FEN/GI/Renal Flashcards
Formula for anion gap?
Anion gap = [Na+] — ([Cl-] + [HCO3-])
Acute renal failure —
AGMA or NAGMA?
Anion gap metabolic acidosis (AGMA)
CAH — AGMA or NAGMA?
Non-anion gap metabolic acidosis (NAGMA)
Congenital hypothyroidism — AGMA or NAGMA?
Non-anion gap metabolic acidosis (NAGMA)
High protein formula — AGMA or NAGMA?
Non-anion gap metabolic acidosis (NAGMA)
MUDPILES — AGMA or NAGMA?
List
Anion gap metabolic acidosis Methanol Uremia — Acute renal failure* DKA Paraldehyde Iron, isoniazid, inborn errors of metabolism*, galactosemia* Lactic acidosis, organic academias* Ethanol, toxins* Salicylates
VACTERL
Vertebral anomalies Anal atresia Cardiac anomalies Tracheoseophageal atresia Esophageal atresia Renal anomalies Limb anomalies
Causes of respiratory alkalosis (7)
CNS-Lung-Metabolic-Meds:
Hypoxia
Parenchymal lung disease
Hyperventilation syndrome
Mechanical ventilation
CNS disorders
Metabolic disorders
Medications (salicylates, xanthines, catecholamines)
If respiratory alkalosis persists, how long before renal compensation?
What are the compensatory mechanisms? (2)
2-6 hours
Decrease H+ secretion (increases pH)
Increase HCO3 excretion (decrease bicarb)
By how much does plasma HCO3- decrease with the decrease in pCO2?
A 10 mmHg decrease in pCO2 causes a decrease of plasma HCO3- by 4 mEq/L
How much kcal/g in carbohydrates?
3.4 kcal/g
How much kcal/g in protein?
4 kcal/g
How much kcal/g in lipids?
9 kcal/g
Which immunoglobulins are preserved in donor milk?
IgA
IgG
Which immunoglobulins are destroyed by pasteurization of donor milk?
IgM
Neonatal ascites - type of fluid in hydrops infant with cardiac arrhythmia or CHF?
Transudative
Neonatal ascites - type of fluid in hydrops infant with hepatosplenic trauma?
Peritoneal blood
Neonatal ascites - type of fluid in hydrops infant with meconium peritonitis?
Exudative
Neonatal ascites - type of fluid in hydrops infant with posterior urethral valve or bladder perforation?
Urine
RTA - NAGMA or AGMA?
Non-anion gap metabolic acidosis (NAGMA)
Type I RTA pathophys
Urine pH high/low?
Diminished H+ secretion in distal tubule -> high urine pH
Which RTA type?
RTA I and II - high or low serum K+? Why?
Low serum K+
K+ lost in urine as cation replacement for H+
Which RTA type?
Which RTA type causes hypercalciuria? Why?
Type I RTA
Increased Ca release from bone as buffer
Downregulation of Ca transport proteins in kidney
High distal Na delivery -> Ca excretion
Type I RTA treatment?
Bicarb
Type II RTA pathophys?
Reduction in threshold for bicarb reabsorption in proximal tubule -> urinary bicarb loss
Type II urine pH high/low?
Initial high urine pH (due to bicarb loss)
Over time kidney compensates -> distal acidification -> lower urine pH
Treatment for Type II RTA?
bicarb
Type IV RTA pathophys?
Aldosterone deficiency or aldosterone resistance (psuedohypoaldosteronism)
What happens to electrolytes in Type IV RTA?
Na / K / H+
Hyponatremia
Hyperkalemia
Metabolic acidosis
Urine pH in Type IV RTA high or low?
Low, < 6.5
Treatment for mastitis?
Dicloxacillin
Treatment for mastitis if PCN resistant?
Erythromycin
At what GA is lactase at adult levels?
36 wks GA
What is the whey-to-casein ratio of mature breast milk?
55:45
What is the whey-to-casein ratio of preterm formulas?
60:40
What is the whey-to-casein ratio of colostrum?
80:20
ARPKD fetal presentation in utero?
It commonly presents in the neonatal period with a history of oligohydramnios and pulmonary hypoplasia as a consequence of poor fetal urine production, along with enlarged kidneys.
ARPKD ultrasound features?
Autosomal recessive polycystic kidney disease is an inherited disorder characterized by bilateral renal cysts and enlarged kidneys without dysplasia.
Renal ultrasonography demonstrates bilaterally enlarged kidneys with poor corticomedullary differentiation. The renal cysts are small (<3 mm) and cannot be visualized on ultrasonography.
ARPKD associated with which anomaly? What gene is involved?
All patients with autosomal recessive polycystic kidney disease have abnormalities of the bile ducts and congenital hepatic fibrosis.
This is because of mutations in the gene PKHD1, which encodes a protein expressed in the cilia of renal tubular and hepatic bile duct epithelial cells.
How is hyponatremia related to preterm growth? What’s the pathophysiology?
Hyponatremia leads to poor growth by inhibiting function of the sodium/hydrogen (Na+/H+) antiporter.
Sodium is an important somatic and brain growth factor in early infancy, stimulating cell proliferation, increased cell mass, and protein synthesis.
Hyponatremia restricts infant growth not only because of decreased extracellular volume, but also through direct restriction of skeletal muscle and tissue growth.
The Na+/H+ antiporter is found in cells throughout the body, including a large number found in the nephrons. Numerous growth factors, including epidermal growth factor, insulin, and angiotensin stimulate the Na+/H+ antiporter.
Decreased extracellular sodium results in inhibition of the Na+/H+ antiporter, leading to decreased pH of the intracellular space, decreased function of intracellular Na+ K+ ATPase, and inhibition of cell division and growth.
How do term newborns adapt to lower sodium content of breastmilk?
The term infant is well adapted to the naturally low-sodium diet provided by human milk.
In the neonatal period, the term infant has a lower glomerular filtration rate (GFR) and reduced proximal tubular reabsorption of sodium and water compared with adults.
The term newborn is able to maintain sodium homeostasis through renal vascular vasoconstriction which decreases the GFR. This avoids overloading immature tubular cells and the risk of exceeding their transporting capabilities, which would result in loss of electrolytes.
Decreased GFR in the period after birth is protective against hyponatremia. This effect is even more important in the immature kidney which has an anatomical preponderance of glomeruli and thus is more susceptible to increased sodium excretion.
4 reasons why preterms are susceptible to hyponatremia?
- Increased sodium loss — high FeNa
- Low sodium intake — human milk and donor milk even lower
- Hormonal factors — preterm kidney tubule less sensitive to aldosterone; intact volume contraction response to RAAS given low sodium diet
- Meds — caffeine and loop diuretics. Caffeine increases FeNa in proximal tubule and distal nephron
The preterm infant of less than 34 weeks’ gestation is particularly susceptible to hyponatremia for several reasons.
First, there is increased sodium loss because of a high absolute and fractional sodium excretion rate. It has been shown that this loss can be overcome through sodium supplementation at 3 to 5 mmol/kg per day to achieve a normal serum sodium concentration.
Second, there is low sodium intake in infants given exclusive human milk diets, and donor human milk tends to have lower sodium concentration than milk provided by a mother who has recently delivered a preterm infant.
Third, hormonal factors contribute to low sodium. The preterm kidney tubule is less responsive to aldosterone than a term kidney. This results in natriuresis despite relatively elevated aldosterone concentrations. At the same time, the preterm infant has an intact volume contraction response to the renin-angiotensin-aldosterone pathway. This suggests that the typical very premature infant receiving a low-sodium diet is volume contracted to an unphysiologic degree and exists in a state of sodium depletion.
Finally, medications such as caffeine and loop diuretics have natriuretic effects. Caffeine affects sodium balance by increasing fractional excretion of sodium in the proximal tubule and distal nephron.
Gastroschisis msAFP level — high or low? Oomphalocele?
Gastroschisis is associated with very high maternal serum AFP concentrations (up to 7 to 9 multiples of the median).
Oomphalocele is usually associated with more modest elevations in maternal serum AFP (nearly 4 multiples of the median).
Gastroschisis fetal mortality causes?
In addition to poor fetal growth, there is an increased rate of fetal mortality (15%) that is thought to be related to midgut volvulus or acute umbilical blood flow restriction.
Frequently, patients with gastroschisis have malrotation. Postnatal mortality is nearly 10%. Infants with gastroschisis are at high risk for feeding intolerance, prolonged ileus, necrotizing enterocolitis, short bowel syndrome, sepsis, and complications related to prolonged parenteral nutrition.
