endocrinology Flashcards

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1
Q

precocious puberty - age definitions?

A

boys < 9, girls <8

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2
Q

central precocious puberty - what is it?

A

early maturation of the hypothalamic-pituitary-gonad axis

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3
Q

peripheral precocious puberty - what is it?

A

excess sex hormone (androgen) production from gonads, adrenals, or exogenous source

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4
Q

classic congenital adrenal hyperplasia - what is the defect - and what does it cause?

A

21-hydroxylase completely deficient (leads to salt wasting or virilization due to glucocorticoid or mineralicorticoid deficiencies)

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5
Q

nonclassic CAH - what is the defect?

A

21-hydroxylase reduced, therefore NO salt wasting. Signs of precocious puberty after infancy.

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6
Q

nonclassic CAH - symptoms?

A

hyperfunctioning endocrine syndrome
cafe-au-lait spots
fibrous dysplasia
early signs of puberty

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7
Q

drugs that increase thyroid binding globulin (therefore need higher dose of synthroid)?

A

tamoxifen
estrogen
raloxifene
methadone, heroin

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8
Q

drugs that reduce thyroid binding globulin (therefore need lower dose synthroid)?

A

androgens
danazol
anabolic steroids
glucocorticoids

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9
Q

patients with thyroid nodule and low TSH - next study?

A

radionucleotide uptake scan

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10
Q

patients with thyroid nodule and normal/high TSH - next study?

A

FNA

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11
Q

MEN Type I - features?

A

DIAMOND

  • pituitary tumors
  • hyperparathyroidism
  • enteropancreatic tumors
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12
Q

what is ASCVD risk level to start statin?

A

> 7.5% @ 10 years

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13
Q

who should start a statin?

A
  • 40-75 w/DM
  • ASCVD risk >7.5% @ 10 years
  • LDL >190
  • ACS
  • stable angina
  • arterial revasc (stent, CABG)
  • stroke, TIA, PVD
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14
Q

sick euthyroid - what is pathophys?

A

impaired conversion of T4 –> T3

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15
Q

what about sick people impairs conversion of T4 to T3?

A
  • high endogenous cortisol
  • inflammatory cytokines (TNF)
  • starvation
  • certain meds (amio, glucocorticoids)
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16
Q

subclinical hyperthyroid - clinical characteristics?

A
  • suppressed TSH
  • normal thyroid hormone levels
  • +/- hyperthyroid symptoms
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17
Q

subclinical hyperthyroid - causes?

A
  • exogenous thyroid hormone
  • graves dz
  • nodular thyroid dz
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18
Q

subclinical hyperthyroid - indications for tx?

A
  • TSH persistently <0.1
  • TSH 0.1-0.5 AND 1 of:
  • – age >65
  • – heart dz
  • – osteoporosis
  • – nodular thyroid dz
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19
Q

subclinical hypothyroidism - what is it?

A
  • increased TSH

- normal T4

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20
Q

subclinical hypothyroidism - when to tx?

A
  • TSH > 10
  • TSH < 10 but high AND pt has anti-TPO Ab
  • TSH < 10 but high AND pt has one of following:
  • – goiter
  • – symptoms
  • – pregnancy
  • – ovulatory dysfunction
  • – hypercholesterolemia
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21
Q

why is serum T3 Unhelpful in hypothyroidism?

A

T4 –> T3 coversion is regulated by TSH, therefore in hypothyroidism, pts have increased TSH and therefore increased conversion of T4 –> T3

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22
Q

maternal changes to thyroid hormones in 1st trimester? (TSH, T4, FT4)

A

TSH - decreased
T4 - increased
FT4 - same/mild increase

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23
Q

which 2 hormones in pregnancy affect TSH/T4?

A

Estrogen = stimulated production of thyroxine-binding globulin = increased bound thyroid hormone, so increased production
- hCG = directly stimulates TSH receptors to make more thyroid hormone and suppresses pituitary signals for TSH release

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24
Q

which antithyroid drug should be used in pregnancy?

A
  • PTY in 1st trimester

- methimazole in 2nd and 3rd

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25
Q

chronic autoimmune thyroiditis - what is the other name?

A

Hashimoto thyroiditis

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26
Q

Hashimoto thyroiditis (chronic autoimmune thyroiditis) - clinical features?

A
  • hypothyroid symptoms

- diffuse goiter

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27
Q

treatment for subacute thyroiditis?

A

NSAID + BB

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28
Q

what is definitive tx in Graves disease?

A

radioiodine thyroid ablation

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29
Q

acromegaly suspected - which tests do you send?

A
  • GH suppression test s/p glucose load (nonsuppression in acromegaly)
  • serum IGF1 levels
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30
Q

patients w/T1DM are predisposed to what conditions?

A
  • thyroid dysfunction
  • adrenal failure
  • primary hyogonadism
  • atrophic gastritis
  • celiac disease
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31
Q

causes of hypercalcemia with low PTH?

A
  • malignancy
  • vit D or A toxicity
  • granulomatous dz
  • drug-induced (thiazides)
  • milk-alkali syndrome
  • thyrotoxicosis
  • immobilization
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32
Q

causes of hypercalcemia with normal/high PTH?

A
  • primary (or tertiary) hyperparathyroidism
  • familial hypocalciuric hypercalcemia
  • lithium
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33
Q

in pregnancy, free thyroid and total thyroid hormone is corrected up to a factor of what?

A

1.5

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34
Q

hashimoto’s thyroiditis - what does TSH do?

A

GO UP

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35
Q

thyroid lymphoma - risk factor?

A

preexisting Hashimotos thyroiditis

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36
Q

follicular thyroid cancer - presentation?

A

palpable thyroid nodule

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37
Q

medullary thyroid cancer - assoc w/what syndrome?

A

multiple endocrine neoplasm

38
Q

how treat pt w/hypoparathyroidism?

A

vitamin D (calciferol) or 1,25-vitD (calcitriol) but 1,25 more expensive and normal vit D works

39
Q

what does PTH do?

A
  • converts 25-OHvitD to 1, 25-OHvitD

- increases renal calcium reABSORPTION

40
Q

what do in hypopara pt w/high Ca+ in urine, low Ca+ in blood?

A

add thiazide diuretic

41
Q

how do SGLT-2 inhibitors work?

A

lower blood glucose by reducing reabsorption of glucose in the kidney which leads to low insulin-to-glucagon ratio

42
Q

what is euglycmic ketoacidosis?

A

associated with SGLT-2 inhibitior use,

43
Q

name an SGLT-2 inhibitor?

A

canaglifloin

44
Q

women w/GDM should be tested with which test how long after birth?

A
  • glucose tolerance test

- 6-12 weeks

45
Q

primary hyperparathyroid - caused by what?

A
  • parathyroid adenoma (most common)
  • hyperplasia
  • carcinoma
46
Q

what puts pts @ risk for primary hyperparathyroidism?

A

MEN 1 & 2a

47
Q

primary hyperparathyroidism - ab abnormalities?

A
  • hypercalcemia
  • high or inappropriately normal PTH
  • high 24-hr urinary calcium excretion
48
Q

parathyroidectomy in pts w/primary hyperparathyroid - indications?

A
  • age < 50
  • symptomatic hypercalcemia
  • osteoporosis (T < -2.5, fragility fracture)
  • nephrolithiasis/calcinosis
  • high risk of complications: calcium > 1mg/dl above normal, urinary calcium excretion >400 mg/day
49
Q

in person w/adrenal insufficiency and hypoT - what do you need to be careful of in treatment?

A

dont give levothyroxine before addressing the adrenal insufficiency

50
Q

when do you measure reverse T3?

A

in hospiitalized pt to ditinguish euthyroid sick syndrome from central hypothyroidism

51
Q

what happens to reverse T3 in sick euthyroid?

A

it is elevated

52
Q

if you diagnose someone w/central hypoT, what else should you do?

A
  • workup for other pituitary hormones- pituitary MRI
53
Q

hormonal abnormalities in PCOS?

A
  • high testosterone
  • high estrogen
  • LH/FSH imbalance
54
Q

why do pts w/PCOS have infertility?

A

anovulation

55
Q

SIADH associated w/which lugn cancer/

A

small cell

56
Q

SIADH - treatment?

A

1 - fluid restriction
2 - may need salt tabs
3 - loop diuretics WITH hypertonic saline or salt tabs
4 - demeclocycline or lithium (blunts response of collecting tubule cells to ADH)

57
Q

primary hyperaldo - how diagnose?

A
  • plasma renin low

- aldo inapprop high

58
Q

autosomal dominant polycystic kidney disease these pts are @ higher risk for what intraacranial abnormality?

A

berry aneurysm

59
Q

raloxifene - what is it?

A

selective estrogen modulator - stimulates estrogen on bone cells, but ANTAGONIZES other estrogen-responsive tissues

60
Q

familial hypocalcuric hypercalcemia - how treat?

A

no treatment needed

61
Q

RET proto-oncogene - most common cause of what?

A

MEN types 2A and 2B

62
Q

how distinguish familial hypocalcuric hypercalcemia from hypereparathyroid?

A

in FHH = low calcium urine excretion

in hyperparathyroid = high urine calcium excretion

63
Q

thyroid effects of amiodarone

A
  1. decreased T4–> T3 conversion
  2. inhibition of thyroid hormone synthesis
  3. amiodarone induced thyrotoxicosis 2/2 increased thyroid hormone synthesis or destructive thyroiditis
64
Q

how treat amio induced TFT abnormalities?

A

you dont - give it time

65
Q

most common cause of primary hyperpara?

A

parathyroid adenoma

66
Q

second line agent for pts who have failed bisphosphonate therapy?

A

teriparatide

67
Q

prolactinoma - treatment?

A
  • dopamine agonists (cabergoline, brmoocriptime)

- surgery

68
Q

dulaglutide, exenatide, liraglutide - what class of meds are these?

A

GLP-1 receptor agonists

69
Q

which antihyperglycemics can cause weight loss?

A
  • biguanides (metformin)

- GLP-1 agonists (-tides)

70
Q

canagliflozin, dapagliflozin, empagliflozin - what class of meds are these?

A

SGLT-2 inhibitors

71
Q

linagliptin, sitagliptin, saxagliptin - what class of meds are these?

A

DPP-4 inhibitors

72
Q

pioglitazone - what class of med is this?

A

thiazolidinediones

73
Q

side effects of thiazolidinediones?

A
  • edema, HF

- bone fractures

74
Q

sulfonylureas (glimepriride), meglitinidies (repaglinide, nateglinide) - what class of meds are these?

A

insulin secretagogues

75
Q

which oral antihyperglucemics can cause hypoglycemia?

A

insulin secratagogues

  • sulfonylureas (glimepiride
  • meglitinides (repaglinide, nateglinide)
76
Q

what are the causes of low Ca?

A
  • vit D deficiency
  • hypopara
  • pseudohypopara
  • hyperphosphatemia
77
Q

vit D deficiency - phos and PTH are low/high?

A
  • phos low

- PTH high

78
Q

hypopara - phos and PTH are low/high?

A
  • phos high

- PTH low

79
Q

pseudohypopara - phos and PTH are low/high?

A
  • phos high

- PTH high

80
Q

hyperphosphatemia - phos and PTH are low/high?

A
  • phos high

- PTH high

81
Q

pseudohypopara - what is mechanism?

A

end organ resistance to PTH

82
Q

plasma ACTH are always measured at the same time as what other test?

A

cortisol

83
Q

what age start screening for osteoporosis?

A

65 unless risk factors (fam history, steroid use, smoking, malabsorption, body weight <127lb)

84
Q

what is secondary hyperpara?

A

increase in PTH 2/2 low calcium

85
Q

in what condition do you most commonly see secondary hyperpara?

A

CKD

86
Q

what is tertiary hyperpara?

A

parathyroid has hypertrophied from being stimulated so long in secondary hyperpara that it begins to produce PTH autonomously

87
Q

incidental adrenal mass - what workup need to send?

A
  • BMP
  • dex suppression test
  • 24h urine catecholamine
  • metanephrine
  • vanillylmandelic acid
  • 17-ketosterid
88
Q

when to excise adrenal mass?

A
  • > 4cm
  • functional tumors
  • malignant tumors (heterogenous appearance on imaging)
89
Q

osteitis fibrosa cystica - what is it? what causes it?

A
  • increased bony turnover causing fibrous tissue replacement

- caused by primary hyperpara or secondary hyperpara (as in CKD)

90
Q

to keep organs of braindead patient alive - what do?

A
  • fluids
  • vasopressin prn
  • methylpred
  • thyroid hormone