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Endocrine / MSK / Repro > Week 1 > Flashcards

Week 1 Flashcards

1
Q

What should prompt a work up of mineralocorticoid excess?

A

HTN with hypokalemia

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2
Q

What do you expect to see in primary hyperaldosterism? (aldosterone / renin)

A

increased aldosterone

decreased renin

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3
Q

What do you expect to see in renal artery stenosis? (renin / aldosterone)

A

Both increased since kidneys are not being perfused well enough

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4
Q

What do you expect to see in renin producing adenoma?

A

increased renin and increased aldosterone

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5
Q

What do you expect to see in increased cortisol? (aldosterone / renin)

A

aldosterone and renin decrease (don’t want an even higher BP)

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6
Q

What do you expect to see in increased DOC? (aldosterone / renin)

A

it acts like a mineralocorticoid

so you would expect decreased renin and decreased aldosterone

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7
Q

What do you expect to see in Liddle syndrome?(aldosterone / renin)

A

decreased aldo and renin since ENaC function is already increased

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8
Q

What is a form of secondary hyperaldosteronism?

A

renal artery stenosis causes (high renin and high aldosterone)

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9
Q

What is the treatment for hyperaldosteronism if there is a bilateral adenoma?

A

spironolactone

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10
Q

How can you determine between the classic and non-classic form of CAH?

A

classic is much more severe and presents early with cortisol deficiency, aldosterone deficiency and excess adrenal hormones

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11
Q

What can males with classic CAH develop?

A

early virilization

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12
Q

What is elevated in 21a-hydroxylase def?

A

androgens

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13
Q

What is elevated in 11B-hydroxylase def?

A

androgens

(you do not see aldosterone def. because it blocks lower down in the pathway)

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14
Q

What is elevated in 17a-hydroxylase deficiency?

A

aldosterone is increased since you can’t shunt to make cortisol (fasc.) or androgens (retic.)

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15
Q

What types of glucocorticoids should be avoided in pregnancy?

A

dexamethasone

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16
Q

What is the inheritance pattern of CAH?

A

autosomal recessive

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17
Q

CYP21A2 is implicated in

A

CAH

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18
Q

What are the three tests for Cushing’s syndrome? (remember that 2 out of 3 need to be positive)

A

1mg overnight dex suppression test
24-hour urine free cortisol
Midnight salivary cortisol

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19
Q

If a low dose dex suppression test does not decrease ACTH what do you know is true?

A

you have a ACTH-dependent Cushing’s syndrome

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20
Q

What is the next step for a ACTH-dependent Cushing’s syndrome?

A

use a high dose dex. suppression test

if ACTH decreases, you have a pituitary adenoma

if ACTH does not decrease, you have ectopic ACTH

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21
Q

Can you see hypokalemia in Cushings?

A

yes!

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22
Q

What are causes of low ACTH Cushing’s syndrome?

A

Adrenal adenomas

Exogenous steriods

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23
Q

What are causes of high ACTH Cushing’s syndrome?

A

Cushing’s disease

Ectopic ACTH

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24
Q

What are you at risk with following removal of adrenal gland s/o low ACTH Cushings?

A

secondary adrenal insufficiency

(low levels of ACTH since the pituitary is not used to having to produce them)

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25
Q

What does plasma ACTH do in adrenal adenoma?

A

it is low since cortisol is being secreted in high amounts by the adrenal adenoma

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26
Q

What drugs can you use if surgery is not an option in Cushings?

A

ketoconazole

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27
Q

What type of tumor results in high levels of epinephrine and norepinehprine?

A

pheochromoctyoma

28
Q

Does 21a-hydroxylase def cause both non-classic and classic CAH?

A

yes

29
Q

What is the pre-op management for pheos?

A

alpha blocker

then a beta blocker along with volume expansion

30
Q

What happens when you suddenly withdrawal exogenous steroids?

A

you have low ACTH and low cortisol levels

(secondary adrenal insufficiency)

the body is not used to producing these things

31
Q

Name 3 alpha 1 blockers

A

phenoxybenzamine, doxazosin, prazosin

32
Q

Do you see hypertension or hypotension in Addison’s ?

A

hypotension from lack of cortisol

33
Q

Do you see hypertension or hypotension in ectopic ACTH?

A

hypertension, you are excreting too much cortisol

34
Q

What is the link between cortisol and ADH?

A

cortisol deficiency can cause increased release of ADH

35
Q

If you involve the pituitary stalk and posterior pituitary what can you develop?

A

SIADH

36
Q

What form of disease is Klinefelter’s?

A

primary hypogonadism

37
Q

What testing should you do for Klinefelters?

A

testosterone in morning

karotype for confirmation (47XXY)

38
Q

What hormones (FSH/LH and testosterone) do you see in Klinefelters?

A

low testosterone (underdeveloped testes)

high FSH / LH

39
Q

What hormones (FSH/LH and testosterone) do you see in secondary hypogonadism?

A

low testosterone

low FSH / LH

40
Q

What hormones (FSH/LH and testosterone) do you see in anabolic steroids?

A

low testosterone

low FSH / LH (the body thinks testosterone is there)

41
Q

What signs should you look for in hypercalcemia?

A

stones, bones, moans, grones and psychiatric overtones

also on the throne (polyuria)

42
Q

What happens to reflexes in hypocalciuria?

A

become hyperreflexive due to increased calcium raising the membrane threshold

43
Q

What 2 mechanisms cause polyuria (and dehydration) in hypercalciema?

A

1) osmotic diuresis from more calcium in urine

2) calcium inhibits ADH receptors

44
Q

What are the 3 differentials for PTH-mediated hypercalecemia?

A

1) Primary hyperparathyroidism

2) Familial hypocalciuric hypercalcemia (FHH)

3) Tertiary hyperparathyroidism (only in ESRD)

45
Q

What is true of FHH?

A

it is protective against kidney stones

46
Q

What should be the first step in working up hypercalcemia?

A

1) measure PTH levels

47
Q

If you have PTH dependent hyperparathyroidism (high / normal PTH), what should be next test?

A

24 hr urine Cr and Ca

48
Q

Do you need to treat FHH?

A

no

49
Q

What two conditions does 24 hr urine Cr and Ca separate?

A

1) High urine Cr / Ca = primary hyperparathyroidism

2) Low urine Cr / Ca = FHH

50
Q

What do you expect labs to look like if they are from malignancy, sarcoidosis or excessive calcium?

A

these are PTH independent processes

so you would see increased calcium with a low PTH

(the PTH is not what is driving the increase in calcium)

51
Q

What 2 signs are seen in hypocalcemia?

A

1) CHVOSTEK’S SIGN: facial contraction

2)TROUSSEAU’S SIGN: spazing after placing the BP cuff

52
Q

What other lab do you always need to check with calcium?

A

albumin

(albumin binds free calcium)

53
Q

What can hypocalcemia cause on EKG?

A

prolongation of QT interval

54
Q

What accounts for most causes of primary hypercalciema?

A

malignancy

55
Q

What does PTH look like in primary hypercalciema?

A

low (PTH is responding normally)

56
Q

When is hypocalciema due to hypoparathyroidism mostly seen?

A

after thyroid or parathyroid surgery

57
Q

What does vitamin D deficiency lead to?

A

defect in skeletal mineralization

58
Q

What is the relationship between vitamin D deficiency and PTH?

A

since vitamin D impairs absorption of Ca2+, PTH increases

59
Q

What is the relationship between vitamin D deficiency and phosphate?

A

see a decreased phosphate level

60
Q

Gastrinoma should make you think …

A

MEN1

60
Q

What are 3 secondary causes of bone loss?

A

1) vitamin D deficiency

2) hyperparathyroidism

3) hyperthyroidism (low TSH with high T4)

61
Q

Thyroid tumor should make you think …

A

MEN2

62
Q

What type of parathyroid does a tumor secrete (like squamous cell)?

A

PTHrP

(then, low PTH)

63
Q

What can MEN1 cause in endocrine?

A

primary hyperparathyroidism with a prolactinoma

64
Q

How do you remember where MEN1 can manifest?

A

the 3Ps

65
Q
A

Endocrine / MSK / Repro (8 decks)

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