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GI Review (sb)

Quiz yourself by thinking what should be in each of the black spaces below before clicking on it to display the answer.
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Question
Answer
cirrhosis   architectural distortion of liver parenchyma due to fibrosis  
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progression of alcoholic liver injury   fatty liver, alcoholic hepatitis, alcoholic cirrhosis  
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steatosis   triglyceride fat accumulation in HC  
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focal/ spotty necrosis   limited to scattered cells within lobules  
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interface hepatitis   between periportal parenchyma and portal tracts  
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submassive necrosis   entire lobules  
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massive necrosis   most of the liver  
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fibrosis cause   response to inflammation or toxic insult (irreversible)  
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maddreys discriminant function and composite clinical laboratory index   shows mortality risk during that hospitalization  
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early cirrhosis s/sx   usually asymptomatic, low platelets, hyperbilirubinemia, hypoalbuminemia, weakness, fatigue, hepatosplenomegaly (maybe)  
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late cirrhosis s/sx   lots of symptoms  
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histological appearance of cirrhosis   chicken wire  
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portal hypertension (definition)   hypertension to the portal system result of liver contraction and impeded blood flow  
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portal hypertension causes   mainly cirrhosis and alcoholic hepatitis  
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variceal hemorrhage and cirrhosis   1/3 of pts with cirrhosis die to EVH  
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s/sx of EVH   fatigue, pallor, tachycardia, hematemesis, melena, hematochezia  
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EVH prevention   beta blockers  
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ascites (fact)   most common clinical manifestation of decompensation  
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ascites sx   increase abdominal girth, weight gain, early satiety, sob, peripheral edema  
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ascites tx   sodium restriction, diuretic therapy, paracentesis  
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spontaneous bacterial peritonitis   infection of ascites (fever is alarming sx)  
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spontaneous bacterial peritonitis sx   fever, abd pain, mental status changes, rigors, n/v, diarrhea, malaise, hypotension, tachycardia, leukocytosis, azotemia, increased bili  
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Heptorenal syndrome (HRS)   renal failure defined by increase creatine in pts with advanced liver disease and portal hypertension  
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heptorenal syndrome types difference   type 1 lives 2 weeks, type 2 lives longer  
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HRS tx   nothing really good  
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Hepatic encephalopathy   4 stages of decreasing mental status  
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Hepatic encephalopathy testing   ammonia (most common used)  
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Hepatic encephalopathy tx   avoid excess protein, lactulose, rifaxamin  
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transplantation   necessary outcome of cirrhosis  
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Transjugular intrahepatic portosystemic shunt (TIPS)   treatment used for variceal hemorrhage (risky), ascites (90% effective), hepatorenal syndrome (type 1), hepatic encephalopathy (but could induce it too?)  
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HAV/HEV transmission   fecal oral transmission  
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HBV/HCV transmission   blood and body secretion transmission  
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prodromal syndrome   anorexia, n/v, fatigue, maliase, arthralgias, headache, photophobia, pharyngitis, cough, coryza, itching  
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mild hepatitis (symptoms)   elevated ast/alt, jaundice, RUQ pain, dark urine, clay colored stools, fever (a and e)  
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acute hepatitis (clinical presentation)   signs and sx of hepatitis, duration less than 6 months  
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chronic hepatitis (clinical presentation)   does not resolve in 6 months, most pts asymptomatic, can progress to cirrhosis  
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HAV (suspect when)   acute onset of s/sx recent shellfish ingestion, foreign travel, sick contacts  
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HBV (suspect when)   Acute: acute onset of s/sx, recent sexual history, IVDA, MSM, tattoos, blood transfusions Chronic: same with mild elevation of transaminases NOTE: highest risk of vertical and sexual transmission  
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Jaundice (when visible)   when bilirubin exceeds 2.5 mg/dL  
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Acute liver failure (symptoms)   coagulopathy, encephalopathy, bilirubin greater than 15  
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HAV (facts)   RNA virus, fecal-oral transmission, persists for months (rarely beyond 6 months)  
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HEV (facts)   high mortality in pregos, viral RNA in serum lasts only weeks while stool contains viral particles for several more weeks  
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HBV (facts)   DNA virus, natural immunity not possible (can reactivate), virus can survive outside human for 6 mo; not cytopathic  
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Childhood-onset HBV   results in chronic infections  
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Adult-onset HBV   usually clears  
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indications to order hep markers   flu-like sx & abd pain faint icterus, dark urine, clay-colored stools risk factors: sexual promiscuity, IVDU, h/o surg before '85 or transfusion/transplant before '92 end-stage liver disease  
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HAV (incubation period)   15-45 days (avg 30)  
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HBV/HDV (incubation period)   30-180 days (avg 60-90)  
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HCV (incubation period)   15-160 days (avg 50)  
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HEV (incubation period)   21-56 days (avg 40)  
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HCV (suspect when)   Acute: rarely found; h/o sexual promiscuity, MSM, IV/IN drug use, tattoos (esp colorful) Chronic: same but with mild elevations of transaminases  
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HDV (suspect when)   initial HBV sx worse than expected or stable chronic HBV infection worsens; foreign travel  
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HEV (suspect when)   same clinical presentation as HAV, but HAV markers negative; consumption of undercooked pork or boar  
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Lab Values   increased AST/ALT (acute disease) increased bili (if >20 or prolonged=severe disease) alk phos normal/inc PT/INR prolonged (acute liver failure)  
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Acute Hepatitis (Management)   tx of symptoms: fever, pain; nausea; dehydration; itching (if HBV, consider nucleosides) imaging: US (initial to r/o), CT/MRI (f/u on abnormal findings), elastogram (if fibrosis)  
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HAV (serology)   Acute infection: IgM Resolved: IgG remains positive for life providing immunity  
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HBV (serology)   HBsAg appears first HBc IgM positive in acute infection HBeAg positive in active replication HBV DNA= viral load HBsAb positive if recovered or if vaccinated  
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HCV (serology)   HCV antibody= exposure, not necessarily infection Must also use HCV RNA by PCR for viral load  
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HEV (serology)   HEV RNA detection in serum or stool Presence of HEV IgM or increased HEV IgG is indicative of infection  
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Chronic Hepatitis (clinical presentation)   Usually asymptomatic • If not, symptoms (see acute) will not resolve within 6 months • Jaundice, first noted in sclera • Spider angiomas/palmer erythema • Caput medusa • Hepatosplenomegaly • Ascites • Neurologic changes • Gynecomastia in males  
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HCV (facts)   RNA virus, rarely causes symptoms, almost never fulminant hepatitis don't let patients wait until sick can be re-infected  
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Tylenol   Most common cause of drug-induced hepatitis  
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False   True/False Steroids are treatment for drug-induced hepatitis  
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Hepatocellular Carcinoma Etiology   Male > Female High assoc. w/ cirrhosis High prevalence with HBV & HCV infection  
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HCC Clinical Presentation   asympt until large or mult abd pain w/ palpable mass friction rub/bruit over liver blood tinged ascites  
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HCC Diagnosis   Alpha-Feto Protein (>1000 is diagnostic)-NOTE: False increase with ascites, PBC, testicular cancer, prego Ultrasound with f/u MRI  
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HCC Treatment   Early detection is key Surgical resection/transplant is the only cure TACE (chemo), thermal/cold ablation, Sorafenib NO radiation!  
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Liver Transplant   Needed mostly in patients with HCV Others: decomp CLD, newly dx HCC, non-alcoholic steatohepatitis  
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MELD Score   Helps determine eligibility for liver transplant Based on INR, bili, creatinine  
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polyps   more prevalent with age, can be present with bleeding, less than 1% become malignant  
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adenomas   greater than 1 cm  
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most common adenoma   tubular adenomas  
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high risk of cancer adenoma   villious adenomas  
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pedunculated   polyps with a stalk  
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sessile   polyps without a stalk  
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colon cancer risk factors   age, colorectal polyps, IBD, inherited syndromes, lifestyle factors (smoking, alcohol, obesity)  
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colorectal cancer at an early age makes you think of   hereditary non polyposis colon cancer  
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with no risk factors how often should you get a colonoscopy   every 10 years  
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staging meaning T   extent of primary tumor invading the wall  
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staging meaning N   lymph node involvement  
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staging meaning M   metastasis to other organs  
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neoadjuvant therapy   treatment given as a 1st step to shrink tumor before main treatment  
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adjuvant therapy   additional cancer treatment given after the primary treatment to lower the risk of recurrence  
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colorectal metastasis most common location   liver  
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Hernia   A profusion of a body structure through a rupture in the wall of the cavity in which it is normally enclosed  
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Causes of hernias   congenital, acquired (surgery or trauma)  
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Inguinal hernia   most common hernia  
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indirect inguinal hernia   lateral to epigastrics, failure to close processes vaginalis  
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direct inguinal hernia   medial to epigastrics, acquired, floor weakness (more common in elderly)  
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Femoral hernia   more common in multiperous women, repair with a plug  
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femoral hernia complications   injury to femoral vein, artery, nerve, DVT, recurrence, and infection  
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Umbilical hernia   failure of closure of umbilical ring after birth  
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Umbilical hernia causes   overweight, ascites (bad news), large abd tumor, pregos  
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Incisional hernia   most common in midline but can occur at any location  
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Incisional hernia predisposing factors   Post op infection, pulmonary disease, obesity, smoking, immune disease, surgery for AAA  
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Repairing hernias   MESH  
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seroma   fluid in old hernia location (post repair)  
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most common type of stone   cholesterol stone  
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by product of hemolytic state common in sickle cell, heart valve pts, cirrhosis   black pigment stone  
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associated with infection of the biliary tree, common in asians   brown pigment stone  
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Risk factors for gallstones   age, women, obesity, rapid weight loss, (fat old lady that joins jenny Craig), TPN, pregos, diabetics  
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sonography pros and cons   detects gallstones, cholelithiasis, not good for detecting CBD stone  
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endoscopic retrograde cholangio-pancreatography pros and cons   dx choledocholithiasis, invasive and can cause pancreatitis (so yikes) if suspicion is high then gold standard  
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Biliary colic   intermittent obstruction of the cystic duct by one or more stones, upper abd pain increases over 1 hour then stops  
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Acute cholecystitis   outlet obstruction of the gallbladder due to a gallstone obstructing the cystic duct, gall bladder neck, or Hartmans pouch  
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Acute cholecystitis sx   like biliary colic but lasts more than 6 hours, vomiting, low grade fever, jaundice, murphys sign  
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cholangitis   kills! pus under pressure in the bile duct leads to rapid spread of bacteria via the liver into the blood, impacted stone in CBD  
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cholangitis sx   charcots triad (ruq pain, fever, jaundice) labs show elevated WBC, bili high, alk phos elevated  
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cholangitis tx   ERCP, IVF, antibiotics  
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choledocholithiasis   stones in the common bile duct rest at the ampulla of cater increases pressure in the bile ducts  
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choledocholithiasis sx   like biliary colic, jaundice, bilirubin and alk phos rise  
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choledocholithiasis tx   ERCP  
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Ligament of treitz   tissue that connects the duodenum to the diaphragm, divides the GI tract into and upper and lower portion  
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Melena   black tarry and foul smelling stools usually mean UGI bleed  
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Hematochezia   passage of bright red blood or maroon stools from the rectum usually LGI or very brisk UGI  
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Peptic ulcer disease   most common cause of UGI bleeding  
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Peptic ulcer disease sx   melena or hematemsis, hx of GERD, n/v, abd pain (gastric= w/ food, duodenal= better w/ food bad 2-5 hrs after)  
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Esophageal varices   association with cirrhosis, high mortality rate  
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Esophageal varices s/sx   abnormal LFTS, hematemesis, melena, hemodynamically unstable  
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mallory weiss tears   longitudinal mucosal laceration in the distal esophagus or proximal stomach usually associated with forceful wrenching/vomiting  
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Mallory weiss tears sx   melena, almost always give a hx of non-bloody vomiting before hematemesis, heavy alcohol use  
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Gastritis   injury to gastric mucosa with inflammation defined endoscopically as mucosal hemorrhages, erythema, and erosions  
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Gastritis causes   H. pylori, stress, NSAID use, alcohol  
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Gastric cancer s/sx   wt loss, abd pain, nausea, dysphagia, early satiety, ulcer type pain, palpable abd mass  
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Anatomy of the gut (3 layers)   mucosa, muscular layer, serosa  
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Bowel obstruction sx   progressive nausea, vomiting (after eating then without eating), feculent (if distal), colicky abd pain, obstipation  
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Bowel obstruction physical findings   colicky abd pain, abd distention, bowel sounds with tinkles and rushes  
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bowel obstruction management   IVF, bowel decompression  
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LaPlaces law   thinner the wall, larger radius = more tension  
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Appendicitis   most common emergency general surgical procedure  
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Appendicitis sx   vague pain referred to umbilicus, anorexia and vomiting, point tenderness in the RLQ  
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Appendicitis tx   IVF, antibiotics, pain management, appendectomy  
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Large bowel obstruction cause   cancer 90% of the time  
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anal fissures sx   pain with defecation, hematochezia, constipation  
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hemorrhoids risk pop   chronic strainers, pregos, low fiber dieters  
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Hemorrhoids treatment   sclerotherapy, band ligation (internal only), coagulation, hemorrhoidectomy  
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colon tics   protrusions of mucosa thru muscularis medium sized arteries associated with diverticula  
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colon tics (cause)   low fiber diet, motility abnormalities, changes of the colon wall with aging  
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uncomplicated acute diverticulitis   small perforation, infection contained, limited to wall of the colon and adjacent adventia likely to develop chronic sx of abd pain, bloating, alt bowel habits  
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complicated acute diverticulitis   abscess, fistula, stricture, bleeding, free perforations rare and results in an acute abd  
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acute diverticulitis (diagnosis)   lower abd pain for days, nausea, change in bowels, abd distention, low grade fever, low abd mass possible  
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uncomplicated acute diverticulitis (treatment)   antibiotics should improve sx w/n 48-72 hours, colonoscopy in 6 weeks (contraindicated in acute phase)  
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complicated acute diverticulitis (treatment)   NPO, IVF, antibiotic coverage, CT scan (to detect complications), surg consult  
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Fistulae (diagnosis)   polymicrobial UTIs, air or stool per urethra or vagina, air in bladder  
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MC cause of lower GI bleed   colon tics  
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diverticular bleeding   painless, bright red to maroon, stops spontaneously  
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colon tics (location)   West: 95% in left colon (sigmoid) Asia: right colon  
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Indications for surgery   no improvement with treatment within 24-72 hours abscess not accessible by IR drainage air on KUB or CT (free perf) acute abdomen (ruptured abscess or free perf)  
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Rome symptom criteria   abd pain discomfort/pain at least 2-3 days per month (improved with defecation, onset associated with a change in frequency and/or form of stool) and present for 3 of the last 12 months  
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IBS stool pattern   irregularly irregular, periods of constipation alternating with periods of diarrhea  
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SIBO (small intestinal bacterial overgrowth)   may occur after acute gastroenteritis and lead to dysmotility, immune response may cause antibody to ICC and cause loss of the SI migrating motor complex which causes bacterial overgrowth increased freq of IBS after GE  
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Pathophysiology   gut is over-reactive (effected by cognitive, emotional, autonomic, endocrine, infections, and immune system)  
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SIBO (diagnosis)   breath test  
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SIBO (IBS-type treatment)   certain abx i.e. metronidazole, neomycin, doxycycline #1=Rifaximin  
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Alarm Signals   Fever, GI bleed, weight loss recent consistent change in bowel habits >45 yo onset of sx FHx or CRC, IBD, celiac disease abnormal physical findings  
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Tegaserod   tx for constipation and abd pain  
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Lubiprostone   tx for constipation (esp with IBS)  
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Linzess   tx for constipation with IBS and abdominal pain  
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Alosetron   tx for females with IBS and diarrhea must report use (severe constipation or ischemic colitis)  
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FODMAP Diet   fermentable oligosaccharides, disaccharaides, monosaccharides, and polyols includes fructose, lactose, polyols, fructans, galacto-oligos  
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Loperimide/Diphenoxylate   tx of diarrhea  
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Tricyclics   tx of pain and diarrhea (worsen constipation)  
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SSRIs   tx for pain (worsens diarrhea and GI symptoms)  
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Acute pancreatitis   inappropriate activation of pancreatic enzymes within the pancreas causing auto digestion and release of inflammatory mediators  
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alcohol caused pancreatitis   premature activation of pancreatic enzymes, directly toxic to cells, generation of toxic metabolites (acetaldehyde)  
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Dx pancreatitis   abd pain (RUQ radiating to back) amylase/lipase elevated, characteristic finding on CT  
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Chronic pancreatitis   chronic inflammatory process leading to irreversible fibrosis, loss of function and structure  
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pancreatic adenocarcinoma (risk factors)   tobacco use, chronic pancreatitis, diabetes in non-obese, hereditary  
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Pancreatic adenocarcinoma in head of pancreas   painless jaundice  
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pancreatic adenocarcinoma in tail of pancreas   abd pain, incidental finding  
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Inflammatory bowel diseases   Ulcerative colitis and crohns disease  
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Ulcerative colitis   chronic inflammatory disorder that affects the colon, most common in young adults  
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Where does ulcerative colitis begin   rectum  
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ulcerative colitis symptoms   diarrhea, rectal bleeding, mucous in stool, tenesmus, urgency, abd pain, fever, wt loss  
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ulcerative colitis signs   if mild to moderate- deceptively well looking, may have tenderness and blood on exam, if severe- pt looks ill with tachycardia, fever, orthostasis, wt loss, diffuse, abd tenderness  
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UC and cancer   Increases risk!! screening 8-10 years after diagnosis  
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Toxic megacolon   potentially fatal complication of UC, acts like severe colitis with abd distention, reduced bowel sounds, pain, and constipation  
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Crohn's disease   can involve any portion of the GI tract from mouth to anus  
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skip areas   Crohns  
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granulomas (totes classic)   crohns disease  
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Presentations of CD   ileal or ileocolonic disease, colonic disease, perianal disease  
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ileocolonic disease sx (CD)   small bowel obstruction, anorexia, frequent loose stools, wt loss, acute RLQ pain, mimicking appy  
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colonic disease sx (CD)   diarrhea often bloody, wt loss, abd pain,  
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perianal disease sx (CD)   fissures, fistulas, ulcers, stenosis, abscess  
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Skin lesions of IBD: pyoderma gangrenosum   appears as a papule, pustule, or nodule mostly on leg, progresses to an ulcer with undermined borders, development of large ulcer with minor trauma (often occurs w/o association of bowel sx)  
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Skin lesions of IBD: erythema nodosum   women! tender subcutaneous nodules with erythematous appearance (associated with flares)  
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Skin lesions of IBD others   psoriasis, metastatic crohns disease, sweets syndrome (fever leukocytosis tender red plaques with neutrophilic infiltrate) epidermolysis bulosa acquisita  
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Extra-intestinal manifestations of IBD   eye (episcleritis, scleritis, uveitis) joints (arthritis) primary sclerosing cholangitis  
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Primary sclerosing cholangitis   chronic inflammation of biliary tree involving intrahepatic and/or extra hepatic ducts (consider in UC pts with abnormal liver tests)  
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Microscopic colitis s/sx   chronic watery diarrhea, abd pain, wt loss, endoscopically and radiologically normal colon, histology shows mucosal inflammation  
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Diarrhea pathophysiology   an increase in intestinal fluid and/or transit time secondary infection, structural change, alteration in GI milieu, iatrogenic, endocrinopathy, systemic illness, malabsorptive conditions  
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Acute Diarrhea   less than 2 weeks duration could be infectious, viral, protozoal, or bacterial  
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Rotavirus primarily infects   children 6m-2yrs  
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Rotavirus   invades epithelium and damages villi of proximal small intestine, 2-3 day prodrome of fever, vomiting, non-bloody diarrhea for 1-5 days  
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Norovirus   could be airborne, fecal oral, or waterborne 24-48 hour incubation 12-60 hour illness, vomiting common  
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Protozoal Giardia lamblia   relapse diarrhea, fever vomiting uncommon, profuse watery diarrhea then in chronic phase foamy greasy foul smelling diarrhea, abd cramps, distention, flatulence, malaise  
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food poisoning sx w/n 1-6 hours   preformed toxin, staph aureus, vomiting major complaint no fever  
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food poisoning sx in 8-16 hours   organism in food toxin after ingestion, clostridium perfringens, vomiting less, abd cramps, no fever  
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ETEC   contaminated water or food gives watery diarrhea and abd cramps, fever, n/v, incubation 1-3 days sx lasts 3-4 days  
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Leading cause of travelers diarrhea   ETEC  
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Vibrio cholera   water with stool, shellfish can give rice water stool (hyper secretion of H2O and Cl) dehydration with hypokalemia, metabolic acidosis, shock  
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Treat (shorten) vibrio   tetracycline  
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Acute inflammatory diarrhea   caused by invasive or toxin producing bacteria, fever bloody diarrhea, usually less than 2 weeks, diarrhea in small volume cramps urgency tenesmus  
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EHEC   cause by unpasterized milk, under cooked meat, course varies from asymptomatic to diarrhea to hemorrhagic colitis, self limiting to 5-7 days  
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Treating EHEC   NOOO can increase risk of hemolytic uremic syndrome  
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C. diff   7-10 days after antibiotics, greenish could smelling watery diarrhea with abd cramps some with fulminant disease (fever, hemogynamic instability, abd distention, pain, tenderness)  
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Dx C. diff   stool glutamate colitis if positive test a toxin specific testing  
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Shigella   elevated WBC, high fever, seizures, mostly self limiting 3-5 days  
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Treat shigella   bactrim- resistance? azithro or FQ  
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Campylobacter jejuni   most pts recover in less than 1 week, 20% relapse, associated with severe pain like appendicitis can mimic IBD  
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Salmonella enterica (S typhi)   enteric fever, maliase, HA, cough, n/v, abd pain, bradycardia, splenomegaly, abd distension...raw eggs  
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Entamoeba histolytica   tropic or subtropic conditions, fecal oral route, ingestion of cysts from contaminated food, if penetrates intestinal walls diarrhea, dysentery  
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Intestinal amebiasis   incubation 1-4 weeks, gradual abd pain, diarrhea, fever is uncommon, remission and recurrence, if severe: dysentery, fever, vomiting, abd pain, tenderness, hepatomegaly, hypotension  
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Intestinal amebiasis extraintestinal complications   amebic liver abscess, less common: brain, lung, GU involvement  
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Chronic diarrhea: Meds   LOTS! antibiotics, SSRIs, NSAIDs, PPIs, Metformin, ARBs, Cholinesterase inhibitors  
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Chronic diarrhea: Osmotic conditions   retention of luminal fluid, elevated osmotic gap, stool volume decrease with fasting, bloating, abd distention, flatulence  
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Chronic diarrhea: Secretory Conditions   increase volume watery diarrhea with normal osmotic gap, increased intestinal secretions or decreased absorption, excess NaCl secreted into lumen (neuroendocrine tumors that stimulate intestinal or pancreatic secretion, zollinger ellison)  
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Chronic diarrhea: inflammatory conditions   malignancy- hematochezia, abd pain, wt loss, +/- fever IBD  
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Chronic diarrhea: malabsorptive conditions   wt loss, osmotic diarrhea, high fecal fat, abnormal labs (small mucosal intestinal diseases, intestinal resections, SIBO, pancreatic insufficiency)  
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Malabsorptive: celiac disease   gluten intolerance autoimmune destruction of villi, constipation, diarrhea, fatty foul smelling, abd pain, gas, N/V, mouth ulcers, wt loss, fatigue, derm hepetiformis  
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Chronic diarrhea: motility disorders   history of systemic disease or prior abd surgery, IBS (dx of exclusion)  
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Chronic diarrhea: chronic infections   abd pain +/- fever +/- wt loss +/- BRBPR  
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Chronic diarrhea: factitious   artificially created, laxative dependence?  
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Most common cause of CRAP   constipation (Chronic recurrent abd pain)  
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Tx constipation   dietary and life style changes, review all meds and discontinue problematic ones, prescribe meds if needed  
🗑
when to refer for constipation   alarm sx, refractory sx, needs anorectal testing  
🗑


   

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