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Endocrine Flashcards

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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
Explain salt wasting crisis
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.
24
Formula has more Calcium than breastmilk, BUT breastfed fed infants have higher Calcium levels than breastfed infants? How is this possible?
Formula has higher phosporous content, which results in higher phosphorus levels, which results in lower CA levels
25
True or False: Fetal mineral homeostasis requires parathyroid hormone?
True
26
What are common findings of CAH?
hyponatremia, hypokalemia, hypoglycemia, dehydration
27
what does 21 hydroxylase do?
converts progesterone to deoxycorticosterone and 17 hydroxyprogesterone (aldosterone) to 11 deoxycortisol (Cortisol)
28
What does ACTH stim test measure?
if cause is adrenal (low aldosterone and cortisol production) or if it is pituitary (low ACTH)
29
What is the primary nutritional cause of metabolic bone disease in preterm infants?
phosphorus deficiency
30
Where is mutation in CAH ?
CYP21A2 gene
31
What is most common presenting symptom of hypocalcemia?
asymptomatic
32
Fetal glucose is maintained by facilitated or simple diffusion across placenta?
FACILITATED
33
What are 4 substrates of glucose?
lactate/pyruvate gluconeogenic amino acids (And alanine glycerol propionic acid
34
What is risk of using diazoxide to surpress insulin release?
pulmonary hypertension
35
How can lipids cause hyperglycemia?
lead to high amount of free fatty acids
36
Embryology Pituitary derives from where?
Pituitary (Ectodermal tissue)
37
What does posterior pituitary do?
stores and secretes ADH and oxyctocin
38
Why does growth hormone deficiency not affect length at birth?
because insulin induces fetal growth and insulin levels are normal
39
What does calcitriol due in maternal state?
increases Calcium absoprtion from intestine, and decreases Ca renal excretion
40
What affect do cortisol and thryoid hormones have on bone?
Cause release of Calcium and phosphate from bone
41
Where is majority of Ca absorbed
proximal small intestine
42
What is affect of PTH on Phosphate?
Decreases Phosphate reabsorption, increases release of Phosphate from bone (increases bone resorption)
43
What affect does PTH have on kidney?
increases renal calcitriol production (vitamin D)
44
What does calictriol do?
increases PTH affect on bone affects kidney by inreases reabsoprtion of Ca
45
How does alkalosis lead to hypocalcemia?
HCO3 causes increased CA binding to albumin think of tingling feeling with hyperventiliation
46
Best anatomical sites to image for hypocalcemia?
wrist or knee due to increased metabolic activity
47
Lab values of Calcium and Phosphate in metabolic bone disease of prematurity?
Serum CA usually normal Serum Phosphate decreasd alk phos also increased
48
Affects of Calcium and Phosphate in primary hypoparathyroidism
decreasedCA, increased Phopshate may have hyperchloremic metabolic acidosis due to renal affect of PTH
49
Affects of Calcium and Phosphate in primary hypoparathyroidism
Decreased, CA, increased Phopsphate, decreased calictriol synthesis Alkalosis
50
How do you treat Central DI
Vasopressin or Desmopressin
51
How do you treat nephrogenic DI?
Thiazide diuretics
52
How do you treat SIADH?
Free water restriction if NA is < 120 then replace with NaCL may also consider furosemide
53
How does ADH act extrarenally?
aterial vasoconstriction, decrease renin secretion, and increase ACTH secretion
54
How does hypokalemia occur with alkalosis?
when H+ leaves cell to compensate, K+ enters cell
55
At Birth PTH is _______ (and) Calcitonin is ___________ ?
decreased, increased
56
How does Aldosterone affect acid/base status?
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
How does asphyxia cause hypocalcemia?
increases phosphate load from cellular injury and reduces calcium.
58
how does hypernateremia lead to possible brain hemorrhage?
cerebral cellular dysfunction causes cell shrinkage, leading to physical separation of brain from meninges, resulting in rupture of bridging veins
59
Is Na supplementation a way to treat SIADH?
No, ADH acts on reasbsoprtion of water not Na
60
What are clinical signs of CAH?
Hypotension, hyponatremia, hyperkalemia, metabolic acidosis
61
What causes hypocalcemia in IDM?
Reduced transplacental transfer of calcium secondary to increased urinary excretion of Ca2+ and mg 2+
62
What distinguishes psuedohypoadlosteronism from CAH?
elevated aldosterone and not super elevated K with pseduo

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