High Yield GI Notes Clinical outcomes of H.

. pylori: duodenal ulcers (significant), gastritis (majority), and gastric cancer (rare/end stage). Risk factors for developing NSAID ulcers: age > 60, prior hx of ulcer, high NSAID dose, concomitant use of anticoagulants, short duration of therapy, serious systemic illness, smoking, alcohol abuse, concomitant H. pylori infection Antacids (Mg, Al, Ca) relieve pain faster than any other group of drugs for GERD (but also wear off fast) Loss of inhibitory motor neurons (NO releasing) to smooth muscle sphincter = tightens LES = achalasia (bird beak sign)! Enteric motor neurons are final pathways from ENS to GI muscles [(-) neurons: NO/VIP; (+) neurons: ACH, Substance P] Interpreting malabsorption tests: 1) Fat malabsorption only: luminal maldigestion (panc insufficiency, bile salt deficiency) 2) Fat and B12 malabsorption: luminal maldigestion (ileal loss of bile salts) bacterial overgrowth (deconjugation of bile acids + bact consumption of B12) 3) Specific disaccharide malabsorption: mucosal maldigestion (disaccharidase deficiency) 4) Fat + d-xylose malabsorption: mucosal malabsorption (celiac dz, tropical sprue, bacterial overgrowth, severe Crohn's, Whipple's dz) Key Points on Colorectal Cancer: # of mutational events occurring during tumor evolution from benign to malignant is much larger than thought Types of mutations differ between colon cancer and breast cancer (many CRC genes unknown) FAP: auto dominant, APC mutation, 1/3 of FAP pts have de novo, sporadic germline mutations. CRC risk is 100% in untreated FAP patients, thus need to scope them frequently and do colectomy prophylactically. Lynch Syndrome/HNPCC: auto dominant, MLH1/MSH2 mutations, problem with DNA mismatch repair, early, frequent colonoscopies improve survival, consider checking other places for cancer (endometrium). MYH Polyposis: auto recessive, MYH mutation, MYH gene normally repairs mispairing between 8-OxoG and adenine (mutated MYH cannot repair this polyps), looks like FAP. Serious IBS Red Flags: onset of symptoms after age 50, GI bleeding/iron deficiency anemia, nocturnal diarrhea, weight loss, family hx of organic GI dz (colorectal cancer, IBD, celiac dz) Hepatitis A/E: + IgM anti Hep A/E (acute), + IgG anti Hep A/E (resolved) Hepatitis B: Interpretation of Hepatitis B Serologic Test Results Tests Results Interpretation HBsAg negative anti-HBc negative Susceptible anti-HBs negative HBsAg positive anti-HBc positive Acutely infected IgM anti-HBc positive anti-HBs negative HBsAg positive Chronically infected anti-HBc positive IgM anti-HBc negative

anti-HBs HBsAg anti-HBc anti-HBs HBsAg anti-HBc anti-HBs

negative negative positive negative negative positive positive

Resolved infection (most common)

Immune due to natural infection

HBsAg negative Immune due to Hepatitis B anti-HBc negative vaccination anti-HBs positive Hepatitis B surface antigen (HBsAg): A protein on the surface of HBV; it can be detected in high levels in serum during acute or chronic HBV infection. The presence of HBsAg indicates that the person is infectious. The body normally produces antibodies to HBsAg as part of the normal immune response to infection. HBsAg is the antigen used to make Hepatitis B vaccine. Hepatitis B surface antibody (anti-HBs): The presence of anti-HBs is generally interpreted as indicating recovery and immunity from HBV infection. Anti-HBs also develops in a person who has been successfully vaccinated against Hepatitis B. Total Hepatitis B core antibody (anti-HBc): Appears at the onset of symptoms in acute Hepatitis B and persists for life. The presence of anti-HBc indicates previous or ongoing infection with HBV in an undefined time frame. IgM antibody to Hepatitis B core antigen (IgM anti-HBc): Positivity indicates recent infection with HBV (6 months). Its presence indicates acute infection. Hepatitis C: + RNA (acute), + RNA + IgG (chronic), - RNA + IgG (resolved). Hepatitis D: + HBsAg (acute/chronic), + IgM anti Hep D (acute), + IgG anti Hep D (chronic), HDV RNA (chronic) Hep A/E are acute, fecal-oral, and don't lead to cancer; Hep B/C/D are parenteral, become chronic, and can lead to cancer High SAAG (Serum-Ascites Albumin Gradient): albumin diff > 1.1g/dL cirrhosis, cardiac disease, massive liver mets, hepatic failure, hepatic outflow block, portal vein thrombosis Low SAAG (Serum-Ascites Albumin Gradient): albumin diff < 1.1 g/dL peritoneal cancer, TB peritonitis, panc duct leak, biliary leak, nephrotic syndrome, serositis Cancers arise as result of genetic alterations (acquired/inherited). Efficacy of therapies in CRC depends on key mutations (Cetuximab does NOT work on tumors with K-ras mutations). Pancreatic bicarb (HCO3) juice dependent on acid and pH of lumen (only secreted in response to pH below 4.5) needed to neutralize HCL so panc enzymes work properly CCK = most important mediator of panc enzyme secretion, release stimulated by presence of amino acids/fatty acids in duodenum lumen. Thus, we use panc enzyme supplements to reduce CCK stimulus related pain in chronic pancreatitis patients.

 Secretin = most potent stimulant of panc fluid/bicarbonate. Regulated by duodenal pH (released when pH drops below 4.5). Below 4.5, panc bicarb juice is exactly proportional to acid in duodenum. Acute pancreatitis (need 2 of 3): 1) Abdominal pain 2) inc panc enzymes in serum 3) radiologic evidence Amylase in AP peaks and falls early; thus degree of elevation is not correlated with severity of illness. Cleared by renal system. Prolonged elevation should prompt eval for pseudocyst/cancer. Look at patient first, THEN the amylase! For AP, antibiotics indicated for the following: 1) infected necrosis 2) pancreatic abscess 3) infected pseudocyst. Use of abx for prevention of infection is controversial. Chronic pancreatitis patients can develop diabetes over the long term (15 years). Calcifications + positive history for chronic panc = start treatment, no further imaging needed! Weight loss in CP: early is due to food avoidance secondary to pain, late is due to fat malabsorption. May complain of nausea/vomiting (further weight loss). Malabsorption in CP: low fecal water/weight (due to ability to absorb water but not fat), can observe fat soluble vitamin deficiencies (ADEK) which can lead to bone disease. Lipase reduction prior to amylase reduction. Aggravated by low pancreatic bicarb excretion and occurs when secretion < 10% baseline (or 90% of exocrine pancreas function lost). Takes 10-20 years to develop. Endocrine insufficiency in CP: diabetes. Endocrine insufficiency later than exocrine (occurs in 60% of CP patients). Lack of glucago/insulin brittle diabetes (glucose levels hard to control). Ketoacidosis/nephropathy rare, while retinopathy/neuropathy develop in time frame similar to routine type 1 DM. Indications for pseudocyst drainage: rapid enlargement, compression of surrounding structures symptoms, pain, infection, hemorrhage. Pancreatic cancer risk factors: cigarette smoking, hereditary pancreatitis, chronic pancreatitis, type 2 DM, family hx of panc cancer, high fat intake, exposure to non-chlorinated solvents/DDT Most common location of pancreatic cancer: head (thus most common presenting sign: painless JAUNDICE) Elderly patient presenting with unexplained epigastric pain radiating to back, weight loss, or obstructive jaundice = red flags for panc cancer! New presentation of diabetes in non-obese adult = red flag for panc cancer!