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Pediatric Gastroenterology & Hepatology For Undergraduate. Dr Hatem Hussein Professor of Pediatrics Associate member of Royal College Of Paed.&Child Health-UK Zagazig Faculty of Medicine-Egypt Mar. 2008. Hepatitis D Virus • Associated exclusively with HBV infection
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Pediatric Gastroenterology & Hepatology For Undergraduate Dr Hatem Hussein Professor of Pediatrics Associate member of Royal College Of Paed.&Child Health-UK Zagazig Faculty of Medicine-Egypt Mar. 2008
Hepatitis D Virus • Associated exclusively with HBV infection • Incomplete virus that required HB surface antigen for packaging • Infection with HDV – Can occur simultaneously with HBV (coinfection) – Can occur following HBV infections (superinfection) • Superinfection of a HBV carrier with HDV increase the severity of chronic disease
DNA virus Uses HBsAg as an outsider coat. Usually parenteral or perinatal IP 3-10 wks Followed by hepatocellular damage,and hepatitis picture. HBsAg clears up followed by the HDV .
Hepatitis C Virus Infection • The most common cause of chronic hepatitis, cirrhosis and hepatocellular carcinoma – HCV infection accounts for > 90% of non-A, non-B hepatitis secondary to blood transfusions – The incidence of HCV infection due to blood transfusions has declined by >95% since 1989. – >50% of all cases are community acquired with no known risk factors
• The cloned virus was used to develop the immunoassay used to detect anti-HCV antibody • At least 6 different genotypes have been recognized with type 1 being the most common (72%). • Diagnosis is made by serology and PCR
RNA virusRoutes of infection:ParenteralSexualVertical???Incubation 1-5 mo.Immune mediated hepatocellular necrosis
C/P1-Prodroma Arthritis,RashHepatitis short preicteric stage(Fever,Abd. Pain,Tender heptomegaly,AH,M,Slpenomeg.) 2- 1-2 wks icteric stageMilder S.&S. than HAV and HBVMost patients are not jaundiced
3- Hepatic compl. A- Chronic persistent hepatitis Pathology involves the portal areas.mod. Enzymopathy.may resolve or procceds to B- Chronic active hepatitis Rec. Jaundice and enzymopathy. May progress to C- Liver failure , either fulminant OR subacute D- Hepatocellular carcinoma 25 fold risk of norms.
Investigations1- High ALT,which coincides with high direct bili.2-AntiHCV abs appears after 1-8 months3-Viral load. RNA can be detected after 2 wks of infectionManagement!- supportive.2- Alpha interferonfor 6-12 mos.Curative in 25%
VOMITING IN INFANTS&CHILDHOOD 1- FEEDING RELATED: OVER- ,Mechanical ,Formula intoler. 2-INFECTIONS: OM,Pnum.,Pyelo.,Mening…etc 3- GASTROENTERITIS: Aetiolgy, electrolytes related 4- Obstructive : Volvolus, Intussception
5-DRUGS: Aspirin,NSAID,Poison,Antibiotics 6- METABOLIC : Renal, DKA,Galactosemia,Urea cyc- le,Fructosemia etc 7- Psychogenic
CONSTIPATION: 1- UNDERFEEDING. 2- ANAL FISSURES,HEMORROIDES. 3- INTESTINAL OBSTRUCTION. 4- HYPOTHYROIDISM 5- NEUROLOGIAL e.g. MENINGOCELE,TETHERED SPINAL CORD 6-HABITUAL??? FEEDING,LIFE STYLE,STRESSES
CONGENITAL MEGACOLON( HIRSCHSPRUNG’S DISEASE) Functional intestinal obstruction Can affect any part of the colon. 1/5000 High incidence in trisomy 21 Aetiology: Failure of segmental relaxation due to defective innervations. Leads to proximal empty segment, hypertonic segment and distally hugely dilated segment.
Clinically: Failure to pass meconium up to 24h. Progressive constipation Huge distension Complicated by Diarrhea, Malnutrition, ent- erocolitis, anaemia Investigations: P/R Ba enema (cone shaped) Rectal biopsy Treatment: 1- manual evac. 2- supportive care 3- surgical management
Chronic Abdominal Pain in Childhood: Diagnosis and Management
Affects more than third of the children. Becomes chronic if it lasts more than 2 weeks. Needs simple approach before rushing to sophosticated investigations. Needs a 5 steps approach based on history,cl. exam.,investig.,individual imagings and interventions.
ACUTE CAUSES: 1-INFECTIONS URTI.,GE,Pancreatitis,Pyelo.,Appendicitis,Hepatitis. 2- ACUTE OBSTRUCT. 3- AUTE DISEASES: e.g. HSP, DKA,RHEUMATIC ,PNUMONIA RECURRENT CAUSES: 1-Irritable bowel 2-Parasitic e.g. Giardia 3-Chronic constipation 4- Chronic pancreatitis 5-Malabsorption 6-Chronic hepatitis 7-Acid peptic disorders 8-H.pylori 9-IBD 10-Renal stones 11-Gynecological DIFF. DIAG. OF PAEDIATRIC AGE ABDOMINAL PAIN
History Location, intensity, character and duration of pain, time of day or night . Appetite, diet, satiety, nausea, reflux, emesisStool pattern, consistency, completeness of evacuationReview of systems: weight loss, growth or pubertal delay, fever, rash Medications and nutritional interventionsFamily history, travelInterference with school, play, peer relations and family dynamics
Physical examinationWeight, height, growth velocity, pubertal stage, blood pressureComplete physical examinationObjective abdominal findings: location, rebound, mass, psoas signLiver, spleen and renal size, ascites, flank painPerianal findings: rectal and pelvic examinations, stool testing for occult blood
Laboratory tests • Complete blood count with differential, erythrocyte • sedimentation rate • Urinalysis and urine culture • Laboratory tests • --Stool testing and culture for parasites, Giardia • antigenSerum chemistry profile, amylase level • --Pregnancy test, cultures for sexually transmitted • Diseases, Breath hydrogen test: lactose, fructose • -Serologic testing for amebae, Helicobacter pylori
Imaging studies individualized according to indication Abdominal and pelvic sonographyUpper gastrointestinal contrast study with small bowel testing, abdominal computed tomographyUpper endoscopy, colonoscopy, laparoscopy
Empiric interventions Patient and parent educationSymptom diary of pain, bowel pattern, diet and associated features, response to intervention Constipation investigated as a factorDietary interventions, including adjusted fiber intake, reduced lactose intake, reduced juice intakeTrial of peptic management