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Endo > Endo Path II > Flashcards

Endo Path II Flashcards

1
Q

Embryologic origin of the adrenal cortex

A

intermediate mesoderm

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2
Q

Embryologic origin of the adrenal medulla

A

Neural crest ectoderm

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3
Q

Which is the largest layer of the adrenal cortex?

A

Zona fasiculata

-large cells containing large fat-droplets as the precursors to glucocorticoid hormone production

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4
Q

Where are the two locations of testosterone production in the male?

A

Adrenal medulla and testicles

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5
Q

What is cortisol so important as a regulatory hormone in the HPA axis?

A

B/c cortisol is the only hormone from the zona fasiculata and zona reticularis that feeds back to negatively inhibit the hypothalamus and pituitary and decrease production of CRH and ACTH

-androgens from reticularis do not inhibit HPA axis

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6
Q

Differentiate the regulation system of the 3 zones of the adrenal cortex

A
  • zona glomerulosa produces aldo which is regulate by the RAAS => works independent of ACTH
  • zona fasiculata and reticularis (cortisol and andreogens) stimulated by ACTH
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7
Q

Conn Syndrome

A

presence of Aldo-secreting tumor => primary hyperaldosteronism => HTN and hypokalemia

  • small, circumscribed yellow nodule
  • causes 70% of primary hyperaldosteronism (other 30% idiopathic)
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8
Q

Spironolactone bodies

A

Distinctive histological finding of Conn syndrome = tumor secretion aldosterone => hyperaldo

Hyperaldo => HTN which is treated w/ spironolactone (diuretic)

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9
Q

Hyperplasia of glomerulosa seen in what functional disorder of the adrenal gland?

A

Seen in hyperaldosteronism

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10
Q

What causes secondary hyperaldosteronism?

A

Excess stimulation of RAAS

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11
Q

Name 3 types of hyperadrenalism

A
  • hyperaldosteronism (often Conn syndrome)
  • hypercortisolism (Cushing syndrome)
  • adrenal virulism
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12
Q

Distinguish Cushing Syndrome from Cushing disease

A

Cushing syndrome is the general term for the presence of hypercortisolism (high cortisol from adrenal zona fasiculata)

While Cushing disease is the cause of 60-70% of endogenous cases of Cushing syndrome. Mostly due to a pituitary adenoma that secretes ACTH

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13
Q

Most common cause of Cushing syndrome

A

taking exogenous cortisol

ex: steroids, iatrogenic

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14
Q

Differentiate Cushing disease and Adrenal Cushing Syndrome

A

Cushing disease = tumor in pituitary causing excess secretion of ACTH

Adrenal Cushing Syndrome = neoplasm or idiopathic hyperplasia of the adrenal that causes excess cortisol release, independent of ACTH

-differ by their dependence on ACTH

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15
Q

Differentiate the pathological findings in

a) Cushing disease
b) Adrenal Cushing Syndrome
c) Ectopic ACTH-secreting tumor
d) Exogenous Cushing syndrome

-is ACTH high or low in the above?

A

Pathological findings

a) Cushing disease = pituitary tumor, high ACTH, bilateral cortical hyperplasia
b) Adrenal cushing syndrome = cortical tumor or cortical hyperplasia, unilateral hyperplasia (side w/o mass), low ACTH
c) Ectopic ACTH-secreting tumor => ACTH high => bilateral cortical hyperplasia
d) Exogenous intake of corticosteroids => ACTH low => normal size or even smaller adrenal gland

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16
Q

Crooke hyaline degeneration

A

Typical histological finding in Cushing Syndrome (hypercortisolism)

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17
Q

What lab finding do you need to diagnose Cushing Syndrome

A
  • elevated cortisol levels (serum, urine)

- then you dig deeper to find the cause (look at ACTH levels, examine adrenal gland if can)

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18
Q

Symptoms of Cushing Syndrome

A

Truncal obesity, moon face, osteoporosis

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19
Q

What is adrenal virilism?

What is the most common clinical presentation?

A

Increased adrenal cortex production of androgens => disorders of sexual differentiation

-female w/ ambiguous genitalia :-(

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20
Q

Two causes of adrenal virilism

A
  • androgen-secreting adrenocortical neoplasm

- congenital adrenal hyperplasia

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21
Q

What is mutated in congenital adrenal hyperplasia?

A

Mutation in 21-hydroxylase = enzyme in the cortical steroid biosynthesis pathway necessary when converting cholesterol –> aldo and cortisol

-Since 21-hydroxylase is mutated, its substrates are shunted to the androgen pathway (recall that cholesterol is the common beginning substrate for all three adrenal cortex main products

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22
Q

Describe the mechanism of adrenal hyperplasia due to congenital adrenal hyperplasia

A

Enzymatic mutation in 21-hydroxylase => inability to make aldo and cortisol and precursors are therefore shunted into the andren pathway

-low cortisol => no negative feedback on HPA => very high CRH and ACTH => hyperplasia of the adrenal gland

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23
Q

What is the main cause of hypoadrenalism? What are the other causes?

A

Main cause = Addison’s = autoimmune or idiopathic

Other causes are really anything (infection, metastatic carcinoma, drugs) that destroy the adrenal gland

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24
Q

What is Addison’s disease?

A

Autoimmune or idiopathic disease causing hypoadrenalism due to destruction of the adrenal cortex

=> get deficiency in glucocorticoids and mineralocorticoids

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25
Q

Symptoms of Addison’s disease

A

No aldo => hyponatremia and hyperkalemia

High ACTH => hyperpigmentation

26
Q

What is a physical exam finding of high ACTH

A

Hyperpigmentation of the skin

27
Q

Describe the pathologic findings of the adrenal cortex and medulla in Addison’s disease

A

Addison’s = autoantibodies against the cortex => fibrous tissue and chronic inflammation replaces the normal cortex tissue
-see a shrunken cortex

Autoantibodies are not against the medulla => normal medulla

28
Q

What is the most common clinical presentation of congenital hypoplasia of the adrenal cortex

A

Very rare to have congenital hypoplasia of the adrenal, but since there is low cortisol => high ACTH

High ACTH => hyperpigmentation

=> newborns present w/ hyperpigmentation

29
Q

What is an infectious cause of Addison’s disease?

A

Recall: Addison’s = chronic adrenal insufficiency

Infectious cause = Tb
-granulomas replace the normal cortex and medullary tissue

30
Q

Waterhouse-Friderichsen syndrome

A

= acute adrenal insufficiency

  • catastrophic overwhelming bacterial infection
  • DIC (blood clots in small vessels) and rapid hypotension

=> massive adrenal hemorrhage and adrenocortical insufficiency

-In addition to treating the infection, need to immediately give hormone replacement (cortisol)

31
Q

Gross pathological findings of Waterhouse-Friderichsen Syndrome

A

The adrenal glands look like sacs of clotted blood

-just tons of hemorrhage

32
Q

What is secondary adrenal insufficiency?

A

Anything (ex: surgery, radiation) that reduces ACTH output and therefore secondarily causes low cortisol and androgens

33
Q

Distinguish primary and secondary adrenal insufficiency by

a) Skin pigmentation
b) Prominence of hyponatremia

A 
Primary = something wrong w/ the adrenal cortex => ACTH is high
Secondary = lack of ACTH and adrenal cortex is fine

a) Primary has high ACTH => hyperpigmentation of skin. secondary has low ACTH => lack of hyperpigmentation

b) Primary = no aldo => prominent hyponatremia
Secondary- aldo is not controlled by ACTH secretion (controlled by RAAS) => aldo is normal and hyponatremia is not prominent

34
Q

Cortical adenoma vs. cortical carcinoma

a) size
b) likelihood of being functional
c) necrosis
d) mitosis
e) vascular/capsular invasion

A

Can be hard to distinguish, especially if they are both small (carcinoma more likely to be larger but can be small)

Favors carcinoma if the tumor is

a) Large in size
b) functional
c) contains necrosis
d) contains mitotic figures
e) contains vascular/capsular invasion

35
Q

Myelolipoma

a) most common location
b) contents
c) benign or malignant

A

Myelolipoma

a) can be anywhere but most classically present in the adrenal cortex
b) made of mature adipose tissue and haematopoietic elements (basically a mix of blood and fat)
c) incidental benign tumor

36
Q

Chromaffin cells on histology

A

= neuroendocrine cells containing catecholamines (aka adrenal medulla cells)

-these cells stain yellow/brown when treated w/ chromium salts b/c the salts oxidize catecholamines to form a a brownish color

37
Q

Differentiate the effects of adrenalin and norepi

A

Adrenalin (epi) has systemic effects while norepi acts as a local neurotransmitter

38
Q

What are extra-adrenal paraganglia?

A

Clusters of chromaffin cells (neuroendocrine cells similar to those found in the adrenal medulla) dispersed throughout the body

-mainly located close to the sympathetic trunk

39
Q

Pheochromocytoma- what are they?

a) most commonly benign or malignant?
b) location
c) associated w/ which familial syndromes

A

Uncommon tumor of chromaffin cells that produces catecholamines

a) most are benign, 10% in the adrenal are malignant
b) most occur in the adrenal medulla while 10% occur in the extra-adrenal paraganglia
c) associated w/ MEN 2a and 2b

40
Q

What germline mutation is characteristic of MEN?

A

Mutation in RET protooncogene

41
Q

Differentiate MEN 2A and MEN 2B

A

-both are associated w/ medullary carcinoma while MEN2A is associated w/ parathyroid hyperplasia and MEN2B is not

42
Q

How to diagnose a pheochromocytoma

A

Pheochromocytoma = chrommafin cell tumor that produces catecholamines

Excess urinary catecholamines or catecholamine metabolites

43
Q

What is the classic pathological finding of a pheochromocytoma

A

The tumor turns brown when oxidized (b/c of its catecholamine contents)

44
Q

What is the only way to diagnose a malignant pheochromocytoma?

A

Malignancy can only be diagnosed in the presence of metastases

-b/c there can be very malignant-like characteristics (ex: vascular invasion or pleomorphism) w/o the tumor being malignant

45
Q

Neuroblastoma- what are they?

a) more common in what age group
b) most common location

A

Neuroblastoma = neuroendocrine tumor arising from any neural crest element of the SNS

a) common tumor of childhood
b) up to 35% are found in the adrenal medulla

46
Q

What are ganglioneuroblastomas?

A

A variant of neuroblastoma surrounded by ganglion cells

-non-malignant

47
Q

Bizarre nuclei

A

Histological finding in parathyroid adenoma

48
Q

Microfollicular pattern

A

Histological finding in parathyroid adenoma that makes the parathyroid look similar to thyroid tissue

49
Q

Most common cause of primary hyperparathyroidism

A

Sporadic causes 70%

Other 30% from familial (MEN or other mutations)

50
Q

Most common cause of secondary hyperparathyroidism

A

chronic renal failure

=> kidneys cannot get rid of excess phosphate and can’t activate vitamin D

51
Q

Common cause of hypoparathyroidism

A

Surgery- parathyroid glands accidentally removed during thyroidectomy

52
Q

Intranuclear inclusion

A

Histological finding in papillary thyroid carcinoma

53
Q

DiGeorge syndrome and the parathyroid gland

A

DiGeorge syndrome includes congenital absence of the parathyroid gland => tetralogy of fallot, hypocalcemia

54
Q

What is pseudohypoparathyroidism?

A

Target organ (kidney, bone) unresponsiveness to PTH

-so PTH levels normal (being normally secreted by parathyroid) but the end organs aren’t listening

55
Q

What are crucial clinical signs of hypoparathyroidism?

A

Tetany,neuromuscular irritability, seizures

56
Q

What is parathyromatosis?

A

Ectopic parathyroid tissue embedded in normal tissue

-causes recurrent hyperparathyroidism

57
Q

Carcinoid tumor

a) most common location
b) most common location of metastatic carcinoid tumor

A

Carcinoid tumor = neuroendocrine tumor

a) most commonly found at the tip of the appendix
b) 90% are benign, but of the 10% malignant most are from the midgut (jejunum, ileum)

58
Q

Trabeculae and nests

A

Histological finding or carcinoid (neuroendocrine) tumors

59
Q

Zollinger-Ellison Syndrome associated w/ what tumor?

A

Gastrinoma

60
Q

What is more commonly malignant: insulinoma or gastrinoma?

A

Insulinoma only malignant 10% of the time

Gastrinoma malignant 60-90%

Endo (4 decks)

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