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Pathology > Endocrine > Flashcards

Endocrine Flashcards

1
Q

MCC of hyperpituitarism

Associated with distinct endocrine signs and symptoms

A

FUNCTIONING ANTERIOR PITUITARY ADENOMA

1 cm - limit size to determine micro/macroadenoma

Prolactin cell adenoma - MC

Somatotroph adenoma - 2nd MC

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2
Q

2nc MC pituitary adenoma

present with mass effects - visual disturbance

A

NON-FUNCTIONING ADENOMA

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3
Q

Microscopic findings in pituitary adenoma

A

Uniform (monomorphic)

Sparse reticulin network

Few mitosis

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4
Q

Sine qua non of Pituitary Carcinomas

atypical adenoma + metastases (CSF/systemic)

A

METASTASES (craniospinal/systemic)

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5
Q

Occurs at ~75% parenchymal loss

CAUSES:
tumors/mass lesions
PITUITARY APOPLEXY
SHEEHAN SYNDROME
Empty sella syndrome

A

HYPOPITUITARISM

GH and gonadotropin (FSH and LH) lost FIRST –> TSH and ACTH –> prolactin (lost LAST)

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6
Q

ADH DEFICIENCY

CAUSES:
CNS disorders

A

Central Diabetes Insipidus

serum osmolality - N - H
urine osmolality - L
serum ADH - L

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7
Q

Unresponsiveness of renal tubules to ADH

CAUSES:
drugs
renal disorders

A

Nephrogenic Diabetes Insipidus

serum osmolality - N - H
urine osmolality - L
serum ADH - H

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8
Q

ADH EXCESS

CAUSES:
SCLC
CNS disorders

A

SIADH

serum osmolality - L
urine osmolality - N - H
serum ADH - H

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9
Q

slow-growing tumors account for 1% to 5% of intracranial tumors

suprasellar, with or without intrasellar extension

bimodal age distribution - one peak in childhood (5 to 15
years) and a second peak in adults 65 years of age or older

ADULTS - headaches and visual disturbances

CHILDREN - growth retardation due to pituitary hypofunction and GH deficiency

A

CRANIOPHARYNGIOMA

from vestigial remnant of RATHKE’S POUCH

Adamantinomatous - compact, lamellar
*WET KERATIN
*DYSTROPHIC CALCIFICATION

Papillary
*papillae

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10
Q

MCC of primary hyperthyroidism

Autoantibodies against TSH receptor

A

GRAVES DISEASE

symmetrically enlarged thyroid

MICROSCOPIC:
diffuse hypertrophy and hyperplasia of thyroid follicular epithelial cells
pseudopapillary structures
pale, scalloped colloid

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11
Q

MCC of congenital hypothyroidism

A

IODINE DEFICIENCY

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12
Q

MCC of hypothyroidism in iodine-sufficient areas

A

AUTOIMMUNE

i.e. Hashimoto

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13
Q

MCC of hypothyroidism in iodine-sufficient areas

autoimmune disease that results in destruction of the thyroid gland and gradual and progressive thyroid failure

T cell mediated injury

Autoantibodies against THYRPGLOBULIN and TPO

COMPLICATIONS:
development of neoplasms (marginal zone B cell lymphoma, papillary thyroid ca)

A

HASHIMOTO THYROIDITIS

PAINLESS thyroid enlargement

diffusely enlarged thyroid

HURTHLE cell changes
GERMINAL CENTERS
(+) FIBROSIS

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14
Q

Autoantibodies against TPO

Family history of autoimmunity

(+) URTI

A

SUBACUTE LYMPHOCYTIC

thyroid grossly normal

PAINLESS thyroid enlargement

(-) fibrosis
(-) Hurthle cells

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15
Q

Antigen-mediated immune damage to follicular cells

(+) URTI prior to thyroiditis

believed to be triggered by a viral infection

majority of patients have a history of an URTI just before the onset of thyroiditis

A

Granulomatous thyroiditis (also called De Quervain thyroiditis)

unilateral or bilaterally enlarged and firm thyroid

PAINFUL thyroid enlargement

multinucleate giant cells enclose pools of colloid

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16
Q

TRIAD of GRAVES DISEASE

A

Hyperthyroidism
Exophthalmos - fibrosis (orbit and EOM)
Dermopathy - pretibial myxedema (dermal thickening)

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17
Q

Thyroid enlargement caused by IMPAIRED THYROID HORMONE synthesis

MASS EFFECT

LOW incidence of malignancy

A

GOITER

iodine deficiency –> compensatory increase in TSH –> trophic effect of TSH on thyroid –> enlargement of the thyroid gland

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18
Q

Phases of Goiter

A

HYPERPLASTIC
*diffuse, symmetrical enlargement
*columnar

COLLOID
*brown, glassy, translucent
*flattened and cuboidal
*abundant

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19
Q

TYPES OF GOITERS

A

Diffuse Nontoxic (Simple)
*areas of iodine insufficiency and intake of goitrogens (cassava - thiocynate)

Multinodular
*irregular enlargement of thyroid
*repeated hyperplastic and colloid phases –> nodularity
*unencapsulated nodular architecture

Toxic Multinodular (PLUMMER SYNDROME)
*autonomous nodule in a long standing multinodular goiter
*(+) hyperthyroidism
*(-) ophthalmopathy, (-) dermopathy

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20
Q

Clinical Factors Favoring Malignancy in Solitary Thyroid Nodule

A

Solitary nodule
Young, Male
History of radiation therapy
NON-FUNCTIONAL - COLD nodules

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21
Q

Shares morphological features with ADENOMATOUS NODULE and FOLLICULAR CARCINOMAS

A

FOLLICULAR ADENOMA

encapsulated lesions
uniform-appearing follicles
little pleomorphism
rare mitosis

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22
Q

HALLMARKS of thyroid adenoma

A

intact, well formed capsule encircling the tumor

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23
Q

MC thyroid cancer

account for the majority of thyroid carcinomas associated with previous exposure to IONIZING RADIATION

A

PAPILLARY CA

(RET/PTC, BRAF)

papillary fronds with fibrovascular cores
ORPHAN ANNIE NUCLEI
PSAMMOMA BODIES - calcifications
LYMPHATIC METASTASIS

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24
Q

2nc MC thyroid cancer

A

FOLLICULAR CA

(RAS, PAX 8, PPAR y)

invading thyroid capsule and vasculature
oncoytic type of Hurthle cells

25
Q

2nc MC thyroid cancer

A

FOLLICULAR CA

(RAS, PAX 8, PPAR y)

invading thyroid capsule and vasculature
oncoytic type of Hurthle cells
HEMATOGENOUS METASTASIS

26
Q

represent aggressive neoplasms of the thyroid
follicular epithelium

less than 5% of thyroid tumors, but with a high mortality rate

RAPID ENLARGEMENT
LARGE MASS

A

ANAPLASTIC CA

pleomorphic GIANT CELLS
SARCOMATOUS appearance - spindle shaped cells

(+) CYTOKERATIN
(+) PAX - 8

27
Q

Neuroendocrine neoplasms derived from the parafollicular cells (C cells)

(+) calcitonin

A

MEDULLARY

RET

small, polygonal to spindle shaped cells
acellular AMYLOID deposits

28
Q

FAVORABLE prognosis

A

papillary thyroid ca
minimally invasive follicular ca

29
Q

UNFAVORABLE prognosis

A

widely invasive follicular ca
medullary thyroid ca
anaplastic thyroid ca

30
Q

Most helpful thyroid differentiation marker in anaplastic ca

A

PAX-8

31
Q

Used to diagnose parathyroid gland pathologies

A

TECHNETIUM 99 radionuclide scan
SCINTIGRAPHY
SESTAMIBI SCANS

32
Q

Clinical manifestations of symptomatic primary hyperparathyroidism

A

STONES, THRONES, BONES, GROANS, PSYCHIATRIC OVERTONES

kidney stones
polyuria and polydipsia
bone pain
weakness, constipation, abdominal/flank pain
confusion, hallucinations, irritability

33
Q

Hallmark of Severe Hyperparathyroidism

A

increased osteoclast activity
peritrabecular fibrosis
cystic brown tumor

34
Q

HALLMARK of HYPOCALCEMIA

A

TETANY

35
Q

ABSOLUTE insulin deficiency
B cell destruction
TYPE IV
HLA - CHROMOSOME 6
antibodies against islet cells (anti-insulin, anti-GAD, anti-ICA2)

A

TYPE I DM

36
Q

RELATIVE insulin deficiency
insulin resistance
B cell dysfunction
genetic, environmental, proinflammatory

A

TYPE II DM

37
Q

Acute Complications of DM

A

hypoglycemia
DKA
HHS

38
Q

Macrovascular diseases in DM

A

Coronary Heart Disease - MI - MCC of death
Peripheral Arterial Disease
Cerebrovascular Disease

39
Q

Microvascular diseases in DM

A

Retinopathy
Nephropathy
Neuropathy

diffuse BM thickening and leaky capillaries
NODULAR GLOMERULOSCLEROSIS - KIMMELSTIEL WILSON LESION

pyelonephritis, necrotizing papillitis
NERVES - glove and stocking pattern - MC

40
Q

Insulin deficiency sufficient to develop KETOACIDOSIS

<7.25

(+) KETONES

usually VISCERAL (nausea, vomiting, abdominal pain)

A

DKA

41
Q

Insulin deficiency insufficient to develop KETOACIDOSIS

> 7.30

usually NEUROLOGIC (altered mental status)

A

HHS

42
Q

MC Pancreatic Neuroendocrine Tumor

A

INSULINOMA

43
Q

Hyperinsulinism

WHIPPLE TRIAD
hypoglycemia (<50 mg/dl)
neuroglycopenic symptoms
relief upon parenteral glucose administration

A

INSULINOMA

pancreas
BENIGN

(+) amyloid deposition

44
Q

Hypergastrinemia

pancreatic islet tumor
hypersecretion of gastric acid
severe peptic ulceration

A

GASTRINOMA (Zollinger Ellison Syndrome)

gastrinoma (Passaro) triangle

usually MALIGNANT

45
Q

Ovoid, spherical, laminated nodules of matrix observed in diffuse and nodular diabetic glomerulosclerosis

A

KIMMELSTIEL-WILSON DISEASE

46
Q

Hallmark of macrovascular disease in DM

A

ACCELERATED ATHEROSCLEROSIS

MI - MCC of death in diabetes

47
Q

Abdominal striae, obesity, dorsocervical fullness (buffalo hump), moon facies

LAB FEATURES: increased 24 hr urine free cortisol

ACTH-independent - increased cortisol –> decreased ACTH
ACTH dependent - increased ACTH –> increased cortisol

pituitary (Cushing disease) or ectopic (SCLC) - increased ACTH

A

CUSHING SYNDROME

Exogenous steroids - MCC overall
ACTH secreting pituitary adenoma (Cushing disease) - MC endogenous cause

48
Q

Crisis in patients with CHRONIC adrenocortical insufficiency
Rapid withdrawal of steroids in patients maintained on steroids

MASSIVE ADRENAL HEMORRHAGE - Waterhouse Friedrichsen syndrome

A

Primary Acute Adrenocortical Insufficiency

49
Q

MCC of primary hyperaldosteronism (CONN DISEASE)

INCREASED ALDOSTERONE

PRIMARY - increased aldosterone – decreased renin
SECONDARY - increased aldosterone and renin

A

Bilateral idiopathic hyperaldosteronism

50
Q

Primary Chronic Hypoaldosteronism (ADDISON DISEASE)

A

(-) mineralocorticoid
(-) glucocorticoid

(+) HYPERPIGMENTATION - secondary to collateral increase in MSH that accompanies the increase in ACTH to low adrenal cortisol output

NO response to ACTH stimulation test

51
Q

Bilateral adrenal hemorrhage as a complication of DISSEMINATED bacterial infection

N. meningitidis

A

WATERHOUSE-FRIEDRICHSEN SYNDROME

52
Q

Eosinophilic, laminated cytoplasmic inclusions in aldosterone secreting adenomas

A

SPIRONOLACTONE BODIES

53
Q

Morphology of Addison Disease

A

irregular shrunken glands with LYMPHOID INFILTRATES

54
Q

Chronic adrenal insufficiency (Addison Disease) in the developed world

A

secondary to autoimmune adrenalitis

55
Q

Other important causes of chronic hypoadrenalism

A

Tuberculosis and infections due to opportunistic pathogens
associated with the human immunodeficiency virus and tumors metastatic to the adrenals

56
Q

TRIAD
diaphoresis
headaches
palpitations

from CHROMAFFIN cells of MEDULLA

releases catecholamines

INCREASED urinary excretion of free catecholamines and metabolites (VANILLYLMANDELIC ACID (VMA) and METANEPHRINES)

A

PHEOCHROMOCYTOMA

Rule of 10’s

10% - extra-adrenal
10% - bilateral
10% - biologically malignant
10% - NOT associated with HPN

25% - have germline mutations

57
Q

Histologic findings in Pheochromocytoma

A

ZELLBALLEN - clusters of polygonal or spindle shaped chromaffin or chief cells surrounded by sustentacular cells (like paraganglioma)

METASTASIS - only reliable criterion for malignancy

lymph nodes
liver
lungs
bone

58
Q

MEN 1 (WERMER SYNDROME)

A

3PS

pituitary - prolactinoma - MC
parathyroid
pancreas

59
Q

MEN 2 (SIPPLE SYNDROME)

A

2A

pheochromocytoma
parathyroid hyperplasia
medullary thyroid ca

2B

pheochromocytoma
medullary thyroid ca
neuromas
ganglioneuromas
marfanoid habitus

Pathology (24 decks)

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