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Block 8 - Endo & Repro > Path: Adrenal & Pancreas > Flashcards

Path: Adrenal & Pancreas Flashcards

1
Q

What causes most cases of Cushing syndrome?

A

iatrogenic (exogenous) - drugs force pituitary through negative feedback to reduce ACTH, ZF and ZR atrophy
too much cortisol, not necessarily too much ACTH

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2
Q

Other than pituitary adenoma, what can cause Cushing dz?

A

corticotroph hyperplasia w/o a mass - pituitary defect or hypothalamus releasing excess CRH

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3
Q

What would the adrenals look like in Cushing dz?

A

hyperplastic ZF and ZR, compressed ZG, unaffected medulla
maybe nodules, brown or yellow cortical thickening
larger, more vacuolated cells

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4
Q

What findings are present in both primary adrenocortical hyperplasia and neoplasia?

A

elevated cortisol with low ACTH

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5
Q

What are the characteristics of primary (bilateral) adrenal hyperplasia?

A

micronodular or macronodular

micronodular - familial, pigmented adrenal nodules, large cortical cells

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6
Q

What are the characteristics of adrenocortical neoplasia?

A

benign or malignant
almost always unilateral
encapsulated, yellow to black

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7
Q

What are the more common non-endocrine neoplasms that make ACTH?

A 
SCC of lung
carcinoid tumor
medullary thyroid carcinoma
pancreatic islet cell tumors
can release CRH, ACTH or mimics = paraneoplastic syndrome
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8
Q

What are some of the normal effects of glucocorticoids?

A

makes glucose, inhibits insulin action
liver gluconeogenesis and protein catabolism
lipid mobilization
anti-inflammation and stress protection
mineralocorticoid-like effects (due to shared receptor)

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9
Q

What are the clinical manifestations of hypercortisolism?

A 
HTN (due to aldo-like effects)
weight gain, truncal obesity, moon facies, fat depo in neck and back
atrophy of fast twitch muscles
hyperglycemia - due to gluconeogenesis
osteoperosis and bone fractures
stria, easy bruising
immunosuppression (suppresses cytokines)
hyperpigmentation
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10
Q

What are the effects of hyperaldosteronism?

A

causes Na retention and K excretion - pts volume overloaded and hypokalemic
renin and angiotensin down due to feedback on JG cells

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11
Q

What is Conn’s syndrome?

A

aldo secreting adenoma in adrenal
do not usually suppress ACTH - no atrophy
look for new onset HTN
most common primary hyperaldo

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12
Q

What is the second cause of primary hyperaldo?

A

primary adrenocortical hyperplasia - ZG
idiopathic
mostly children and young adults
possible CYP11B2 gene overactivity

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13
Q

What causes secondary hyperaldo?

A

stimulation of RAAS, higher rates of aldo than primary
decreased blood flow to kidney
hypovolemia and edema from other dz
pregnancy

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14
Q

What are the signs and symptoms of hyperaldo?

A

Na retention
HTN
volume overload
hypokalemia

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15
Q

What is adrenogenital syndrome?

A

adrenocortical hyperplasia from increased ACTH, may be mixed w Cushings

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16
Q

What can cause adrenogenital syndrome?

A

adrenocortical adenoma
adrenocortical carcinoma - virilization more often
CAH

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17
Q

What is CAH?

A 
AR
mutated CYP21B (21-hydroxylase) enzyme
hypocortisolemia stimulates ACTH then bottle neck at defective enzyme and divert down androgen synthetic pathway
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18
Q

What types of adrenal insufficiency are there?

A

acute and chronic (Addisons) primary

secondary

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19
Q

What can cause acute primary adrenal insufficiency?

A

Waterhouse-Friderichsen syndrome: massive hemorrhage, children, sepsis by meningococcus (also pseudomonas, staph, strep), maybe endotoxins damage vessels
adults - hemorrhage, stress in setting of chronic

20
Q

What can cause chronic primary adrenocortical insufficiency?

A

autoimmune - most common, Ab to 21-hydroxylase or ACTH receptor
inf - tb, fungi w granulomas
AIDS
metastases - bronchogenic, breast

21
Q

What are signs and symptoms of Addisons dz?

A

weak, fatigued
dark skin pigment - ACTH released w proopiomelanocortin
nausea, anorexia, weight loss
Na wasting, volume loss, hypotension
hyperkalemia
crisis b/c can’t handle stress - coma or death

22
Q

What causes secondary adrenocortical insufficiency and what are its signs and symptoms?

A

reduced pituitary ACTH output

same as primary but no skin pigment or loss of aldo

23
Q

What are the basics of adrenal adenomas?

A

can secrete any of the hormones, mixes, or none (rare)
associated w Cushings - <500g, pink ovoid cells
cut surface is yellow

24
Q

What are findings specific to adenomas causing Cushings?

A

remaining normal adrenal and contralateral atrophic due to feedback

25
Q

What are findings specific to adenomas causing Conns?

A

unencapsulated, adrenals not atrophic, spironolactone bodies

26
Q

What is important to remember about lesions in the adrenals?

A

histology alone does not help predict whether adenoma is functioning or not and which hormone it is secreting

27
Q

What are the basics of adrenal carcinomas?

A

can secrete everything but aldo, mixed syndromes more common than adenomas
poor prognosis - metastasis to lung common
metastatic tumors more common than primary

28
Q

What are pheochromocytomas?

A

adrenal medulla tumor
release catecholamines sporadically –> HTN, tachycardia, headaches, sweating, tremors
risk for MI, stroke, renal injury, death

29
Q

What factors distinguish an adrenal carcinoma from an adenoma?

A

venous invasion
necrosis
frequent mitoses
metastases

30
Q

How is pheo diagnosed?

A

detecting elevated urinary catecholamines and their metabolites (vanillylmandelic acid, metanephrines)

31
Q

What is the rule of 10?

A 
followed by pheo
10% familial (MEN and neurofibromatosis)
10% extradrenal (carotid body, neural crest cells)
10% bilateral
10% malignant
32
Q

What does pheo look like histologically?

A

Zellballen - nests of cells encased by rich vascular network

33
Q

What is the treatment for pheo?

A

give adrenergic blockers and resect

34
Q

What contributes to the pathogenesis of type II diabetes?

A

FFA and TGs inhibit insulin signalling
adipokines promote insulin resistance
adipocytes have PPARgamma that promotes insulin sensitivity - maybe mutated

35
Q

What could cause type I diabetes?

A

HLA-DR3 or DR4 are associated
maybe inf or environmental trigger
overload hypothesis - sedentary and overeating children make beta cells vulnerable

36
Q

What are the 3 criteria for diagnosing diabetes?

A

any 1 of the following:
random glucose >200 w signs and symptoms
fasting glucose >125 >1 time
abnormal glucose tolerance test

37
Q

What happens in both types of diabetes that cause the complications?

A

excess glucose binds and glycosylates proteins
Blood vessels-cross-linked glycosylated collagen entraps lipoprotein → atherosclerosis
Glycosylated capillary basement membrane entraps plasma proteins
Glycosylated plasma proteins affect endothelial permeability, coagulation, extracellular matrix production
Elevated blood glucose causes increased intracellular sorbitol → oxidative cell damage

38
Q

What are diabetic complications in the kidneys?

A

ESRD
BM and mesangial thickening
Kimmelsten-Weilson - hyaline nodular glomerulosclerosis
micro –> macroproteinuria and nephrotic syndrome

39
Q

What is the role of diabetes in infections?

A

more prone to severe inf - malignant otitis media from pseudomonas, mucormycosis (mucor or rhizopus fungi in nose and brain)

40
Q

What are pancreatic endocrine tumors?

A

benign (2cm)
functional more likely benign
arise in islets

41
Q

What is Whipple’s triad of symptoms?

A

in insulinoma:
hypoglycemic attacks with serum glucose <50
attacks characterized by stupor, confusion, loss of consciousness, slurred speech, coma
brought on by fasting/exercise, relieved by eating

42
Q

What happens with an insulinoma?

A

episodic release of insulin and catecholamines

only small percentage secrete enough to be symptomatic

43
Q

What are gastrinomas?

A

most malignant
gastrin causes gastric ulcers (Zollinger-Ellison)
25% in MEN-1 pts

44
Q

What is a glucagonoma?

A

from alpha cells
usually malignant
necrolytic migratory erythema - esp in areas w lots of friction

45
Q

What are somatostatinomas?

A

from delta cells, most malignant

diabetes, gallstones, steatorrhea

46
Q

What are MEN syndromes?

A

AD inherited disorders w hyperplasias, adenomas, and carcinomas in several endocrine organs
manifest at younger age
multifocal w/i individual organ
tumors preceded by asymptomatic hyperplasia
more aggressive

47
Q

What are the MEN1 and MEN2 mutations?

A

MEN-1: tumor suppressor gene mutations

MEN-2A,2B: RET proto-oncogene mutations –> prophylactic thyroidectomy

Block 8 - Endo & Repro (27 decks)

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