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Neo Board Review > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Thyroid dysgenesis T4 & TSH

A

T4 low or normal

TSH high

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2
Q

Organification, thyroglobulin defects and deiodinase deficiency T4 & TSH

A

T4 low

TSH high

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3
Q

Thyroid hormone resistance T4 & TSH

A

T4 high

TSH normal or high

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4
Q

TSH deficiency T4 & TSH

A

T4 low

TSH normal or low

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5
Q

TRH deficiency T4 & TSH

A

T4 low

TSH low

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6
Q

Transient hypothyroidism T4 & TSH

A

T4 low or normal

TSH variably high

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7
Q

TBG deficiency T4 & TSH

A

T4 low

TSH normal

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8
Q

Transient hypothyroxinemia of prematurity T4 & TSH

A

T4 low

TSH normal or low

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9
Q

Sick euthyroid T4 & TSH

A

T4 low or normal

TSH normal

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10
Q

Draw adrenal cortex pathway

A

Google picture for confirmation

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11
Q

Causes of virilized female

A

Increased androgen production (CAH d/t 21H def, 11B def, 3B def), abn androgen metabolism (aromatase def), increased maternal androgen exposure

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12
Q

Causes of undervirilized male

A

Decreased testosterone synthesis (CAH d/t 17a def, 3B def; abn leydig cell production of testosterone)
Abn testosterone metabolism (5 alpha reductase deficiency)
Defect of testosterone action (androgen resistance or androgen insensitivity)

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13
Q

What substrates maintain glycogenolysis and gluconeogenesis

A

Lactate/pyruvate from anaerobic glycolysis
Gluconeogenic amino acids
Glycerol
Propionic acid

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14
Q

Etiologies of neonatal hypoglycemia

A

Prematurity
Sepsis
Hyperinsulinemia (IDM, SGA or LGA, discordant twins, perinatal depression, BWS, pancreatic islet adenoma)
Hormonal abn (panhypopit, GH def, cortisol def)
IEM (carbohydrate disorders, protein abnormalities, organic acidemias, fatty acids abn)

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15
Q

Carbohydrate disorders that can cause hypoglycemia

A

Galactosemia
GSD
Hereditary fructose intolerance

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16
Q

Protein abnormalities that can lead to hypoglycemia

A

Maple syrup urine disease

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17
Q

Organic acidemias that can cause hypoglycemia

A

Propionic acidemia, methylmalonic acidemia, beta methylcrotonyl glycinuria, glutaric aciduria type I and II

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18
Q

Fatty acid abnormalities that can lead to hypoglycemia

A

Long chain 3 hydroxyacyl coA deficiency

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19
Q

Calcium and the preterm infant

A

Accretion occurs during third trimester so they have low stores, abnormal calcium absorption from the intestines, increase losses of Ca and P from kidney, and physiologic hypoparathyroidism

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20
Q

Causes of early hypocalcemia

A

Birth-72h
Maternal: diabetes (bc leads to dec calcium which leads to less transfer), pet (leads to increased maternal mag and decreased PTH release), hyperparathyroidism
Prematurity, growth restriction, perinatal depression, infection, hypomagnesemia, blood product transfusion

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21
Q

Causes of late neonatal hypocalcemia

A

> 72h
Hypoparathyroidism (22q11.2, familial AD, AR, x-linked recessive)
Transient neonatal pseudohypoparathyroidism 2/2 blunted phosphaturic response to PTH
Hypomag
But D def, renal insufficiency, high phosphate milk diet, malabsorption, alkalosis, liver or renal disease, drug induced

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22
Q

Assessment of hypocalcemia

A

Total serum ca, ionized ca, phosphate, creatinine, ALK-P, urine ca excretion, calcitriol, CD4 count, skeletal radiographs, chest XR for thymic shadow

23
Q

Schizencephaly

A

Abnormal clefts in the brain

24
Q

Lissencephaly

A

Underdevelopment of gyri - smooth brain

25
Q

Pachygyria

A

Broad and abnormally large gyri leading to less sulci

26
Q

Polymicrogyria

A

Numerous small convolutions

27
Q

Colpocephaly

A

congenital abnormality in which the occipital horns of the lateral ventricles are larger than normal because white matter in the posterior cerebrum has failed to develop or thicken

28
Q

Thyroid hormone function

A

Basal metabolic rate
Thermogenesis
Stimulates normal growth
Increases bone mineralization and skeletal muscle activity
Increases HR, contractility and cardiac output
CNS maturation

29
Q

Neonatal hyperthyroidism presenting secondary to maternal graves - timing and length of symptoms

A

Symptoms typically present by 14 days of age (up to 29 days)
If mom not on anti thyroid meds then present as early as 1-3 days

Symptoms can last 3-6 months

30
Q

Cortisol production pathway

A

Hypothalamus secretes corticotropin releasing hormone (CRH)
Anterior pituitary secretes adrenocorticotropic hormone (ACTH)
Adrenal gland produces cortisol which does a feedback loop

31
Q

Cortisol functions

A

Induces, gluconeogenesis and antagonizes insulin, leading to increase glucose and lipolysis

Increases calcium and phosphate released from bone

Critical for vascular responses to catecholamines

Decreases inflammation and suppresses immune system

Inhibits a DH, increases gastric acid, secretion, increases production of red blood cells

32
Q

Important enzymes in adrenal cortex pathway

A

3 beta hydroxysteroid dehydrogenase
17 alpha hydroxylase
21 hydroxylase
11 beta hydroxylase
17 beta hydroxysteroid dehydrogenase
Aromatase
5 alpha reductase

33
Q

Laboratory characteristics of 21 OH deficiency

A

Elevated 17 OH P
Elevated 17 OH P following ACTH administration
Can have salt wasting (75% of cases)

34
Q

11 beta hydroxylase deficiency lab characteristics

A

Increased DOC and deoxycortisol
Not salt wasting because DOC acts as mineralcorticoid

35
Q

17 alpha hydroxylase deficiency lab characteristics

A

Elevated DOC and corticosterone
Low 17 OH progesterone and 17 OH pregnenolone
Not impacting enzyme of aldosterone pathway

36
Q

Lab characteristics of 3 beta hydroxysteroid dehydrogenase deficiency

A

Rare
Elevated 17 OH pregnenolone and DHEA
(All shunted to sex hormone pathway)
Salt wasting

37
Q

Ambiguous genitalia

A

Clitromegaly, inguinal mass, labial mass, posterior labial fusion
Micropenis with bilateral cryptorchidism
Hypospadius with undescended testes
Peniscrotal Hypospadius

38
Q

Ambiguous genitalia workup

A

Gonads palpable:
US for mullerian structures
17 OHP
karyotype

39
Q

Infant response to cut of maternal glucose

A

3-5 fold increase in glucagon
Decrease insulin
Increase catecholamines

All leads to increased gng, glycogenolysis, lipolysis, and ketogenesis

40
Q

Substrates of gluconeogenesis

A

Lactate/pyruvate from anaerobic glycolysis
Gluconeogenic amino acids (alanine is very important)
Glycerol
Propionic acid

41
Q

Etiologies of hypoglycemia

A

General: prematurity and sepsis

Hyperinsulinism: IDM, SGA, LGA, discordant twin, perinatal depression, BWS, pancreatic islet adenoma

Hormonal abnormalities: panhypopit, GH deficiency, cortisol deficiency

IEM: carbohydrate disorders, protein abnormalities, organic acidemias, fatty acid abnormalities

42
Q

Review book proposed critical labs for hypoglycemia

A

Blood gas, BHOB, serum lactate, FFA, insulin level, urine for non glucose reducing substances, urine for ketones

Others: GH and cortisol

43
Q

Increase in PTH related hormone results in

A

Increase in calcitriol which leads to maternal increase in calcium absorption from guy and decrease renal calcium excretion

44
Q

What crosses the placenta with regards to calcium and phosphate metabolism

A

Calcium, phos and magnesium cross placenta which is greatest in the 3rd trimester
Calcidiol (25OH Vit D) also crosses placenta

45
Q

Fetus control of calcium

A

High fetal serum calcium levels leads to increased calcitonin and suppressed fetal PTH
fetal kidney is capable of converting calcidiol to calcitriol (the active form)

46
Q

Postnatal calcium patterns

A

Ca level decreases rapidly in first 6 hours with nadir 24-48 hours
PTH increases during 1st day and peaks at 48 HOL
Calcitriol increases and remains constant after 24 HOL
Phosphate is high in first few days and slowly declines
Calcitonin increases after birth and then slowly decreases

47
Q

Causes of early hypocalcemia

A

Up to 72 HOL
maternal illness (diabetes bc of less calcium and calcium transfer, preE because of high mag and low pth, hyperpara)
Prematurity, FGR, perinatal depression, infection, hypomag, transfusion, phototherapy?

48
Q

Causes of late hypocalcemia

A

After 72 HOL
Hypoparathyroidism, transient neonatal pseudohypoparathyroidisms secondary to blunted phosphaturic response to PTH
Hypomag, Vit d deficiency, renal insufficiency, high phos milk diet, malabsorption

49
Q

Labs with metabolic bone disease of prematurity

A

Serum calcium usually normal (but can be increased or decreased)
Serum phos low
Vit 1,25 OH D increased
Alk Phos often increased

50
Q

Labs of primary hyperparathyroidism

A

Serum Ca increased
Serum phos decreased
Maybe have hyperchloremic acidosis due to renal effect on PTH

51
Q

Labs of hypoparathyroidism

A

Serum ca decreased
Serum phos increased
Pth low
Calcitriol synthesis low
Alkalosis

52
Q

Paeudohypoparathyroidism labs

A

serum calcium decreased
Serum phos increased
Tissue resistance to pth
Increased pth
Low calcitriol

53
Q

Labs of chronic renal failure

A

Serum ca decreased
Serum phos increased
Pth increased to compensate for low serum ca

54
Q

Labs of malabsorption

A

Serum ca decreased
Serum phos decreased
Multiple nutrient deficiency

Neo Board Review (12 decks)

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