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PATHOLOGY OFENDOCRINESYSTEMDepartment of Pathology GMUSM
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Hypophysis
A. Anterior pituitary (adenohyphophysis)
1. Anterior pituitary hyperfunction
a. Prolactinomawith hyperprolactinemia
- is most common/30% pituitary tumor- staining chromophobe
- in women amenorrhea &
galactorrhea
- caused by hypothalamic lesions or
mediations methyl dopa, reserpine
interfere with dopamine
(prolactin-inhibitory factors) secretion
- can also be associated with estrogen
therapy
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b. Somatotropic adenoma with hypersecretion of growthhormone
- 2ndmost common pituitary tumor
- staining acidophyl
- causes secondary hyperfunction of somatomedins by the
liver. End organ effects are caused by both growth
hormone and somatomedins, especially somatomedin C
(insulin-like growth factor 1/IGF-1)
- results gigantismif adenoma develops before epiphyseal
closure and acromegaly if adenoma develops after
epiphyseal closure- acromegalyovergrowth of jaws, face, hands and feet,
and general enlargement of viscera with hyperglycemia,
osteoporosis and hypertension
- can also result in local compression effects due to
expansion of the tumor within the sella tursica
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Anterior pituitaryhypofunctiona. Pituitary cachexia (Simmonds disease)
- is generelized panhypopituitarism
- characterized by marked wasting
- can result from any process that destroy the
pituitaryEtiology:
(1) Pituitary tumors
(2) Post partum pituitary necrosis (Sheehan
syndrome)
- is caused by ischemic necrosis of pituitarygland,
characteristically associated with hemorrhage
and shock during childbirth
- clinical manifestations are due at first to loss of
gonadotropins, then to subsequent loss of TSH
and ACTH
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b. Selective deficiency of one or more
pituitary hormones
(1) deficiency of growth hormone
- in children, result in growth retardation (pituitary dwarfism)
- in adults, may result in increased insulin sensitivity with
hypocalcemia, decreased muscle strength and anemia(2) deficiency of gonadotropins
- in preadolescent children, results in retarded sexual
maturation
- in adults, results in loss of libido, impotence, loss of muscular
mass, and decreased hair in men, and amenorrhea and vaginal
atrophy in women
(3) deficiency of TSH
- result in secondary hypothyroidism
(4) deficiency of ACTH
- results in secondary adrenal failure
- does not result in hyperpigmentation of the skin, probably
because of lack of both ACTH and -MSH; this is in contrast to
primary adrenal failure (Addison disease), in which ACTH isincreased and hyperpigmentation is the rule
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Growth hormone containing cell in adenoma ofadenohyphophysisImmunoperoxidase staining method
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POSTERIOR HYPOPHYSISNEUROHYPOPHYSIS) HORMONES
- are synthesized in the hypothalamus and
transported via axons to the posterior
pituitarya. Oxytocin: induces uterine contarction
during labor and ejection of milk from
mammary alveoli
b. Anti diuretic hormone(ADH, vasopressin)- promotes water retention through action
on the renal collecting ducts
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Syndrome of inappropriate ADH(SIADH)secretion is
most commonly caused by ectopic production of ADH
by various tumors, especially small cell carcinoma of
lung. Results in retention of water with consequentdilutional hyponatremia, reduced serum osmolality,
and inability to dilute urine
Deficiency of ADH: results in diabetes insipidus;
characterized by polyuria, with consequent
dehydration and insatiable thirst- can be caused by tumors, trauma, inflammatory
processes, lipid storage disorders, and other
conditions characterized by damage of the
neurohypophysis or hypothalamus
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C. NON FUNCTIONINGPITUITARY TUMORS Non secreting pituitary adenomas
- are most often chromophobe
- result in dysfunction because of local
pressure phenomena- are clinically variable ;manifestations
include hypopituitarism, headache,visual
disturbance (bilateral hemianopsia / loss of
peripheral visual fields due to pressure onoptic chiasm), and palsies caused by
cranial
nerve damage
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Craniopharyngioma- is benign childhood tumor derived from remnants of
the Rathke pouch
- is not a true pituitary tumors- similar to ameloblastoma of the jaw
- is characterized by nests and cords of squamous orcolumnar cells in loose stroma, closely resembling theappearance of the embryonic tooth bud enamel organ
- is often cystic; lining epithelium of flat or columnar cellsoften expands into papillary projections
- is often detected radiographically because of calcification
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Craniopharyngioma : masses of keratin within tumourmasses composed of loosely packed stellate epithelialcells surrounded by a pallisaded basal layer bordering anoedematous stroma
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PATHOLOGY OFTHYROID ANDPARATHYROID GLANDHarijadi
Department of Pathology GMU SM
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NORMAL THYROIDGLAND
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Autoimmune disease of thyroidgland
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HYPERTHYROIDISM GRAVES THYROIDITIS
FUNCTIONAL ADENOMA
TOXIC NODULAR GOITRE
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GR VES DISE SE
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Gross specimen of Graves disease
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MICROSCOPIC SPECIMEN OF GR VESdisease
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Papillary carcinomathyroid
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Follicular carcinoma ofthyroid
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Anaplastic carcinoma ofthyroid
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Medullary carcinoma ofthyroid
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Parathyroid adenoma
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Parathyroid adenoma
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Pathology ofadrenal glandsHarijadi
Department of Pathology GMUSM
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Normal adrenal gland
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NORMAL CORTEXADRENAL
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Adrenal glands CORTEX
- Hypercorticism / Cushing syndrome
- Hyperaldosteronism- Adrenal virilsm
- Hypocorticism
MEDULLA- Pheochromocytoma
- Medulloblastoma
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ADRENOCORTICAL HYPERPLASIA
The adrenal cortex are yellow, thickened and multinodular
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ADRENOCORTICAL ADENOMASOLITARY, CIRCUMSCRIBED
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ADRENAL CORTICALADENOMA
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Cells in adrenocorticaladenoma
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Compact adenoma
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Black cortex adenoma inCushing syndrome
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Morphologic changes inadrenal glands Bilateral hyperplasia of adrenal zona fasciculata occurs
when the syndrome results from ACTH stimulation
Adrenal cortical atrophy is seen when exogenousglucocorticoid medication is cause
Adrenal cortical adenoma or carcinoma
- Adenoma is more common- cannot be supressed by exogenous adrenal steroids in
dexamethasone supression test, in contrast, hypercorticismof
pituitary origin can usually be supressed useful diagnosis
measures in determining the cause of hypercorticism.- ACTH increased in pituitary hypercorticism and in ectopic
ACTH production, and it is low when hypercorticism isadrenal
origin
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Clinical characteristics ofhypercorticism Redistribution of body fat with round
moon face, dorsal buffalo hump, oftenwith relatively thin extremities caused
by muscle wasting; skin atrophy witheasy bruishing and purplish striae,especially over abdomen , and
hirsutism Muscle weakness, osteoporosis,
amenorrhea, hypertension,hyperglycemia, and psychiatric
d sfunction
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HYPERALDOSTERONISM Primary aldosteronism ( Conn syndrome)
- is caused by primary hyperfunction od adrenal
mineralocorticoids
- usually results from an aldosteron-producing
adrenocortical adenoma (aldosteronoma)- can results from hyperplasia of the zonaglomerulosa
- may rarely caused by adrenocortical carcinoma
- is characterized clinically by hypertension, sodium
and water retention, and hypokalemia, often withhypokalemic alkalosis
- demostrates decreased serum renin due tonegative
feedback of increased blood pressure on renin
secretion
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Secondary aldosteronism
- is secondary to renal ischemia, renal tumors, and
edema( e.g. cirrhosis, nephrotic syndrome, cardiac
failure)
- is caused by stimulation of the renin-angiotensin
system
- demonstates increased serum renin. In contrast to
primary aldosteronism. Renin synthesized in the
juxta glomerular apparatus of the kidney promotes
the conversion of angiotensigen to angiotensin I,
which converted catalytically by angiotensin
converting enzyme (mainly in lung) to AT II. The
release of aldosterone is facilitated by AT II.
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Adrenal virilismadrenogenital syndrome) Causes
a. Congenital enzyme defectresult in deminished
corticol production and compensatory increased
ACTH, with resultant adrenal hyperplasia with
androgenic steroid production(1) 21- hydroxylase deficiencymost common
result in salt loss and hypotension
(2) 11- hydroxylase deficiency less common
results in salt retention and hypertension
b. Tumor of the adrenal cortex
Clinical characteristic:
- produces virilism in females and precocious puberty
in males
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HYPOCORTICISMadrenal hypofunction) Can be primary adrenal cause or
secondary to hypothalamic or
pituitary hypofunction Is characterized by deficiency of
glucocorticoid (primary cortisol) ,
often associated with
mineralocorticoid deficiency
1. ADDISON DISEASE
2. Waterhouse Friderichsen
syndrome
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ADDISON DISEASE Is most commonly due to idiopathic adrenal
atrophy ( autoimmune lymphocyticadrenalitis)
Can also be caused by tuberculosis,metastatic tumors and various infections.
Is characterized by hypotension; increasedpigmentation of skin; decreased serumsodium, chloride, glucose, and bicarbonate;and increase of serum potasium
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Waterhouse Friderichsensyndrome Is catastrophic adrenal insufficiency
and vascular collapse due to
hemorrhagic necrosis of the adrenalcortex
Is often associated with disseminated
intravascular coagulation
Is characteristically due to
meningococcemia, most often in
association with meningococcal Adrenals in Waterhouse-
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Friderichsensyndromedestroyed by hemorrhage
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Tumors of adrenalmedulla1. Pheochromocytoma
Is derived from chromaffin cells of adrenal
medulla( if derived from extra-adrenal chromaffincells, called paraganglioma
Most often benign, only 10% malignant
Is characterized by increased urinary excretion of
catecholamines (epinephrine or norepinephrine)
and their metabolites ( metanephrine,
normetanephrine, and vanillymandelic acid (VMA)
Can also cause hyperglycemia
Can be part of MEN IIa or MEN IIb(III)
Can also be associated with bneurofibromatosis or
with von Hippel-Lindau disease
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Pheochromocytomathe adrenal medulla is expanded by a darked-coloured
tumour with areas of degeneration and hemorrhage
Pheochromocytoma
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left right normaladrenal
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Chromaffin cells inpheochromocytoma
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2. Neuroblastoma Is highly malignant catecholamine producing tumor in early
childhood. Urinary catecholamine and cathecolaminemetabolites are the same as in pheochromocytoma
Causes hypertension
Usually originates in the adrenal medulla and often presents
as a large abdominal mass Occasionally converts into a more differentiated form termed
ganglioneuroma
Is characterized by amplification of the N-myc oncogene withthousands of gene copies per cell
a. Amplification results in karyotypic changes homogenous
staining regions or double minutes chromosomes
b. the number of N-myc gene copies is related to the
aggressiveness of the tumor
c. the malignant neuroblastoma sometimes differentiate into
benign cells, and this changes is reflected by a marked
reduction of gene amplification
Microscopic appearance of
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neuroblastoma neurogenic primitivecells
MULTIPLE ENDOCRINE
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NEOPLASIA MEN)SYNDROMES Are a group of autosomal dominant
syndromes in which more than one
endocrine organ are hyperfunctional May be associated with hyperplasia or
tumors
MEN I ( Werner syndrome)MEN IIa (Sipple syndrome)
MEN IIb / III
MEN I WERMER
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SYNDROME) Includes hyperplasia or tumors of the
pituitary, parathyroid, or pancreatic islets(3Ps)
Additionally may include hyperplasia ortumors of the thyroid or adrenal cortex
May manifest its pancreatic component bythe Zollinger-Ellison syndrome,
hyperinsulinism, or pancreatic cholera Is linked to mutations in the MEN I gene
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MEN IIa (Sipple syndrome)
- includes pheochromocytoma, medullary
carcinoma of thyroid, and hyperparathyroidismdue to hyperplasia or tumor
- is linked to mutations in the retoncogene MEN IIb / III
- Includes pheochromocytoma, medullarycarcinoma,
and multiple mucocutaneous neuroma organglioneuroma. In contrast to MEN IIa, does not
induce hyperparathyroidism.
- is linked to different mutations in the retoncogene
than is MEN IIa
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NORMAL PANCREAS
Staining of immunoperoxidase technique
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for insulin insulin containing cells aredarkly stained
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TYPES OF DM
TYPE I VERSUS TYPE II
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DM
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DIABETES MELLITUS Classification and general features
A. Type 1 (insulin-dependent diabetes mellitus / IDDM),
juvenile or ketosis-prone diabetes mellitus
- often begins early in life, before age 30
- is less common than type 2
- is due to failure insulin synthesis by beta cells of the pancreas
islets- a genetic predisposition complicated by
autoimmune inflammation / insulinitis triggered by a viral
infection or environmental factors. Family history lessfrequently
than type 2 DM
- Increased incidence with specific point mutation of HLA- DQ
gene, and incidence markedly increased in HLA-DR3- and
HLA-DR4-positive individuals
- marked carbohydrate intolerance with hyperglycemia, leading
polyuria, polydipsia, weight loss despite increased appetite,
ketoacidosis, coma and death
- ketoacidosisketon bodiesincreased catabolism of fat
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B. Type 2 (non-insulin dependent diabetesmellitus / NIDDM, adult onset, ketosis-
resistent DM
- More common than type 1 DM
- Most often in middle age
- due to increased insulin resistance
mediated by decreased cell membrane
insulin receptors or post receptordysfunction, impaired processing of pro-
insulin to insulin, decreased sensing of
glucose by beta cells, or impaired
function of intracellular carrier proteins
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(1) Etiologic factors
(a) positive family history more frequent than type 1
(b) most often associated with mild to moderate
obesity
(2) Characteristics
(a) normal, often increased, plasma insulin
concentration
(b) mild carbohydrate intolerance, most often
managed by oral antidiabetic agents; insulin
therapy is not usually required
(c) ketoacidosis is unsual but does occur,characteristically precipitated by unusual stress
such as infection or surgery
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C. Maturity-onset diabetes mellitus of the young (MODY)
- an autosomal dominant syndrome characterized by
mild hyperglycemia and hyposecretion of insulin, but
without loss of beta cells
- onset earlier than type 2 DM
- is caused by a diverse group of single gene defects
D. Secondary DM occurs as a secondary phenomenon in pancreaticand other endocrine disease and pregnancy
(a) pancreatic disease
- hereditary hemochromatosis (bronze diabetes)
excess iron absorption and parenchymal deposition of
hemosiderin, with reactive fibrosis in various organs,
especially pancreas, liver and heart
(b) pancreatitisacute pancreatitis hyperglycemia,
chronic pancreatitis islet cell destruction and secondary DM
(c) carcinoma of pancreas DM may be the presenting sign
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Other endocrine diseases Cushing syndrome produces
hyperglycemia a s a result of increased
gluconeogenesis and impaired peripheral
utilization of glucose
Acromegaly produces hyperglycemia due
to the anti- insulin like effect of GH
Glucagon hypersecretion promotes
glycogenolysis is characteristically caused
by an islet alpha cell tumor (glucagonoma)
Phaeochromocytoma and hyperthyroidism
are sometimes associated with
hyperglycemia
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Pregnancy May associated with transient DM
(gestational diabetes)
Is characteristically associated with
increased fetal birth weight and increasedfetal mortality, notably from neonatal
respiratory distress syndrome (hyaline
membrane disease)
When the mother has hyperglycemia can
result in an infant born with hyperplasia of
the pancreatic islets and hypoglycemia
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Pathologic changes in DM Pancreas islets
(1) Type 1 DM islets are small and beta cells are
greatly decreased in number or absent; insulinitis
marked by lymphocytic infiltration is highlyspecific
early change
(2) Type 2 DM focal islet fibrosis and
hyalinization due to deposit amylin are
characteristic but not specific. Amylin (islet
amyloid polypeptide/IAPP) deposition inpancreatic islet is characteristic of type 2 DM and
thought to interfere either with conversion of
proinsulin to insulin or with the sensing of insulinby
beta cells
Amyloid of a pancreatic
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islet
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Hyaline arteriolosclerosis of
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afferent arteriole of kidney
Nodular
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glomerulosclerosis
Nephrosclerosis in long
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standing diabetes
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Diabetic retinopathy
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ISLET CELL TUMOR Insulinoma (beta cell tumor)
- is most common islet cell tumor
- benign / malignant
- characterized by greatly increased of
insulin- clinically Whipple triad
1. episodic hyperinsulinemia and
hypoglycemia
2. CNS dysfunction temporally related tohypoglycemia (confusion, anxiety,
stupor, convulsion, coma)
3. Dramatic reversal of CNS abnormalities
by glucose administration
Insulinoma : ribbon or brown stained cells
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resembling those of the normal islet ofLangerhans
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Gastrinoma
- is often a malignant tumor, sometimes
occuring in extrapancreatic sites
- results in gastrin hypersecretion andhyper-
gastrinemia
- is associated with Zollinger-Ellison
syndrome ( marked gastric hypersecretion
of HCl, recurrent peptic ulcer disease and
hypergastrinemia