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GI Board Review

GI Board Review. Steven Klein, MD Wilmington Gastroenterology. Pearls. Specialists write questions Endoscopy usually the answer Emphasis on outpt. Eval of common GI disorders When to refer for endoscopic evaluation. Outline. CRC Screening/Hereditary cancer syndromes Common UGI disorders

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GI Board Review

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  1. GI Board Review Steven Klein, MD Wilmington Gastroenterology

  2. Pearls • Specialists write questions • Endoscopy usually the answer • Emphasis on outpt. Eval of common GI disorders • When to refer for endoscopic evaluation

  3. Outline • CRC Screening/Hereditary cancer syndromes • Common UGI disorders • IBD • Abnormal Liver enzymes

  4. Colorectal Cancer Screening • Risk Assessment • Family hx of CRC • Family hx of adenomatous colon polyps • Possible HNPCC/FAP • Important factors • First degree relatives • Age at diagnosis • Younger than 60?

  5. Hereditary CRC Syndromes • HNPCC • Account for 2-3% of CRC • 50 -70 % risk of CRC, early in life (30’s) • Average number of polyps, but more aggressive • Germline mutation in MMR Gene • Associated Malignancies • Endometrial (70%) • Ovary,stomach,SI, panc, GU • Surveillence – colonoscopy every 1-2 yrs starting at age 20

  6. Hereditary CRC Syndromes • Familial Adenomatous Polyposis • Autosomal dominant germline mutation APC • Greater than 100 polyps • Cancer risk 100% by age 45 • Attenuated version with fewer polyps • Management • Total proctocolectomy • Surveillence for extracolonic lesions – gastric/duodenal carcinoma, thyroid ca, CNS tumors

  7. Hereditary CRC Syndromes • MUTYH Associated Polyposis • Autonomic recessive (MYH gene) • Similar to FAP • Peutz-Jeghers Syndrome • Autosomal Dominant • Pigmentation of buccal mucosa, harmatomatous polyps throughout GI tract

  8. UGI Disorders • GERD • Emperic tx with PPI in those that are young without alarm symptoms • Endoscopy for those with alarm symptoms – age greater than 50, dysphagia, blood in stool, anemia, vomiting, hemetemesis, wt.loss, failure of sx. To respond to PPI

  9. UGI Disorders • Barrett’s esophagus • Intestinal metaplasia of squamous epithelium • Caucasions, Hispanic >> Blacks,Asians • Male:Female 2:1 • 8-15% of those undergoing EGD for GERD • 5% in those without!!

  10. UGI Disorders • Barretts • associated with dysplasia (1%) , adenocarcinoma (0.5%) • HGD – 4 – 6% risk of cancer within the year • Screening – chronic GERD, those > 50? • Scant evidence to support mortality benefit • Most people die for other reasons

  11. UGI Disorders • Barretts • Screening controversisal • If found, 4 quadrant biopsy q 2 cm • Repeat endo in 1 year, if no dysplasia, then q 3 yrs • Low grade dysplasia – 6 months then yearly • High grade dysplasia – repeat endo in 3 months • Ablative techniques, vs. surgery

  12. UGI Disorders • Dysphagia – difficulty swallowing • Oropharyngeal – neurogenic/myogenic origin • Esophageal – body, or LES, motility vs. obstruction • Solids vs liquids? • Odynophagia – pain with swallowing

  13. UGI Disorders • Eosinophilic esophagitis • Young adults, hx. of atopy • Multiple rings, often present with food bolus obstruction

  14. UGI Disorders • H. Pylori infection • 50% of world population • More prevalent in developing world • Acquired at early age • Associated diseases • Chronic gastritis • Duodenal ulcer • Gastric ulcer • Gastric cancer • dyspepsia

  15. UGI Disorders • H Pylori – Diagnostic testing • Non invasive – urea breath test (most accurate), serology(perhaps best initial test) stool antigen • “test and treat” - dyspepsia, no alarm symptoms, young pt. • Invasive – CLO, histology – reserved for those undergoing diagnostic endoscopy • Confirm eradication – with breath test off PPI 1 month later for those with complications

  16. IBD • Epidemiology • prevalence • CD 201 per 100,000 • UC 238 per 100,000 • Peak incidence • Between 15 – 30 yrs • Second peak between 50 – 80 • Smoking • Negative correlation with UC, positive for CD

  17. IBD • UC • Chronic colonic inflammation limited to mucosa • Presentation • Mild – tenesmus, mucous, < 4 BM/day • Moderate – mild anemia, up to 10BM/day • Severe – fever, cramps, wt loss, >10 stools per day • Diagnosis • Hx. + endoscopy with bx • Chronic inflammation • Infectious, ischemic colitis in differential

  18. IBD

  19. IBD • Crohns Disease • Transmural inflammation – leading to fibrosis, obstruction, fistulae • Can involve the entire GI tract • Presentation • More variable than UC • Fatigue, abdominal pain, wt. loss. • 10% without diarrhea • Diagnosis • Chronic inflammation, skip lesion, granuloma

  20. IBD

  21. IBD • Treatment • Goals are induction and maintenance of remission • Similar for both UC/Crohns • Mild disease • Mesalamine, SSZ for colitis • Abx , entocort for CD • Moderate disease • Add steroids, consider immunomodulator (AZA/6MP)

  22. IBD • Treatment • Severe Disease • Hospitalizaion • Consider TPN • IV Corticosteroids • Rapid improvement – add immunomodulator • Steroid Refractory • CD – biologic agent (infliximab), • UC – biologic, cyclosporine, surgery

  23. IBD • Treatment • Fistulizing CD • No role for steroids • Abx, AZA/6MP, biologic • Surgery • UC – proctocolectomy with IPAA • CD – limited resection based on disease extent • No pouch • Extraintestinal Manifestations • 40% of pts

  24. Elevated Liver Tests • Liver performs a wide variety of biochemical, synthetic, and excretory function • No one test provides a global assessment • Recognition of common patterns of abnormalities will help guide further evaluation

  25. Markers of Hepatocyte Necrosis • Aminotransferases • Aspartate aminotransferase (AST/SGOT) • Not specific for liver – present in muscle, kidney, RBC • Present in both hepatocyte cytosol and mitochondria • Alanine aminotransferase (ALT/SGPT) • Relatively specific for liver • Present in the cytosol

  26. Markers of Hepatocyte Necrosis • AST/ALT ratio • Usually less than or equal to one • Greater than 2 in several settings • ETOH – secondary to pyridoxine deficiency • Cirrhosis • Wilson’s disease (ratio greater than 4)

  27. Markers of Hepatocyte Necrosis • AST and ALT levels • Levels < 500 are found in wide variety of liver diseases • Massive elevations (>2000 IU) are almost exclusively related to acute viral hepatitis, drug induced liver disease, or ischemia

  28. Markers of Hepatocyte Necrosis • Lactate Dehydrogenase (LDH) • Very wide tissue distribution, so rarely helpful • Extreme elevation with ischemia (greater than 5000 IU)

  29. Markers of Cholestasis • Alkaline phospatase (AP) • Present in a variety of tissues (liver, bone, intestine, leukocytes) • Elevation results from increased synthesis induced by cholestasis • Striking elevations seen in infiltrative liver disease, intra or extrahepatic biliary obstruction

  30. Markers of Cholestasis • Gamma Glutamyl Transpeptidase (GGTP) • Also found in a variety of other tissue, but not bone • Can confirm hepatic origin of elevated AP • Induced by EtoH and drugs – GGTP/AP ratio > 2.5 suggests EtoH

  31. Markers of Cholestasis • 5’ – Nucleotidase • Again has wide tissue distribution, but sig elevations are fairly specific for liver disease • Less sensitive compared to GGTP to confirm hepatic origin of elevated alk phos

  32. Markers of Cholestasis • Bilirubin • Product of heme metabolism • Serum concentration usually < 1mg/dl, is unconjugated • Normally, less than 5% conjugated • Jaundice evident with bilirubin > 3

  33. Markers of Cholestasis • Hyperbilirubinemia • Impaired biliary excretion – conjugated hyperbilirubinemia • Biliary obstruction • With choledocholithiasis, bilirubin rarely exceeds 8 mg/dl • Hepatocellular disease • Increased production usually results in an unconjugated hyperbilirubinemia • Hereditary disorders of bilirubin metabolism

  34. Markers of Synthetic Capacity • Prothrombin Time (PT) • Liver synthesizes all coagulation factors except VIII • Vit K required for carboxylation of II, VII, IX, X • Diff dx of prolonged PT includes Vit K def, DIC, and Liver disease • Measurement of factor VIII is low in DIC, nml or high in liver disease • If malabsorption, Vit K should reduced the PT by 30% within 24 hrs

  35. Markers of Synthetic Capacity • Albumin • About 10gm synthesized and secreted by hepatocytes daily • Synthesis decreases with progressive liver disease • Other factors such as nutrition, renal or GI losses, important as well • Half life of 20 days, so less helpful for acute liver disease

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