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Neo Board Review > Endocrine > Flashcards

Endocrine Flashcards

(54 cards)

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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

Study These Flashcards
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

Study These Flashcards
A

Abnormal clefts in the brain

24
Q

Lissencephaly

Study These Flashcards
A

Underdevelopment of gyri - smooth brain

25
Pachygyria
Broad and abnormally large gyri leading to less sulci
26
Polymicrogyria
Numerous small convolutions
27
Colpocephaly
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
Thyroid hormone function
Basal metabolic rate Thermogenesis Stimulates normal growth Increases bone mineralization and skeletal muscle activity Increases HR, contractility and cardiac output CNS maturation
29
Neonatal hyperthyroidism presenting secondary to maternal graves - timing and length of symptoms
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
Cortisol production pathway
Hypothalamus secretes corticotropin releasing hormone (CRH) Anterior pituitary secretes adrenocorticotropic hormone (ACTH) Adrenal gland produces cortisol which does a feedback loop
31
Cortisol functions
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
Important enzymes in adrenal cortex pathway
3 beta hydroxysteroid dehydrogenase 17 alpha hydroxylase 21 hydroxylase 11 beta hydroxylase 17 beta hydroxysteroid dehydrogenase Aromatase 5 alpha reductase
33
Laboratory characteristics of 21 OH deficiency
Elevated 17 OH P Elevated 17 OH P following ACTH administration Can have salt wasting (75% of cases)
34
11 beta hydroxylase deficiency lab characteristics
Increased DOC and deoxycortisol Not salt wasting because DOC acts as mineralcorticoid
35
17 alpha hydroxylase deficiency lab characteristics
Elevated DOC and corticosterone Low 17 OH progesterone and 17 OH pregnenolone Not impacting enzyme of aldosterone pathway
36
Lab characteristics of 3 beta hydroxysteroid dehydrogenase deficiency
Rare Elevated 17 OH pregnenolone and DHEA (All shunted to sex hormone pathway) Salt wasting
37
Ambiguous genitalia
Clitromegaly, inguinal mass, labial mass, posterior labial fusion Micropenis with bilateral cryptorchidism Hypospadius with undescended testes Peniscrotal Hypospadius
38
Ambiguous genitalia workup
Gonads palpable: US for mullerian structures 17 OHP karyotype
39
Infant response to cut of maternal glucose
3-5 fold increase in glucagon Decrease insulin Increase catecholamines All leads to increased gng, glycogenolysis, lipolysis, and ketogenesis
40
Substrates of gluconeogenesis
Lactate/pyruvate from anaerobic glycolysis Gluconeogenic amino acids (alanine is very important) Glycerol Propionic acid
41
Etiologies of hypoglycemia
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
Review book proposed critical labs for hypoglycemia
Blood gas, BHOB, serum lactate, FFA, insulin level, urine for non glucose reducing substances, urine for ketones Others: GH and cortisol
43
Increase in PTH related hormone results in
Increase in calcitriol which leads to maternal increase in calcium absorption from guy and decrease renal calcium excretion
44
What crosses the placenta with regards to calcium and phosphate metabolism
Calcium, phos and magnesium cross placenta which is greatest in the 3rd trimester Calcidiol (25OH Vit D) also crosses placenta
45
Fetus control of calcium
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
Postnatal calcium patterns
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
Causes of early hypocalcemia
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
Causes of late hypocalcemia
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
Labs with metabolic bone disease of prematurity
Serum calcium usually normal (but can be increased or decreased) Serum phos low Vit 1,25 OH D increased Alk Phos often increased
50
Labs of primary hyperparathyroidism
Serum Ca increased Serum phos decreased Maybe have hyperchloremic acidosis due to renal effect on PTH
51
Labs of hypoparathyroidism
Serum ca decreased Serum phos increased Pth low Calcitriol synthesis low Alkalosis
52
Paeudohypoparathyroidism labs
serum calcium decreased Serum phos increased Tissue resistance to pth Increased pth Low calcitriol
53
Labs of chronic renal failure
Serum ca decreased Serum phos increased Pth increased to compensate for low serum ca
54
Labs of malabsorption
Serum ca decreased Serum phos decreased Multiple nutrient deficiency

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