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Metabolic/Endocrine > NCC content > Flashcards

NCC content Flashcards

1
Q

About glucose

A
  • received completely from mom
  • crosses placenta
  • fetal glucose levels are 80% of maternal
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2
Q

do insulin and glucagon cross the placenta?

A

NO

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3
Q

What is gluconeogenesis?

A

production of glucose from non-glucose sources

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4
Q

When do glycogen stores start being stored in the fetus?

A
  • don’t begin until 27 weeks

- this is the major form of stored glucose

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5
Q

How quickly are glycogen stores depleted?

A

in 3-12 hours

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6
Q

What doe insulin do?

A

changes cell wall permeability so that glucose can enter and become active

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7
Q

What does glucagon do?

A

promotes glycogenolysis and gluconeogenesis

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8
Q

What do catecholamines do?

A
  • increases glycogenolysis, gluconeogenesis and glucagon secretion
  • decreases secretion of insulin
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9
Q

When is the glucose nadir?

A

30-90 minutes after birth

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10
Q

Describe Beckwith-Wiedemann Syndrome

A
  • macroglossia
  • abdominal wall defects
  • macrosomia
  • organomegaly including pancreas
  • severe unremitting hypoglycemia
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11
Q

Iatrogenic causes of hyperinsulinemia

A
  • excess administration

- UAC placement: placed too low and can put dextrose straight into artery going to pancreas

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12
Q

Endocrine deficiencies associated with hyperinsulinemia

A
  • panhypopituitarism
  • adrenal hemorrhage
  • hypothyroidism
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13
Q

symptoms of hypoglycemia

A
  • *most symptoms are nonspecific**
  • *most infants are asymptomatic**
  • apnea
  • irritability
  • lethargy
  • tachycardia and tachypnea
  • abnormal neuro exam
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14
Q

How does hydrocortisone help hypoglycemia?

A
  • decreases peripheral glucose utilization
  • increases blood glucose concentration
  • consider using with glucose requirements > 15 mg/kg/min
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15
Q

How does diazoxide help hypoglycemia?

A

-decreases insulin secretion

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16
Q

Does mother become more or less insulin resistance through pregnancy?

A

MORE

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17
Q

Why do IDMs have respiratory distress?

A

-decreased surfactant production in IDM

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18
Q

How high is the risk for congenital anomalies in IDMs?

A

3-4x the normal risk

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19
Q

Name clinical manifestations of IDM

A
  • congenital anomalies
  • neural tube defects
  • congenital heart disease (VSD, TGV)
  • hypertrophic cardiomyopathy
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20
Q

Describe hypertrophic cardiomyopathy

A

large left ventricle; septum between ventricles may be large enough to obstruct blood flow through the aorta and body has decreased perfusion and hypotension

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21
Q

How do you treat hypertrophic cardiomyopathy

A

supportive; septum will shrink and condition will improve

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22
Q

Describe caudal regression syndrome

A

happens in IDM

  • abnormalities in lower extremities ranging from scoliosis to “mermaid syndrome”
  • other common anomalies include anal atresia, myelomeningocele, GI abnormalities, GU abnormalities
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23
Q

Describe small left colon syndrome

A

happens in IDM

  • constriction at the sigmoid and descending colon
  • symptoms of intestinal obstruction; abdominal distention, emesis, no stool
  • diagnosis and treatment is contrast enema
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24
Q

pathophysiology behind hyperglycemia in ELBW infants

A

-failure of glucose auto regulation

hepatic and pancreatic immaturity

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25
Q

clinical manifestations of hyperglycemia is ELBW infant

A
  • usual onset prior to three days
  • glycosuria due to low renal threshold
  • osmotic diuresis occurs d/t lack of tubular reabsorption; this can lead to fluid and electrolyte problems
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26
Q

calcium function

A
  • maintenance of cell membrane permeability
  • activation of enzyme reactions for muscle contraction
  • nerve transmission
  • blood clotting
  • normal skeletal function and development
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27
Q

How does the fetus get calcium?

A

completely dependent on the placenta

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28
Q

Which babies get hypocalcemic at birth?

A
  • all of them are to some degree when the Ca supply from the placenta ceases at birth
  • nadir at 24 hours
  • hypocalcemia is exaggerated in unstable or very small babies
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29
Q

When and how do babies start producing Ca?

A

-at 48 hours, PTH and vitamin D increase and calcitonin decreases

30
Q

What does PTH do?

A
  • mobilizes Ca and phos from the bone

- decreases renal excretion of Ca

31
Q

What does vitamin D do?

A
  • required for PTH to work

- increases GI absorption of Ca and phos

32
Q

What does calcitonin do?

A
  • inhibits calcium mobilization from bone

- increases calcium excretion

33
Q

What does phosphorus do to Ca absorption?

A

phosphorus INHIBITS the absorption of Ca
-high Ca level = low phos level (may need to increase the amount of phos being given if Ca level is too high but appropriate amount is being given for nutritional purposes)

34
Q

How is magnesium level related to Ca?

A

-normal magnesium level is mandatory for PTH to function

35
Q

When are majority of Ca stores transferred to the fetus?

A

during the third trimester

36
Q

Why are babies with IDM hypocalcemic?

A

inadequate amounts of PTH initially

37
Q

Lab levels for hypocalcemia

A
  • total calcium less than 7 mg/dL

- iCal less than 3-4.4 mg/dL or 0.75-1.1 mmol/L

38
Q

Treatment of hypocalcemia

A
  • unknown if asymptomatic infant should be treated

- for the symptomatic infant: give 10% calcium gluconate over 20-30 min, given until symptoms subside

39
Q

symptoms of hypocalcemia

A

-hyperexcitability of the central and peripheral nervous system (jittery, increased sensory response, seizures)

40
Q

lab levels for hypercalcemia

A
  • total calcium over 11 mg/dL

- iCal over 5.8 mg/dL

41
Q

symptoms of hypercalcemia

A
  • hypotonia or irritability
  • poor feeding
  • constipation
  • seizures
  • polyuria and dehydration
  • renal stones
  • bradycardia and arrhythmias
42
Q

causes of hypercalcemia

A
  • iatrogenic
  • hyperparathyroidism
  • decreased phosphorus
  • familial infantile hypercalcemia
43
Q

treatment of hypercalcemia

A
  • hydrate
  • promote excretion with lasix
  • decrease calcium and vitamin D intake
  • increase phosphorus intake
44
Q

function of magnesium

A
  • maintenance of muscle and nerve function
  • supports the immune system
  • important for bone formation
  • involved in energy metabolism and protein synthesis
45
Q

etiology of hypomagnesemia

A
  • low maternal level
  • placental insufficiency
  • prematurity and IUGR
  • increased losses with renal or intestinal disorders
  • hypoparathyroidism?
46
Q

symptoms of hypomagnesemia

A
  • tremors
  • irritability
  • hyperreflexia
  • seizures
  • hypocalcemia
47
Q

treatment of hypomagnesemia

A

administer magnesium IV or PO

48
Q

what is the function of the adrenal medulla?

A
  • secrete catecholamines (epi and norepi)

- “fight or flight” response

49
Q

what is the function of the adrenal cortex?

A
  • glucocorticoids (cortisol)
  • mineralocorticoids (aldosterone)
  • androgens
50
Q

What is the function of cortisol?

A
  • regulates blood sugar
  • important for growth
  • maintains cardiovascular function
  • released in times of stress (increases glucose, cardiac output and vascular tone)
51
Q

What is the function of aldosterone?

A
  • regulates fluid and electrolyte balance
  • stimulates reabsorption of sodium and water in the distal collecting tubules
  • promotes secretion of potassium
  • maintains blood pressure, intravascular volume, cardiac function and electrolytes
52
Q

Describe adrenal insufficiency

A
  • a transient phenomenon in the ELBW infant
  • related to hypothalamic-pituitary-adrenal immaturity
  • cortisol levels decreased in ELBW infants and do not increase during times of stress
  • cortisol suppression r/t exogenous steroid administration
53
Q

Clinical manifestations of adrenal insufficiency

A
  • glucose abnormalities
  • refractory hypotension
  • decreased cardiac output, acidosis, shock
  • decreased UOP
  • hyponatremia, hyperkalemia
  • tachycardia
54
Q

How to diagnose adrenal insufficiency?

A

-cortisol level below 15 mcg/dL

55
Q

complications of adrenal insufficiency

A
  • recovery by 14 days

- association with BPD

56
Q

What is the function of TSH (thyroid stimulating hormone)?

A
  • secreted from anterior pituitary

- stimulates secretion of thyroid hormones

57
Q

What is the most common neonatal endocrine disorder?

A

-congenital hypothyroidism

58
Q

etiology of congenital hypothyroidism

A
  • maternal iodine deficiency
  • dysgenic or absent thyroid gland
  • deficient synthesis of thyroid hormones
  • maldevelopment or absence of the anterior pituitary gland
59
Q

what chromosomal defect is associated with hypothyroidism?

A

-trisomy 21

60
Q

How is congenital hypothyroidism diagnosed?

A
  • state screen
  • low T4 and high TSH
  • free T4
61
Q

What is hypothyroxinemia of prematurity?

A
  • a transient phenomenon d/t immaturity

- T4 levels increase with advancing gestation

62
Q

What are the lab levels in hypothyroxinemia of prematurity?

A
  • T4 low
  • TSH normal
  • Free T4 may be low or normal
  • persists for 4-8 weeks
63
Q

What maternal condition is associated with neonatal thyrotoxicosis (hyperthyroidism)?

A

maternal graves disease:

  • transplacental transfer of thyroid stimulating immunoglobulins
  • considered a medical emergency
64
Q

What are the lab levels in neonatal thyrotoxicosis?

A
  • high T4

- low TSH

65
Q

treatment for neonatal thyrotoxicosis?

A
  • chronic treatment: Lugol’s solution

- acute treatment: PTU (prophlthiouracil)

66
Q

When does bone mineralization happen?

A
  • 80% of bone mineralization occurs during third trimester

- calcium and phos are maximally acquired

67
Q

etiology of osteopenia of prematurity

A
  • poor nutrition
  • lasix (increases renal calcium loss, stimulations calcium reabsorption from bone)
  • phenobarbital and dilantin (enhance vitamin D metabolism)
  • steroids (inhibits bone growth and longitudinal growth)
  • immobility
68
Q

what do we need to make bones?

A
  • vitamin D (stimulates intestinal absorption of calcium and phos)
  • phosphorus (stimulates bone formation, inhibits reabsorption from bone)
  • calcium
69
Q

clinical manifestations of osteopenia of prematurity

A
  • normal calcium levels
  • normal to low phosphorus (499): elevated value precedes radiographic changes; >700 IU/L at 3 weeks is predictive of osteopenia
70
Q

osteopenia of prematurity on xray

A
  • decreased bone density apparent with 20% reduction in mineralization
  • cupping and fraying of metaphysis
71
Q

pathophysiology of congenital adrenal hyperplasia

A
  • 21-hydroxylase deficiency prevents conversion of progesterone to cortisol and aldosterone
  • in the absence of cortisol, ACTH stimulates the adrenal cortex resulting in adrenal hyperplasia
  • cortisol precursor (17-OHP) accumulates in the blood and takes the unblocked androgen metabolic pathway, virilizing external genitalia of female fetus
  • aldosterone deficiency leads to salt-wasting and hypovolemia
72
Q

how is CAH passed on?

A

autosomal recessive

Metabolic/Endocrine (2 decks)

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