurysm or intussusception.

Pearls & Pitfalls

Gastrointestinalbleeding studies

• The best way to pinpoint the

bleeding site is to find an

image in which there is adefinite abnormality and then

to look at the earlier images

and find the first image in

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and find the first image in

which the activity can be seen.

This is necessary because

activity seen as a result of

bleeding can go anterograde orretrograde in the bowel.

Pearls & Pitfalls

Gastrointestinalbleeding studies

• Bladder activity from free Tc-

99m pertechnetate can be

confusing and sometimes it isnecessary for the patients to

void or catheterized.

• If bleeding is intermittent use

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• If bleeding is intermittent, use

Tc-99m RBC. If the bleeding is

active, either Tc-99m RBC or

Tc-99m sulfur colloid can be

used.

Pearls & Pitfalls

Gastrointestinalbleeding studies

• False positives:

Free pertechnetate seen at

stomachRenal excretion of breakdown

products

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Penile blood pool,transplanted kidney and

varices.

Pearls & Pitfalls

Gastrointestinalbleeding studies

• False negatives:

Small bowel bleeding

Rectal bleeding obscured bybladder activity

A stationary abnormal focus

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could represent clotted blood

 

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Gastroesophageal reflux : Milk studyPatient preparation Overnight fasting

Radionuclide Tc-99m SC (0.2 – 1 mCi)

Feeding meal The radionuclide is mixed with half of the

meal and fed the child. The second “cold”

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meal and fed the child. The second cold  

half of the meal is then fed to the child.Orange juice for adults and children

Imaging After blurping infant, place supine with

gamma camera and radioactive marker at

the mouth

Acquire delayed image of the chest

 

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Cimetidine

• Histamine H₂ receptor antagonis 

Increases uptake of Tc-99m pertechnitate• Inhibit releasing of gastric mucosa

• Dose 20 mg/kg orally 2 days prior of the study

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Pentagastrin

• Increases rapidity, duration and intensity of Tc-

99m pertechnitate uptake• Increased mucin producing cells

• Increases intestinal motility

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Glucagon

• Antiperistalsis

Decreased bowel peristalsis• Prevent tracer washout from diverticulum

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Tc-99m RBC

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Criteria for

diagnosis of

bleeding site with

Focal activity appears

Activity increases over time

activity movement confirm

to intestinal anatomy

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Tc-99m RBC Movement may beantegrade or retrograde

Tc-99m RBC in vitro

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Tc-99m RBC

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Tc-99m SC

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Tc-99m SC

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Meckel’s Diverticulum 

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Pearls & Pitfalls

Meckel’s diverticulumimaging

• These scan are performed with

Tc-99m pertechnetate which

concentrates in normal and

ectopic gastric mucosa

• Most Meckel’s  diverticula do

not contain ectopic gastric

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mucosa but the ones that

bleed almost always do.

• A Meckel’s  diverticula should

be seen anteriorly, lateral or

oblique.

Pearls & Pitfalls

Meckel’s diverticulumimaging

• Cimetidine can be used to fixthe radiotracer andpentagastrin can increase

uptake in the gastric mucosa,thus increasing the sensitivityof the study.

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Bladder activity from the Tc-99m pertechnetate is normal.The patient may need to voidor be catheterized if there is a

suspicious lesion nearby.

Pearls & Pitfalls

Meckel’s diverticulumimaging

False positives:Confounding urinary system

activity, GI obstruction, tumor

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and inflammation.

Pearls & Pitfalls

Meckel’s diverticulumimaging

• False negatives:Lack of sufficient gastric

mucosa.

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Recent barium study orbladder.

 

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Meckel’s 

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Tc-99m pertechnitate (Meckel’s) 

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Hepatobiliary

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Pearls & Pitfalls

Hepatobiliary

• The most common indications for

hepatobiliary study are to

differentiate between acute or

chronic cholecystitis, to look forsuspected bile leaks or biliary

obstruction and in the setting of

neonatal jaundice to

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neonatal jaundice, todifferentiate neonatal jaundice or

biliary atresia.

• Tc-99m (IDA) agents are cleared

and excreted by hepatocytes but

not conjugated.

Pearls & Pitfalls

Hepatobiliary

• Cardiac blood pool activity

should clear by 5 to 10 minutes.

Lack of clearance indicates poorly

functioning hepatocytes.

• If there is persistent cardiac

blood pool activity and no biliary

excretion the DD includes

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excretion, the DD includeshepatitis and biliary obstruction.

• Renal and bladder activity may

be seen if the liver cannot

efficiently excrete the

radiotracer.

Pearls & Pitfalls

Hepatobiliary

• Bowel activity should be seen by1 hour. Delayed biliary to boweltransit can be result of a number

of entities, including commonduct calculous, tumor, stricture,morphine, sphincter dyskinesiaand chronic cholecystitis.

• For hepatobiliary scans

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For hepatobiliary scansperformed to differentiate biliaryatresia from neonatal hepatitis,delayed 24 hours images to look

for evidence of excretion intobowel are often necessary.

Pearls & Pitfalls

Hepatobiliary

• The normal GB with patent

cystic duct is usually seen by

30 minutes and should always

be seen by 1 hour.

• Nonvisualization of the GB is

most likely the result of acute

or chronic cholecystitis

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or chronic cholecystitis.

• Nonvisualization of the GB at 4

hours or after given morphine

at 1 hour is most likely due toacute cholecystitis.

Pearls & Pitfalls

Hepatobiliary

• Nonvisualization of the GB at 1hour but visualization at 4hours after morphine is most

likely due to chroniccholecystitis.

• Look for either RIM sign or

cystic duct sign of acuteh l titi if th GB i t

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cystic duct sign of acutecholecystitis if the GB is notseen by 1 hour. A RIM signincreases the likelihood of

complicated cholecystitis(gangrene, abscess or rupture)

Pearls & Pitfalls

Hepatobiliary

• Bile leaks often pool in the regionof the porta hepatis, along rightlateral aspect of the liver. If the

GB was recently removed, thebile may pool in the GB fossa andmimic a GB.

• An unequivocally GBEF after CCK

is more than 50% Borderline 35

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is more than 50%. Borderline 35 – 50% and abnormal < 35%.

• A recent meal may cause GBcontraction and result innonvisualisation of GB,simulating acute cholecystitis.

Pearls & Pitfalls

Hepatobiliary

• False positive

Fasting longer than 24 hours

may cause GB distend withviscous bile. CCK can contract

GB,

Severe illness, pancreatitis,

h i h l titi d id

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chronic cholecystitis and rapid

biliary to bowel transit.

Pearls & Pitfalls

Hepatobiliary

• False negatives:

Mistake with duodenum, renal

pelvis and cystic or common

bile duct

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Left hepatic duct

Right hepatic duct

Common hepatic duct

Common bile duct

Cystic duct

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Gallbladder 

Common bile duct

Spincter of oddi

 

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Patient preparation NBM for 4 hours before study

If fasting longer than 24 hours, infuse sincalide

Radiopharmaceutical Tc-99m HIDA/ mebrofenin/ disofenin

IV

Adults bilirubin < 2mg/dl : 5 mCi

2-10 mg/dl : 7.5 mCi

>10 mg/dl : 10 mCi

Children 200 µCi/kg (no less than 1 mCi)

Patient positioning Supine

Instrumentation Collimator: LEGP

Window : 15% 140 keV

Imaging protocol Inject Tc-99m IDA IVAt 60 min, acquire right lateral and left anterior oblique

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If GB not filled and acute cholecystitis suspected, inject IV

morphine sulfate (0.04 mg/kg over 1 min)

Perform delayed imaging 2 to 4 hour if:

1. Morphine sulfate is not administered and GB has not

filled

2. Hepatic insufficient/ suspected biliary leak/ partialcommon duct obstruction

 

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Radiopharmaceutical Mechanism of uptake Indication

Tc-99m sulfur colloid Kupffer cell uptake Focal nodular hyperplasia

Tc-99m HIDA Hepatocyte uptake Cholescintigraphy

Tc-99m RBC Blood pool distribution Cavernous hemangioma

Tc-99m MAA Blood flow & capillary

blockage

Hepatic arterial perfusion

Xe-133 Lipid soluble Focal fatty tumor uptake

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Gallium-67 citrate Lactoferrin transport and

iron binding

Tumor/abscess

F-18 FDG Glucose metabolism tumor

CCK• 33- amino acid polypeptide

• Gallbladder contraction

• Relaxation of sphincter of oddi

• Sincalide = synthetic form of CCK

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Gastrointestinalactions of CCK

Contracts gallbladder

Relaxes sphincter of Oddi

Stimulates intestinal

motilityInhibits gastric emptying

Reduces gastrointestinal

sphincter tone

Stimulates hepatic bile

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secretion

Stimulates pancreatic

enzyme secretion

Morphine sulphate• Constricting sphincter of Oddi

• Increases intraluminal biliary pressure

• IV 0.04 mg/kg when GB not filled by 60

minutes

Should not be given to :1 Poor clearance to the bowel

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1. Poor clearance to the bowel

2. Significant retention of radiotracer in biliary

duct

 

False positive of

Acute

Cholecystitis

Fasting < 4 hour

Fasting > 4 hour

concurrent severe illness

Chronic cholescystitis

hepatic insufficient

hyperalimentation

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Alcoholism/pancreatitis (?)

Drugs a/w poor GB

contraction

Diseases a/w poor GB

contractionMorphine DM

Atropine Sickle cells disease

Nifedipine (CCB) IBS

Indomethacin Pancreatic insufficiency

Progesterone Crohn’s disease

Oral contraception Celiac disease

Octreotide Achalasia

Theophylline Obesity

Benzodiazepine Cirrhosis

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Phentolamine Pregnancy

Dyspeptic syndrome

Truncal vagotomy

Differential diagnosis of Primary

Hepatic tumor with Tc-99m HIDA

Lesion Flow Uptake Clearance

Focal

nodular

hyperplasia

Increased Immediate Delayed

Hepaticd

Normal none -

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adenoma

Hepatocellul

ar carcinoma

Increased Delayed Delayed

 

Causes of FocalLiver Defects

Cyst

Benign and malignant

tumor

Abscess

Hematoma

Laceration

Radiation therapy

Infarctionh

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Cirrhosis

Fatty infiltration

Dilated bile duct

 

Increased focal

uptake in Tc-99m SC

Arm injection

Leg injection

focal nodular hyperplasia

Budd-Chiari syndrome

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Cirrhosis

 

Liver heterogeneity

of Tc-99m SC

Metastases

Lymphoma/leukemia

Hepatitis

Chronic passive congestion

Cirrhosis

Parenchymal liver disease

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y

Fatty metamorphosis

Normal HIDA

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Normal HIDA

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HIDA scan, GB visualized after

morphine

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Acute cholecystitis

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What are two FDA approved IDA in use

and how are they different?

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What are two FDA approved IDA in use

and how are they different?• Tc-99m DISIDA and Tc-99m mebrofenin.

Mebrofenin has better hepatic extraction 98%

and renal excretion is 1 %. The higherextraction of mebrofenin is preferable in

patients with hepatic insufficiency.

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What is the most important Q to ask

the patient before startingcholescintigraphy for suspected acute

cholecystitis?

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What is the most important Q to ask

the patient before startingcholescintigraphy for suspected acute

cholecystitis?• When did you last eat. If the patient has eaten

in the last 4 hours, the GB may be contracted

secondary to endogenous stimulation of CCK

and therefore tracer cannot enter into GB.• If the patient has not eaten > 24 hours the GB

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• If the patient has not eaten > 24 hours, the GB

may not have had the stimulus to contract and

will be full of thick, concentrated bile whichmay prevent tracer entry.

What are 5 indication for CCK

infusion?

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In what clinical settings are false

positive HIDA studies likely to occurwhen performed to rule out acute

cholecystitis.

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In what clinical settings are false

positive HIDA studies likely to occurwhen performed to rule out acute

cholecystitis.

• In patients who have fasted less than 4 hours

or more than 24 hours, patient receiving

hyperalimentation and those who havechronic cholecystitis, hepatic insufficiency or

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y p y

severe illness.

What is the rim sign sometimes seen

with cholescintigraphy and what is itssignificance?

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In what clinical settings are false

positive HIDA studies likely to occurwhen performed to rule out acute

cholecystitis.

• The rim sign is increased uptake and delayed

clearance of activity in the hepatic

parenchyma adjacent to the GB fossa. It hasbeen associated with an increased incidence

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of complications e.g.. perforation and

gangrene.

At what time after HIDA injection is

nonfilling of the GB diagnostic of acutecholecystitis

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At what time after HIDA injection is

nonfilling of the GB diagnostic of acutecholecystitis

• One hour is defined as abnormal. However,

nonfilling of the GB is diagnostic of acute

cholecystitis if delayed images show no filling

by 2 to 4 hours or 30 minutes after morphine

administration.

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What is the mechanism of morphine

augmented cholescintigraphy?

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What is the mechanism of morphine

augmented cholescintigraphy?• Morphine increases tone at the sphincter of

Oddi, resulting in increased intraductal

pressure. This result in bile flow through thecystic duct, if it is patent.

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What is the most common scan finding

in chronic cholecystitis?

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What is the most common scan finding

in chronic cholecystitis?• A normal study. < 5% of patients with chronic

cholecystitis have delayed filling. Other

associated findings include delayed biliary tobowel transit time and rarely nonvisualization

of GB or intraluminal filling defects.

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What is acute acalculous cholecystitis?

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What is acute acalculous cholecystitis?

• Cholecystitis without a stone occluding the

cystic duct. The obstruction may caused by

debris or inflammatory changes or thecholecystitis may be limited to the GB wall

because of infection, ischemia or toxins. It

occurs in hospitalized patients who havesustained trauma, burns, sepsis or other

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sustained trauma, burns, sepsis or other

serious illness.

What are the cholescintigraphic

findings of high grade common ductobstruction?

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What are the cholescintigraphic

findings of high grade common ductobstruction?

Persistent hepatogram with no clearance intobiliary ducts.

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What are the cholescintigraphic

findings of partial common ductobstruction?

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What are the cholescintigraphic

findings of partial common ductobstruction?

• Prominent retention of activity in the common

duct, delayed biliary to bowel clearance and

most important, poor ductal clearance on

delayed imaging or with CCK.

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What is the difference in clinical

presentation and clinical course ofpatients with FNH and hepatic

adenoma

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What is the difference in clinical

presentation and clinical course ofpatients with FNH and hepatic

adenoma

• FNH is asymptomatic and found incidentally,

whereas hepatic adenomas often present with

hemorrhage and can be life threatening.

Adenomas are closely associated with the useof OCP which must be discontinued

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of OCP which must be discontinued.

What are the Tc-99m SC scan findings

in FNH and hepatic adenoma?

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What are the Tc-99m SC scan findings

in FNH and hepatic adenoma?• Hepatic adenomas do not show Tc-99m SC

uptake because they do not usually have

Kupffer cells. FNH is associated with increasedblood flow. Uptake may be increased, normal

or nonexistent. Two thirds of cases of FNH

show some Tc-99m SC uptake.

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What are the characteristic

scintigraphy findings in liverhemangioma?

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What are the characteristic

scintigraphy findings in liverhemangioma?

•Blood flow is normal. Immediate images showa cold defect, whereas delayed images

acquired 1 to 2 hours after tracer

administration show increased uptake withinthe lesion compared with the normal liver,

f l k h l d h

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often equal to uptake in the spleen and heart.

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Beside FNH, what are other causes of

increased focal uptake on Tc-99m SCimaging?

• Superior vena cava syndrome (with arm

injection), inferior vena cava syndrome (withleg injection), Budd-Chiari syndrome and

cirrhosis with a regenerating nodule.

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What is functional asplenia?

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What is functional asplenia?

• Nonvisualization of the spleen on a Tc-99m SC

when the spleen is anatomically present and

when functions other than reticuloendothelialextraction are intact. Functional asplenia is

caused by an acquired dysfunction of the

reticuloendothelial system e.g.. sickle cellanemia or by a disruption of the blood supply

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(splenic artery occlusion).

What is achalasia and how can

radionuclide studies help in makingthe diagnosis and following the

patient’s course? 

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What is achalasia and how can

radionuclide studies help in makingthe diagnosis and following the

patient’s course? 

• Achalasia is characterized by absence ofperistalsis in the distal two thirds of theesophagus, increased lower esophageal sphincter

pressure and incomplete sphincter relaxationafter swallowing. The diagnosis can be confirmedby esophageal manometry Radionuclide

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by esophageal manometry. Radionuclideesophageal transit studies have a high sensitivity

for making the diagnosis and evaluate theeffectiveness of esophageal dilatation.

In regard to reflux and aspiration

studies?A. The milk study is a sensitive method for

diagnosing gastroesophageal reflux.

B. The milk study is a sensitive method for

diagnosing aspiration.

C. Frequent image acquisition improves the

sensitivity of milk study.

D The salivagram is a sensitive method for

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D. The salivagram is a sensitive method for

diagnosing aspiration.

In regard to reflux and aspiration

studies?• TFTT

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Which anatomical portion of the

stomach are responsible for solid

emptying and which for liquid

emptying

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Which anatomical portion of the

stomach are responsible for solid

emptying and which for liquid

emptying

• Liquid emptying is largely caused by the slow

contractions of the proximal fundus whereas

the distal stomach or antrum is responsible for

the grinding and sieving solid food.

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Which of these factors will affect the

rate of gastric emptying?A. Meal content

B. Time of day

C. Gender

D. Position

E. StressF. Exercise

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Which of these factors will affect the

rate of gastric emptying?• TTTTTT

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Regarding gastric emptying studies?

A. Attenuation results in an underestimation ofgastric emptying when performed in the

anterior viewB. A solid gastric emptying time activity curve

shows a rise in activity after ingestion in theanterior view

C. The geometric mean method of attenuationcorrection is considered the reference standard

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D. The left anterior oblique method of attenuationcorrection is superior to the geometric mean.

Regarding gastric emptying studies?

• TTTF

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When might the use of Tc-99m SC

offer advantages over Tc-99m RBCs forthe diagnosis of acute GI bleeding?

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When might the use of Tc-99m SC

offer advantages over Tc-99m RBCs forthe diagnosis of acute GI bleeding?

With very rapid GI bleeding and vascularinstability, the radiotracer can be injected and

the study completed in 15 to 20 minutes. It is

likely to be positive with the rapid

hemorrhage when transfusion cannot keep up

with the bleeding rate The patient can then

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with the bleeding rate. The patient can then

go directly for angiography.

List in increasing order the labeling

efficiency for method to label Tc-99m

RBCs; in vivo, in vitro or in vivtro

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List in increasing order the labeling

efficiency for method to label Tc-99m

RBCs; in vivo, in vitro or in vivtro

• In vivo 75%, in vivtro 85% and in vitro 98%

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Why is the Tc-99m RBC for detecting GI

bleeding more sensitive than the Tc-

99m SC?

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Why is the Tc-99m RBC for detecting GI

bleeding more sensitive than the Tc-

99m SC?

• Delayed images can be performed up to 24

hours with RBC labeling

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What are the criteria needed to

diagnose confidently the site of

bleeding on a radionuclide study?

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What are the criteria needed to

diagnose confidently the site of

bleeding on a radionuclide study?

a. Hot spot appears where there was none and

conforms to bowel activity

b. Activity increases over time

c. Activity moves antegrade and retrograde

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Ectopic mucosa is most often seen

clinically in Meckel’s diverticulum.

What other gastric abnormalities may

contain gastric mucosa?

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Ectopic mucosa is most often seen

clinically in Meckel’s diverticulum.

What other gastric abnormalities may

contain gastric mucosa?

• Duplication of GI tract

• Barrett’s esophagus 

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What is the origin of Meckel’s

diverticulum?

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What is the origin of Meckel’s

diverticulum?• Failure of closure of the omphalomesentric

duct of the embryo, which connects the yolk

sac to the primitive foregut via the umbilicalcord

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Concerning Meckel’s diverticulum 

A. Ectopic gastric mucosa in a Meckel’s diverticulum can be reliably distinguished fromectopic mucosa elsewhere in the small intestine

B. Cimetidine given before the scan to blocks thesecretion of pertechnetate from gastric mucosa

C. Children are more likely to have a positive testthan adults

D. Diverticulitis is a common cause of false positiveresult

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E. A false negative result may be obtained if therehas been a recent barium study

Concerning Meckel’s diverticulum 

• FTTFT

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Concerning GI bleeding studies

A. Hepatic hemangioma is a recognised cause offalse positive Tc-99m RBS study

B. A rejecting transplanted kidney is a recognisedcause of a false positive Tc-99m tin colloid study

C. Anemia is a cause of visualization of the GB inlabeled RBC study

D. Diffuse colonic activity in a labeled RBC studyindicates colonic bleeding

E. When reporting a study. It is not necessary to

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view the dynamic images that provide allinformation

Concerning GI bleeding studies

• TTTFF

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GI bleeding studies

A. Tin colloid studies are better at detecting bleedingsites proximal to the ligament of Treitz than distal to it

B. Delayed images on a tin colloid scan may be of valuein separating liver and spleen activity from bowelactivity

C. In vitro labeling of RBC gives fewer false positive teststhan in vivo

D. Bleeding must be continuous to be detected on alabeled RBC study

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E. 51 Cr-chromate labeled RBC can detect bleedingdown to 1-2 mls per day

GI bleeding studies

• FFTFT

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Concerning cholescintigraphy

A. Failure to visualize the GB by 4 hr with normal activityappearing in the bowel is highly suggestive of GBdisease

B. Chronic Cholecystitis can be distinguished fromacalculous cholecystitis

C. Giving CCK before isotope is more likely todemonstrate the GB than giving morphine

D. Common duct obstruction should be excluded ifvisualization of bowel activity is delayed beyond 1h

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hour

E. GB emphysema has a typical rim sign appearance

Concerning cholescintigraphy

• TFTTT

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Concerning cholescintigraphy

A. Cholescintigraphy has greater specificity thanultrasound at detecting bile duct obstruction

B. Following cholecystectomy, an abnormalaccumulation of HIDA outside biliary tree likelydue to bile leak

C. US is more sensitive than cholescintigraphy atdetecting bile leak

D. Cholescintigraphy can diagnose afferent loopobstruction after gastroenterostomy

i b d d

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E. Ascites can be detected

Concerning cholescintigraphy

• TTFTT

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In pediatric cholescintigraphy

A. Phenobarbitone is used to maximise hepatic oftracer

B. Neonate hepatitis can be distinguished fromRotor syndrome

C. Choledocal cyst can be distinguished frompancreatic cyst

D. Cholescintigraphy is more accurate in diagnosingbiliary atresia in children > 3 months than inneonates

E Dil d i h i d f i

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E. Dilated intrahepatic ducts are often seen inpatients with biliary atresia

In pediatric cholescintigraphy

• TTTFF

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Concerning GI transit studies

A. It is easier to detect abnormalities of gastricemptying for solids than for liquids

B. DM is a common cause of delayed gastricemptying

C. Hyperthyroidism is the commonest of rapidgastric emptying

D. Scleroderma affects esophageal transit throughthe whole esophagus

E. Achalasia has a specific appearance on adi lid h l t it ti

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radionuclide esophageal transit time

Concerning GI transit studies

• TTFFF

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Concerning Milk Studies

A. Reflux is more likely to be detected if the infantis placed prone

B. The longer the test the more sensitive itbecomes

C. Labeled milk studies are better at detectingpost-prandial reflux than 24 hour pH monitoring

D. A normal study excludes significant lungaspiration

E. Reflux detected by scintigraphy is more likely tob i ifi t

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be significant

Concerning Milk Studies

• FTTFF

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3. False positive for Tc-99m RBC

• TTTFF

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6. Tc-99m HIDA

• TTTTF

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8. Sulphur colloid scan

• FFFFT

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9. Colloid shift is seen in

• TTTTF

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12. Focal defect in sulphur colloid scan

is seen in• TTTTT

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What physiologic molecules does Tc-

99m IDA most closely mimic?

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What physiologic molecules does Tc-

99m IDA most closely mimic?• Bilirubin

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What is the main difference between

Tc-99m IDA and bilirubin?

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What is the main difference between

Tc-99m IDA and bilirubin?• Tc-99m IDA is not conjugated

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What level of bilirubin is required to

interfere with the quality of HIDAscan?

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What level of bilirubin is required to

interfere with the quality of HIDAscan?

> than 20 to 30 mg/dl

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How does prior CCK administration

affect the biliary to bowel transit time?

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How does prior CCK administration

affect the biliary to bowel transit time?• CCK delays biliary to bowel transit time

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How can one distinguish acute from

chronic cholecystitis as a cause of non

visualization of the GB at 1 hour ?

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How can one distinguish acute from

chronic cholecystitis as a cause of non

visualization of the GB at 1 hour ?

• Obtain delayed image and perform morphine

augmentation

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What 2 findings on scan increased

likelihood that nonvisualisation of GB

is caused by acute cholecystitis ?

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What 2 findings on scan increased

likelihood that nonvisualisation of GB

is caused by acute cholecystitis ?

1. Hyperemia in GB fossa on early images

2. Rim sign on later images

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What is the prognostic implication of

rim sign in scan?

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What is the prognostic implication of

rim sign in scan?• It is associated with GB gangrene and

perforation

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How does morphine augmented

cholescintigraphy work?

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How does morphine augmented

cholescintigraphy work?• Morphine increases the tone of sphincter of

oddi

• Raising common bile duct pressure• Facilitating GB filling if cystic duct is patent

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How does one perform morphine

augmented cholescintigraphy?

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How does one perform morphine

augmented cholescintigraphy?• If GB does not fill by 60 minutes

• Give 0.04 mg/kg IV morphine

• If GB does not fill by 30 minutes means thepatient has cystic duct obstruction

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What is the major cause of a false

negative scan for acute cholecystitis in

scan ?

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What is the major cause of a false

negative scan for acute cholecystitis in

scan ?

• Acute acalculous cholecystitis

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How does one perform GB ejection

fraction?

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How does one perform GB ejection

fraction?• Administer IV sincilide 0.02 µg/kg

• Normal GB ejection fraction = 35%

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What patient preparation is requires

before scan for biliary atresia?

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Tc-99m colonic bleeding

1. Tc-99m labeled RBCs.

2. A. left colon, rectosigmoid region

3. B. Right colon, hepatic flexure. It movesrapidly to the left colon.

4. RBC scintigraphy, 0.1 mil/min; contrast

angiography 1 ml/min.

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Meckel’s Diverticulum 

1. Meckel’s  can. The radiopharmaceutical is taken up andsecreted by gastric mucosa.

2. Pentagastrin increases rapidity, intensity and duration ofuptake. It is used with glucagon, which is antiparistalticthat inhibits rapid dispersion effect of pentagastrin.Cimetidine, a histamine antagonist, increases andprolonged uptake because of inhibition of Tc-99mpertechnetate secretion from gastric mucosal cells.

3. Increasing focal uptake in the mid abdomen suspicious forMeckel’s diverticulum, however, atypical timing of uptakelessens the certainty. The uptake should be coincidentwith gastric uptake in cases of Meckel’s diverticulum. Thismay be false positive scan.

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4. Acid and pepsin secretion by the gastric mucosa producesinflammation and ulceration of adjacent bowel mucosa.

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Diabetic gastroparesis

1. Consistent with severe diabetic gastroparesis. Obstructioncannot be ruled out.

2. Normal values are meal specific and depend on itsvolume/composition, the method of acquisition,attenuation correction, processing and quantification.Normal values must be determines in each clinic or resultsof a published method should be followed closely.

3. Solid or semisolid gastric emptying meals are moresensitive for detection of mild to moderate delay inemptying than studies conducted after a liquid meal.

4. Activity is detected with greatest efficiency close to thecamera. The anterior view alone underestimates emptyingand posterior view overestimates it because of variable

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attenuation as the meal moves through the stomach fromthe posterior gastric fundus to the more anterior gastricantrum.

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Gastroesophageal reflux

1. Vomiting, pulmonary symptoms, asthma,

pneumonia, sudden death, failure to thrive

and anemia.2. 24 hours pH monitoring.

3. Tc-99m sulfur colloid 1 mCi in the child’s 

usual feeding, formula or milk4. 5 to 10 second/frame.

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Gastrointestinal bleeding

1. Tc-99m labeled RBC study. Abnormal focaluptake appearing simultaneously at two sitesin the right abdomen, increasing in intensityand changing in pattern with time.

2. Caecum and ascending colon.

3. Review images an a computer in cinematic

mode.4. Acute bleeding due to angiodisplasia,

diverticula, neoplasm, IBD and ischemia.

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Axillobifemoral bypass graft

1. Tc-99m labeled RBC or sulfur colloid

2. Evidence of current or recent bleeding

3. Tc-99m RBCs4. The vascular flow and delayed static images

show no active bleeding seen. Labeled RBCsare shown in a tubular shape in the rightabdomen that connects after a Y bifurcationto the two iliac vessels as a result of anaxillobifemoral vascular bypass graft. The

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patient has prominent splenomegaly.

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Free pertechnetate vs gastric bleeding

1. Tc-99m RBC

2. In both studies the stomach visualize

promptly. The chest and neck image showsthyroid and salivary gland uptake in study Abut not in study B

3. A. Free pertechnetate. Negative for

gastrointestinal bleeding. B. Active bleedingoriginating from the stomach

4. In vitro

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Rectal bleeding

1. Abnormal activity accumulate early in the lowermidline pelvis. The appearance is changing overtime and seems to decrease and then increase

again.2. To differentiate activity in the rectum from

bladder and penis, in this patient the activity isseen in the rectum.

3. Positive for gastrointestinal bleeding is not theanswer. Localization is critical. The 90 minutelateral view confirms that this is rectal bleeding.

4. New activity, increases in amount over time and

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moves intraluminally.

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Small bowel bleeding

1. Tc-99m RBCs. The in vitro method of labelingwas used.

2. Evidence of active bleeding, first seen at 5minutes, starting in the left upper abdomenand moving across the mid to lowerabdomen to the right lower and then right

mid abdomen.3. Small bowel bleeding originating from the

region of the jejunum.

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4. Arteriovenous malformation or tumors

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Pulmonary aspiration

1. Recurrent pneumonia, cough, asthma, apnea orsudden infant death.

2. Tc-99m sulfur colloid in a small volume of fluid

placed on the tongue and allowed to mix withoral secretion and swallowed.

3. Poor bolus progression noted in the dynamicesophageal swallow study with entrance into

the main bronchi bilaterally and then into theright lower lobe.

4. The milk study is very sensitive for reflux,however it is insensitive for aspiration. The

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salivagram is sensitive for small amounts ofpulmonary aspiration.

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Choledocal cyst

1. A. Good hepatic uptake and clearance into thegallbladder, common hepatic and proximal commonbile duct at 60 minutes. No biliary to bowel transit. B.the gallbladder contracts with sincalide infusion,however focal increasing accumulation of radiotracer

occurs just medial to the proximal portion of thecommon bile. The proximal common duct activityempties into the duodenum.

2. Likely choledocal cyst. Partial biliary obstruction alsowould cause radiotracer retention within the moreproximal biliary duct.

3. Cholangitis, sepsis, pancreatitis or obstruction.

4. Congenital anomaly. Localize dilatation of the biliarytract, either fusiform or diverticular outpouching.

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, p g

Surgery is the appropriate therapy.

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Chronic acalculous cholecystitis

1. CAC is clinically and pathologically identical to chroniccalculous cholecystitis, except for absence ofgallstone.

2. Anatomical imaging diagnosis depends heavily onvisualization of gallstones. CCK cholescintigraphyallows quantification of gallbladder contraction.Diseased gallbladders do not contract.

3. Findings consistent with chronic acalculouscholecystitis in patient B but not A.

4. A low GBEF has a positive predictive value of morethan 90% that cholecystectomy will cure the patient’s 

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symptoms and that diagnosis will be confirmed bypathological gallbladder examination.

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Post cholecystectomy syndrome

1. Prompt hepatic uptake, clearance into biliary ducts by 15to 30 minutes, retention of activity in ducts, apparentlydilated proximal hepatic and common ducts, biliary tobowel clearance but prominent retention in common duct

with apparent cutoff distally.2. 60 minutes: partial common duct obstruction versus post

biliary duct obstruction surgery with nonobstructedpersistent bile duct dilatation. 120 minutes: suspectedpartial obstruction.

3. Common duct stone, inflammatory stricture of thecommon duct, sphincter of Oddi dysfunction, inflamedcystic duct remnant.

4. Sphincter of Oddi dysfunction is a partial biliaryobstruction at the level of the sphincter of Oddi not

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obstruction at the level of the sphincter of Oddi not

caused by atones or stricture.

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Focal nodular hyperplasia

1. Increased uptake that corresponds to the lesionseen on CT. the uptake is retained after liverwashout.

2. Benign and malignant tumors that havehepatocytes e.g.., hepatic adenoma, hepatomaand FNH. The letter is the correct diagnosis.

3. FNH usually requires no specific therapy. Hepaticadenoma requires discontinuation of oralcontraceptives and surgical removal andhepatoma requires resection.

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4. Tc-99m sulfur colloid.

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Hot spot Tc-99m sulfur colloid imaging

1. Uptake by reticuloendothelial system.

2. 85% by Kupffer cells, 10% by the spleen and

5% by the bone marrow.3. A. the central large cold region may becaused by an intrahepatic mass but thepattern has been stable and CT shows

cirrhosis. B. increased uptake in the region ofthe quadrate lobe, consistent with FNH.

4. Superior vena cava syndrome, inferior vena

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cava obstruction, Budd-Chiari syndrome.

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Cholescintigraphy – normal study

1. No oral intake for 3 to 4 hours before

injection.

2. Tc-99m disofenin or Tc-99m brida.3. Both are iminodiacetic acid analogues,

extracted and excreted by hepatocytes into

biliary system. Mebrofenin has higherhepatocyte extraction (98%)

4. Yes. Acute cholecystitis is ruled out with a

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high degree of certainty.

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Acute cholecystitis

1. A. Abnormal. B. No. C, yes

2. A. Sensitivity 98%, specificity 95%, B greater

than 90%.3. The few direct comparisons published have

shown cholescintigraphy superior to US.

4. Prolonged fasting, hyperalimentation, chroniccholecystitis and hepatic insufficiency.

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Morphine augmented

cholescintigraphy

1. Morphine produces contraction of the sphincterof Oddi, which increases intraluminal commonbile duct pressure. Bile and excreted radiotracer

then preferentially flow through the cystic ductinto the GB if the cystic duct is pattern.

2. Exclude drug allergy. Do not give if evidence ofcommon duct obstruction.

3. The accuracy is at least as good, if not betterthan the delayed imaging method.

4. IV 0.04 mg/kg morphine. Images are acquired

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for an additional 30 minutes.

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Biliary leak

1. Rapid bile leakage probably originating fromthe region of the ligated cystic duct andextending toward the right colonic gutter

with time, over the dome of the liver.

2. Rapid biliary leak.

3. Cystic duct ligature after cholecystectomy,

surgical anastomosis, trauma andinflammatory processes.

4. Confirm that fluid collection seen by

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anatomical imaging modalities are biliary innature.

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Cavernous hemangioma of the liver

1. Tc-99m RBCs

2. Immediate images show no definite

abnormality. Delayed images show increasedfocal uptake in the left lobe consistent with

cavernous hemangioma.

3. At least 2 cm4. Very specific (>99%) for hemangioma. Poor

sensitivity for small lesions.

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Biliary atresia

1. Phenobarbital, 5mg/kg/day for 3 to 5 daysbefore study.

2. Inflammatory, infections and metabolic causes

for neonatal hepatitis and biliary atresia.3. A. delayed blood pool clearance as the result of

hepatic insufficiency. Biliary clearance at 50minutes and increasing through 120 minutes. B.

good liver function. No secretion into biliaryduct during the initial 120 minutes or at 5 and24 hours. Case B consistent with biliary atresia.Case A with neonatal hepatitis.

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4. Sensitivity 97% and specificity 82%.

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RIM sign

1. Increased incidence of false positive in patients whohave been fasting more than 24 hours

2. Nonvisualization of GB after 60 minutes. After

morphine, no filling of the GB occurs. Increaseduptake is seen in the region of the GB fossa, whichpersists after most of the liver has washout (RIM sign)

3. Nonvisualization of the GB after morphine is

consistent with acute cholecystitis. The RIM sigh isvery specific for acute cholecystitis and confirmsdiagnosis.

4. The RIM sign indicates severe acute cholecystitis

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which is associated with an increased incidence of GBgangrene and perforation.

Genitourinary scan

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Pearls & Pitfalls

General

The common indications forradionuclide scan for kidneys

include allergy to iodinated

contrast material, assessment

of possible renal artery

stenosis and differentiation of

obstruction from collecting

system. In children corticalscanning agents are used for

evaluation of pyelonephritis.

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Pearls & Pitfalls

General

Tc-99m DTPA reflects glomerularfiltration, Tc-99m MAG3 isessential a tubular agent.

• Tc-99m DMSA is renal cortical

agent.• Tc-99m glucoheptonate is used

to evaluate both renal corticaland collecting system.

• Maximum parenchymal activity isseen at about 3 to 5 minutes andbladder activity is seen by 4 to 8

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minutes.

Pearls & Pitfalls

General

Half of the renal activity shouldbe cleared in about 8 to 12minutes.

• On a postcaptopril renogram

using Tc-99m MAG3 , the kidneythat has delayed clearance withsignificant renal cortical retentionshould be the one with the renal

artery stenosis.• Bilateral delayed clearance can

be caused by bilateral stenosis,obstruction, renal disease,

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dehydration or hypotension.

Pearls & Pitfalls

General

ATN perfusion is usuallynormal with bilaterally

increased renal cortical activity

and rising renogram curves

when Tc-99m MAG3 is used.

• When faced with abnormal

time activity curves, look at the

images to see if the problem is

parenchymal or related to the

collecting system.

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Pearls & Pitfalls

Renal transplant

Common indication are todifferentiate rejection from

ATN.

ATN is usually seen within thefirst week after

transplantation. It usually has

preserved renal perfusion with

progressive accumulation of

tubular agents (Tc-99m MAG3)

in the renal parenchyma. It

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should improved with time.

Pearls & Pitfalls

Renal transplant

Severe ATN can present withenough edema immediatelyafter surgery to have reducedperfusion and therefore look

similar to acute rejection.• Cyclosporin toxicity can look

like ATN but is usually not seen

in the immediatepostoperative period.

• Rejection usually has poorperfusion and poor tubular

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excretion.

Pearls & Pitfalls

Renal transplant

Look for photopenic defectsaround the transplant on the

blood pool image that may be

caused by urinomas,

hematomas and lymphoceles.

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Pearls & Pitfalls

Testicularimaging

Common indications are todifferentiate between

epididymitis and acute or

delayed torsion.

• The initial problem is to

determine whether blood flow

is increased or decreased.

• The best way to determine

which side is abnormal is to

obtain a patient history.

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Pearls & Pitfalls

Testicularimaging

Epididymitis should bediffusely hot on all images and

frequently focal hot in the

region of the epididymitis.

• Increased flow to one

hemiscrotum and a rim of

testicular activity with a cold

center (halo sign) can be a

delayed torsion but also can be

testicular abscess, hematoma

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or tumor

 

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Glomerular filtration 100 % DTPA

Tubular secretion 100% MAG 3

Tubular secretion 80%Glomerular filtration 20%

HIPPURAN

Cortical binding 40% DMSA

Glomerular filtration 80%

Cortical binding 15%

GLUCOHEPTONATE

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Tc-99m DTPA Tc-99m MAG 3

Glomerular filtration 100% -

Tubular secretion - 100%

Extraction fraction

20% 40 – 50%Target to back ground

ratioPoor Good

Protein bound No Yes

Time for imaging Immediate Immediate

Heating for labeling No Yes

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30 – 60 SECONDS

1-3 MINUTES

COLLECTING

SYSTEMCORTICAL

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lungs

LIVER

KIDNEY

ADRENAL

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RVH with DTPA

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RVH with MAG 3

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Renogram pattern with ACE

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Renogram pattern with ACE

• A = normal TAC curve (grade 0)

• B = peak mildly delayed but greater than 5 minand with delayed excretion (grade 1)

• C = very delayed uptake but some wash out(grade 2A)

• C = extremely delayed uptake with no wash out

(grade 2B)• D = complete renal failure where blood pool

moves through the kidney without an extractionphase

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Complication of

renal transplant

Pre surgical

insult

Autoimmune

rejection

Surgical

Vascular

Vasomotor nephropathy

resolution ATNMinutes to hours

Hyperacute rejection

Accelerated rejection

Acute rejection

Chronic rejection

Cyclosporine rejection

Urine leak

Hematoma 

Infection 

Lymphocyle 

Renal artery stenosis

Vascular occlusion

Infarct 

Renal obstruction

Vesicoureteroreflux

Minutes to hours

1 – 5 hours

After 5 days – first 3/12

Months to years

Months 

Days or weeks

1st few days

1st few days

2 – 4 months

After 1st months

Days/months/years

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1. Static radionuclide imaging of

kidney

A. Tc 99m DMSA is the radionuclide of choice

B. Tc 99m DMSA is the best for imaging

pseudotumor of kidney

C. DMSA can measure relative tubular mass

D. DMSA can detect of areas of renal ischemia

E. Optimum time for DMSA scanning is oneweek after onset of symptoms in infection

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1. Static radionuclide imaging of

kidney

• TTFFF

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2. MAG 3 scintigraphy

A. Best method for assessment of scarring in

children

B. Prolonged transit time in dilated system

C. Reliable for diagnosis of obstruction in renal

failure

D. Prolonged parenchymal transit time in renal

artery stenosis

E. Patients are dehydrated before study

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2. MAG 3 scintigraphy

• FTFTF

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3. Renal scintigraphy

A. For captopril test, ACE inhibitors should on

the day of the test

B. MAG 3 is used for assessing renal scarring

C. DMSA is superior to MAG 3 for both dynamic

and structural assessment

D. Radiation is lower for MAG 3

E. 100% of MAG 3 is excreted by tubular

secretion

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3. Renal scintigraphy

• FTFTF

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4. Renal scintigraphy

A. DMSA images are acquired within one hourof injection to avoid artifacts

B. DTPA is isotope of choice for dynamic renal

scansC. Kidney/background ratio is better for MAG 3

than DTPA

D. I 123 can be produced only by cyclotronE. Hippuran is completely cleared by glomerular

filtration

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4. Renal scintigraphy

• FFTTF

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5. Renal scintigraphy

A. The glomerular filtration rate of DTPA is 500ml/min

B. DTPA is completely cleared by tubular

filtrationC. The maximum diuresis occurs within 2

minutes of diuretic administration

D. Images are acquired between 5-10 minutesfor perfusion in transplants

E. Post void film is indicated in cases of stasis

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5. Renal scintigraphy

• FFFFT

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6. Static renal scans are indicated in

the following instances

A. Horseshoe kidney

B. Renal agenesis

C. Column of bertin

D. Individual renal function

E. UTIs

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6. Static renal scans are indicated in

the following instances

• TTTTT

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7. Recognised indication of dynamic

nuclear scanning

A. Hypertension

B. Renal transplantation

C. Renal trauma

D. Reflux

E. Tumor

d d f d

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7. Recognised indication of dynamic

nuclear scanning

• TTTTF

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9. Abnormal bone uptake in kidney

A. Radiation

B. Chemotherapy

C. Papillary necrosis

D. Multiple myeloma

E. Amyloidosis

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9. Abnormal bone uptake in kidney

• TTFTF

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10. In urinary tract obstruction

A. A DMSA scan always estimates renal function moreaccurately than DTPA scan

B. Evan if a kidney contributes less than 10% to the totalGFR, it’s  function will usually improve if the

obstruction is relievedC. Failure of the collecting systems to empty on standingconfirms the presence of obstruction

D. Lower urinary tract obstruction may be missed on aDTPA study

E. Giving furosemide during a DTPA study results in agreater specificity for diagnosing PUJ obstruction thangiving it at the start of the study

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10. In urinary tract obstruction

• FFFFTF

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11. Concerning radionuclide studies

A. DMSA gives an accurate assessment of overallrenal function in renal tubular acidosis

B. DTPA studies can reliably exclude obstruction indehydrated patient

C. A tissue injection can give a false positive resultfor obstruction

D. An aortic aneurysm can be excluded if a dilatedaorta is not seen on the blood flow renogram

imagesE. Visualization of a ureter on a renogram is

abnormal

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11. Concerning radionuclide studies

• FFTFF

12 C i di lid t di i

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12. Concerning radionuclide studies in

acute renal failure

A. ATN typically can be distinguished from othercauses of acute renal failure

B. On a DTPA study in pre renal failure, there isimpaired renal blood flow, poor uptake, delayed

intrarenal transit and little or no excretionC. A rising T/A curve on DTPA study confirms

obstruction

D. In ATN , a horizontal third phase to the T/A curve

in a DTPA study indicates that recovery isoccurring

E. MAG 3 is agent of choice

12 C i di lid t di i

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12. Concerning radionuclide studies in

acute renal failure

• TFFTT

13 C i d l

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13. Concerning renogram and renal

transplants

A. On a DTPA scan, rejection can be distinguished fromcyclosporine A toxicity

B. Arterial thrombosis can be distinguished from venousocclusion

C. A high perfusion index means that there is a good bloodsupply to the transplant

D. Arterial occlusion can be detected on a DTPA study even ifan earlier one has shown ATN from which the patient hasnot yet recovered

E. Vesicoureteric reflux is the commonest cause ofpelviureteric dilatation

F. A urinary leak can be excluded if it is not shown in earlyimages

13 C i d l

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13. Concerning renogram and renal

transplants

• FFFTTF

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14. Concerning MAG 3

A. A kit reconstituted first thing in the morningremains usable until the 99m-Tc decays

B. MAG 3 has a smaller volume of distribution

than DTPAC. Liver and biliary activity may be seen

D. MAG 3 measures GFR more accurately than

DTPAE. The radiation dose from a MAG 3 study is

less than from DTPA

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14. Concerning MAG 3

• FTTFF

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15. In renal tract infections

A. In acute pyelonephritis, there may be area ofdecreased perfusion on the flow study

B. In a patient with UTI, a small smooth kidney is unlikelyto be due to chronic pyelonephritis alone

C. The overall sensitivity of DMSA is increased by SPECTD. A recognised feature of established scars is that they

become more prominent with time

E. Renal parenchymal involvement can be predictedfrom clinical and lab parameters

F. Most acute parenchymal defects develop into corticalscars

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15. In renal tract infections

• TFFTFF

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16. Concerning vesicoureteric reflux

A. In patients who reflux, 20% reflux only during micturitionB. Reflux seen on direct scintigraphy cystography correlates

closely with the results of an MCUG

C. Any reflux is a risk factor for pyelonephritis

D. Renal scarring occurring after an episode of acutepyelonephritis is independent of continued reflux

E. A recognised appearance on a DMSA scan of a kidneydamaged by infection is a normal size kidney with reducedfunction

F. Reflux occurring after the age of 3 yrs in patients withnormal DMSA scans is probably irrelevant

G. A 1 yr old with their first proven UTI and hydronephrosison US should have a DMSA and an MCUG

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16. Concerning vesicoureteric reflux

• TFFFTTF

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17. In ACE I renography

A. With longstanding total occlusion of the renalartery, there can be no uptake in the affectedkidney

B. Branch arterial stenosis can be detected

C. In a patient with solitary kidney, ACE Irenography may result in acute renal failure

D. Furosemide is recommended at the start of thetest to improve specificity

E. In a MAG 3 study, a continually rising curveindicates a haemodynamically significantstenosis

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17. In ACE I renography

• FTTTT

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18. Renal radionuclide imaging

A. Can distinguish between renal contusion andinfarction

B. Can detect radiation nephritis 3 wks aftertreatment

C. Can detect central cysts more easily thanperipheral ones

D. A phantom kidney may be seen afternephrectomy

E. A phantom kidney, if due to mesenteric vesselsmore commonly occurs on the right

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18. Renal radionuclide imaging

• TTFTF

19 The following are causes of a

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19. The following are causes of a

flattened DTPA curve

A. Hypovolaemia

B. Hypoplastic kidney

C. Recent contrast angiogram

D. After extracorporeal shock wave lithotripsy

E. Severe cyclosporine toxicity

19 The following are causes of a

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19. The following are causes of a

flattened DTPA curve

• TTTTT

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20. In DTPA renal scan

A. The examination is contraindicated in renalfailure

B. Fluid restriction is mandatory

C. Vascular phase is acquired immediately afterinjection

D. The acquisition is performed with patient

facing the cameraE. Calculation of GFR takes the background into

consideration

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20. In DTPA renal scan

• TFTFT

What percentage of renal plasma flow

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p g p

is filtered through the glomerulus and

what percentage is secreted by thetubules

What percentage of renal plasma flow

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p g p

is filtered through the glomerulus and

what percentage is secreted by thetubules• 20% of renal plasma flow is cleared by

glomerular filtration.• 80% by tubular secretion.

Which radiopharmaceuticals are most

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often used clinically for measurement

of GFR and ERPF?

Which radiopharmaceuticals are most

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often used clinically for measurement

of GFR and ERPF?

• GFR : Tc-99m DTPA

• ERPF : I-131 OIH (iodohippurate) or Tc-99m

MAG3• However Tc-99m MAG3 does not actually

measure ERPF and a correction factor based

on proportional clearance compared with I-131 OIH must be applied.

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What is the percentage of cortical

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binding of Tc-99m DMSA and Tc-

99mGH?

• Tc-99m DMSA :40-50%

• Tc-99m GH : 10-20%

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What is Webster’s rule? 

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What is Webster’s rule? 

• Pediatric radiopharmaceutical doses can beestimated using the formula (age + 1)/(age +

7) x adult dose.

The time to peak activity of a renal

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The time to peak activity of a renal

time activity curve (TAC) represents:

A. The end of extraction

B. The beginning of renal clearance

C. The time point at which the amount of

cortical uptake of the radiopharmaceutical is

equal to clearance

The time to peak activity of a renal

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The time to peak activity of a renal

time activity curve (TAC) represents:

• FFT

What are the general method for

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What are the general method for

calculating absolute GFR?

What are the general method for

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What are the general method for

calculating absolute GFR?

• Blood sampling, blood sampling and urinecollection and camera based methods.

At what step in the renin-angiotensin-ld d d il

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aldosterone cascade does captopril

work?

At what step in the renin-angiotensin-ld d d il

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aldosterone cascade does captopril

work?

• Captopril blocks the conversion of angiotensin

I to angiotensin II in the lung.

Which of these factors effects the

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Which of these factors effects the

accuracy of diuresis renography?

A. State of hydration

B. Renal function

C. Dose of diuresis

D. Radiopharmaceutical

E. Bladder capacity

Which of these factors effects the

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accuracy of diuresis renography?

• TTTTT

What is the most sensitive technique

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q

for diagnosing scarring secondary to

reflux?

What is the most sensitive technique

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q

for diagnosing scarring secondary to

reflux?• Tc-99m DMSA

How can radionuclide imaging

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g g

differentiate upper from lower UTI?

How can radionuclide imaging

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g g

differentiate upper from lower UTI?

• Upper UTI or pyelonephritis , Tc-99m DMSAshows tubular dysfunction, manifested bydecreased uptake.

This is a reversible process.• With appropriate therapy, tubular will return

in 3 – 6 months.

• Upper UTI has prognostic implication becauseit may lead to subsequent renal scarring, HPTand renal failure.

What is meant by direct vs indirect

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cystography and which is the preferred

method in detecting VUR?

What is meant by direct vs indirect

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cystography and which is the preferred

method in detecting VUR??• Direct cystography is sensitive, requiring

urinary tract catheterization and infusion of

radiotracer into the bladder. Reflux can bedetected during bladder filling and voiding.

• Indirect method, where a routine renogram is

initially performed, cannot be used to detectreflux during the bladder filling stage becauseradiotracer is flowing through the collectingsystem antegrade.

What is the common development

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p

abnormality leading testicular torsion?

What is the common development

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p

abnormality leading testicular torsion?

• The bell-clapper testis

What is the difference in blood supply

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pp y

to the testis and scrotum?

What is the difference in blood supply

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to the testis and scrotum?

• The testes receive the blood from testicularartery.

• Scrotum receives supply from the pudendal

vessels.

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Urinoma

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Urinoma

1. A photopenic region, best seen on early images, involvesmost of the left renal fossa. Only the upper pole isfunctioning. Urinary clearance into the left renal pelvisappears displaced medially by the photopenic defect. Theright pelvic and uppe2/3 of the ureter fill. Poor clearance

bilaterally. Delayed images show increased uptake in theregion of the initial cold defect and inferior to it.

2. The cold defect is a urinoma with an attenuating masseffect. Over time the radioactive urine enters this spaceand mixed with the nonradioactive urinoma. Activity in

the region of the urinoma increases over time while theearlier seen kidney and background activity have cleared.

3. Activity urinary leak and urinoma.

4. Urinary tract obstruction.

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Bilateral obstruction

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Bilateral obstruction

1. Left kidney; delayed and decreased cortical uptake, noclearance into the calyces or pelvis. Right kidney;prompt uptake and clearance into the collectingsymptom, faint persistent visualization of the rightureter and, poor response to furosemide.

2. Before furosemide; high grade obstruction on the leftand HN on the right, suspicious of obstruction. Afurosemide high grade obstruction on the left andobstruction on the right.

3. Filling of the renal collecting system.4. Percent radiopharmaceutical uptake by each kidney

divided by total renal uptake between 1 and 3minutes (before clearance into the pelvicalycialsystem)

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Torsion of testicular appendage

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Torsion of testicular appendage

1. A, Mildly increased flow and mild focal left upperscrotal uptake on the static image. B, Increased flowand increased distribution on the left hemiscrotum. C,Increased flow and delayed halo sign of the right

hemiscrotum.2. A, Torsion of a testicular appendage. B, Acute

epididymitis/orchitis. D, Delayed testicular torsion.

3. A, Loss of blood supply to the appendage of the

testicle. B, Infection, viral or bacterial. C, Infarction ofthe testicle caused by torsion more than 24 hoursduration.

4. Testicular torsion, 35%; torsion of the appendix testis,

35%; acute epididymitis, 25%.

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Radionuclide cystography

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Radionuclide cystography

1. Tc-99m DTPA and Tc-99m SC2. Radionuclide cystography is more sensitive in detection of

VUR and results in 50 to 200 times less radiation exposureto gonads compared with the contrast study.

3. The direct method is commonly used and requires urinary

catheterization and installation of radiotracer into thebladder through catheter. The indirect method isperformed after routine DTPA/MAG3. when the bladder isfull, a prevoiding image is obtained, followed by dynamicimages during and after voiding.

4. Grading criteria are similar to those used with contrastcystography, however the radionuclide study’s  limitedresolution does not permit assessment of calycealmorphology. Mild reflux; confined to the ureter.Moderate; reaches the pelvicalyceal system. Severe;

distorted collecting system and dilated tortuous ureter.

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Unilateral obstruction

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Unilateral obstruction

1. Good symmetrical cortical uptake and promptexcretion into collecting systems bilaterally.Retention of activity in left renal collectingsystem, apparent cutoff in the upper ureter and

very poor response of furosemide. The right sideshows a prominent collecting system but washesout spontaneously before furosemide.

2. HN of the left kidney. TRO obstruction.

3. Consistent with significant obstruction of the leftkidney.

4. Dehydration, renal insufficiency, inadequatediuretic dose, full bladder and large collecting

system.

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Renal scan

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Renal scan

1. Tc-99m DTPA, Tc-99m MAG3 and I-131 hippuran.2. DTPA; glomerular filtration, MAG3; tubular secretion

and hippuran; 20% glomerular and 80% tubular.

3. DTPA is inexpensive, provides a good image quality

but has low extraction efficiency (10-20%) and poorpoor quality images with renal insufficiency. MAG 3has a high extraction rate (60%), good target tobackground and good quality images with renalinsufficiency. Hippuran has good extraction efficiency,

high target to background, poor image quality, poorcortical/collecting system differentiation and deliversa high radiation dose in renal insufficiency.

4. No . A dose of 5 mCi is needed for good blood flowimages.

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Diuretic renography

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Diuretic renography

1. Bilateral cortical uptake and excretion into collectingsystems. Retention in the right collecting system at 30minutes with good post furosemide washout.

2. Good response to surgical correction with no obstruction.

3. Not with certainty. Ureteral nonvisualization is not

diagnostic of ureteropelvic junction obstruction because astanding column of ureteral urine can prevent radiotracerentry.

4. It measures pressure flow relationships and requiresfluoroscopically guided trocar or spinal needle insertion

into the renal pelvis. Basal and pressure measurementsduring infusion of a contrast solution at a rate arerecorded. Obstruction pressure is defined as greater than15cm water, no obstruction as less than 10 to 12 cmwater.

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Transplanted kidney

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Transplanted kidney

1. Rapid leakage of urine just inferior to thetransplanted kidney and extravasating into the

scrotum.

2. Urinary leak caused by disruption of surgicalanastomosis.

3. Hematomas and abscess occur in the early

postoperative course, whereas lymphoceles

generally are noted 4 to 8 weeks after surgery.

4. ATN, acute rejection or obstruction. Cyclosporin

toxicity usually occurs months after transplant.

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Non viable kidney after

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transplantation

1. No blood flow to the transplanted kidney. Norenal uptake. A photopenic region in the

shape of the transplanted kidney.

2. Nonviable kidney3. Arterial or venous thrombosis, severe

irreversible rejection and acute cortical

necrosis.4. Removal of nonviable transplanted kidney

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ATN

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ATN

1. ATN, accelerated acute rejection, urinary leakand urinary obstruction.

2. The second postoperative week. Acceleratedrejection may occur during the first week in

patients who have had previous transplants orreceived multiple transfusion.

3. Normal blood flow, very poor function, no

excretion. Base of penis seen inferiorly.4. The pattern of normal blood flow but poor

function during the first week aftertransplantation is typical of ATN

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Testicular torsion

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Testicular torsion

1. Tc-99m pertechnetate, initial blood flow andthen tracer distributes in the extracellular fluidspace.

2. Acute epididymitis, testicular torsion or torsion

of the testicular appendage.3. Developmental abnormality of testicular

descent and attachment predisposes tospermatic cord torsion. The most common

anatomical abnormality is “bell clapper” testis.4. Decreased blood flow to the right testicle and aphotopenic right testicle consistent with acutetesticular torsion.

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Acute renal transplant rejection

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Acute renal transplant rejection

1. Very decreased and delayed blood flow andpoor transplant function.

2. Acute rejection.

3. Fever, transplant tenderness andenlargement, decreased urinary output and

rising serum creatinine level.

4. Biopsy.

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Captopril renography

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Captopril renography

1. With renal artery stenosis, glomerular filtration decreasesand GFR drops. Renin released from juxtaglomerularconvert angiotensin I to angiotensin II. Angiotensin IIcauses vasoconstriction of the glomerular efferentarterioles, rising filtration and maintaining GFR. ACE

inhibitor blocks conversion of angiotensin I to II resultingin decreased in a decrease GFR.

2. The right kidney is small but with good function. Withcaptopril cortical retention persists, consistent with renindependent renovascular HPT of the right kidney. This isconfirmed by the renal cortical time activity curves.

3. Yes. The accuracy of I-131 hippuran, Tc-99m DTPA and Tc-99m MAG 3 are similar.

4. Sensitivity 90% and specificity 95%. Sensitivity is less fordetection of renin dependent HPT if the patient has been

taking an ACE inhibitor chronically or renal insufficiency.

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Pyelonephritis

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y p

1. 40% of DMSA binds and fixes to functioningproximal cortical renal tubules.

2. Diagnosis of pyelonephritis or renal scarring.

3. Decreased uptake in the lower half of theright kidney on initial imaging (A). RepeatSPECT show normalization of uptake. A,Pyelonephritis. B, Renal scarring

4. DMSA in the early stages of infection is thebest predictor of renal sequalae.Identification of pyelonephritis will increase

the duration of antibiotic therapy

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Lung scintigraphy

Pearls & Pitfalls

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Lungs perfusion

• Unless it is completely and

absolutely normal, neverinterpret a V/P scan without a

recent chest radiograph.

•A normal perfusion lung scanessentially excludes clinically

significant PE.

An abnormal ventilation scanor chest radiograph will not

change this assessment.

Pearls & PitfallsOth f f i

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Lungs perfusion

• Other causes of perfusiondefects are COPD, asthma,tumor, mediastinitis, mucousplug, fat emboli and vasculitis.

• Most perfusion defects caused

by PE are wedge shaped andextend to the periphery,usually bilateral and multiple.

An unmatched defects refers toone that is seen on theperfusion scan withoutventilation abnormality.

Pearls & Pitfalls

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Lungs perfusion

• Even a low probability scan has

a 15% to 20% probability of PE.• A very low probability scan has

a positive predictive value of

less than 10%.• Asthma, mucous plugs and

COPD can cause segmental

defects, but they should nothave normal ventilation scans.

Pearls & Pitfalls

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Lungs perfusion

• A stripe sign of peripheral activity

around a perfusion defect isfrequently seen with COPD and

indicates a very low probability

defect.

• When there is an infiltrate on the

CXR and a small perfusion defect,

pneumonia is a common cause.

• When there is a small infiltrateand a relatively larger perfusion

defect, PE should be considered.

Pearls & Pitfalls

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Lungs perfusion

• If there is ventilation of one

whole lung but no perfusion, thedifferential diagnosis includescongenital absence of thepulmonary artery, massive

central PE, mediastinal fibrosis orhilar neoplasm.

• A focal hot spot in the lung is dueto an injected labeled clot that

was either formed in the syringeor dislodged from the end of thecentral line through which Tc-99m MAA was injected.

Pearls & Pitfalls

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Lungs perfusion

• On an aerosol ventilation scan,

collection of activity in thecentral bronchi is an indication ofCOPD.

• Poor perfusion to the lung apices

may be normal after lungtransplantation.

• Large segmental V/Q mismatchesare more likely to represent PE

than the small ones.

• Multiple irregular tiny perfusiondefects can be due to COPD, fat

emboli and vasculitis

Pearls & Pitfalls

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Lung perfusion

• Parenchymal renal activity on a

Tc-99m MAA scan indicates apossible right to left shunt.

• This can be confirmed by

noting activity in the brain.• V/Q scans remain useful for

renal failure patients and

contrast allergies.

Lungs

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Lungs

Perfusion ventilation

Radioactive

gasesRadioaeresols

Tc-99m human

Albumin microspheres

Tc-99m MAA

Macroaggregated

albumin

Xenon 133 Xenon 127 Krypton 81m Tc-99m DTPA Tc-99m

technigas

Xenon 133 Tc-99m DTPA

Mode of decay Beta minus Isometric

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Mode of decay Beta minus Isometric

Half life 5.5 days 6 hours

Biological half life 30 seconds 45 minutes

Photo energy 81 keV 140 keV

Multiple view imaging No Yes

Useful for severe

COADYes -/+

Used after perfusion

scan

No No

Tc-99m MAA

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Size 10 – 90 µm

Minimum number of particles to

be used in adults

100000 unless pulmonary

hypertension and right to left

shunt

Ideal number of particles 200000 - 500000

Biological half life 4 – 8 h

Injection Care should be taken not to

cause particle aggregates that

can produce hot spot

Safety Particles block <1/1000 of thecapillaries and precapillary

arterioles

Terminology

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V/Q match defect Both scans abnormal in same area

and equal size

V/Q mismatch Abnormal perfusion

Normal ventilation

Triple match

V/Q matching with CXR

Segmental defect

Wedge shape and pleural base

Large > 75%

Moderate 25 -75%

Small < 25%

Reversed mismatch Abnormal ventilation

Normal perfusion

Xenon-133 ventilation scintigraphyPatient preparation None

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Patient preparation None

Dosage 10-20 mCi inhale

Collimator LEGP

Photopeak 20% window centered at 81 keV

Positioning Patient is seated

Place nose clamps on patient and connect

mouthpiece for several minutesCenter camera over chest posteriorly

Patient breathes continuously through

mouthpiece for several minutes

Acquisition First breath- patients exhales fully and is ask to

minimally inspire and hold it long enough to

obtain 100000 count or 10-15 secondsEquilibrium-obtain 2 sequential 90 seconds

images while patient breath normally

Washout-turn system to exhaust

Obtain 3 sequential 45 seconds posterior

images then right and left posterior oblique

and final posterior image

Tc-99m DTPA ventilation scintigraphy

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Patient preparation None

Dosage 30 mCi Tc-99m DTPA nebulizer

Collimator LEGP

Photopeak 20% window centered at 140 keV

Positioning Place nose clamps on patient and connect

mouthpiece for several minutes

Center camera over chest posteriorly

Patient breathes continuously through

mouthpiece for several minutes

Acquisition Acquire posterior image for 250k and

mark time

Views: posterior/anterior/right and left

lateral/right and left posterior oblique

Tc-99m MAA perfusion scintigraphy

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Patient preparation None

Patient precaution Pulmonary hypertension : reduces

particle to 100000

Right to left cardiac shunt : reduced

particle number

Dosage 2-5 mCi IV over several respiratory cycle

with patient supine

Collimator LEGP

Photopeak 20% window centered at 140 keV

Acquisition Acquire posterior image for 500k

counts/image

Views: posterior/anterior/right and left

lateral/right and left posterior oblique

Understanding the report

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Mismatched or matched V/Q scan

Mismatched  –  decreased perfusion with

normal ventilation

Matched  –  abnormal perfusion and

abnormal ventilation

Ventilation abnormal image shows  – 

slow to wash in/ slow to wash out (wash

in images are obtained in all ventilation

agent but wash out only with xenon gas)

Understanding probability

Normal scan- low probability of PE (0-5%)

Low probability scan -PE (10-15%)

Intermediate probability -PE (25-30%)

High probability –PE (80-100%)

Qualitative lung scan

Describe the percent contribution to

global perfusion of each lung

Combined with pulmonary function test

Potential problemsFalse positive Conditions that can mimic high probability-

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pvasculitis / pulmonary arterial anomalies i.e.

hypoplasia and stenosis

Clinical pretest probability of PE Useful for deriving post test probability

Interpretations of defect size High probability  –  2 moderate / large

mismatched perfusion defects

If patient with cardiopulmonary disease- 4

mismatched defects

Moderate – 25-27% area lung segment

Large 75% segment2 defects each 50% of segment can be counted

as 1 large defect

Widespread ventilatory abnormalities Widespread ventilatory abnormalities =

intermediate probability of PE

i.e. pulmonary infarction or pneumonia showedmatched V/Q and matched CXR infiltrate

Right to left shunt Number of particle can be reduced for

patients with right to left shunt i.e.

children.

 

V/Q scan

b bili f

Clinical pre scan probability

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probability for

PE High Intermediate Low

High 97% 88% 56%

Intermediate 66% 28% 16%

Low 40% 16% 4%

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Technegas (ventilation)

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DTPA (perfusion)

Patient with COPD

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  Primary vascular lesionPE

Vasculitis

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Causes of perfusion

defect

Septic/fat/air emboli

Pulmonary artery hypoplasia or atresia

Primary ventilation

abnormalityPneumonia

Atelectasis

Pulmonary edema

Asthma

COPD

Bullae

Mass effectTumor

AdenopathyPleural effusion

IatrogenicSurgery

Radiation fibrosis

Acute PE

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V/Q mismatched

defect

Chronic PE

Vasculitis

Mediastinal or hilar

adenopathy

hypoplasia or aplasia ofpulmonary artery

Post radiation therapy

Bronchogenic carcinoma

Septic/drug abuse

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V/Q matched defect

COPDAir space disease

Tumor

Pleural effusion

Asthma

Lung infarction

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V/Q reversed

mismatched defect

Pneumonia

Mucus plugging

Alveolar pulmonary edema

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Unilateral lung

perfusion

abnormality

Pneumonectomy

Mediastinal fibrosis

Pneumothorax

Tumors

Mucous plug

Pulmonary embolus

Pulmonary artery stenosis

Swyer-James syndrome

Massive pleural effusion

  Pacemaker

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Non segmental

defect

Bullae

Trauma

Tumors

Hemorrhage

CardiomegalyHilar adenopathy

Atelectasis

Pleural effusionPneumonia

Perfusions defect ventilation CXR Probability category

Moderate to large

≥ 2 segments Mismatch clear high

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≥ 2 segments  Mismatch clear high

< 2 Mismatch clear Intermediate

Match LL zone Intermediate

Match UL zone Low

Multiple Match Clear Low

Small (<25% of a segments)

> 3 N/A Clear Low

1 - 3 N/A Clear Very low

Non segmental

N/A Shows anatomicalreason for perfusion

abnormality

Very low

None

N/A N/A Normal

Wells clinical prediction rule for the diagnosis of pulmonary embolism (PE)

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Variable Points

Clinical signs and symptoms of DVT 3

Alternative diagnosis is less likely than PE 3

Heart rate > 100 bpm 1.5

Immobilization or surgery in the previous 4 weeks 1.5

Previous DVT or PE 1.5

Hemoptysis 1

Malignancy 1

Risk categories based on Wells score

(version used in PIOPED II)

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Risk category Cumulative score

Low <2

Intermediate 2-6

High >6

Risk categories based on Wells score

(version used in Christopher study)

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Risk category Cumulative score

PE unlikely ≤4 

PE likely >4

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 Most common symptoms of

PE (PIOPED study)

Dyspnea (73%)

Pleuritic chest pain (66%)

Coughing (37%)

Hemoptysis (13%)

Abdominal/ pelvic pain

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Atypical

presentations of PE

bdo a / pe c pa

Decreasing level ofconsciousness

Fever

Productive cough

Seizures

Syncope

Wheezing

  AMI

Acute stroke

DIC

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Conditions

associated with D-

Dimer production

Advanced age

Heart failure

Connective tissue disease

Infection

Malignancy

Post operative

Pregnancy

Renal failure

Trauma

Sickle cells

DVT

The following associated with matchedventilation/perfusion defects of lung

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scans

A. IV drug abuse

B. Congenital rubella syndrome

C. Histoplasmosis

D. Thymolipoma

E. Haematogenous metastases

The following associated with matchedventilation/perfusion defects of lung

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scans

• TFTFF

The following may cause perfusion

defects on lung scan

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A. SLE

B. TB

C. SarcoidosisD. Retrosternal goitre

E. Radiation pneumonitis

F. Anomalous pulmonary artery

G. Bronchial carcinoma

H. Congenital lobar emphysema

I. Haemangioendoliomatosis

The following may cause perfusion

defects on lung scan

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•TTTTTTTTT

Concerning PE

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A. A single perfusion defect separated from thepleural surface by a rim of normal perfusion israrely due to embolus

B. Normal perfusion exclude clinically significant PE

C. The combination of clinical impression and lungscan results is a better predictor of PE thaneither taken alone

D. Patients with a low probability scan and no

evidence of venous thrombosis may be safelyleft untreated

E. He particle count of Tc-99 MAA may need to beincreased in patients with pulmonaryhypertension to achieved diagnostic images

Concerning PE

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•TTTTF

Total loss of perfusion to one lung

occurs in

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A. Bullous emphysemaB. Beckwith-Wiedmann syndrome

C. Following a Blalock-Taussig shunt

D. Pleural effusion

E. Swyer-James syndrome

Total loss of perfusion to one lung

occurs in

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•TFTTT

Regarding V/Q scanning in the

following up of confirmed PE

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A. Perfusion defects may clear at 24 hoursB. A perfusion defect still present at three

months is likely in persist indefinitely

C. A persistent defect implies lung infarctionD. Underlying heart failure may enhance the

resolution f perfusion defects

E. A repeat V/Q scan should be performed priorto stopping anticoagulation

Regarding V/Q scanning in the

following up of confirmed PE

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•TTFFT

The fissure sign occurs in

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A. Sub pulmonic effusionB. Cystic fibrosis

C. Sarcoidosis

D. PE

E. Emphysema

The fissure sign occurs in

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•TTFTT

Reverse V/Q mismatched occurs in

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A. Pulmonary atelectasisB. PE

C. Alveolar proteinosis

D. Bronchogenic carcinoma

E. Pleural effusion

Reverse V/Q mismatched occurs in

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•TFFTT

The visualization of the kidneys on Tc-99m MAA perfusion scan can be

caused by:

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caused by:

A. Right to left shunt

B. Free Tc-99m

C. MAA particle less than 10 µm in sizeD. Kidney obstruction

E. Less dehydration

The visualization of the kidneys on Tc-

99m MAA perfusion scan can be

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caused by:

• TTTFF

A. Low probabilityB. Intermediate probability

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C. High probability1. Clear CXR with multiple matched V/Q defects

2. Single large segmental V/Q mismatch

3. Perfusion defect < radiological infiltrate

4. Multiple small perfusion defect

5. Perfusion defects equal to radiographic

infiltrate

6. Lobar V/Q mismatch

A. Low probabilityB. Intermediate probability

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C. High probability1. Clear CXR with multiple matched V/Q

defects. A

2. Single large segmental V/Q mismatch. B

3. Perfusion defect < radiological infiltrate. A

4. Multiple small perfusion defect. A

5. Perfusion defects equal to radiographic

infiltrate. B

6. Lobar V/Q mismatch. C

Stripe sign generally is reflective of

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A. PEB. Non embolic disease such as COPD

C. Pulmonary hypertension

D. Pleural fluid

E. Asthma

Stripe sign generally is reflective of

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FTFFF

Matched absence or near absence ofperfusion and ventilation in the entire

lung may be associated with?

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lung may be associated with?

A. Lung carcinoma

B. Aspirated foreign body

C. Swyer James syndrome

Matched absence or near absence ofperfusion and ventilation in the entire

lung may be associated with?

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lung may be associated with?

• TTT

Regarding V/Q

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A. Kr-81m is generator producedB. Rb-81 is cyclotron produced

C. Albumin macroaggregates remain in thepulmonary capillary bed for weeks, limiting the

number of follow up perfusion scans that can besafely performed.

D. The biologic half life of MAA is longer thanalbumin microspheres

E. A patient with high pretest probability of PE, thenegative predictive value of a normal scanexceeds 95%

Regarding V/Q

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TTFFT

Regarding V/Q

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A. In a patient with low pretest probability of PE,the positive predictive value of positive scanexceeds 95%

B. The presence of the triad has a positive

predictive value of PE exceeding 95%C. V/Q scan is nondiagnostic in most patients with

pulmonary edema

D. Most patients with PE show infiltrate or effusionon properly exposed CXR

E. Absence of perfusion to an entire lung iscommon with PE

Regarding V/Q

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FFFFF

What are two commonly used

radiopharmaceuticals for ventilation

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imaging? What are their advantagesand disadvantages

What are two commonly used

radiopharmaceuticals for ventilation

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imaging? What are their advantagesand disadvantages

• Xenon-133 and Tc-99m DTPA aerosol. Xenon-133

demonstrates more clearly the physiology ofrespiration and is very sensitive to detection ofobstructive airways disease manifested by slowwashout. The disadvantages is the rapid washout, itssuboptimal view due to low photopeak (81 keV) andpoor count rate image.

• Tc-99m DTPA aerosol allows high count images in allprojections, however the images are comparable onlyto the inspiratory phase of xenon-133.

What is minimum number of particlesrecommended for pulmonary

perfusion imaging?

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perfusion imaging?

What is minimum number of particlesrecommended for pulmonary

perfusion imaging?

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perfusion imaging?

• This requires at least 100,000 particles in

normal adults and many authorities

recommend a minimum of 200000  –  500000

particles.

What is the size range of MAAparticles?

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What is the size range of MAAparticles?

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In commercial preparations the majority ofparticles are 20 to 40 υm with a range of 10 – 

90 υm.

What is the biological fate of MAAparticles?

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What is the biological fate of MAAparticles?

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MAA particles are easily broken down in thelung. Delayed imaging performed several

hours after pharmaceutical administration

demonstrates activity in the

reticuloendothelial system because of

phagocytosis of the breakdown particles.

Pearl

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One way to determine whether radioactivityoutside of the lungs is caused by free Tc-99m

or shunted Tc-99m MAA is to image the brain.

Free pertechnetate should localize in the

brain, whereas Tc-99m MAA particles that gain

access to the systemic circulation will lodge in

the first capillary bed that they encounter,

including the capillary bed in the brain.

What is the preferred patient positionduring administration of Tc-99m MAA?

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What is the preferred patient positionduring administration of Tc-99m MAA?

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Administering Tc-99m MAA with the patientsupine results in a more homogenous

distribution of particles in the lung than when

the patient is sitting or standing.

What is the stripe sign?

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What is the stripe sign?

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Stripe sign refers to a stripe or zone of activityseen between a perfusion defect and the

closest pleural surface. Because PE are

typically pleura based, the stripe sign suggests

another diagnosis, often emphysema.

What is physiological basis forperfusion defects in areas of poor

ventilation?

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ventilation?

What is physiological basis forperfusion defects in areas of poor

ventilation?

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ventilation?

• The classic response to hypoxia at the alveolar

level is vasoconstriction. Shunting a blood

away from the hypoxic lung zone maintains

oxygen saturation.

What is the shrunken lung sign?

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What is the shrunken lung sign?

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The lung may appear smaller than usual inpatient sustaining multiple small emboli, such

as fat emboli, that distribute uniformly around

the lung periphery

What is the classical appearance ofmultiple PE on lung perfusion

scintigraphy?

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scintigraphy?

What is the classical appearance ofmultiple PE on lung perfusion

scintigraphy?

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scintigraphy?

• Multiple pleura-based, wedged shaped areas

of significantly diminished or absent

perfusion. The size of the defect may varyfrom subsegmental to segmental or may

involve an entire lung or lobe.

What is the sensitivity of the highprobability scan category for detecting

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pulmonary embolism?

What is the sensitivity of the highprobability scan category for detecting

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pulmonary embolism?• In the PIOPED study, 41 % of patients with PE

had a high probability scintigraphy pattern.

What are the most common clinical

signs and symptoms in patients with

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confirmed PE?

What are the most common clinical

signs and symptoms in patients with

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confirmed PE?• In PIOPED, the three most common presenting

symptoms, dyspnea 80%, pleuritic chest pain

60% and cough 40%.• On physical examination, lung crackles 60 %,

leg swelling 30% or pleural friction rub 5%.

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High probability of PE

1 Perfusion is decreased in the right lower lobe

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1. Perfusion is decreased in the right lower lobeexcept for the superior segment. Ventilation istruncated in the right lower lobe consistent withsubpulmonic effusion

2. High probability for PE. Mismatch between

perfusion and ventilation is evident in the basalsegment. The perfusion defect is considerablylarger than the effusion on the X-ray

3. > 90%

4. Most common : Normal5. Next most common : atelectasis

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Hot spots on lung scan

1 Multiple hot spot are present in the upper and lower

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1. Multiple hot spot are present in the upper and lowerlobes, predominately in the right lung field

2. Radioactive emboli as a result of poor techniquecaused by drawing back blood into the syringecontaining the Tc-99m MAA before injection of the

radiotracer, causing clumping

3. The lungs, the target organ, received 5 mCi from Tc-99m MAA. Approximately 0.2 rads to the lung from a20 mCi xenon study

4. The biological half life is brief. The patient breathesXe-133 gas to equilibrium, then expels it into a trap.Only Xe-133 absorbed as a result of fat solubility hasany appreciable biological half life

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Ventilation perfusion stripe sign,emphysema

1 Decreased upper lobe ventilation is seen on the

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1. Decreased upper lobe ventilation is seen on thesingle breath with air trapping in both upperlobes and the right lower lobe on washoutimages

2. Decreased perfusion to the majority of bothlungs, with preserved perfusion in thesubpleural lung, most evident at the lung basesand medial aspect of both upper lobes

3. Low probability4. Stripe sign

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Hampton’s Hump – intermediateprobability

1. Posteroanterior and lateral chest radiographs

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1. Posteroanterior and lateral chest radiographsdemonstrate a pleural based opacity in the lateralright lung base

2. A single wedge shape, pleural based defect in thesame location as the radiographic abnormality,

probably the anterobasal segment of the right lowerlobe. Normal Xe-133 ventilation study

3. Intermediate probability for PE

4. CXR findings in PE without infarction are uncommon.When present, they are usually associated with alarge, central embolus. Discoid atelectasis is the nextmost common finding

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Emphysema caused by alfa 1antitrypsin deficiency

1. Single breath or wash in, equilibrium and wash out phase

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g , q p

2. Single breath : patient breathes in and holds a singlemaximum deep inspiration while a 100000 count image isacquired. Equilibrium : patient breathes a mixture of airand xenon while serial images are obtained every 60  – 90seconds for 3 minutes. Washout : patient breathes room

air and exhales xenon while serial images are obtained3. Ventilation : nonuniform in the upper lung zones

bilaterally, initial near absent at the bases. As upper lobeswash out, xenon fills and is retained in both basesindicating severe air trapping. Perfusion : heterogeneous

to both upper lung zones that match the early ventilationimages. The extensive perfusion abnormalities in bothlower lung zones are matched with areas of washout airtrapping

4. Low probability for PE, alfa 1 antitrypsin deficiency

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Tc-99m DTPA ventilation study withaerosol clumping

1. Multiple perfusion defects in upper and lower lung fields. Many appear

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segmental e.g.., the lateral of the right lower lobe, superior segment ofthe left lower lobe. Ventilation shows extensive diffused clumping withinthe air ways throughout both lung fields making determination ofmatching or mismatching difficult. The study was interpreted asintermediate probability since ventilation study could not be interpreted,however the segmental perfusion defect pattern is suspicious forembolus

2. Tc-99m DTPA aerosol provide (0.1  –  0.5 υm) normally distribute on firsimpact within alveoli. With airway turbulence e.g.., asthma or COPD,particles impact proximally within bronchi and appear as focal hot spot

3. Tc-99m DTPA aerosol ventilation is performed first. The patient breathesin less than 1 mCi at tidal volume until an adequate count rate isobtained the sixfold larger Tc-99m MAA perfusion dose (5 mCi)

overwhelms the retained ventilation dose, allowing the two consecutiveTc-99m studies

4. Xe-133 an inert gas, is advantageous for patients with COPD and asthma.Delayed filling and clearance in regions of obstructive disease can beseen. Disadvantage : only posterior views are possible because of rapidexhalation

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Low probability V/Q scan

1. Bilateral inhomogeneous distribution. Matched

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gperfusion and ventilation abnormalities throughoutthe upper and lower lobes, especially in the rightlower lobe basal segments. Minimal atelectasis in thelower lobes in chest x-ray. Low probability for PE

2. < 20%3. < 1 %

4. Large (segmental): > 75% of a segment

Moderate (subsegmental): 25% to 75% of a segmentSmall (small subsegmental):< 25% of a segment

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Intermediate probability andpregnancy

1. Bronchodilator therapy before V/Q scan as an asthmatic

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therapeutic trial2. PE are life threatening to the patient and fetus. The radiation

dose to the patient and fetus is low (< 2 rads). The benefit/riskratio is high. No change in procedure is required. In young,nonsmoking patients without cardiopulmonary disease, one

might reduce the dose, conduct only a perfusion study or both3. Hypoperfusion of the left lower lobe, except the superior

segment. Better ventilation than perfusion with mismatching inthe anterior basal and part of the lateral basal segments. Noventilation in the posterior basal and part of the lateral basal.

Costrophenic angle loss seen in the left lateral and LPO views.CXR: atelectasis/ infiltrate with elevation of the left diaphragm

4. Intermediate probability for PE. One large/ one moderatesegmental mismatch and one large and one moderate segmentalmatch corresponding to the x-ray atelectasis/infiltrate

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High probability of PE

1. Perfusion: decreased right lower lobe except for

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the superior segment. Ventilation: normalexcept for mildly truncated right lower lobeconsistent with subpulmonic effusion

2. High probability of PE. Mismatch between

perfusion and ventilation in the basal segments.The perfusion defect is considerably larger thanthe pleural effusion on the radiograph

3. > 80%

4. Most common: normal, next most common:atelectasis

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Stripe sign

1. Decreased perfusion in the right upper lobe

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(apical and anterior segment). Stripe sign of theposterior segment of the right upper lobe. Normalventilation

2. Two segmental mismatched. High probability of PE

3. Its presence signifies perfused lung tissuebetween a perfusion defect and the adjacentpleural surface. Its presence can be use to classifya segment as not related to PE.

4. Usually a manifestation of airway obstruction. Thesign has been correlated with CT and PET showingspared perfusion of the cortex of the lung inasthma and emphysema

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Unilateral matched V/Q abnormality

1. Perfusion: global decreased perfusion to the

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g pentire left lung, more striking than theventilation. Xe-133 ventilation images:decreased and delayed ventilation of the entireleft lung. Washout images show no significantair trapping

2. Low probability

3. Hilar mass, severe unilateral parenchymal lung

disease, prior shunt for congenital heart disease4. Lung cancer

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PET and oncology

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• A : without

attenuation

corrected

• B : with attenuation

corrected

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HG = high grade

If spleen > liver = post chemo

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Ur Metser, MD, Einat Even-Sapir, MD, PhD, Semin Nucl Med 37:206-222 © 2007

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Ur Metser, MD, Einat Even-Sapir, MD, PhD, Semin Nucl Med 37:206-222 © 2007

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Ur Metser, MD, Einat Even-Sapir, MD, PhD, Semin Nucl Med 37:206-222 © 2007

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Ur Metser, MD, Einat Even-Sapir, MD, PhD, Semin Nucl Med 37:206-222 © 2007

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Ur Metser, MD, Einat Even-Sapir, MD, PhD, Semin Nucl Med 37:206-222 © 2007

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Ur Metser, MD, Einat Even-Sapir, MD, PhD, Semin Nucl Med 37:206-222 © 2007

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Ur Metser, MD, Einat Even-Sapir, MD, PhD, Semin Nucl Med 37:206-222 © 2007

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Brown Fat

• Sedation

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• Adrenergic blocking agents

  Higher tumor grade

Large number of variable

cells

Increased tumor blood flow

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High FDG uptake

Increased tumor blood flow

Inflammation

Tumor hypoxia

Acute radiation

Recent chemotherapy

Recent surgery

  Benign lesion

Necrosis

Mucinous bronchoalveolar

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Low FDG uptake

Mucinous , bronchoalveolar

carcinoma

Hyperglycemia

High insulin

Chronic radiation

Scar

Prior chemotherapy

History Course of action

Prior surgery Delay scan 4-6 weeks

Chemotherapy Delay scan several weeks or schedule

scan just before next cycle

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scan just before next cycle

Radiation therapy Delay scan at least 3 months

Colony stimulating factor Delay scan for 1 week for short actingagents or several weeks for long

acting agents

Serum glucose > 200 Reschedule scan

Insulin administration Wait at least 2 hours

Breastfeeding Discontinue scan at least 6 hours

 

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Which of these statements is trueregarding F-18 FDG PET?

A. F-18 FDG uptake is normally high in brain and

heart

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heart

B. The mechanism of F-18 FDG uptake and

metabolism is identical to that glucose

C. Oncology patients should fast for at least 4

hours prior to injection

D. Unlike glucose, F-18 FDG is excreted through

the genitourinary system

Which of these statements is trueregarding F-18 FDG PET?

• TFTT

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The sensitivity of FDG PET is high fordetection of many malignancies. For

which of the following tumors is the

sensitivity of FDG PET not high?

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sensitivity of FDG PET not high?

A. Colorectal cancer

B. MelanomaC. Hepatocellular carcinoma

D. Renal cell carcinoma

E. Lymphoma

The sensitivity of FDG PET is high fordetection of many malignancies. For

which of the following tumors is the

sensitivity of FDG PET not high?

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sensitivity of FDG PET not high?

FDG PET has poor sensitivity for primary

hepatocellular carcinoma, renal cell carcinomaand prostate cancer.

This is less true of metastatic disease than

primary tumors.

Concerning F-18 FDG PET in lungcancer staging

A. The sensitivity for detection is high for

tumors of 5mm and greater size

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tumors of 5mm and greater size.

B. Sensitivity and specificity of FDG PET is

higher than CT for mediastinal staging for

lung cancer.

C. False negatives may be seen with

hyperglycemia.

D. False negatives may occur with

bronchoalveolar carcinoma

Concerning F-18 FDG PET in lungcancer staging

• FTTT

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What are the advantages CT PET overPET alone?

A. Automated hardware and software fusion for

anatomical fusion

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anatomical fusion

B. Diagnostic CT at the same time as the PET

scan.

C. CT is used for more rapid attenuation

correction.

D. Eliminates false positive interpretation.

What are the advantages CT PET overPET alone?

• TFTF

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What are some limitations of FDG PETin tumor staging?

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What are some limitations of FDG PETin tumor staging?

• PET imaging does not detect microscopic

metastases tumor involvement in local LNs

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metastases, tumor involvement in local LNs

may be obscured by activity in an adjacent

tumor, concurrent infection/inflammatory

process may cause false positive andsensitivity for intracranial metastases is low.

What are limitations of tumorrestaging by PET?

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What are limitations of tumorrestaging by PET?

• Posttherapy effect of surgery, chemotherapy

and radiation therapy may cause increased F-

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and radiation therapy may cause increased F-

18 FDG uptake, which can be confused activity

from active tumor.

• Even patients scheduled for imaging after an

appropriate delay after therapy may require

follow up imaging.

What are some differences between

nonattenuation corrected and

attenuation corrected PET images?

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What are some differences between

nonattenuation corrected and

attenuation corrected PET images?

Nonattenuation

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• Structures near surface more intense

• The skins more intense

• The lungs more intense

Nonattenuationcorrected

Lung carcinoma

• PET sensitivity in 1 node is 75%

• Pet sensitivity for mediastinal involvement is

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• Pet sensitivity for mediastinal involvement is

91%

• Adrenal is most common metastasis site

Lung carcinoma

Epidemiology 

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UK = 38000 cases

22000 men and 16000 women Death = 34000 per annum

Peak incidence in Europe 60-70 years

3 x more common in men

Lung carcinoma

Small cell carcinoma Non small cell carcinoma

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25% 75%

Oat cell Intermediate cell Squamous cell

50%

Adenocarcinoma

15%

Large

Cell

Anaplastic

10%

Bronchoalveolar Acinar

Papillary

Solid

Bronchial derived

Lung carcinoma

Symptoms 

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Cough

Hemoptysis Dyspnea

Chest pain

Recurrent chest infection

Lung carcinoma

Signs

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Finger clubbing

Nicotine staining Cervical sympathetic (Horner’s  syndrome)=

partial ptosis/ miosis (pupil constriction)/

enopthalmos/ anhydrosis Wasting of hand

Lung carcinoma

Differential diagnosis

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Benign tumors-papilloma/ carcinoid/

leiomyoma

Metastasis

Primary malignant-mesothelioma/ soft tissue

sarcoma Chronic lung abscess

Radiographic artifact-nipple shadow

Lung carcinoma

Investigation

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CXR

Sputum cytology

Bronchoscopy CT

MRI

Bone scan Indirect laryngoscopy

Lung function test

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Stage TNM

Ia T1 N0 M0

Ib T2 N0 M0

Staging lung carcinoma based on TNM classification scheme

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IIa T1 N1 M0

IIb T2 N1 M0

T3 N0 M0

IIIa T3 N1 M0

T1-3 N2 M0

IIIb T4 N0-2 M0

T1-4 N3 M0

IV Any T Any N M1

Based on AJCC staging system 1997

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Single pulmonary nodule

1. Only 20% to 30% are malignant. Higher for

smoker 50%.

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2. CXR/CT criteria, 30% - 40% are

indeterminate, 50% are benign.

3. High.

4. False negative: lesion < 1cm, bronchoalveolar

carcinoma and carcinoid tumors. False

positive: benign tumor, inflammatory,

infection (TB).

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Lung carcinoma staging

1. Focal increased uptake corresponding to the

nodule on CT. abnormal uptake is seen in thei ht d l ft t h l i th i ht

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right and left paratracheal regions, the rightand left hilum and mediastinum.

2. FDG PET has preoperatively upstaged thepatient, who is no longer a surgicalcandidate.

3. 65%

4. 85%

Breast carcinoma

Epidemiology

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UK = 45000 cases

325 arising in men

12000 death per annum

Peak age incidence 50-70 years

Breast carcinoma

Etiology

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Family history

Menstruation > 12 or stop >55 years

On HRT

Women with no borne children

Women have had children late > 30 years

Overweight

Alcohol

Breast carcinoma

Classification

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Ductal carcinoma in situ

Lobular carcinoma in situ

Inflammatory breast carcinoma

Paget’s disease of the breast 

Basal cancers

Male breast cancer

Breast carcinoma

Differential diagnosis

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Fibroadenoma

Breast abscess

Fat necrosis

Galactocoele

Breast carcinoma

Investigations

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Mammography

FNA

Ultrasound

MRI

Excision biopsy

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(ipsilateral mobile axillary nodes)

(ipsilateral fixed axillary nodes)

(ipsilateral internal mammary nodes metastasis)

GIST

Mesenchymal neoplasm

70% arise from stomach

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25% arise from small intestine

Express growth factor receptor with tyrosinekinase activity (c-kit) – detect by CD117

Highly malignant

Resistant to conventional treatment

Staging TNM(Gastrointestinal)

Tis – carcinoma in situ

T0 – no evidence of primary TX – primary cannot be assessed

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p y

T1 – involving lamina propria/submucosa

T2 – involving muscularis propria/subserosa

T3 – penetrates serosa T4 – involving adjacent structures

N0 – 1 – 6 nodes involved

N2 – 7 -15 nodes involved

N3 - > 15 nodes M0 – no distant metastasis

M1 – distant metastasis

Colon carcinoma

Epidemiology

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UK = 36000 cases, 22000 men and 16000

women

3rd commonest

16000 deaths per annum

Occur 50 years of age

Colon carcinoma

Etiology

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Diet – high meat/fat/calorie/alcohol

First degree

Polyps

Chronic Crohn’s colitis 

Colon carcinoma

Symptoms

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Change in bowel habit

Blood per rectum

Mucus per rectum

Tenesmus

Obstructive symptoms

Iron deficiency anemia

Colon carcinoma

Investigations

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Digital PR examination

Double contrast barium enema

Colonoscopy

CT

MRI

Colon carcinoma

DUKES Staging

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Dukes’  A/ stage A  –  invasion into but not

through bowel wall

Dukes’  B/ stage B  –  involving bowel wall but

not lymph nodes

Dukes’ C/ stage C – involvement of nodes

Dukes’ D/ stage D - metastasis

TNM colorectal carcinoma

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TNM colorectal carcinoma

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Colorectal carcinoma

1. Increased uptake consistent with tumor in the

liver corresponding to CT mass. No other liverlesions or metastases are seen elsewhere.

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2. Surgical resection is planned. The preoperativeFDG PET scan is used to determine the presence

of any other metastases in the liver orelsewhere.

3. a. increased serum CEA with normalconventional imaging. b. equivocal lesion withconventional imaging. c. preoperative stagingbefore curative resection.

4. Negative scan. No evidence of tumor.

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Colorectal carcinoma

1. Large abnormal region of increased uptake in

the pelvis consistent with recurrent tumor. Alarge tumor is present in the left pelvis adjacentt th bl dd i dditi t lti l ll it

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to the bladder in addition to multiple small sitesof tumor uptake.

2. Tc-99m CEA is superior to CT in extrahepaticabdomen and pelvis but equal to CT in detectingtumor in the liver.

3. Rising serum CEA level with negative CT findings.Potentially resectable recurrent disease, usuallyin the liver, done to exclude other metastasesthat would preclude surgery.

4. In-111 Oncoscint and FDG PET

Prostate carcinoma

Epidemiology

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UK = 35000 cases = 12% cancer cases and

10000 deaths per annum

Age over 70 years

2nd most common after lung carcinoma

Prostate carcinoma

Symptoms

P t ti tfl b t ti t

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Prostatic outflow obstructive symptoms: poorstream/ frequency/ terminal dribble/ nocturia

Erectile dysfunction Haematospermia

Bone pain

Hypercalcemia

Prostate carcinoma

Investigations

PSA l 4 / l

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PSA = normal 4 ng/ml

Blood test = hypercalcaemia

Biopsy

IVU

CT scan

Bone scan

MRI

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Prostate carcinoma

1. In-111 labeled monoclonal antibody directed

against the prostate specific membrane antigen,a glycoprotein expressed by normal and prostatecancer cells

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cancer cells.

2. CT and MRI sensitivity ranges from 5% - 20%.

Accuracy of In-111 ProstaScint is 70%.3. Paraaortic upper abdominal uptake consistentwith tumor adenopathy. Focal uptake in the leftupper chest consistent with tumor.

4. Recurrent tumor limited to the prostate bed ormetastatic pelvic nodes require radiation ports.Extrapelvic metastases require systemic therapy.

Cervical carcinoma

Epidemiology

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UK = 2700 cases, 900 deaths per annum

Age 40 – 50 years

24000 carcinoma in citu (CIN III)

Cervical carcinoma

Etiology

HPV

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HPV

Intercourse at early age

Lower socioeconomic group

Oral contraceptive

Miscarriage

Smoking

Cervical carcinoma

Symptoms

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Vaginal bleeding

Vaginal discharge

Hematuria

Low back pain

Renal failure due to bilateral ureteralobstruction

Cervical carcinoma

Investigations

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Cervical cytology

Biopsy

CT scan

MRI

Cervical carcinoma

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Cervical carcinoma

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Ovarian carcinoma

Epidemiology

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UK = 6600 cases

2.3 % of all cancer cases

4400 cases deaths per annum

Ovarian carcinoma

Pathology

Common appearance

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Common appearance

• Psedomucinous cyst

• Serous cyst

Microscopic appearance

• Epithelial adenocarcinoma• Germ cell tumors

Ovarian carcinoma

Investigation

S CA 125

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Serum CA 125

CXR

Ultrasound

CT scan

Ovarian carcinoma staging

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Hodgkin’s Lymphoma

Epidemiology

UK 1500 850 d 650

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UK = 1500 cases, 850 men and 650 women

with 350 deaths per annum

Two peak incidence in young 20  –  30 years

and over 70 year

Hodgkin’s Lymphoma

Etiology

E t i B i

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Epstein Barr virus

Hodgkin’s Lymphoma

Symptoms

B t

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B symptoms:

1. Fever > 38⁰C 

2. Weight loss > 10%

3. Night sweat

Hodgkin’s Lymphoma 

Sign

E l d t k

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Enlarge nodes at neck

Hepatospleenomegaly

Abdominal mass

Inguinal nodes

Hodgkin’s Lymphoma 

Differential diagnosis

I f ti i / TB i l

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Infection: pyogenic/ TB or viral

Leukemia

carcinoma

Hodgkin’s Lymphoma 

Investigations

Bl d t

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Blood count

ESR

Serum LDH

Alkaline phosphatase

Marrow

CXR

CT/ MRI

PET scan

Biopsy

Non Hodgkin’s lymphoma 

Epidemiology

UK 10000 cases 5300 for men and 4800 for

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UK = 10000 cases, 5300 for men and 4800 for

women with 4500 deaths per annum

Occurs equally in men and women

More 50 years of age

Non Hodgkin’s lymphoma 

Epidemiology

UK 10000 cases 5300 for men and 4800 for

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UK = 10000 cases, 5300 for men and 4800 for

women with 4500 deaths per annum

Occurs equally in men and women

More 50 years of age

Non Hodgkin’s lymphoma 

Etiology

Infective agents : EBV/ helicobacter/ human T

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Infective agents : EBV/ helicobacter/ human T

cell lymphotropic virus/ HIV

Altered immune status

Irradiation

Non Hodgkin’s Lymphoma 

Sign

Enlarge nodes at neck

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Enlarge nodes at neck

Hepatospleenomegaly

Abdominal mass

Inguinal nodes

Non Hodgkin’s Lymphoma 

Investigations

Blood count

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Blood count

ESR

Serum LDH

Alkaline phosphatase

CSF - DLBCL

Marrow

CXR

CT/ MRI

PET scan

Biopsy

Hodgkin’s Lymphoma 

Classic HD

Nodular Lymphocyte rich

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Nodular sclerosis

Mixed cellularity

Lymphocyte depleted

Nodular

lymphocyte

predominant

Lymphocyte rich

Non Hodgkin’s lymphomaLow grade

Indolent

High grade

CurableAggressive and urgent

treatmentFollicular

Lympho

plasmacytoid

DLBCLBurkitt’s 

Lymphoblastic

Sezary syndrome

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Non Hodgkin s lymphoma Indolent

Respond well to chemo but

difficult to cure

T cellMantle cell

MALT

Lymphocytic

Peripheral T cell

Anaplasticlarge cell

Angiocentric

Adult T cellleukemia

Angioimunoblastic

Mycosis fungoides

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Hodgkin’s disease 

1. FDG is glucose analog. Increased FDG uptake occurs

with increased glucose metabolism. Is taken upintracellularly and phosphorylated similar to glucose,however, unlike glucose, it can not be metabolized

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further and is intracellularly trapped.

2. a. intense multifocal uptake bilaterally in the neck,upper chest and parasternal regions. b. uptake limitedto the left neck. Study a. abnormalities are caused bymuscle tension. Diazepam 5 mg was take just beforestudy b.

3. 110 minutes. 2. 10 and 20 minutes. It is important toremember that the half life of positron are very short.

4. 3.2 rads/ 5 mCi to urinary bladder. Brain and heart.

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Intracranial lymphoma

1. Tl-201 was used. Tc-99m sestamibi also can

be used, however it is taken up by choroidplexus and could pose diagnostic problems in

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some cases.

2. Tumor, particularly lymphoma, versusinfection, usually toxoplasmosis or infection

e.g.. CMV or herpes simplex.

3. Malignant lymphoma.4. 90% sensitivity and false negative < 10%.

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Lymphoma

1. CT scan is in indeterminate, but FDG PETdemonstrates a complete response.

2. CT assessment of tumor response is based on adecreased in the size of the mass or completeresolution Post therapy residual masses are common

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resolution. Post therapy residual masses are commonand CT cannot differentiate residual tumor from post

therapy fibrosis and necrosis.3. Multiple high energy photopeak: 185, 300, 394

resulting poor image resolution, need delayed imagesfrom 2 to 3 days.

4. Study completed 2 hours after injection. FDG PETtarget to background ratio higher and image qualitysuperior to Ga-67.

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Hodgkin’s disease 

1. The bone scan shows mild increased uptake

at L3. The Ga-67 scan shows abnormaluptake in the L3 vertebral body, bilateralneck mediastinum right paratracheal

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neck, mediastinum, right paratrachealregions, posterior thorax, right lung base and

liver.2. Bone scan.

3. Hodgkin’s  disease, TB or atypical

mycobacteria; Hodgkin’s disease likely.4. Stage IV.

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Non Hodgkin’s lymphoma 

1. Adult dose is 10 mCi. Imaging performed 48 to

72 hours after injection.2. CT provides better sensitivity for initial staging.

Ga-67 is superior to CT after therapy and

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Ga-67 is superior to CT after therapy andresidual masses after therapy.

3. a, large mass in the anterior mediastinumextends to supraclavicular regions. b. completeresponse to therapy. The residual chest mass onCT caused by necrosis and fibrosis, not tumor.

4. Laxative may be given, and imaging may bedelayed as needed at 4 to 7 days after injection.

Axillary LNs

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Sentinel node

• Is the first lymph node bed which a tumor cell

would come if it penetrated into lymphaticfluid.

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• If axillary sentinel node is tumor free < 3%

chance of any tumor metastasis• Radiopharmaceutical= Tc-99m SC injected

subdermally/ periareolar/ intradermal or

peritumoral

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Scintimammography

1. Tc-99m sestamibi lipophilicity allows it to enter thecell where it is concentrated in the mitochondrialregion related to charge.

2. Patient A has prominent focal uptake in a right breastmass Patient B has definite focal uptake at the

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mass. Patient B has definite focal uptake at theperiphery of the breast prosthesis.

3. Accuracy of conventional mammography: sensitivity,70% to 95%; positive predictive value for cancer, 20%- 30%. Scintimammography trial: sensitivity/specificity, 75%/83%

4. Most false negative findings are in lesions less than 1cm. False positive findings occur in fibroadenomasand benign and malignant tumors other than breastcancer

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Scintimammography

1. The 5 year survival rate for breast cancerdecreases with axillary node involvement.Adjuvant chemotherapy is indicated.

2. A sentinel node biopsy drained by thel h i i d l b i

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lymphatics in a nodal basin.

3. If the sentinel node biopsy is tumor negative, noaxillary dissection is needed. If positive, axillarydissection is performed.

4. Tc-99m sulfur colloid is often used. It is injectedaround the lesion or biopsy site. Imaging usuallyis performed. At surgery a gamma probe is usedto help locate the sentinel node.

Head and neck carcinoma

• PET sensitivity for recurrence is 76-96%

• Negative predictive value > 90%

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Thyroid carcinoma

• PET sensitivity for poorly differentiated

carcinoma > 90%• Benefits for: anaplastic and Hurtle cell variant

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of follicular

Medullary thyroid carcinoma

• Arises from parafollicular cells

• Does not accumulate I-131• PET sensitivity 78% and specificity 79%

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• Can evaluate with :1. Somatostatin

2. DMSA pentavalent

3. Thallium 2014. Tc-99m sestaMIBI

Esophageal carcinoma

• PET sensitivity 95%

• LNs involvement sensitivity >70%

• LNs involvement specificity >90%

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p y

• Distant metastasis accuracy 83%

Colorectal carcinoma

• Primary sensitivity >90% : CT 60%

• LNs involvement sensitivity 85 – 99%

• LNs involvement specificity 71 – 87%

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• Alter management 29 – 36%

Melanoma

• PET sensitivity > 90% and specificity 87%

• PET alter treatment 20 – 26%

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• Α feto protein for hepatocellular carcinoma

• Ca 19-9 for pancreatic carcinoma

• PET less sensitive for hepatocellular carcinoma

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Breast carcinoma

• PET sensitivity 88% and specificity 79%

• > 2-5 cm PET sensitivity 92%• < 2 cm PET sensitivity 68%

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• LNs involvement sensitivity 79-100% and

specificity 66-100%

• False negative:

1. Well differentiated2. Slow growing : lobular/tubular/DCIS

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PET false – ve in

Mucinous

cystadenocarcinoma

Well differentiated

cystadenocarcinoma

Di i d i l

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PET false   ve in

ovarian carcinoma

Disseminated peritoneal

carcinomatosis

Borderline tumors

Stage I tumors confined to

the ovary

Testicular carcinoma

• PET sensitivity 84%

• PET negative predictive value is 94%

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Neuroendocrine tumor

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Radionuclide therapy

Bone metastasis

Intra articular therapy

Intra vascular therapyHepatocellular ca

Phosphorus 32 phosphate

Rhenium 188 lipiodol

Rhenium 188

Rhenium 188 HEDP

Phosphorus 32 phosphate

Phosphorus 32 phosphate

Yittrium 90 microsphere

I-131 lipiodol

Samarium 153 EDTMP

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Non Hodgkin’s LymphomaIntra cavity therapy

Polycythemia vera

Hyperthyroid / thyroid ca

Phosphorus 32 phosphatePhosphorus 32 phosphate colloid

I-131 NaI

Yittrium 90 citrate

I-131 anti CD 20 antibody

Strontium 89 chloride

PeptideNon specific

Tumor specific

Tumor imaging

Monoclonal

Thyroid ca

Tc-99m

Thallium-201

FDG

Gallium - 67

MIBI/tetrofosmin

MTC

Breast

MTC

Breast

Brain

Bone

MTC

Karposi sarcoma

I-131

HD

NHD

Hepatocellular

Melanoma

LungsHead & neck

Soft tissue sarcoma

Abd & pelvic tumors

MIBG

Adrenal medulla

NP-59

Adrenal cortex

DMSA(V)

MTC

Tc-99m CEA

Colorectal

I-111 pentreotide

Somatostatin

MTC

Tc 99m Neo Tect

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Organ specific

HotCold

ThyroidBone Brain

I-123

Tc-99m pertechnetate

Tc-99m SC Tc-99m DTPA

Tc-99m glucoheptonate

Hepatocyte

Tc-99m MDP

Tc-99m HDPTc-99m HIDA

In-111 satumomab (onco scint)

Ovarian

colorectal

In-111 capromab

Prostate

Liver

I-111 zevalin

NHD

Tc-99m Neo Tect

Somatostatin

Lungs ca

What is the mechanism of G-67 uptake

in tumors?

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What is the mechanism of G-67 uptake

in tumors?

• It’s binds to serum iron transport molecules suchas transferrin, which transport Ga-67 to thetumors.

• Ga-67 enters the extracellular fluid space via thetumor’s leaky capillary endothelium.

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• It’s bound to the tumor cell surface by transferrinreceptors and then transported into the cell,where it binds to proteins such as ferritin andlactoferrin, which are increased concentration in

tumors.

Ga-67 uptake is normally seen in which

of the following organs: salivaryglands, lacrimal glands, thymus,

spleen, breast and heart?

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Ga-67 uptake is normally seen in which

of the following organs: salivaryglands, lacrimal glands, thymus,

spleen, breast and heart?

• Normal uptake : salivary glands and lacrimal

glands. Spleen has uptake but is low level.

B t t k i i bl d t i t

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Breast uptake is variable and most prominent

in post partum.

• Children after chemo : thymus

Not normal : heart due to myocarditis andpericarditis.

Which malignant tumors useful for Ga-

67 for diagnosis, staging and restaging?

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Which malignant tumors useful for Ga-

67 for diagnosis, staging and restaging?

• Hodgkin’s disease• Lymphoma

• Hepatoma

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Hepatoma

• Melanoma

Which of the following statement

associated with Hodgkin’s and nonHodgkin’s lymphoma? 

A. Contagious spread of LN involvement in youngpatients.

B. Multicentric disease with a highly variable clinicalcourse and high incidence of extranodal tumorinvolvement

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involvement.

C. Mediastinal masses are common.D. Abdominal involvement of mesenteric and

retroperitoneal nodes is common.

E. High cure rate.

F. Variable clinical course that can be indolent or rapidlethal

Which of the following statement

associated with Hodgkin’s and nonHodgkin’s lymphoma? 

HD

• Contagious spread of LN

involvement in young

patients.

Non HD• Multicentric disease with a

highly variable clinical course

and high incidence of

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p

• Mediastinal masses arecommon.

• High cure rate.

extranodal tumorinvolvement.

• Abdominal involvement of

mesenteric and

retroperitoneal nodes is

common.• Variable clinical course that

can be indolent or rapid lethal

Tc-99m sestamibi has been used for

determination of malignancy of breastmasses.

A. Its accuracy is higher for palpable than fornon palpable masses.

B. Its sensitivity is poor for lesions less than 1

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cm in size.C. Fibroadenomas are always negative.

D. Useful for dense breast patients, previous

surgery, radiation therapy and breastimplants.

Tc-99m sestamibi has been used for

determination of malignancy of breastmasses

TTFT

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Regarding In-111 capromab pendetide

(ProstaScint)

A. Murine monoclonal antibody against aprostate specific membrane antigen expressby more than 95% of prostateadenocarcinomas.

B. Its main indication is for localization of soft

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tissue metastases after prostactomy inpatients with a rising PSA and negative bonescan.

C. Elevated human murine antibody (HAMA)titers are observed in 50% of patients.

D. SPECT is mandatory for the pelvis.

Regarding In-111 capromab pendetide

(ProstaScint)

• TTFT

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Regarding In-111 Octreoscan

A. It is somatostatin receptor imaging agent.

B. The sensitivity for all NET is very high.C. Highest uptake is seen in the spleen and

kidneys.

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D. Only NET have somatostatin receptors.

Regarding In-111 OctreoScan

• TFTF

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Lacrimal drainage study

Inner canthus

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Using 2 - 4 MBq Tc-99m pertechnetate

Face in front collimator

Imaging time 5,10, 15, 20 minutes

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Dacryoscintigram : Normal drainage on the left eye with obstruction on

the right eye at the level of common canaliculus

Radiosynovectomy

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