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8/10/2019 AZIMAT NUCLEAR PDF .pdf
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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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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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j p
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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p g p
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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p j (p )
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
2
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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