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Endocrinology Flashcards

1
Q

Posterior pituitary hormones

A

Oxytocin, ADH

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2
Q

Anterior pituitary hormones

A

TSH, ACTH, FSH/LH, GH, prolactin, endorphins

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3
Q

Direct secretion of hormones from the hypothalamus

A

Posterior pituitary - oxytocin, ADH

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4
Q

Zones of the adrenal gland

A

Glomerulosa, Fasiculata, Reticularis, Medulla

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5
Q

Mineralocorticoids

A

Aldosterone
Secreted by glomerulosa in response to RAS
Increases Na and HCO3, decreases K

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6
Q

Glucocorticoids

A

Cortisol (high AM, low at MN)
Secreted by fasiculata in response to ACTH
Increases glucose and BP

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7
Q

Most common defect in CAH

A

21-hydroxylase deficiency (95%)

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8
Q

Classic CAH

A

salt wasting (no aldo), hypotension (no cortisol), virilization (excess DHEA)

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9
Q

Primary causes of adrenal insufficiency

A

Congenital (x-linked)
Adrenal damage
Defects in cholesterol synthesis (Smith-Lemli-Optiz)
Peroxisomal disorders (ALD, Zellweger)

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10
Q

Secondary adrenal insufficiency

A

No salt-wasting or hyperpigmentation

Due to lack of ACTH

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11
Q

Triple A syndrome (Allgrove)

A

ACTH resistance, achalasia, alacrima

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12
Q

Autoimmune Polyglandular Syndrome (type 1)

A

Hypoparathyroidism, adrenal insufficiency, candidiasis

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13
Q

Autoimmune Polyglandular Syndrome (type 2)

A

Hypothyroidism, adrenal insufficiency, DM type 1

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14
Q

Liddle syndrome

A

Activation of Na channel causes mineralocorticoid excess and hypertension

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15
Q

Pheochromocytoma rule of 10’s

A

10% = extra-adrenal, malignant, children, bilateral

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16
Q

Syndromes associated with pheochromocytoma

A

MEN 2A, 2B
Von Hippel-Lindau
Neurofibromatosis

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17
Q

Causes of congenital hypothyroidism

A

Dysgenesis (75%), enzyme defects (10%), transient (10%), HPT axis (5%)
Only 2% have goiter!

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18
Q

Diagnosis of Hashimoto’s thyroiditis

A

anti-microsomal Ab’s

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19
Q

Diagnosis of euthyroid sick syndrome

A

low T4, T3, TSH

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20
Q

% of thyroid nodules that are malignant

A

33%

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21
Q

Iodine scan findings

A

Graves - high update, subacute thyroidisits - low uptake

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22
Q

Linear growth rate (after 3 years)

A

5-7 cm/yr

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23
Q

GH therapy side effects

A

pseudotumor, SCFE, rapid growth of nevi, worsening scoliosis

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24
Q

Diagnosis of GH deficiency

A

low IGF-1

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25
Q

Pubertal progression (girls)

A

Breast (8-13)
Pubic hair (8-14)
Growth spurt (10-14)
Menarche (10-16)

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26
Q

Pubertal progression (boys)

A 
Growth of testes (10-17)
Penis lengthens (11-15)
Pubic hair (11-14)
Growth spurt (12-17)
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27
Q

LH function

A

Men - stimulates Leydig cell to produce testosterone

Women - ovulation

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28
Q

FSH function

A

Stimulates Sertoli cell to produce inhibin
Women - initiates follicular development
Both - stimulates maturation of germ cells

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29
Q

Testosterone production

A

Testes (Leydig cells), ovaries, adrenal gland

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30
Q

Estrogen production

A

Granulosa cells of the ovary

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31
Q

Stimulation of FSH/LH

A

GnRH from hypothalamus

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32
Q

Pubertal delay

A

Boys - 14 yo

Girls -13 yo

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33
Q

Most common cause of pubertal delay in boys

A

Constitutional delay

34
Q

Constitutional delay of puberty findings

A

Delayed bone age, testes < 4 mL and penis < 7 cm, positive family history

35
Q

Kallman syndrome

A 
Hypogonadotropic hypogonadism (delayed puberty, micropenis, cryptorchidism)
Anosmia
36
Q

Swyer syndrome

A

46 XY but female phenotype due to mutation of SRY gene

37
Q

Swyer syndrome presentation

A

Tall women with primary amenorrhea. U/S with normal female internal anatomy. Streak gonads

38
Q

Premature puberty definition

A

Boys < 9 yo

Girls < 8 yo

39
Q

Precious puberty findings

A

Bone age > chronological age

40
Q

Causes of precocious puberty

A

Hypothalamic hamartoma, CAH, ovarian cyst, McCune-Albright, adrenal tumors

41
Q

Premature thelarche age

A

bimodal (< 2 yo and > 6 yo)

42
Q

McCune-Albright Syndrome

A

cafe-au-lait macules, fibrous dysplasia of bone, peripheral precocious puberty

43
Q

Vitamin D forms

A

D3 formed in skin
25-D3 in liver
1,25-D3 in kidney (stimulates intestinal absorption of Ca)

44
Q

PTH function

A

Stimulated by drop in iCa

Causes Ca mobilization from bones, increased vit D production, decreased PO4 absorption

45
Q

Rickets findings

A

tetany, growth retardation, frontal bossing, rachitic rosary, widening of wrists

46
Q

X-ray findings in Rickets

A

widening and fraying of epiphyses

47
Q

Causes of Rickets

A

Vitamin-D deficiency
Vitamin-D dependent
Hypophosphatemic (vitamin-D resistant)
Renal failure

48
Q

Causes of vitamin D deficiency

A

Lack of sunlight, vitamin D, phenobarb, malabsorbtion

49
Q

Hypophosphatemic rickets cause

A

phosphate leak in the proximal tubule

50
Q

Findings of renal failure rickets

A

Elevated PO4 (failure of vitamin D and PTH systems)

51
Q

MEN type 1

A

Hyperparathyroidism, pancreas islet cell tumor, pituitary tumors

52
Q

Findings of vitamin D deficiency

A

Low/normal Ca, PO4, elevated AP, PTH

53
Q

Most common cause of acquired adrenal insufficiency

A

Autoimmune adrenalitis

54
Q

2nd most common cause of CAH

A

11-hydroxylase deficiency

55
Q

11-hydroxylase deficiency findings

A

virilization, HTN, hypokalemia

56
Q

CAH genetics

57
Q

MEN type 2A

A

Pheochromocytoma, hyperparathyroidism, medullary cell thyroid cancer

58
Q

MEN type 2B

A

Pheochromocytoma, medullary cell thyroid cancer, mucosal neuromas

59
Q

Rate of congenital hypothyroidism

A

1 in 4000 births

60
Q

Factors associated with decreased IQ in congenital hypothyroidism

A

Low T4 at birth, delayed bone age at birth, delayed treatment, low T4 during first year of therapy

61
Q

Pseudohypoparathyroidism

A

Genetic resistance to PTH (low Ca, high PO4 and PTH)

62
Q

Pseudohypoparathyroidism findings

A

Round facies, spade-like hands, short stature, DD

63
Q

Causes of hyperparathyroidism

A

Sarcoidosis, immobilization, Vit D intoxication, cancer, Williams syndrome

64
Q

Familial hypocalciuric hypercalcemia genetics

65
Q

Familial short stature findings

A

Bone age = chronological age, normal onset of puberty

66
Q

Tumor associated with GH deficiency

A

craniopharyngioma

67
Q

Diagnosis of Cushing syndrome

A

urinary free cortisol

68
Q

Most common cause of Cushing syndrome in infants

A

adrenocortical tumor

69
Q

Septo-optic dysplasia findings

A

panhypopituitarism, hypoplastic optic discs, microphallus (boys)

70
Q

Treatment of choice for Grave’s disease

A

Methimazole

71
Q

Pubertal trigger

A

pulsatile release of GnRH

72
Q

Premature adrenarche onset

A

6 to 8 years

73
Q

Premature adrenarche management

A

follow-up every 4-6 months to confirm non-progressive nature

74
Q

CNS lesion causing central precocious puberty

A

hypothalamic hamartoma (benign - no resection), septo-optic dysplasia, neurofibroma

75
Q

Causes of peripheral precocious puberty

A

CAH, McCune-Albright, severe primary hypothyroidism, adrenal tumor

76
Q

PE findings of estrogen stimulated vaginal mucosa

A

pinkish (glistening red = non-estrogen stimulated)

77
Q

Areolar breast mounding - Tanner Stage

78
Q

Androgenic changes

A

body odor, body hair, acne

79
Q

Gynecomastia seen during what Tanner Stage

80
Q

1st sign of puberty in boys

A

testicular enlargement (4 cc!)

81
Q

Diagnosis of PCOS

A

amenorrhea/oligomenorrhea, elevated serum androgen/hirusitism/acne, polycystic ovaries on U/S

82
Q

Mid-parental height calculation

A

(maternal height + paternal height +/- 5 in)/2

Pediatrics (14 decks)

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