Endocrine Flashcards

1
Q

Which Thyroid hormone is highest in fetus?

A

Reverse T3
(fetus metabolizes T4 to rt3)

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2
Q

When can fetus begin converting T4 to t3?

A

About 30 weeks gestational age

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3
Q

How does fetus maintain iodide needed for thyroid hormone production?

A

transplacental transfer

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4
Q

Why do maternal T4 and T3 increase in pregnancy?

A

hcg structurally similar to TSH

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5
Q

Does TSH cross placenta?

A

No

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6
Q

Describe steps of thyroid hormone production

A

TRH made in hypothalamus, acts on anterior pituitary to release TSH, TSH acts on thyroid gland

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7
Q

Why is Free T4 a good measure of thyroid function?

A

only free form can enter cells

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8
Q

What decreases TBG?

A

Essentially anything that makes you sick, prematurity, or glucocorticoids.

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9
Q

What does iodine exposure due to T4 levels?

A

decreases

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10
Q

Why do neurologic deficiencies manifest with hypothyroidism?

A

delayed myelination and abnormal neuronal cell membrane synthesis.

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11
Q

What is medication used for Graves in first trimester?

A

Propylthiouracil

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12
Q

What is medication used for Graves in third trimester?

A

Methimazole
avoid during first trimester due to cutis aplasia

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13
Q

Postnatal management of Hyperthyroidism?

A

Methmiamzole, PTU (2nd choice, due to liver failure), Beta blocker (inhibits T4 to t3), iodine (stops TRH), Glucocorticoids, block T4 to 3

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14
Q

Pathway of cortisol production

A

Hypothalamus secretes CRH, induces anterior pituitary to secrete ACTH, which than leads to production by adrenal gland

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15
Q

Cortisol deficiency would lead to

A

Hypoglycemia, hypotension, anemia

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15
Q

What is function of cortisol?

A
  1. Induces gluconeogenesis and antagonizes insulin
  2. Increases CA and phosphate release from bone
  3. Decreases inflammation and suppresses immune system
  4. Inhibits ADH, increases RBC production
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15
Q

21 hydroxylase deficiency leads to what?

A

Increase 17-OHP
increased testosterone production

salt wasting and hypotension because of aldosterone deficiency
(17-OHP can’t be converted to 11 DOC)

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16
Q

Laboratory findings CAH

A

hyponatremia, hyperkalemia, hypoglycemia, and elevated 17-OHP

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17
Q

In 11 Beta Hydroxylase deficiency why is there no salt wasting?

A

DOC can still function as mineralocorticoid

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18
Q

How do you diagnose 11 Beta Hydroxylase deficiency

A

High DOC and 11-deoxycortisol levels with increased response to ACTH

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19
Q

Maternal exposure to fetal androgens (female fetus) what happens before 13 weeks gestation

After 13 weeks gestation

A

Before 13, posterior fusion of vagina, scrotilization of labia

After, clitoromegaly

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20
Q

What is 5 alpha reductase deficiency?

A

AR disorder can’t convert testosterone to dihydrotesterone

there is absence of Mullerian structures, and presence of Wolffian (just poorly developed)

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21
Q

What causes hydrocele?

A

persistence of processus vaginalis, which usually involutes
communicating (increases with increase abdominal pressure) vs non-communicating

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22
Q

Do you see alkalosis or acidosis in CAH?

A

Acidosis due to deficiency of aldosterone

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23
Q

Explain salt wasting crisis

A

deficiencies in both glucocorticoid and mineralocorticoid activities

glucocorticoid deficiency can cause hypotension and hypoglycemia (which can lead to siezures)

mineralocorticoid deficiency can ause worsening urinary salt loss, dehydration and potassium retention.

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24
Q

Formula has more Calcium than breastmilk, BUT breastfed fed infants have higher Calcium levels than breastfed infants? How is this possible?

A

Formula has higher phosporous content, which results in higher phosphorus levels, which results in lower CA levels

25
Q

True or False: Fetal mineral homeostasis requires parathyroid hormone?

A

True

26
Q

What are common findings of CAH?

A

hyponatremia, hypokalemia, hypoglycemia, dehydration

27
Q

what does 21 hydroxylase do?

A

converts progesterone to deoxycorticosterone and 17 hydroxyprogesterone (aldosterone) to 11 deoxycortisol (Cortisol)

28
Q

What does ACTH stim test measure?

A

if cause is adrenal (low aldosterone and cortisol production)

or if it is pituitary (low ACTH)

29
Q

What is the primary nutritional cause of metabolic bone disease in preterm infants?

A

phosphorus deficiency

30
Q

Where is mutation in CAH ?

A

CYP21A2 gene

31
Q

What is most common presenting symptom of hypocalcemia?

A

asymptomatic

32
Q

Fetal glucose is maintained by facilitated or simple diffusion across placenta?

A

FACILITATED

33
Q

What are 4 substrates of glucose?

A

lactate/pyruvate
gluconeogenic amino acids (And alanine
glycerol
propionic acid

34
Q

What is risk of using diazoxide to surpress insulin release?

A

pulmonary hypertension

35
Q

How can lipids cause hyperglycemia?

A

lead to high amount of free fatty acids

36
Q

Embryology
Pituitary derives from where?

A

Pituitary (Ectodermal tissue)

37
Q

What does posterior pituitary do?

A

stores and secretes ADH and oxyctocin

38
Q

Why does growth hormone deficiency not affect length at birth?

A

because insulin induces fetal growth and insulin levels are normal

39
Q

What does calcitriol due in maternal state?

A

increases Calcium absoprtion from intestine, and decreases Ca renal excretion

40
Q

What affect do cortisol and thryoid hormones have on bone?

A

Cause release of Calcium and phosphate from bone

41
Q

Where is majority of Ca absorbed

A

proximal small intestine

42
Q

What is affect of PTH on Phosphate?

A

Decreases Phosphate reabsorption, increases release of Phosphate from bone (increases bone resorption)

43
Q

What affect does PTH have on kidney?

A

increases renal calcitriol production (vitamin D)

44
Q

What does calictriol do?

A

increases PTH affect on bone

affects kidney by inreases reabsoprtion of Ca

45
Q

How does alkalosis lead to hypocalcemia?

A

HCO3 causes increased CA binding to albumin

think of tingling feeling with hyperventiliation

46
Q

Best anatomical sites to image for hypocalcemia?

A

wrist or knee due to increased metabolic activity

47
Q

Lab values of Calcium and Phosphate in metabolic bone disease of prematurity?

A

Serum CA usually normal
Serum Phosphate decreasd
alk phos also increased

48
Q

Affects of Calcium and Phosphate in primary hypoparathyroidism

A

decreasedCA, increased Phopshate
may have hyperchloremic metabolic acidosis due to renal affect of PTH

49
Q

Affects of Calcium and Phosphate in primary hypoparathyroidism

A

Decreased, CA, increased Phopsphate, decreased calictriol synthesis
Alkalosis

50
Q

How do you treat Central DI

A

Vasopressin or Desmopressin

51
Q

How do you treat nephrogenic DI?

A

Thiazide diuretics

52
Q

How do you treat SIADH?

A

Free water restriction
if NA is < 120 then replace with NaCL
may also consider furosemide

53
Q

How does ADH act extrarenally?

A

aterial vasoconstriction, decrease renin secretion, and increase ACTH secretion

54
Q

How does hypokalemia occur with alkalosis?

A

when H+ leaves cell to compensate, K+ enters cell

55
Q

At Birth PTH is _______ (and) Calcitonin is ___________ ?

A

decreased, increased

56
Q

How does Aldosterone affect acid/base status?

A

stimulates renal secretion of H+, regulating bicarb levels.

acts on distal tubules and collecting ducts to increase reabsorption of NA and Water, and secretion of K

57
Q

How does asphyxia cause hypocalcemia?

A

increases phosphate load from cellular injury and reduces calcium.

58
Q

how does hypernateremia lead to possible brain hemorrhage?

A

cerebral cellular dysfunction causes cell shrinkage, leading to physical separation of brain from meninges, resulting in rupture of bridging veins

59
Q

Is Na supplementation a way to treat SIADH?

A

No, ADH acts on reasbsoprtion of water not Na

60
Q

What are clinical signs of CAH?

A

Hypotension, hyponatremia, hyperkalemia, metabolic acidosis

61
Q

What causes hypocalcemia in IDM?

A

Reduced transplacental transfer of calcium secondary to increased urinary excretion of Ca2+ and mg 2+

62
Q

What distinguishes psuedohypoadlosteronism from CAH?

A

elevated aldosterone and not super elevated K with pseduo