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Clinical Medicine > Endocrine > Flashcards

Endocrine Flashcards

1
Q

what most often causes hyperparathyroidism?

A

parathyroid adenoma

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2
Q

s/s of hyperparathyroidism

A

moans, groans, stones, bones

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3
Q

dx hyperparathyroidism

A

elevated serum Ca

PTH assay

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4
Q

tx hyperparathyroidism

A

NS + furosemide

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5
Q

most common cause of hypoparathyroidism

A

iatrogenic: post-thyroidectomy

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6
Q

what deficiency may cause development of hypoparathyroidism?

A

Mg

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7
Q

s/s of hypoparathyroidism

A

muscle cramps, carpopedal spasms, chvosteks & trousseaus sign, hyperactive DTR

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8
Q

dx hypoparathyroidism

A

decreased serum Ca, elevated PO4

EKG: QT prolongation

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9
Q

tx hypoparathyroidism

A

calcium gluconate

oral calcium, vit d, mg

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10
Q

causes of hyperthyroidism

A

graves

hot/toxic nodule

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11
Q

s/s hyperthyroidism

A

irritability, heat intolerance, anxiety, tachycardia

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12
Q

dx hyperthyroidism

A

elevated T3/T4

decreased TSH

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13
Q

tx hyperthyroidism

A

propanolol for sxs
methimiazole & PTH
RAI is definitive tx

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14
Q

what is Graves & who is it more common in?

A

autoimmune hyperthyroidism

8x more common in women (onset 20-40)

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15
Q

what are clinical manifestations of Graves?

A

proptosis/exopthalmosis

orange skinned

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16
Q

causes of hypothyroidism

A

autoimmune -> Hashimotos

iatrogenic -> thyroidectomy

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17
Q

s/s of hypothyroidism

A

cold intolerance, fatigue, bradycardia, constipation

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18
Q

what will the thyroid be like in hypothyroidism

A

diffusely enlarged, firm, finely nodular thyroid

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19
Q

what does congenital hypothyroidism cause

A

mental retardation -> cretinism

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20
Q

dx hypothyroidism

A

decreased T3/T4

elevated TSH

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21
Q

tx hypothyroidism

A

levothyroxine

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22
Q

what is cushings

A

excess cortisol

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23
Q

causes of cushings

A

endogenous: tumor secreting excess cortisol or ACTH
exogenous: drugs

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24
Q

what is cushings syndrome

A

adrenal tumor

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25
Q

what is cushings disease

A

pituitary tumor

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26
Q

s/s of cushings

A

central obesity, moon facies, striae, buffalo hump, DM/glucose intolerance, thin extremities, HTN

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27
Q

dx cushings

A

elevated AM cortisol with loss of diurnal pattern

Dexamethasone suppression test

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28
Q

tx cushings

A

stop drug

remove tumor

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29
Q

what is addison’s disease

A

adrenal insufficiency

autoimmune destruction of adrenal glands

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30
Q

s/s of addison’s disease

A

hyperpigmentation, palmar creases, fatigue, weakness, arthralgias, reduction in axillary & pubic hair

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31
Q

dx addison’s disease

A

low AM cortisol level
ab CT: small, non-calcified adrenals
cosyntropin stimulation test

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32
Q

tx addison’s disease

A

glucocorticoid replacement

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33
Q

how much must you increase maintenance cortisol during periods of stress

A

8-10x

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34
Q

what may precipitate acute adrenal insufficiency/crisis

A

abrupt stop of corticosteroids

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35
Q

s/s of acute adrenal insufficiency

A

confusion, diarrhea, temp > 40, hypotension, cyanosis, hemodynamic collaps

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36
Q

patient w/ hypotension/shock unresponsive to IV fluids & pressors

A

acute adrenal insufficiency

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37
Q

tx acute adrenal insufficiency

A

rapid infusion of isotonic fluids & IV hydrocortisone

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38
Q

what is pheochromocytoma

A

rare adrenal tumor that secretes NE/EPI

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39
Q

s/s pheochromocytoma

A

sustained HTN, palpitations, HA, excessive sweating

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40
Q

dx pheochromocytoma

A

24 hour urine for catecholamines & metanephrines

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41
Q

tx pheochromocytoma

A

laparoscopic removal of tumor

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42
Q

what is pagets disease

A

focal ares of excessive osteoclast-mediated bone resorption preceding disorganized osteoblast-mediated bone repair

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43
Q

what does the bone look like in pagets disease

A

mosaic/jigsaw puzzle

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44
Q

s/s of pagets disease

A

usually asymptomatic

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45
Q

dx of pagets disease

A

x-ray w/ characteristic bone deformities

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46
Q

tx pagets disease

A

NSAIDS for pain

bisphosphonates

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47
Q

what is nephrogenic diabetes insipidus

A

inability for the kidneys to respond to ADH

48
Q

s/s DI

A

polyuria, intense thirst

49
Q

dx DI

A

vasopression challenge

50
Q

what causes acromegaly/gigantism

A

excess GH, usually from a pituitary adenoma

51
Q

effects of GH are mediated by…

A

IGF-1 produciton in the liver

52
Q

s/s of excess GH

A

before closure epiphysis: gigantism

after closure: acromegaly

53
Q

s/s of acromegaly

A

enlarged hands, feet, jaw, coarse facial features, bones of skull enlarge, deep voice

54
Q

associated findings w/ acromegaly/gigantism

A

HTN, cardiomyopathy, insulin resistance/DM

55
Q

dx acromegaly/gigantism

A

serum IGF-1 increased 5x

56
Q

tx acromegaly/gigantism

A

transphenoidal microsurgery

57
Q

what is the most common cause of hyperpituitarism

A

pituitary adenoma

58
Q

s/s of hyperprolactinemia

A

high proactive levels suppress GnRh -> decreases LH/FSH -> hypogonatropic hypogonadism
females: oligomenorrhea, glactorrhea, infertility

59
Q

tx hyperprolactinemia

A

dopamine agonists

60
Q

what is the most common cause of hypoglycemia

A

insulin & sulfonylureas

61
Q

s/s hypoglycemia

A

sweating, tachycardia, hunger, nausea

62
Q

what might mask the symptoms hypoglycemia

A

beta blockers

63
Q

dx of hypoglycemia

A

BS

64
Q

tx hypoglycemia

A

simple sugars (diabetics should always carry)
glucagon injection
IV glucose

65
Q

DKA is more common in T1DM or T2DM

A

T1DM

66
Q

phys behind DKA

A

lack of insulin leads to rapid breakdown of energy stores from muscle & fat -> excess ketoacids

67
Q

what is usually the trigger to DKA

A

something that requires an increased amount of insulin

68
Q

s/s DKA

A

decreased mentation, N/V, coma

fruity smell from volatile ketones

69
Q

dx DKA

A

BS > 300, low pH, volume depletion & electrolyte loss, metabolic acidosis w/ increased anion gap, total body K is low

70
Q

tx DKA

A

insulin + IV fluids

71
Q

who is at risk for developing nonketotic hyperosmolar coma

A

elderly w/ T2DM

72
Q

pathophys of NKHC

A

adequate circulating insulin to prevent fat breakdown, but not enough to control hyperglycemia

73
Q

tx NKHC

A

fluid replacement & insulin by infusion

74
Q

what is osteoporosis

A

compromised bone strength predisposing to an increased risk of fracture

75
Q

osteoporosis leads to an increased bone resorption, especially of _____ bone

A

trabecular

76
Q

when does bone density peak

A

young adults, early 20s

77
Q

when is physiology bone loss accelerated

A

first 5-10 years post menopause

78
Q

definition of osteopenia

A

1-2.5 SD below peak bone density

79
Q

definition of osteoporosis

A

greater than 2.5 SB below peak density

80
Q

dx osteoporosis

A

DEXA scan

81
Q

can you reverse established osteoporosis?

A

no, you can increased BD, decreased fractures, halt/slow progression

82
Q

when do you screen for osteoporosis?

A

all patients at increased risk including early post menopause + risk factors (FH, malnourished, alcoholism, renal failure), older than 65

83
Q

tx for osteoporosis

A

bisphosphonates

84
Q

what do bisphosphonates do?

A

inhibit osteoclastic bone resorption

85
Q

what is important when prescribing bisphosphonates?

A

dental care

86
Q

insulin ____ fat

insulin ____ protein synthesis

A

spares fat

promotes protein synthesis

87
Q

what causes T1DM

A

autoimmune -> presence of islet cell antibodies

causes destruction of beta cells

88
Q

s/s of diabetes

A

polyphagia, polydipsia, polyuria

89
Q

tx for T1DM

A

insulin

90
Q

pathophys of T2DM

A

circulating insulin prevents ketoacidosis, but not hyperglycemia

91
Q

what does the constant state of hyperglycemia in T2DM cause

A

causes increased insulin resistance & eventual destruction of beta cells

92
Q

what is common in people with T2DM & a major factor for insulin resistance?

A

central obesity

93
Q

what does hepatic insensitivity in T2DM cause?

A

increased gluconeogenesis

94
Q

what does glucotoxicity in T2DM cause?

A

chronic hyperglycemia that worsens peripheral insulin resistance & eventually destroyed beta cells permanently

95
Q

what does metabolic syndrome increase your risk of & by how much

A

atherosclerosis

3x

96
Q

what are the 5 factors of metabolic syndrome

A
  1. central obesity
  2. HTN (> 135/85)
  3. hyperglycemia (> 110)
  4. elevated Trig (>150)
  5. decreased HDL (women
97
Q

what are some long term complications of DM

A

retinopathy, neuropathy, nephropathy, proteinuria, HTN, atherosclerosis, PVD

98
Q

what two classes make up the insulin secretagogues

A

sulfonylureas

meglitinides

99
Q

where do the insulin secretagogues act

A

they close the Katp channels & promote insulin secretion

100
Q

sulfonylureas stimulate the release of _____

A

somatostatin

101
Q

SE of the insulin secretagogues

A

hypoglycemia & wt gain

102
Q

what are 4 actions of biguanides

A

decreases hepatic glucose produciton
improves insulin sensitivity
improves lipid profiles
decreases carb absorption from the gut

103
Q

biguanides may impair hepatic metabolism of _____

A

lactic acid

104
Q

C/I for biguanides

A

renal insufficiency, liver failure, major surgery

105
Q

most common SE for biguanides

A

GI issues

106
Q

site of action for TZDs

A

muslce, fate, liver cells

107
Q

what are 3 actions for TZDs

A

improve insulin sensitivity
increase glucose uptake
decrease hepatic glucose production & glycogenolysis

108
Q

what do you need to check before starting TZDs

A

LFTs

109
Q

what is the onset of action for TZDs like

A

slow, 6-14 weeks

110
Q

C/I for TZDs

A

hepatic disease & HF

111
Q

what are 2 actions for alpha-glucosidase inhibitors

A

inhibits intestinal hydrolysis of complex carbs

decreases postprandial digestion

112
Q

main SE of alpha-glucosidase inhibitors

A

flatulence, diarrhea, ab pain

113
Q

GLP-1 agonist is an ___ mimetic

A

incretin

114
Q

what are 3 actions of GLP-1 agonist?

A

promotes insulin secretion in presence of glucose
slows gastric emptying
promotes satiety

115
Q

what is an alternative to insulin without weight gain?

A

GLP-1 agonists

116
Q

what is normally secreted w/ insulin?

A

amylin

117
Q

what are 3 actions of amylin analogues?

A

modulates post prandial glucose
suppressed glucagon secretion
slows gastric emptying

Clinical Medicine (2 decks)

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