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endoII exam2 > Darrow, pheo, hirsuitism, aldosteronism > Flashcards

Darrow, pheo, hirsuitism, aldosteronism Flashcards

1
Q

43 F uncontrolled HTN, rash on wrist, 4th heart sound, K low, HCO3 high,Mg low
acid base state?

A

hypokalemic alkalosis

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2
Q

if you are hypokalemic how does that affect insulin

A

decreases insulin secretion leading to glucose intolerance

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3
Q

what type of DI does hypokalemia cayse

A

nephrogenic because defective activation of renal adenyl cyclase

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4
Q

why is K drawn slowly without vacutainer

A

fast will cause hemolysis

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5
Q

alubuterol affects on K

A

lower serum K by stimulating release of insulin

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6
Q

What stimulates the glomerulosa to produce aldosterone

A

ANG II and K+

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7
Q

what inhibits glomerulosa

A

ANP= less aldosterone

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8
Q

what stimulates the fasiculata and reticularis

A

ACTH

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9
Q

what do you expect renin level to be if aldosterone is high

A

low because neg feedback

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10
Q

what is the standing up test for aldosterone renin

A

keep patient upright for 3 hours to cause rise in renin

if the aldosterone: renin ratio>30 it is most likely primary hyperaldosteronism

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11
Q

Conns syndrome

A

primary hyperaldosteronism

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12
Q

causes of conns syndrome

A

adrenal ademoa
unilateral or b/l hyperlpasia
genetic defect with overly strong effect of ACTH on aldosterone production

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13
Q

what is a good Dx test for primary aldosteronism

A

24 hour urine collection for aldosterone (>12 confirmatory)

Na loading before

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14
Q

how do you differentiate adenoma from b/l adrenal hyperplasia

A

postural sitmulation test

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15
Q

what is postural stimulation test

A

measure aldosterone while patient laying down then walk around 3 hours and if see rise in aldosterone then responding normal so hyperplasia
an adenoma would not respond

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16
Q

how to Tx patient with adrenal hyperplasia causing primary hyperaldosteronisms

A

meds- spironolactone

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17
Q

licorice effects on adrenals

A

inhibits 11betaHSD2 which converts cortisol to cortisone

so allows cortisol to drive mineralocortiocoid R leading to HTN and low renin/aldosterone

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18
Q

increased renin and aldosterone with alkalosis could be what

A

secondary aldosteronism: diuretics, Bartters and Gitelman,
vomiting
nasogastric suction

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19
Q

what are causes of pseudohyperaldosteronisms

A

liddles
cushings exogenous steroids
CAH
licorice

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20
Q

renin and aldosterone levels in pseduohyperaldosteronism

A

both decreased

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21
Q

What is liddles syndrome

A

gain of function in Na channel which inc K secretion and dec aldosterone and renin
pseudohyperaldosteronism

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22
Q

22 y.o F with acne, hirsutism, irregular menses,, acanthosis nigricans and apple shape
lab show inc testosterone with normal DHEA and 17OHP
next test

A

FSH LH

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23
Q

LH/FSH >2 22 y.o F with hirsutism

A

problem with follicular cell development in ovaries, Polycycstic ovary syndrome

24
Q

majority of hirsutism is caused by what

A

decreased sex hormone binding globulin (increased free testosterone)

25
Q

if there is not a dec in sex hormone binding globulin what could cause hirsutism

A

excessive activity of 5 alpha reductase

26
Q

common causes of hirsutism

A

PCOS
drugs: pheytoin
idiopathic/familial

27
Q

common causes virilization

A

ovarian/adrenal tumors

28
Q

What labs will you do for PCOS

A

testosterone, LH/FSH
DHEAS
17 OHP

29
Q

what labs do you do for CAH

A

total testosterone, DHEAS, 17OHP all increased

30
Q

what labs do you do for patients with hirsutism in general

A

TSH, PRL, IGF-1, 24 hr cortisol, testosterone, DHEAS and 17OHP

31
Q

in virilization what labs do you want to order

A

testosterone, DHEA and androstenedioine

32
Q

ovarian utmor will have what lab results

A

increased total testosterone with normal DHEAS and 17OHP

33
Q

adrneal tumor will have what lab results

A

increased DHEAS

34
Q

what will lab results be in CAH

A

total testosterone and DHEAS and 17OHP will be increased

35
Q

if 17 OHP is >500

A

CAH

36
Q

Tx for hirsutism

A

OCPs with progestins to increase estrogen

antiandroges: spironolactone, flutamide, finasteride, metformin, GnRH agonists

37
Q

how does insulin affect androgens

A

triggers ovarian androgen production and reduces SHBG

38
Q

what occurs in 21 hydroxylase deficiency

A

shift to zona reticularis

masculinizaiton and hypotension

39
Q

what occurs in 17 hydroxylase deficiency

A

shift to the glomerulosa, alot of aldosterone, HTN

40
Q

what happens in 11 beta hydroxylase deficiency

A

HTN and masculinization

41
Q

how does congential adrenal hyperplasia happen

A

lose cortisol negative feedback so massive increases of androgens with no feedback from cortisol to hypothalamus or pituitary

42
Q

palpitations, sweating, HA

A

pheochromocytoma

43
Q

cafe au lait spots and nodules

A

neurofibromas

44
Q

Causes of non-essential HTN

A 
aldosteronism
myxedema
hyperCa
pheo
steroid excess
45
Q

how does epi/norepi produce neutrophilia

A

mobilization of neutrophils form vessel walls

46
Q

how does epi/norepi produce hyperglycemia

A

activation of alpha 2 R on islet beta cells with decreased insulin output and icnreased liver glucose production by beta 2 R

47
Q

how does epi/noreepi lead to hypotension

A

vasodilation Beta 2 R

48
Q

pheo can cause hyperCa how

A

releases PTHrP

49
Q

where are tumores that secrete norepi

A

anywhere in paraganglion chain

50
Q

where are epinephrine tumors

A

adrenal gland

51
Q

what is a good test for pheo

A

meta iodobenzylguanadine scintography because pheo takes it up

52
Q

10% pheo

A

b/l 10%malignant

53
Q

when must you investigate incidentalomas

A

25% incidence of having cancer cells if above 6cm so need biopsy if above this size

54
Q

what is a preoperative evaluation for incidentaloma

A

plasam free metaneprhines

1 mg DXM suppression to rule out cushings (low dose DXM)

55
Q

60% incidentalomas associated with

A

some degree of CAH

56
Q

causes of facial flushing

A

carcinoid, medullary carcinoma of the thyroid

pheochromocytoma

endoII exam2 (18 decks)

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