NCC content Flashcards
(72 cards)
1
Q
About glucose
A
- received completely from mom
- crosses placenta
- fetal glucose levels are 80% of maternal
2
Q
do insulin and glucagon cross the placenta?
A
NO
3
Q
What is gluconeogenesis?
A
production of glucose from non-glucose sources
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
5
Q
How quickly are glycogen stores depleted?
A
in 3-12 hours
6
Q
What doe insulin do?
A
changes cell wall permeability so that glucose can enter and become active
7
Q
What does glucagon do?
A
promotes glycogenolysis and gluconeogenesis
8
Q
What do catecholamines do?
A
- increases glycogenolysis, gluconeogenesis and glucagon secretion
- decreases secretion of insulin
9
Q
When is the glucose nadir?
A
30-90 minutes after birth
10
Q
Describe Beckwith-Wiedemann Syndrome
A
- macroglossia
- abdominal wall defects
- macrosomia
- organomegaly including pancreas
- severe unremitting hypoglycemia
11
Q
Iatrogenic causes of hyperinsulinemia
A
- excess administration
- UAC placement: placed too low and can put dextrose straight into artery going to pancreas
12
Q
Endocrine deficiencies associated with hyperinsulinemia
A
- panhypopituitarism
- adrenal hemorrhage
- hypothyroidism
13
Q
symptoms of hypoglycemia
A
- *most symptoms are nonspecific**
- *most infants are asymptomatic**
- apnea
- irritability
- lethargy
- tachycardia and tachypnea
- abnormal neuro exam
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
15
Q
How does diazoxide help hypoglycemia?
A
-decreases insulin secretion
16
Q
Does mother become more or less insulin resistance through pregnancy?
A
MORE
17
Q
Why do IDMs have respiratory distress?
A
-decreased surfactant production in IDM
18
Q
How high is the risk for congenital anomalies in IDMs?
A
3-4x the normal risk
19
Q
Name clinical manifestations of IDM
A
- congenital anomalies
- neural tube defects
- congenital heart disease (VSD, TGV)
- hypertrophic cardiomyopathy
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
21
Q
How do you treat hypertrophic cardiomyopathy
A
supportive; septum will shrink and condition will improve
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
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
24
Q
pathophysiology behind hyperglycemia in ELBW infants
A
-failure of glucose auto regulation
hepatic and pancreatic immaturity
25
clinical manifestations of hyperglycemia is ELBW infant
- 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
26
calcium function
- maintenance of cell membrane permeability
- activation of enzyme reactions for muscle contraction
- nerve transmission
- blood clotting
- normal skeletal function and development
27
How does the fetus get calcium?
completely dependent on the placenta
28
Which babies get hypocalcemic at birth?
- 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
29
When and how do babies start producing Ca?
-at 48 hours, PTH and vitamin D increase and calcitonin decreases
30
What does PTH do?
- mobilizes Ca and phos from the bone
| - decreases renal excretion of Ca
31
What does vitamin D do?
- required for PTH to work
| - increases GI absorption of Ca and phos
32
What does calcitonin do?
- inhibits calcium mobilization from bone
| - increases calcium excretion
33
What does phosphorus do to Ca absorption?
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
How is magnesium level related to Ca?
-normal magnesium level is mandatory for PTH to function
35
When are majority of Ca stores transferred to the fetus?
during the third trimester
36
Why are babies with IDM hypocalcemic?
inadequate amounts of PTH initially
37
Lab levels for hypocalcemia
- total calcium less than 7 mg/dL
| - iCal less than 3-4.4 mg/dL or 0.75-1.1 mmol/L
38
Treatment of hypocalcemia
- unknown if asymptomatic infant should be treated
| - for the symptomatic infant: give 10% calcium gluconate over 20-30 min, given until symptoms subside
39
symptoms of hypocalcemia
-hyperexcitability of the central and peripheral nervous system (jittery, increased sensory response, seizures)
40
lab levels for hypercalcemia
- total calcium over 11 mg/dL
| - iCal over 5.8 mg/dL
41
symptoms of hypercalcemia
- hypotonia or irritability
- poor feeding
- constipation
- seizures
- polyuria and dehydration
- renal stones
- bradycardia and arrhythmias
42
causes of hypercalcemia
- iatrogenic
- hyperparathyroidism
- decreased phosphorus
- familial infantile hypercalcemia
43
treatment of hypercalcemia
- hydrate
- promote excretion with lasix
- decrease calcium and vitamin D intake
- increase phosphorus intake
44
function of magnesium
- maintenance of muscle and nerve function
- supports the immune system
- important for bone formation
- involved in energy metabolism and protein synthesis
45
etiology of hypomagnesemia
- low maternal level
- placental insufficiency
- prematurity and IUGR
- increased losses with renal or intestinal disorders
- hypoparathyroidism?
46
symptoms of hypomagnesemia
- tremors
- irritability
- hyperreflexia
- seizures
- hypocalcemia
47
treatment of hypomagnesemia
administer magnesium IV or PO
48
what is the function of the adrenal medulla?
- secrete catecholamines (epi and norepi)
| - "fight or flight" response
49
what is the function of the adrenal cortex?
- glucocorticoids (cortisol)
- mineralocorticoids (aldosterone)
- androgens
50
What is the function of cortisol?
- regulates blood sugar
- important for growth
- maintains cardiovascular function
- released in times of stress (increases glucose, cardiac output and vascular tone)
51
What is the function of aldosterone?
- 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
Describe adrenal insufficiency
- 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
Clinical manifestations of adrenal insufficiency
- glucose abnormalities
- refractory hypotension
- decreased cardiac output, acidosis, shock
- decreased UOP
- hyponatremia, hyperkalemia
- tachycardia
54
How to diagnose adrenal insufficiency?
-cortisol level below 15 mcg/dL
55
complications of adrenal insufficiency
- recovery by 14 days
| - association with BPD
56
What is the function of TSH (thyroid stimulating hormone)?
- secreted from anterior pituitary
| - stimulates secretion of thyroid hormones
57
What is the most common neonatal endocrine disorder?
-congenital hypothyroidism
58
etiology of congenital hypothyroidism
- maternal iodine deficiency
- dysgenic or absent thyroid gland
- deficient synthesis of thyroid hormones
- maldevelopment or absence of the anterior pituitary gland
59
what chromosomal defect is associated with hypothyroidism?
-trisomy 21
60
How is congenital hypothyroidism diagnosed?
- state screen
- low T4 and high TSH
- free T4
61
What is hypothyroxinemia of prematurity?
- a transient phenomenon d/t immaturity
| - T4 levels increase with advancing gestation
62
What are the lab levels in hypothyroxinemia of prematurity?
- T4 low
- TSH normal
- Free T4 may be low or normal
- persists for 4-8 weeks
63
What maternal condition is associated with neonatal thyrotoxicosis (hyperthyroidism)?
maternal graves disease:
- transplacental transfer of thyroid stimulating immunoglobulins
- considered a medical emergency
64
What are the lab levels in neonatal thyrotoxicosis?
- high T4
| - low TSH
65
treatment for neonatal thyrotoxicosis?
- chronic treatment: Lugol's solution
| - acute treatment: PTU (prophlthiouracil)
66
When does bone mineralization happen?
- 80% of bone mineralization occurs during third trimester
| - calcium and phos are maximally acquired
67
etiology of osteopenia of prematurity
- 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
what do we need to make bones?
- vitamin D (stimulates intestinal absorption of calcium and phos)
- phosphorus (stimulates bone formation, inhibits reabsorption from bone)
- calcium
69
clinical manifestations of osteopenia of prematurity
- normal calcium levels
- normal to low phosphorus (499): elevated value precedes radiographic changes; >700 IU/L at 3 weeks is predictive of osteopenia
70
osteopenia of prematurity on xray
- decreased bone density apparent with 20% reduction in mineralization
- cupping and fraying of metaphysis
71
pathophysiology of congenital adrenal hyperplasia
- 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
how is CAH passed on?
autosomal recessive
