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ER Week 1 > Adrenal Pathology > Flashcards

Adrenal Pathology Flashcards

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1
Q

How many adrenal glands do we have?

A

two - at the upper poles of the kidneys

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2
Q

What are the two separates parts of the adrenal glands?

A

cortex (three zones) and medulla

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3
Q

What are the three zonas of the cortex?

A

zona glomerulosa
zona fasciculata
zona reticularis

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4
Q

What does the zona glomerulosa secrete? THe outside part….

A

mineralocorticoids

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5
Q

What does the zona fasciculata secrete? The middle part….

A

glucocorticoids

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6
Q

What does the zona reticularis secrete? The inside part….

A

sex hormones

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7
Q

What does the medulla secrete?

A

epinephrine and norepinephrine

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8
Q

What are the three disorders that arrise from too much adrenal hormone?

A 
Cushing syndrome (too much cortisol)
Hyperaldosteronism (too much aldosterone)
Adrenogenital syndrome (too much catecholamines?)
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9
Q

What is the mnemonic for what cortisol does?

A

cortisol is BBIIG

maintains Blood pressure
breaks down Bone
suppresses Inflammation
suppresses Immune system
stimualtes Gluconeogenesis
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10
Q

What are the symptoms of cushing syndrome?

A 
hypertension
weight gain
characteristic habitus
weakness
glucose intolerance
thin skin
osteoporosis
infeciton
mental changes
hirsutism
menstrual abnormalities
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11
Q

What lab tests do you use for diagnosis of Cushing’s syndrome?

A

24 hour urine free cortisol

loss of normal diurnal cortisol secretion

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12
Q

What two tests do you use to determine the cause of the cushing syndrome?

A

ACTH level (tells you if the issue is with the pituitary)

Dexamethasone suppression test

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13
Q

What is the most common cause of cushing syndrome?

A

Iatrogenic! Taking steroids

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14
Q

What will lab tests show in iatrogenic cushing syndrome?

A

increased cortisol (with no Dexa supression)

decreased ACTH (the prednisone does feedback inhibition on the pituitary)

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15
Q

What causes cushing DISEASE?

A

pituitary cushing syndrome - a tumor in the atnerior pituitary makes too much ACTH

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16
Q

What will happen to the adrenal cortices in pituitary cushing syndrome (cushing disease)?

A

they will become hyperplastic

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17
Q

What will lab tests show in pituitary cushing syndrome?

A 
increased cortisol (with dexa suppression)
 (note this is surprising, but pituitary adenomas can be turned off with high dose dexa)

increased ACTH

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18
Q

Is the adrenal cortex hypoplastic or hyperplastic in ADRENAL cushing syndrome?

A

can be either

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19
Q

What will lab tests show in adrenal cushing syndrome?

A

increased cortisol (with no dexa suppression)

decreased ACTH

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20
Q

What lung cancer will cause paraneoplastic cuhshing syndrome?

A

small-cell

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21
Q

Will the adrenal cortices be hypoplastic or hyperplastic in paraneoplastic cushings?

A

hyperplastic because of all the fake ACTH stimulation

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22
Q

What will lab tests show in paraneoplastic cushing syndrome

A

increased cortisol (with no Dexa suppression)

increased “fake” ACTH because the test can’t differentiate true ACTH from the cancer’s ACTH

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23
Q

Back to CRRAB…How is the release of aldosterone triggered?

A

angiotensinogen is converted to angiotensin 1 by renin

Ang 1 is converted to Ang II by ACE

Angiotensin II then triggers the release of aldosterone

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24
Q

So increased renin leads to ___ aldosterone

A

increased

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25
Q

What does aldosterone do?

A
  1. retain Na and water
  2. pee out K

so hypernatremia, increased BP and hypokalemia

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26
Q

What will hypertension do to aldosterone levels?

A

decresas renin, so decreased aldosterone

hence, you pee out Na and H20 and retain K, leading to hyponatremia, decreased BP and hyperkalemia

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27
Q

What is the general cause of primary hyperaldosteronism? Two specific causes?

A

you have increased aldosterone release, leading to decreased renin via feedback

caused by a cortical adenoma or cortical hyperplasia

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28
Q

What syndrome is associated with cortical adenoma?

A

Conn syndrome

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29
Q

What are the main symptoms of primary hyperaldosteronism?

A

hypertension (hypernatremia)
weakness
fatigue
psychosis (hypokalemia)

30
Q

What will the lab findings be in primary hyperaldosteronism?

A 
elevated aldosterone
low renin
hypernatremia
hypokalemia
metabolic alkalosis (loss of H+ along with the K+)
31
Q

What is the general cause of secondary hyperaldosteronism?

A

abnormally increased renin

32
Q

What are three causes of the abnormally increased renin that leads to secondary hyperaldosteronism?

A

CHF
decreased renal blood flow (like in RAS)
renin-producing tumors

33
Q

What are the symptoms of secondary hyperaldosteronism?

A

same as primary….

hypertension (hypernatremia)
weakness, fatigue and psychosis (hypokalemia)

34
Q

What will the lab findings be in secondary hyperaldosteronism?

A 
elevated aldosterone
high renin
hypernatremia
hypokalemia
metabolic alkalosis (loss of H along with K)
35
Q

What makes these lab findings different from primary hyperaldosteronism?

A

high renin

36
Q

What are the two general cuases of virilization?

A
  1. primary gonadal disorders

2. primary adrenal disorders

37
Q

What are the two general primary adrenal disorders?

A

adrenocortical neoplasms

congenital adrenal hyperplasia

38
Q

Adrenocortical carcinoma is super rare, but how does it present?

A

you get sudden virilization in a girl or woman

sometimes has a palpable abdominal mass

39
Q

Does an adrenocortical carcinoma have a good or gad prognosis?

A

bad

40
Q

What’s wrong in congenital adrenal hyperplasia?

A

the patient has a deficiency in an enzyme in volved in making either/or the minerlocorticoids of the glucocorticoids, which means you 1. lose the feedback inhibition on the pituitary and 2. have all the hormone precursors being shunted into the sex steroid synthesis pathway

this means they have low aldosteron, low cortisol (with all those symptoms) and high testosterone leading to virilization

41
Q

What is the most common enzyme deficiency that leads to congenital adrenal hyperplasia?

A

21 hydroxylase deficiency, which is required for both cortisol and aldosterone synthesis

42
Q

What are the three types of 21 hydroxylase CAH?

A
  1. salt-wasting (wher eyou get no aldosterone whatsoever)
  2. simple virilizing (some aldosterone)
  3. laste-onset virilizing some aldosteron and some cortisol)

all depends on how much active enzyme you have

43
Q

So in congenital adrenal hyperplasia, which layer of the cortex will be big?

A

the zona reticularis (wince that’s what makes the sex steroids(

44
Q

What are the two general kinds of primary adrenal insufficiency?

A

acute or chronic

45
Q

What is the more common name for primary chronic adrenal insufficiency?

A

Addison disease

46
Q

What is Addison’s disease?

A

typically an autoimmune destruction of the adrenal cortex such that the patient cannot make cortisol and mineralocorticoids

47
Q

What are the main symptoms of addison’s disease?

A

weakness, fatiuge, GI complains

hypotension (no aldosterone)

skin hyperpigmentation

48
Q

Why do you get the skin hyperpigmentation in addisons?

A

You don’t have cortisol or aldosteron feeding back to inhibit the pituitary, so the pituitary just keeps making a ton of ACTH

remember that ACTH is derived from POMC. Remember that melanocyte stimulating factor is also derived from POMC, so you get lots of melanocyte stimulation leading to a bronzing effect

49
Q

What is the management for an acute exacerbation of addison’s?

A

IV Na+ (bc they’re hyponatremic due to lack of aldosterone)

hydrocortisone (since they can’t make cortisol)

dextrose

50
Q

What does Addison’s disease look like on histology?

A

you see very little cortex left and what is there will be filled with lymphocytes

51
Q

Although Addison’s can present in an acute-like manner, it’s really a chronic problem. What are the two most common causes of actual primary acute adrenal insufficiency?

A
  1. rapid steroid withdrawal (because their adrenal glands have hypertrophied)
  2. Massive adrenal hemorrhage
52
Q

What is the classic setting for massive adrenal hemorrhage and what is the syndrome called?

A

waterhouse-friderichsen syndrome

A young child with a N. meningitidis infection presenting in DIC with hypotension and shock

they just get massive bilateral adrenal hemorrhage which rapidly progresses. Often fatal

53
Q

What is secondary adrenal insufficiency typically caused by?

A

pituitary or hypothalamic insufficiency related to tumor, infection, radiation or infarction

54
Q

What are the clinical features of secondary adrenal insufficiency?

A

you have decreased ACTH, so you have decreased adrenal products

you get the symptoms of decreased cortisol and decreased sex steroids

55
Q

Why will mineralocorticoids be normal in secondary adrenal insufficiency?

A

because the renin axis is intact, so the signal for aldosteron release is still there

56
Q

Why don’t you have the hyperpigmentation in secondary adrenal insufficiency?

A

beause the issue is with too little ACTH. If you have no ACTH, then you’re probably not making melanocyte stimulating factor either

57
Q

There are two tumors of the adrenal medulla. What are they?

A
  1. pheochromocytoma

2. neuroblastoma

58
Q

What is a pheochromocytoma a neoplasm of?

A

catecholamine-producing cells in the medulla

59
Q

What are the symptoms of pheochromocytoma?

A

episodic in nature…

pressure (HTN)
pain (headache)
perspiration
palpitations (tachycardia)
pallor
60
Q

What labs can you do to diagnose a pheochromocytom?

A

urine analysis for catecholamien break-down products like VMA and metanephrines

61
Q

Why is a pheochromocytoma called the 10% tumor?

A 
10% are extra-adrenal (paragangliomas)
10% are bilateral
10% are familial
10% are malignant
10% of patients don't have HTN
62
Q

What does a pheochromocytoma look like under histology?

A

littles that hang out in ball-like packets called zellballen

63
Q

What kind of cells is a neuroblastoma derived from?

A

neural crest

64
Q

Neuroblastoma presents in what stage of life?

A

childhood

65
Q

True or false: prognosis for neuroblastoma is better in children over 18 months of age

A

false - better for children less than 18 months

66
Q

True or false: prognosis is better for hyperdiploid tumors

A

true (whichi s unusual)

67
Q

Prognosis is better if the tumor has fewer copies of what tumor promoter gene?

A

N-myc

68
Q

True or false: in really young children, some neuroblastoma (even metastatic) can go away with time.

A

true!

69
Q

What does neuroblastoma look like micrscopically

A

it’s in the calss of small round blue cell tumors

so it has small round blue cells arranged in homer-wright rosettes

70
Q

WHat is in the center of a homer-wright rosette?

A

neuropil

ER Week 1 (11 decks)

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