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Neonatal-Perinatal Boards Review > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Symptoms and signs of adrenal hemorrhage

A
  1. Mild—asymptomatic
  2. Moderate—hypertension (induced transient reactive hyperplasia), unconjugated hyperbilirubinemia
  3. Severe—hypotensive shock, severe anemia, mass

Risks are difficult delivery (especially if infant large/dystocia) and perinatal depression. (Like other highly vascular areas, is at increased risk from those stresses)

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2
Q

Clinical findings in panhypopituitarism

A
  1. hypoglycemia
  2. micropenis
  3. cholestasis
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3
Q

Clinical findings in hypothyroidism

A
  1. hypoglycemia
  2. cholestasis
  3. failure to thrive

(similar to panhypopituitarism, main difference is sexual development)

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4
Q

The system tested by a cortisol stimulation test

A

Hypothalamic-pituitary-adrenal (HPA) axis

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5
Q

Location and stimulants of ADH excretion

A

Posterior pituitary

Primary stimulant: high serum osmolality (>284 mOsm/kg)

Others: hypoxia, hypotension, acidemia

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6
Q

What gene is required for Sertoli cells, and what two hormones do those cells make?

A

SOX9

Anti-mullerian hormone and mullerian-inhibiting hormone

Sertolis are SOX9 fans and Mullerian-haters

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7
Q

What hormone is most responsible for external genitalia development?

A

Dihydrotestosterone (DHT)

Made from testosterone (via 5-alpha-reductase)

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8
Q

Hormone elevated in classic congenital adrenal hyperplasia (CAH)

A

17-hydroxyprogesterone (17-OHP)

Build-up product from 21-hydroxlyase deficiency (most common form of CAH)

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9
Q

Four “basic” laboratory abnormalities in congenital adrenal hyperplasia (CAH)

A
  1. Hyponatremia (salt-wasting from aldosterone insufficiency)
  2. Hyperkalemia
  3. Metabolic acidosis
  4. Hypoglycemia
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10
Q

Which would be potentially higher-risk and require “urgent” labs–a maternal history of hyperthyroidism or hypothyroidism

A

Hyperthyroidism–if mother has Graves disease, antibodies that activate TSH receptors can cross placenta and cause neonatal thyrotoxicosis

(Rare but possibly life-threatening, requires either maternal or cord antibody [TRAb or TSI] titers)

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11
Q

What are features of diabetes insipidus, and the main way to distinguish nephrogenic from neurogenic

A
  1. Polydipsia
  2. High serum osmolality
  3. Low urine osmolality
    * In Neurogenic DI they can’t make ADH, their brain is dumb so ADH doesn’t respond to fluid restriction*
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12
Q

Laboratory findings in hypoparathyroidism

A

Low calcium, high phosphate, low PTH

This last point can help distinguish from pseudohypoparathryoidism

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13
Q

Pseudohypoparathyroidism facts

A
  1. Low Ca, high Phos, high PTH (insensitivity)
  2. Usually autosomal dominant, see short 4th/5th metacarpals and very round face
  3. Associated with inability to respond to TSH as well
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14
Q

What hormone is responsible for sexual differentiation in the first trimester (and where does it come from)

A

hCG from the placenta

(After 12 weeks the fetus’ hypothalamus starts making GnRH that then stimulates LH and FSH from the anterior pituitary)

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15
Q

The only thyroid-related compount that canNOT cross the placenta

A

TSH (thyroid stimulating hormone)

Most of T4 that crosses gets “deactivated” by conversion to rT3

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16
Q

The thyroid gland’s derived from what embryonal tissue

A

Endoderm

As are the lungs and foregut, compared to heart which comes from mesoderm

17
Q

Fetal thyroid starts making thyroglobulin at ___ weeks and secreting thyroid hormone at ___ weeks

A

8 weeks and 12 weeks

Before 12 weeks, thyroid hormone (T3/T4) comes from mother

18
Q

The thyroid hormone that’s most abundant in the fetus (up until term gestation)

A

rT3

Majority of maternal T4 is converted to inactive rT3 at placenta by deiodinase (fetus also has deiodinase)

19
Q

What maternal hormone is structurally similar to TSH and responsible for increased maternal T3/T4 production?

A

bHCG

Whereas placental ESTROGENS are what causes increased production of TBG as well as T3 and T4

20
Q

90% of thyroid hormone secreted by the thyroid is ____

A

T4

Converted to T3 (more potent, shorter half-life) in peripheral tissues and mainly kept intracellular

21
Q

The most common cause of congenital hypothyroidism

A

Thyroid disgenesis (75%), i.e. aplasia, hypoplasia or ectopy

Only 10% 2-2 hypothalamic or pituitary issues

22
Q

The best test to confirm thyroid dysgenesis

A

Radionuclide iodine123 scan “to assess degre of RAIU (radioactive iodine uptake)

Can test TBG, T3, TRH and antithyroid antibodies

23
Q

How long should infants exposed to maternal Graves disease by monitored?

A

Minimum 4-6 weeks outpatient

  • Majority of TSH receptor antibodies are STIMULATING, so will be hypERthyroid*
  • Treatment can include PTU or methimazole, beta-blocker and in emergencies corticosteroids*
24
Q

The two parts of the adrenals (cortex and medulla) make which products

A

CortEX: SEX and other hormones (glucocorticoids, mineralocorticoids)

Medulla: catecholamines (epinephrine, norepinephrine, dopamine)

25
Q

Foremost cause of CAH (congenital adrenal hyperplasia) and lab findings

A

21-hydroxylase deficiency

Hyponatremia, hyperkalemia, VERY elevated 17-OHP, high testosterone

Linked to HLA type/mutations (like DM1 and Celiac)

26
Q

Secondmost cause of CAH and laboratory findings

A

11 beta-hydroxylase deficiency

Elevated DOC (deoxycortisone) and 11-deoxycortisol, high testosterone

DOC has mineralocorticoid effects so not salt wasting

27
Q

Hormone products of two testicular cell types

A

Sertoli cells: MIS (regression of Mullerian ducts)

Leydig cells: testosterone and INSL3 (insulin-like growth factor 3)

_L_uteinizing hormone, like both factors from _L_eydig cells, works on EXTERNAL genitalia

*Testosterone also stabilizes Wolffian ducts (internal)*

28
Q

What should you always test for when you see hypospadias and undescended testes

A

Congenital adrenal hyperplasia (CAH)

29
Q

What do 5 alpha-reductase and aromatase do?

A

5 alpha-reductase: testosterone to DHT (dihydrotestosterone, more active form)

Aromatase: testosterone to estradiol (and androstenedione to estrone)

30
Q

Two problems that can cause a blind vaginal pouch in 46XY people

A

5 alpha-reductase deficiency (no DHT)

Androgen insensitivity syndrome (AIS) (can’t respond to DHT/T)

31
Q

For undescended testes, who ultimately have more orchiopexies–term or preterm males?

A

TERM males

  • Frequency of undescended tests is higher in premature infants (don’t descend until ~28 weeks)*
  • 90% in preemies ultimately descend vs. 75% in term*
32
Q

Glucose crosses the placenta via what mechanism?

A

Facilitated diffusion

“Fetal glucose is maintained entirely by placental transfer…using glucose transporters” (Brodsky 2010).

33
Q

In what timeframe does glucagon surge after birth?

A

Minutes to hours

Along with catecholamine surge and insulin down-trend, all in response to being cut off from maternal glucose

34
Q

“Critical labs” to be drawn when neonates are persistently hypoglycemic (and drawn WHEN hypoglycemic)

A

When glucose <40: insulin, growth hormone, cortisol (and PLASMA glucose [i.e. lab-run] since whole blood glucoses are less accurate)

35
Q

The rate of fetal anomalies when diabetic control is achieved after conception

A
  1. 8%
    vs. 2.5% if control’s achieved pre-conception
36
Q

Three types of cardiac problems most common in infants of diabetic mothers (IDM)

A

Hypertrophic cardiomyopathy

VSD

dTGA

37
Q

The posterior pituitary contains which hormones

A

Antidiuretic hormone (i.e. vasopressin)

Oxytocin

Hypothalamus PRODUCES these, posterior pituitary just stores

38
Q

The hypothalamic-pituitary axis STARTS production at ___ weeks, but isn’t established until ____ weeks

A

12 weeks (same timeframe as fetal T4 production)

18 weeks is when axis is established (same timeframe as fetal [thyroid] being sufficient)

39
Q

When does T4 peak after birth?

A

24-36 hours

In response to TSH surge 30min post-delivery (same as glucagon/catecholamine) 2-2 cold stress

Neonatal-Perinatal Boards Review (11 decks)

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