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Endocrinology Flashcards

1
Q

when does anatomic development begin in thyroid

A

3 wk

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2
Q

what dermal layer does thyroid arise from?

A

median endodermal thickening in the primitive pharyngeal floor at 5-7 weeks

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3
Q

when does trh production begin?

A

6-8 weeks

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4
Q

when does thyroid follicles form?

A

8 weeks

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5
Q

when does thyroglobulin production begin?

A

8 weeks

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6
Q

when does iodide accumulate in fetal thyroid?

A

10 weeks

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7
Q

when does pituitary make tsh?

A

12 weeks

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8
Q

when are thyroid hormones secreted from thyroid gland?

A

12 weeks

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9
Q

T4 levels pattern pre and post delivery

A
  • low until 18-20 weeks
  • then increase with GA
  • increase with TSH surge at birth
  • peak at 24-36 hours then decrease over 1-2 weeks
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10
Q

T3 levels pattern pre and post delivery

A
  • low until 30 weeks when able to convert T4 to T3 with deiodination
  • increase dramatically at birth
  • peak at 24-36 hours then continue to increase over 1-2 weeks
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11
Q

TSH levels pattern pre and post delivery

A
  • low until 18-20 weeks
  • increase proportional to GA
  • surge at birth
  • peak at 30 minutes, decrease over 1-2 weeks
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12
Q

which cross placenta?
TRH
T3
T4
Iodide
TSH
TSH Abs

A

TRH - yes
T3 - partial
T4 - partial
Iodide - yea
TSH - NO
TSH Abs - yes

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13
Q

what placental hormones affect thyroid hormones?

A
  • estrogen increase TBG, T4, T3
  • hCG increase T4 and T3
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14
Q

which is secreted more from thyroid? T3 or T4

A

T4

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15
Q

which is more potent? T3 or T4

A

T3

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16
Q

which has higher blood concentration? T3 or T4

A

T4

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17
Q

which has higher protein binding affinity? T3 or T4

A

T4

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18
Q

which is present more in free form? T3 or T4

A

T3

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19
Q

which has higher plasma half life? T3 or T4

A

T4

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20
Q

where is T3 localized?

A

intracellular

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21
Q

where is T4 localized?

A

extracellular

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22
Q

what does T3 resin uptake measure?

A
  • amount of unsaturated binding sites on TBG
  • radioactive T3 binds to sites; the rest bind to resin which is measured
  • higher resin binding means less open sites
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23
Q

Free T4 index?

A

T4 X (T3 resin uptake/T3 resin uptake control)

corrects for TBG concentration

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24
Q

Pendred syndrome

A
  • AR
  • organification defect with congenital 8th nerve abnormality
  • deafness
  • goiter
  • positive percholate discharge test
  • rapid loss of radioactive iodine from thyroid gland
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25
Q

low T4 and high TSH

A

thyroid dysgenesis
dyshormonogenesis
transient primary hypothyroidism

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26
Q

low free T4 normal TSH

A

transient hypothyroxinemia of prematurity
sick euthyroid syndrome
thyroglobulin deficiency
congenital TSH deficiency

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27
Q

normal free T4 and high TSH

A

transient hypothyroidism
thyroid dysgenesis

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28
Q

best way to give levothyroxine

A

crushed tablets directly - may cling to syringe
small amounts into milk and then mouth
not absorbed well in soy

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29
Q

types of TRAbs

A

thyroid receptor stimulating antibodies (TSIs) and thyroid receptor blocking antibodies (TBAs)

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30
Q

maternal treatment options for graves

A

ptu: during first trimester
methimazole after first trimester

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31
Q

side effects of ptu

A
  • preauricular sinus/fistula
  • GU anomalies
  • LBW
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32
Q

side effects of methimazole

A
  • cutis aplasia
  • choanal atresia
  • GI defects
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33
Q

timing of sending levels on infant with exposure to TRAbs

A

3-5 days
10-14 days;
4 weeks
2-3 months

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34
Q

how does methimazole work?

A

inhibit thyroid peroxidase - decreasing TH synthesis

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35
Q

how does ptu work?

A

inhibits thyroid peroxidase and blocks peripheral conversion of T4 to T3

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36
Q

effect of beta blockers on thyroid hormones

A

inhibits peripheral conversion of t4 to t3

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37
Q

effect of potassium iodide (lugols soln) on thyroid hormones

A

inhibits thyroid hormone release and synthesis

38
Q

effect of glucocorticoids on thyroid hormones

A
  • decrease th secretion
  • block peripheral conversion of t4 to t3
39
Q

what is adrenal cortex derived from?

40
Q

what is adrenal medulla derived from

A

neuroectodermal cells of neural crest

41
Q

when does the gonadal ridge give rise to the steroidogenic gonadal cells and adrenal cortex cells?

A

5-6 weeks before migrating caudally (gonadal cells) and retroperitoneally (adrenal)

42
Q

when do the sympathetic neural cells invade the adrenal cells to form the adrenal medulla

43
Q

when does the adrenal gland become encapsulated?

44
Q

MCC of CAH

A

21 hydroxylase deficiency

45
Q

pathophysiology of 21 hydroxylase deficiency

A

can not convert progesterone to deoxycortisone –> aldosterone deficiency (salt wasting)

cannot convert 17-OH progesterone to 11 deoxycortisol –> cortisol deficiency

increased 17OHP and increased testosterone

46
Q

how does 21 hydroxylase deficiency affect XX and XY

A

XX- ambigious genitalia
XY - normal

47
Q

electrolyte abnormalities in 21 hydroxylase deficiency

A

hyponatremia
hyperkalemia
hypoglycemia

48
Q

pathophys of 11 beta hydroxylase deficiency

A
  • deoxycorticosterone acts as mineralocorticoid so no salt wasting
  • cannot convert 11 deoxycortisol to cortisol –> cortisol deficiency
  • increased 11 deoxycortisol –> increased testosterone
49
Q

2nd MCM of CAH

A

11 beta hydroxylase deficiency

50
Q

how does 11 beta hydroxylase deficiency effect XX and XY?

A

XX - ambiguous
XY - normal

51
Q

how does 17 alpha hydroxylase deficiency effect XX and XY?

A

XX - normal
XY - ambiguous

52
Q

how does 3 beta hydroxysteroid dehydrogenase deficiency effect XX and XY?

A

xx- ambiguous
xy - ambigious

53
Q

pathophysiology of 17 alpha hydroxylase deficiency

A
  • blocks DHEA to androstenediol conversion
  • elevated DOC and corticosterone
  • low 17 OHP and low 17 OH pregnenolone
54
Q

pathophys of 3 beta hydroxysteroid dehydrogenase deficiency

A

elevated 17 OH, pregnenolone, DHEA

55
Q

pathophysiology of aromatase deficiency

A
  • inability to convert testosterone to estradiol and androstenedione to estrone
  • virilized female
56
Q

pathophysiology of 5a reductase deficiency

A

AR
inability to convert testosterone to dihydrotestosterone

undervirilized XY
normal XX

57
Q

what hormones released from Leydig and Sertoli cells?

A

Leydig
- INSL3 - testicular development
- testosterone
» wolfian duct development
» external 2/2 DHT

Sertoli
- MIS/AMH: regression of mullerian duct

58
Q

micropenis is due to hormonal abnormality after what week GA?

A

14; decreased testosterone

59
Q

what is hydrometrocolpos?

A
  • collection of fluid in fetal uterus and vagina 2/2 vaginal blockage (imperforate hymen/high vaginal septum/vaginal atresia/urogenital sinus) and excess vaginal fluid

may require drainage as it can lead to obstruction of other organs

60
Q

how does diazoxide work?

A

suppress insulin release

61
Q

What is pituitary gland derived from

A

ectodermal tissue

62
Q

what is neurohypophysis derived from?

A

floor of forebrain

63
Q

what is adenohypophysis derived from

A

primitive oropharynx; Rathkes pouch

64
Q

when does HPA axis develop

A

18-20 weeks

65
Q

what hormones come from anterior lobe

A

tsh LH FSH prolactin GH ACTH and pro-opiomelaocortin

66
Q

what hormones come from posterior lobe

A

vasopressin and oxytocin

67
Q

when are hypothalamic hormones detected

A

8-12 weeks

68
Q

placental transfer of Ca, Phos and Mag

69
Q

postnatal Ca levels

A
  • rise first 6 hours
  • lowest at 24-48 hours
70
Q

postnatal PTH

A

increases after birth peaking at 48 hours

71
Q

postnatal calcitriol

A
  • increases after birth
  • constant after 24 hours
72
Q

postnatal phosphate levels

A

high first few days then declines

73
Q

postnatal calcitonin levels

A

increases after birth then decreases slowly

74
Q

Ca regulation intestines, kidney, bone

A
  • 20-60% reabsorbed in intestines (proximal SI)
  • filters free in kidney, 98% reabsorbed (60% PT, 35% loop)
  • released from bone 2/2 cortisol and thyroid hormone
75
Q

Phos regulation intestines, kidney, bone

A
  • 70-90% absorption in intestines
  • filters free P, 90% reabsorbed esp PT
  • released from bone 2/2 cortisol and thyroid hormone
76
Q

PTH action intestines, kidney, bone

A
  • Intestines:
    – indirectly increases Ca, Phos absorption via vit D
  • Kidney:
    – increases Ca (ascending loop), decreases P and HCO3 reabsorption (increase Cl)
    – increases renal calcitriol
  • Bone:
    – increases Ca and Phos release from bone with vit D
77
Q

Vit D action intestines, kidney, bone

A
  • increases Ca and slightly P in intestines (1,25)
  • converted to 1,25 in kidney
  • increase effect of PTH on bone
78
Q

Calcitonin action intestines, kidney, bone

A
  • no effect on intestines
  • small increase in Ca, P excretion
  • inhibits release of Ca and P from bone
79
Q

differences between metabolic bone disease, osteopenia, osteomalacia and rickets

A

metabolic bone disease - decreased bone mineral content

osteopenia - decreased osteoid, matrix mineralized

osteomalacia - poorly mineralized osteoid and bone

rickets - inadequate mineralization of growth plates

80
Q

lab findings of metabolic bone disease

A
  • normal Ca (normal PTH)
  • low phos
  • elevated alk phos
  • 25 vit D normal
  • 1,25 vit D elevated
  • normal/elevated PTH
81
Q

increased Ca, decreased P

A

primary hyperPTH

82
Q

decreased Ca, increased P, low PTH

A

primary hypoparathyroid

83
Q

decreased Ca, increased P, high PTH

A

primary pseudohypoparathyroid - PTH resistance

chronic renal failure

84
Q

MCC congenital cardiac defect in IDM

85
Q

what hormones contribute to macrosomia in IDM

A

IGFBP3 and IGF1

86
Q

effect of dopamine on thyroid pathway

A

inhibit secretion of TSH

87
Q

effect of caffeine on thyroid pathyway

A

inhibit secretion of TSH

88
Q

postnatal TSH surge in SGA vs AGA

A

higher TSH surge
lower T4

89
Q

incidence of thyroid disease in infant born to woman with Graves

90
Q

which has more FT or PT?
thyroglobulin
iodide stores
TBG

A

thyroglobulin - PT
iodide stores - FT
TBG - FT

91
Q

critical period of external virilization

A

6-12 weeks

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