May involve only palate but may not be midline Some cases the vomer and nasal

May involve only palate but may not be midline some

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May involve only palate but, may not be midline. Some cases the vomer and nasal septum ae partly or completely undeveloped. Pyloric Stenosis Risk Factors: Affects infants between the ages of 1-2 wks and 3-4 months Incidence is higher in white males.
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Affects full-term infants more than preterm Unknown cause Possible cause is increased gastrin secretion by mother in last trimester of pregnancy Etiology: An obstruction of the pyloric sphincter caused by hypertrophy of the sphincter muscle. Clinical Manifestations: Forceful or projectile vomiting immediately after eating. Emesis contains the bulk of the feeding plus some of previous feeding Almost always BILE FREE Infant will want to eat again after vomiting Prolonged retention of food in the stomach is characteristic and food remains present after 4 hours if no vomiting. Constipation is the rule because most food does not reach the intestine. Patho: The circular muscle of the pylorus is grossly enlarged because of an increase in cell size (hypertrophy) and an increase in cell number (hyperplasia). The mucosal lining of the pyloric the pyloric opening folded and the lumen is narrowed by the encroaching muscle. Neonatal Jaundice Physiologic Pathologic Risk Factors: ABO/Rh incompatability Prematurity Exclusive breast feeding Maternal age >25 Male infants Delayed meconium passage Excessive birth trauma Etiology: Physiological - transient, benign that occurs in the first week of life in otherwise healthy full term infants. Pathological : appears in 24 hours with total serum bilirubin level > 20 or indirect bilirubin >15. Should be suspected if serum bili levels increase > 5 mg/dl per day, persistent jaundice (>7- 10 days in full term infant). Clinical Manifestations: Physiological : develops during 2nd or 3rd day after birth and usually subsides in 1-2 weeks in full term infants and in 2-4 weeks in premature infants. Increasing bili levels beyond this time frame indicated pathological jaundice. Yellowing of skin, dark urine,
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light colored stools, weight loss. Premature infants with resp distress, acidosis or sepsis are at greater risk for encephalopathy. Disabilities of encephalopathy include athetoid cerebral palsy, speech and hearing problems. Patho: Physiological : Caused by mild unconjugated hyperbilirubinemia. Pathological- result from complex interaction of factors that cause: 1. Increase bilirubin production (hemolysis) 2. Impaired hepatic uptake of excretion of unconjugated ed bilirubin 3. Delayed maturation of liver conjugating mechanisms Unconjugated bilirubin is lipid soluble, bound to albumin in blood and is able to cross BBB. Kernicterus or chronic bilirubin encephalopathy deposits of toxic unconjugated bilirubin in brain cells. Late rising indirect bilirubin level may sign of glucose -6- phosphate dehydrogenase deficiency, an enzyme important in red blood cell metabolism. X linked genetic defect. Elevated unconjugated bilirubin levels can cause hemolysis → increasing jaundice even more
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