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22 Cards in this Set
- Front
- Back
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What week of gestation is the GI tract formed
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fourthAppears as 4 mm hollow tubeBuccopharyngeal and cloacal membranes rupture during the third and seventh weeks respectivelyBy end of 2nd trimester, organs well formed and display early function
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Foregut includes:
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Esophagus, stomach, duodenum, liver, gallbladder, pancreas
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Midgut includes:
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jejunum, ileum, ascending colon, transverse colon
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Hindgut includes:
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descending colon, rectosigmoid colon
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Esophageal Atresia and Tracheoesophageal Fistula
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1/3000 to 5000 live births, M=F, 50% of infants have associated anomalies, many varieties
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Associated Anomalies with the foregut:
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Polyhydraminos in 50% of mothers- babies cant swallow amniotic fluid,Cardiovascular-PDA, VSD, ASDGastrointestinal-imperforate anus, duodenal atresiaSkeletal-vertebral anomaliesGenitourinary-hypospadiasOther-trisomy
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EA with distal TEF
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85% of total esophageal defects,Esophageal gap 1 to 2 cm,Distal TEF joins trachea at carina,Diagnosis made by placing nasogastric tube,Cough, choking, aspiration with first feed
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Pure EA
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10% of congenital esophageal defects,Absence of gas within the GI tract*,20% will have Down’s syndrome,If the gap between the esophageal pouches is > 4 cm primary anastomosis is difficult
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H- tracheoesophageal fistula
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3% to 5% of cases,Rarely have other anomalies,Repeated episodes of pneumonia,Esophagus and trachea otherwise normal
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Pyloric Stenosis
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1/900-1000 live birthsdevelopmental disorder- not congenital
nonbilious vomiting, hypochloremic alkalosis, presents 1 week to 5 mos of life, pyloric mass on PE |
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Incidence and heredity of Pyloric Stenosis
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Most frequent surgical disorder of the stomach,Incidence variable 1 per 1,000 live births,Males to females 4-6:1,Positive family history 13% of time
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Pathogenesis of PS
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Pyloric muscle hypertrophy from gastric peristalsis against closed pyloric canal.Hypergastrinemia with hyperacidity.Elevations of prostaglandins leading to smooth muscle constriction
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Clinical Presentation of PS
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Nonbilious, progressive vomitingDehydrationFailure to thrive1 week to 5 months of ageElevated serum bicarbonate, decrease in serum chloride
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Dx of PS
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Physical examination reveals pyloric mass or “olive”UGISonography
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Duodenal Atresia
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Thought to arise from failure of recanalization of duodenal lumina,Incidence is 1 in 10,000,50% infants premature. F to M 2:1Down’s syndrome occurs in up to 30%,Presents with bilious vomiting and abdominal distension
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Duplications of the GI tract
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Rare anomalies consisting of well developed tubular, or spherical structuresLocated on the mesenteric borderSymptoms related to obstruction, intussusception, volvulus, perforation, or hemorrhage
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Malrotation
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Malrotation itself doesnt cause trouble unless a volvulus forms.Failure of midgut to achieve normal position, predisposes to volvulus of midgut, acute bowel obstruction, bilious vomiting, surgical emergency
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Meckel's Diverticulum
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Remnant of vitellointestinal duct, antimesenteric border of ileum, 2-3% of population, painles rectal bleeding in children under 2. Cannot relax the colon. Crampy abdominal pain. Can use nuclear medicine to Dx
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Hirschprungs Disease
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Absence of intramural ganglion cells. 1/5000 births, M>F, assoc w/ Down's, 75% rectosigmoid colon, aganglionic segment permanently contracted.
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Sx of Hirschprung's
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delayed passage of meconium, 83% have problems within first month, 96% have problems within first year, FTT, vomiting, intermittent diarrhea, abdominal distension
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Compare and contrast Regular constipation and Hirschprung's
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soiling, stool in ampulla, large caliber stools, stool witholding behavior all rare with Hirschprungs
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Dx of Hirschprung's
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Unprepared BE, Mucosal suction Bx, Anorectal Manometry
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