GI USMLE
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| etiology of colon cancer | adenocarcinoma
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| risk factors colon cancer (5) | 1) age >50, 2) adenmatous polyps, esp if villous, large size and number, 3) IBD, esp UC, 4) fam hx, 5) high fat, low fiber diet
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| MC place of met for colon cancer | liver (as w all GI cancers)
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| name 6 colon polyp syndromes, location polyps and other features, and relevant cancers | 1)fam adenom polyp-100% col ca, 2)Gardners col polyps+osteomas &benign STS 3)Turcots-col polyps+Cb medullo/glio4)Peutz Jegher-GI hamartomas, incrs other ca but not col, pigment lips/genit, 5)juven polyp-sm risk ca 6)heredit nonpolyp col ca-no polyps ahead
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| clinical features of colon cancers and difft locations | abd pain MC presenting sympt; R side: melena, Fe defic anemia, no change stool; L-side: hematochezia, obstruct more common and change stool; rectal: higher recurrence lower survival, hematochezia MC sympt, tenasmus
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| grading colon cancer | duke's criteria: A=mucosa, B=past mucosa w/o LN, C=regional LN, D=mets
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| tx colon cancer | measure CEA, then surgical resxn; colon stage C: also give 5FU+leucovirin; rectal if B2 or C give 5FU +radiation
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| when use radiation in colon cancer | only rectal, not colon
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| how/when use CEA to monitor recurrence colon cancer, when do recurrences occur | check CEA q3-6mos, 90% recurrences occur within 3yrs
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| types of colon polyps and cancer potl | 1) hyperplastic/metaplastic: usu small, asx, no risk cancer but removed bc hard to tell from ca, 2) inflamm polyps/pseudo polyps in UC, 3) adenomatous polyps-malignant potl, esp if villous (v tubular or tubulovillous), large, flat, and if lots
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| MC location of colon polyps | rectosigmoid
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| cxns of diverticulosis v diverticulitis | diverticulosis: painless bldg, diverticulitis; diverticulitis: obstruction, abscess, fistula
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| risks of diverticulosis (3) | low fiber, fam hx, incrsd age
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| MC location of diverticulosis | sigmoid colon
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| sympt of diverticulosis | (usu asx) vague LLQ discomfort, may have painless bldg that usu stops spont (no tx nec)
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| dx for diverticulosis | ba enema
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| tx for diverticulosis | hi fiber diet or psyllium (has mucilage)
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| sympt of diverticulitis | F, LLQ pain, incrsd WBC
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| dx for diverticulitis | CT scan w contrast--not ba enema or colonoscopy bc risk of perf
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| tx for diverticulitis | IV fluids and Abx, NPO, mild episodes can be outpatient; if sympt persist 3-4d or recurrence need surgery
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| angiodyspl of colon is due to what etiol? Is assoc w what cardiac defect? | AVM, assoc w AV stenosis
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| how does angiodysp of colon present? In whom? Dx, tx? | presents as lower GI bldg in pt>60, dx colonoscopy, tx: stops spont
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| 4 etiologies of acute mesenteric isch in order of freq | 1) arterial embolism (50%)-cardiac emboli; 2)arterial thrombus (25%): occlusion over atheroscl dz; 3) nonocclusive: low CO leading to splanchnic constriction; 4) venous thrombosis in hypercoag pts
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| presentation, tx of arterial embolic acute mesenteric isch | more sudden, painful presentation in pt w cardiac dz (ie A fib, MI, valve dz); tx: papaverine during arteriography +/- thrombolytics or embolectomy
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| presentation, tx of arterial thrombus acute mesenteric isch | more gradual present in pts w CAD, PVD; tx: papaverine during arteriography
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| presentation, tx of nonocclusive acute mesenteric isch | pts w low CO, critically ill, elderly; tx: papaverine during arteriography
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| presentation, risks for, tx of venous thrombosis acute mesenteric isch | sympt present for days/wks get progressively worse; pts have infxn, hypercoag, OCP, portal HTN, malig, pancreatitis; tx: heparin
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| clinical features of acute mesenteric isch | abd pain >> physical findings
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| in addition to arteriography tx for acute mesenteric ischemia, what other tx do all etiol of acute mes isch get | IV fluids and broad spectrum Abx
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| what Rx should be avoided in acute mesenteric isch | vasopressors, they make isch worse
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| what metabolic derangement may be seen in acute mesenteric isch | lactic acidosis
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| cause and presentation of chronic mesenteric isch? Is it more common than acute? | cause: atheroscl of celiac, superior&infr mesenteric arteries; presents w dull pain that increases after meal; less common than acute
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| dx and tx for chronic mesenteric isch | dx: mesenteric arteriography; tx: revasc surgery
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| what's Ogilvie's syndrome? | signs/sympt of large bowel obstruction, but no evidence of mechanical obstruction
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| what's Ogilvie's syndrome assoc w? | recent surgery or trauma, sepsis, malig, Rx (narcotics, psych, antichol)
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| tx for Ogilvie's syndrome? | start w gentle enemas & NG suction, then colonoscopic decompression [stop Rx if that's suspected]
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| when is immed colonoscopic decompression called for in Ogilvie's syndrome | if colon diam >10cm (bowel rupture risk)
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| etiol of pseudomem colitis | C dif overgrowth after Abx
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| MC Abx that lead to pseudomem colitis, when does colitis develop relative to Abx use | clindamycin, ampicillin, cephalosporins [usu get pseudomem colitis w'in 1st wk]
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| clinical present of pseudomem colitis? Cxns? | profuse, watery diarrhea, crampy Abd pain; risk: toxic megacolon
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| dx pseudomem colitis; what other tests should be ordered | C dif toxin in stool; also get abd radiograph to r/o toxic megacolon and colonic perf
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| tx pseudomem colitis | discont Abx, start metronidazole (but not in preg or kids; back up is vanc); cholestryramine can help w diarrhea
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| after pseudomem colitis has been tx, when might it recur | 2-8wks after discont Abx
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| MC location of colonic volvulus | sigmoid colon (same as location colonic polyps), but also can occur in cecum
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| clinical present of colonic volvulus | acute onset colicky abd pain, constipation w abd distension; anorexia N/V
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| tx for 2 types of colonic volvulus | 1) sigmoid: decompress w sigmoidoscopy, elective resxn; 2) cecal: emergent resxn
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| dx of colonic volvulus (2 types) | 1) sigmoid: omega loop sign, dilated sigmoid; 2) cecal: coffee bean sign, air fluid RLQ w distension of cecum and small bowel
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| what would barium enema show for colonic volvulus | bird's beak at location of volvulus
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| when should barium enema NOT be used in colonic volvulus work up | if suspect strangulation
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| grading for liver cirrhosis: name of classif, 5 elements evaluated, scale | Child's classif includes ascites (0, controlled, uncontrolled), bili, albumin, nutrition, encephalpathy; scale A (good) to C (bad)
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| albumin, bili cut-offs for difft Child's classif of liver cirrhosis | bili: <2=A, 2-2.5=B, >3=C; albumin: >3.5=A, 3-3.5=B; <3=C
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| ascites, nutrition, and encephalopathy cut-offs for difft Child's classif of liver cirrhosis | ascites: 0=A, controlled=B, uncontrolled=C; nutrition: excellent=A, good=B, poor=C; encephalopathy: 0=A, min=B, severe=C
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| top 2 causes of liver cirrhosis | 1=EtOH, 2=chronic hep,
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| causes of liver cirrhosis other than 2 (7--divided into 4 categories) | 1) hepatitis: autoimmune hep, non-EtOH steatohep; 2) back up: biliary cirrhosis, hepatic congestion, hepato veno occlusion; 3) Rx; 4) genetic metabolic
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| metabolic/genetic causes of liver cirrhosis | hemochromatosis, Wilson's, alpha-anti trypsin defic
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| Rx causing liver cirrhosis (2) | acetaminophen and methotrexate
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| classic clinical signs of liver cirrhosis | ascites, varices, gynecomastia, palmar erythema, spider angioma, hemorrhoids
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| lab values in liver cirrhosis | coag (incrsd PT, and PTT in severe), low glu, almumin, incrsd ammonia, incrsd bili, LFT [not always incrsd bc decrsd fxnal hepatocytes], +/- CRF lab findings
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| cxns of liver cirrhosis (7) | 1) Portal HTN/varices, 2) ascites/spontaneous bac peritonitis, 3) hepatic encephalopathy, 4) hepatorenal syndrome, 5) hyperestrinism, 6) coag, 7) cancer
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| types of varices in liver cirrhosis and tx | esophageal varices(90%), gastric (10%); esoph: hematemesis, once pt stabilized emergent upper GI endo; tx: variceal ligation/banding (tx of choice), sclerotherapy, IV octreotide splnachnic vasoconstrict decrs portal P, IV vasopresin and nitroglycerin
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| tx of esophageal varices in liver cirrhosis | once pt stabilized emergent upper GI endoscopy; tx: variceal ligation/banding (tx of choice), sclerotherapy, IV octreotide splanchnic vasoconstrict decrs portal P, IV vasopresin and nitroglycerin
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| long term tx for varices in liver cirrhosis | beta blockers to prevent rebleeding
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| pathophysiol and clinical findings of ascites in liver cirrhosis | due to portal HTN and hypoalbumin; abd distension, shifting dullness, fluid wave
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| indications for parecentesis; what in parecentesis indicates portal HTN | new onset, worsening ascites, or r/o SBP; serum:ascites albumin >1.1= portal HTN
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| tx ascites in liver cirrhosis | low Na diet, diuretics (furosemide&spironolactone), parecentesis if short of breath; TIPS (transjugular intrahep portal-system shunt) or peritoneovenous shunt can decrs portal P
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| differential ascites (6) | cirrhosis/portal HTN, CHF, CRF, TB peritonitis, cancer, hypoalbumin
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| gold standard for liver cirrhosis | liver bx
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| clinical findings and tx for hepatic encephalopathy | clinical: decrsd mental fxn, confusion, asterixis; tx: lactulose (prevents absorb ammonia), neomycin (klls bowel bac decrs ammonia); limit protein 30-40mg/d
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| describe hepatorenal syndrome, lab findings, tx | from renal hypoperfusion; incrsd BUN, Cr, decrsd Na and U_Na, hypotension, oliguria; tx: liver transplant
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| clinical findings of spont bac peritonitis | ascites + abd pain, F, vomit, rebound tenderness
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| dx of spont bac peritonitis | paracentesis WBC>500, PMN>250, +cultures [E Coli (MC), Kleb, S Pneu, but also culture - SBP]
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| tx of spont bac peritonitis | Abx, repeat parecentesis 2-3d to see decrsd PMN (<250)
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| lab findings of coag in liver cirrhosis, tx | incrsd PT (+/- PTT), doesn't correct w K, tx: FFP
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| features of Wilson's (4) | 1) Liver: usu 1st presentation, can be hepatitis, cirrhosis; 2) eye: Kayser-Fleischer rings in cornea; 3) CNS: Cu in basal ganglia: Parksonian (resting tremor, rigidity, bradykinesia), chorea, drooling, incoord; Psych; 4) renal
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| tx of Wilson's (2) | 1) penicillamine, 2) Zn prevents Cu uptake [can be used in presympt or preg, or w penicillamine]
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| what do the deposits in hemochromo consist of | ferritin and hemosiderin
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| AD or AR: Wilsons? Hemochromo? Alpha-anti trypsin defic | all AR
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| clinical findings of hemochromo | Liver: cirrhosis; cardiac: CHF, arrhythmias; skin/joints: tanning of skin, arthritis; endo: DM (deposits in pancreas), hypothyr, hypogonad (incl impotence and amenorrhea)
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| lab iron values in hemochromo | incrsd Fe, incrsd ferritin, incrsd transferrin, decrsd TIBC
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| dx of hemochromo | liver bx is reqd
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| presentation and tx of hepatocellular adenoma | benign liver tumor in young women (15-40), assoc OCP and anabolic; tx: discont OCP, resxn tumors >5cm that don't regress after stopping OCP
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| presentation and tx of liver (cavernous) hemangioma | (MC benign liver tumor) usu small and asx (but incrs size w preg and OCP); don't bx (risk bldg); no need tx (unless sympt and high risk rupture)
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| 2 MC benign liver tumor | 1) liver (cavernous) hemangioma, 2) cholangiosarcoma
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| two types of hepatocellular carcinoma incl presentation and prognosis | 1) non-fibrolamellar (MC): assoc Hep and cirrhosis, usu unresectable and short survival; 2) fibrolamellar: seen more in adolescents and young adults, more commonly resectable, longer survival
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| risks of hepatocellular carcinoma (5) | cirrhosis (esp hep or EtOH), chemicals (alfatoxin, vinyl Cl, thorotrast), genetic: hemochromo, Wilsons, AAT defic, glycogen storage dz type1; schistosomiasis; smoking
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| hepatocellular carcinoma clinical findings other than chronic liver dz | painful hepatomegaly, also look for paraneoplastic syndromes (ie incrsd RBC, plts, Ca++, carcinoid)
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| dx of hepatocellular cancer | liver bx; imaging esp MRI/MRA if resxn; AFP used as screening tool (40-70% cases of cancer) and response to therapy
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| % of liver cancer resectable | 10%
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| describe presentation, risks for, and tx of non-EtOH steatohepatitis | histology same as EtOH liver dz, usu asx and benign w mild incrsd ALT and AST; assoc w obesity, incrsd lipids, DM; no clear tx
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| types of liver cysts and tx | 1) polycystic-seen w polycystic kidney dz, usu asx and no tx; 2) hydatid-(Echino granulosus or multilocularis), small are asx, large RUQ pain and can rupture; tx: resxn w mebendazole after
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| organism and location of liver hydatid cysts | Echino granulosus or multilocularis; in R lobe
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| types of liver abscess and organisms | 1) pyogenic: E Coli, Kleb, Proteus, Enteroccoc and anaerobes; 2) amebic: Entamoeba histolytica
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| clinical present of liver amebic abscess | F, RUQ pain, N/V, hepatosplenomegaly, diarrhea
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| dx and tx of liver abscess pyogenic | US, CT w incrsd LFTs, tx: IV Abx and percut drainage
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| dx and tx of liver amebic abscess | dx: Ig G enzyme immunoassay [E Histolytica stool Ag test is not sensitive]; tx: IV metronidazole
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| presentation and risks for Budd Chiari | occlusion hepatic veins, usu gradual course; causes: hypercoag, polycythemia and myloprolifer, preg, chronic inflamm
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| dx and tx of Budd Chiari | dx: hepatic venography; tx: balloon angioplasty w stent in IVC portocaval shunts
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| at what bilirubin level is juandice usu visible | t_bili >2
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| describe bilirubin metabolism | most bili from Hb breakdown; 1)Hb->bili in spleen=unconjugated (indirect,circulat att'd to albumin), not water sol, not in urine but can cross BBB; 2) uptake by liver; conjugated->intestine, bac produce urobilinogen/urobilin, when excess conjugated->urine
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| where is the defect for direct hyperbili? Indirect hyperbili? | indirect (unconjug)=defect before hepatic uptake; direct (conjug)=defect after hepatic uptake
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| LFTs indicating cholestasis v hepatocellular dz | cholestasis: incrsd incrsd AlkP, incrsd ALT/AST; hepatocellular: nml or sl incrsd AlkP, incrsd incrsd ALT/AST
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| ALT or AST more specific to liver | ALT is more sensitive and specific to liver dz, AST found elsewhere
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| different levels of ALT and AST and what indicate | low hundreds: chronic viral hep, acute EtOH hep; high hundreds to low thousands: acute viral hep; >10,000: hepatic necrosis (isch, acetaminophen, severe viral)
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| notes on AlkP levels wrt liver dz | not liver specific, but GGT is; incrsd when bile obstructed
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| Rx that can cause acute hep | acetaminophen, INH, methyldopa, TB meds (rifampin, pyrazinamide), tetracycline
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| types of gallstones | 1) cholesterol (yellow/green), 2) pigmented (black=in GB, hemolysis or EtOH cirrhosis; brown=ducts seen in biliary tract infxn); 3) mixed (majority)
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| causes of black and brown (pigmented) gallstones | black=in GB, hemolysis or EtOH cirrhosis; brown=ducts seen in biliary tract infxn
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| causes of cholesterol stones | obesity, DM, hyperlipid; mltpl preg, OCP; Crohn's, ileal resxn, CF; native american; incrsd age; cirrhosis
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| classic cholelithiasis sympt | RUQ/epigastric pain, classically after eating and at night; pain can go to R subscapula (Boas' sign)
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| complications of cholelithiasis | cholecystitis, choledocholithiasis, gallstone ileus
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| dx of cholelithiasis, tx | RUQ US good sensitivity and specificity for stones >2mm; if recurrent bouts then elective cholecystectomy
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| pathophysiol of acute cholecystitis | obstruction of cystic duct (not infxn) causes inflamm of GB wall (pain persists several days vs. biliary colic)
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| clinical findings of acute cholecystitis | rebound tenderness RUQ [Murphy's sign-inspiratory arrest during deep palp], pain RUQ/epigastric to R shoulder, low grade F, mild incrs WBC
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| dx acute cholecystitis | US-thickened GB wall w distended GB [CT as good as US for dx, but better for assessing cxns]; HIDA if US is inconclusive
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| abbrev for HIDA and describe HIDA for acute cholecystitis | HIDA=hepatoiminodiacetic acid; if HIDA after 4 hrs GB not visualized then acute cholecystitis
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| tx for acute cholecystitis | hydration, NPO, IV Abx and pain meds; surgery 1st 24-48hrs in most pts w sympt gallstones
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| key differences of choledocholithiasis (v cholelithiasis) | jaundice, dx w ERCP (v. US), tx w ERCP, cxns incl cholangitis, acute pancreatitis (v choledocholithiasis, gallstone ileus, cholecystitis)
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| primary v 2ry stone in choledocholithiasis | 1ry=arises in CBD, usu pigmented; 2ry=arises in GB (95%, usu chol or mixed)
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| dx of choledocholithiasis | need ERCP, (RUQ US not sensitive)
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| tx choledocholithiasis | ERCP w sphincterotomy, stone extraction, stent placement
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| pathophys and causes of cholangitis | infxn of biliary tract 2ry to obstruction; 60% stones, other:pancreatic and biliary cancers, strictures from abd surg…
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| clinical findings of cholangitis | Charcots's triad (~60%): RUQ pain, jaundice, F; Reynold's pentad: Charcots + septic shock and altered mental status **emergency!!!
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| labs cholangitis | incrsd bili, incrsd WBC, mild incrs ALT/AST
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| dx of cholangitis | RUQ US initial study (but not sensitive for stones in CBD)
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| tx cholangitis | start IV fluids and Abx, once afebrile 48hrs do ERCP/PTC to decompress
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| how know whether use ERCP or PTC in cholangitis | PTC (percut transhep cholangiography) if US shows dilated ducts, ERCP (endoscopic retrograde cholangiopancreatography) if nml duct
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| present and tx of acalculous cholecystitis | same as acute cholecystitis but w/o stone, seen in pt w severe underlying dz so difficult to recognize--emergent cholecystectomy
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| etiology and pt population for GB cancer | adenocarcinoma in elderly
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| clinical presentation of GB cancer | jaundice, biliary colic, wgt loss, RUQ mass, if palp GB advanced dz
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| risks for GB cancer | gallstones, cholecystenteric fistula, porcelin GB
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| how tx porcelin GB | prophylactically remove (50% develop cancer)
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| tx GB cancer, px | resxn (+/- wedge resxn of liver and LN); poor px bc presents late
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| bead like strictures/dilations on ERCP/PTC indicates | 1ry sclerosing cholangitis
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| 1ry sclerosing cholangitis assoc w | ulcerative colitis
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| tx of 1ry sclerosing cholangitis | no curative, can give cholestyramine for pruritus [sequesters bile acid in GI to prevent reabsorb]
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| location of problem for 1ry biliary cirrhosis | intrahep ducts
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| 1ry biliary cirrhosis assoc w | scleroderma (seen in young women w autoimmune dzs)
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| clinical present of 1ry biliary cirrhosis | pruritus early, jaundice late, xanthoma and xanthelasmata, osteoporosis, portal HTN, RUQ discomfort, fatigue
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| lab of 1ry biliary cirrhosis | cholestatic LFT (incrsd alkP), incrsd chol HDL, incrsd immunoglob M, anti-mitochondrial Abs
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| dx of 1ry biliary cirrhosis | liver bx
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| tx of 1ry biliary cirrhosis | sympt (pruritus, osteoporosis), also ursodeoxycholic acid slows progression [can do liver transplant]
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| types of cholangiosarcinoma | usu adenocarcinoma of bile ducts, 1) prox CBD (MC, Klatskin unresectable), 2) distal extrahep (most likely to be resectable), 3) intrahep (least common)
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| risk for cholangiosarcinoma | MC 1ry scl cholangitis, also UC, choledochal cysts, clonorhic sinensis infxn Hong Kong
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| clinical picture of cholangiosarcinoma, dx | clinical=obstructive jaundice, dx=ERCP/PTC +/- stent placement to relieve obstruct if unresectable
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| px cholangiosarcinoma | very poor, since most are not resectable
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| MC pts with choledochal cyst, worst cxn | more common in women, worst complication is cholangiocarcinoma
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| dx and tx of choledochal cysts | dx: US, ERCP is definitive, tx: resxn with biliary enteric anastamosis
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| what hormone causes relax of sphincter of Oddi and cxn of GB | CCK
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| how dx biliary dyskinesia; tx | HIDA: once GB filled w contrast, give CCK and calculate EF; tx: cholecystectomy or endo sphincterotomy
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| clinical present of biliary diskinesia | recurrent bil colic w/o stones
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| causes of bile duct stricture | iatrogenic, reccurent choledocholith, chronic pancreatitis, 1ry scl chol
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| cxns of bile duct stricture | 2ry bil cirrhosis, liver abscess, asc cholangitis
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| tx bile duct stricture | endostent
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| pathogen of acute appendicitis | 60% hyperplasia of lymphoid, 35% fecolith
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| peak incidence acute appendicitis, highest risk of perf | peak incidence teens-mid20's, highest rate perf in infants and elderly (and delay >24hrs)
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| clinical present of acute appendicitis | pain: epigastric to umbilicus to RLQ w rebound tenderness, low F; anorexia***; N/V
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| named signs in acute appendicitis | McBurney's pt of max pain, Rovsing: deep palp LLQ causes pain RLQ; Psoas: RLQ pain when R thigh extended; obturator: RLQ pain when flexed R thigh internally rotated
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| dx of acute appendicitis | clinical, no imaging nec [if uncertain: CT (98-100% sensitive), US (90% sensitive)]
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| characteristics of carcinoid syndrome | flushing, sweating, wheezing, diarrhea, abd pain, heart valve dysfxn
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| causes of acute pancreatitis (6), MC for kids | EtOH (40%), gallstones (40%), ERCP (10%), viral (mumps, coxB), Rx, scorpion bites; in kids: blunt trauma
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| clinical present of acute pancreatitis | epigastric pain (50% radiate to back), worse supine and after meals, N/V, anorexia; low F, hypotension, incrsd WBC
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| signs of hemorr acute pancreatitis | ecchymoses following fascial planes--Grey Turner's sign, Cullen's sign, Fox's sign
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|
||||
| dx of acute pancreatitis | amylase not sensitive or specific; lipase more specific; LFT can tell if gallstones involved; order all tests for Ranson's criteria; order CT for severe acute pancreatitis (most accurate to dx and for cxns)
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|
||||
| how abd radiograph or US helpful in acute pancreatitis | abd radiograph only helpful r/o other dx, abd US can use for seeing gallstones
🗑
|
||||
| cxns of acute pancreatitis (5) | pancreatic necrosis (sterile or infected), pan pseudo cyst, ARDS, asc cholangitis, pan abscess
🗑
|
||||
| describe 2 types of pan necrosis and how differentiate | steile and infected(hi mortality), can only differentiate w CT guided aspiration
🗑
|
||||
| how to manage pan pseudo cyst | if <5cm observe, >5cm drain
🗑
|
||||
| describe present of pan pseudo cyst | appears 2-3wks after acute pancreatitis, can be remote to pancreas, not a true cyst bc lacks epithelial lining; CT is best for dx [if <5cm observe, >5cm drain]
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|
||||
| name Ranson's criteria for acute pancreatitis | GA LAW Glu>200; age>55, LDH>350, AST>250, WBC>16,000; if >3 acute pancreatitis is likely and admit to ICU
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|
||||
| initial 48 hrs Ranson's criteria for acute pancreatitis | C HOBBS= Ca++<8; Hct decrsd by >10%; PaO2 <60; BUN incrsd >8, Base defic >4; sequest fluid >6L
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|
||||
| causes of chronic pancreatitis | almost all EtOH (80%)
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|
||||
| clinical present of chronic pancreatitis | chronic epigastric pain + Ca++ on plain abd radio=dx; also steatorhhea, DM, Ca++; clinical same as in acute w epigastric pain 50% radiate to back, often N/V, pain can be aggravate by eating, drinking
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|
||||
| dx chronic pancreatitis | CT (can show Ca++ not evident on plain radio; but nml CT doesn’t r/o dx); ERCP is gold standard; labs not helpful bc lipase and amylase are not elevated
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| cxns of chronic pancreatitis | narcotic abuse, DM, malab/steatorrhea (late) B12 defic, pseudocyst, pan cancer
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|
||||
| tx chronic pancreatitis | pain, NPO, insulin, pan enzymes WITH H2 block (so gastrin doesn't degrade enzymes you're supplementing); surgery just for pain management (pancreaticojejunostomy to decompress, also Whipple, pan resxn)
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| describe Whipple procedure | removal of distal 1/2 stom, GB w cystic and CBD, head of pancreas, duo, and prox jejunum; connect pancreas and hepatic duct to duodenum
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|
||||
| describe pt population and anatomy of pan cancer | MC in elderly, more common in AA; pan head (75%), pan body (20%), tail
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|
||||
| risks for pan cancer | **smoking, chronic pan, DM, heavy EtOH, chemicals (benzidine, naphythylamine-both also assoc bladder cancer)
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|
||||
| clinical present of pan cancer | abd pain, jaundice (if head of pan, in adv dz), Couravoiser's sign=palp GB w/o pain (30% cancers of head), migratory thrombophlebitis (Trousseau's sign--also seen adeno of lung)
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|
||||
| dx of pan cancer; tumor mrkrs | ERCP; CA 19-9 & CEA (CA 19-9 much more sensitive and specific)
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|
||||
| tx pan cancer | resxn (Whipple's) but only 10% resectable and poor px even w resxn; should stent during ERCP if non-resectable and bil obstruction
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|
||||
| causes of upper GI bldg (5) | PUD (duo ulcer 25%, gastric ulcer 20%, gastritis 25%), esophag varices 10%, Mallory Weiss, aortoenteric fistula, neoplasm
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|
||||
| tests to order for various types of GI bldg: hematemesis, hematochezia, melena, occult blood | hematemesis: upper GI endo, hematochezia: r/o hemorrhoids then colonoscopy, melena: upper endo, occult blood: colonoscopy
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|
||||
| what does coffee grounds emesis suggest | upper GI bleed, but slower rate
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|
||||
| causes of lower GI bleeding (5) | diverticulosis (40%--MC for pts <60), angiodyspl (40%, MC for pts >60), IBD, polyps, colon cancer
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|
||||
| how dx small GI bleeding; how might present | dx by excluding upper GI and colon bleeding; can present as either melena or hematochezia
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|
||||
| causes of dark stools other than melena (5) | Bismuth (bismuth subsalicylate is Pepto-bismol and kaopectate anti-diarrheal), Fe, spinach, charcoal, licorice
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|
||||
| how does BUN: Cr help dx GI bleeding | BUN:Cr is incrsd in upper GI bleeds if nml renal fxn
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|
||||
| how is NG tube aspirate useful for dx GI bleeding | can tell upper GI bleeding, but doesn't catch duo bleeding
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|
||||
| where is lig of trietz, why impt for GI bleeding | is marker dividing duo and jejunum, prox to lig of Trietx is considered an upper GI bleed
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|
||||
| tx of upper GI bldg | EGD w coag, if bleeding cont may need surgical intervention
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|
||||
| tx of lower GI bldg | colonoscopy-polyp excision and laser/cautery, arteriography can inject vasoconstrict
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|
||||
| indications for surgery for GI bldg (4) | hemo unstable not responsive to fluids, severe initial bldg or recurrence after endo tx, cont'd bldg after 24hrs, visible vessel at base of ulcer (hi risk recurrence)
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|
||||
| types of esophageal cancer and who they occur in | squamos cell-more common in AA, smoking EtOH, usu upper and mid esophag; adeno-more common in Caucasian men with GERD and Barretts in distal 1/3
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|
||||
| risks for squamos cell cancer of esophag | EtOH, smoking, nitrosamines, betel nuts, achalasia, Plummer-Vinson
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|
||||
| risks for adeno esophag cancer | GERD and Barretts
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|
||||
| staging for esophag cancer | I: lamina propria or submucosa, IIa: muscul propria or adventitia; IIb: up to muscul propria w regional LN; III: adventitia w regional LN; IV: mets
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|
||||
| clinical present of esophag cancer | MC: dysphagia, 2nd MC: wgt loss, also odynophagia (late, suggesting extra esophag involvement)
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|
||||
| dx of esophag cancer | Barium swallow to evaluate dysphagia; upper endo w bx and brush cytol for dx, TE US for staging, need full met w/u (CT, CXR, bone scan)
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|
||||
| tx esophag cancer | usu palliation bc often adv dz; chemo and radiation before surgery prolongs survival; I and IIA surgery can be curative
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|
||||
| pathophysiol of achalasia | LES doesn't relax completely w swallowing
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|
||||
| cause of achalasia | usu idiopathic, no. 2 stomach adeno (but Chagas impt world wide)
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|
||||
| clinical present of achalasia | dysphagia of solids=liquids (unlike esophag cancer); may aspriate bc of regurg
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|
||||
| type of dysphagia seen in esophag cancer | solids first, then liquids
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|
||||
| cxns of achalasia | esophag cancer (SCC), so surveillance esophagoscopy
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|
||||
| dx achalasia | mannometry showing 1) incomplete relax of LES, 2) aperistalsis of esophag
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|
||||
| Rx tx for achalasia | injxn botulinum into LES (effective 65%, but rept q2 yrs), subling NG can help early for short-term tx; anti muscarinics, ie dicyclomine) not helpful
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|
||||
| 3 tx strategies for achalasia | 1) Rx (esp botulinum), 2) dilation (5% risk perf), 3) surgical (Heller myotomy, incise muscle of LES, often if dilation doesn't work)
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|
||||
| describe pathophys and dx of diffuse esophag spasm | LES nml, several sections of esophag contract at once (by mannometry)
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|
||||
| clinical present of diffuse esophag spasm | non-cardiac chest pain, dysphagia (but w/o regurg)
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|
||||
| corkscrew esophag indicates? | diffuse esophag spasm (v birds beak of achalasia)
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|
||||
| tx of diffuse esophag spasm | nitrates and CCB (decrs amplit of cxns), TCA may help sympt
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|
||||
| types of esophag hiatal hernias | 1) sliding (>90%, assoc w GERD) both stomach and GEJ; 2) paraesophag: just stomach at risk strangulation so need surgery
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|
||||
| cxns of sliding esophag hiatal hernia | GERD, reflux esophagitis, Barrettes/cancer, aspiration
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|
||||
| dx of esophag hiatal hernia | Ba upper GI + upper endo
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|
||||
| tx of esophag hiatal hernias | 1)sliding: antacids, sm meals, elevate head after eat, may need Niessens fundoplication in 15%; 2) paraeso: sx
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|
||||
| differentiate Mallory Weiss Tears and Boerhaaves | Mallory Weiss=mucosal tear at GEJ; Boerhaaves=transmural esophag perf
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|
||||
| tx of Mallory Weiss tears | 90% stop spont, may do angiographic embol, acid suppression aids healing
🗑
|
||||
| describe Plummer Vinson syndrome | upper esophag web (dysphagia), Fe defic anemia, spoon shaped nails [koilonychia], atrophic oral mucosa
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|
||||
| cxns of Pulmmer Vinson syndrome | risk of SCC or oral, esophag
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|
||||
| tx of Plummer Vinson | esophag dilation, tx of anemia
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|
||||
| describe Shatzki ring and tx | circum ring in distal esophag, always w sliding hernia; usu asympt but if sympt w/o reflux can esophag dilate, w/ reflux use reflux sx
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|
||||
| what is Shatzki's ring assoc w | digestion of toxic agents, acids, bases (alkali are worse bc full thickness liquefactive necrosis)
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|
||||
| types of esophag diverticuli and cause for ea(3) | Zenkers (upper 1/3, failure of cricopharyng mscl relax), epiphrenic (distal 1/3, spastic esphog or achalasia), traction (mid, from mediastinum inflamm, TB)
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|
||||
| tx for ea type of esophag diverticuli (3) | [for ea treat underlying motility dz, diverticulotomy is 2ry] Zenkers-cricopharyngmyotomy; traction-none, asx; epiphrenic-esophagomyotomy
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|
||||
| clinical present of esophag perf | severe retrosternal/chest/shoulder pain, tachycard, tachypnea/dyspnea, F, Hamman's sign (crunch as heart beating ag air filled space)
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|
||||
| dx esophag perf | contrast esophagram using Gatrografin
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|
||||
| tx of esophag perf | if small and pt stable: IV fluids, NPO, Abx, H2 block; if large perf or goes into pleura need surgery w/in 24 hrs
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|
||||
| clinical present of Zenkers diverticul | dysphagia, regurg, halitosis, chronic cough
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|
||||
| cxns of Shatzki | stricture and esophag cancer
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|
||||
| define Hamman's sign | crunching sound as heart beats ag air filled spaces in context of esophag perf
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|
||||
| describe key factors duo ulcers: % of ulcers, acid sxn, cause, age, blood type, pain wrt eating | 75% of ulcers, acid sxn nml or incrsd, cause H Pylori, age younger (40s), blood type O, pain better w eating but then gets worse 2-3 hrs and often nocturnal sympt
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|
||||
| describe key factors gastric ulcers: % of ulcers, acid sxn, cause, age, blood type, pain wrt eating | 25% of ulcers, acid sxn nml or decrsd, cause NSAIDs although also H Pylori, age older (50s), blood type A, pain worse w eating
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|
||||
| describe locations of duo ulcers (1) and gastric ulcers (4) | duo: 1-2 cm distal pylorus; gastric: I(70%) lesser curv, II: gastric and duo, III: prepyloric, IV: near esophagogastric jxn
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|
||||
| dx of PUD | 1) endoscopy (need for bx gastric, for tx acute bleeding) also can dx H Pylori, 2) H Pylori dx: urease breath test, Abs in serum to H Pylori doesn't mean acute infxn, 3) serum gastrin levels if suspect ZES
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|
||||
| tx of PUD--pt care/preventative | no NSAIDs or ASA, no EtOH or smoking, no eating before bed
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|
||||
| tx of PUD--Rx | PPI (prazole), H2 block aids healing ulcers (tidine), antacids just used supplement for sympt; tx of H Pylori infxn as nec
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|
||||
| tx of PUD--cytoprotective Rx | sucralfate, misoprosol (use w NSAID)
🗑
|
||||
| if pt on NSAID and develop PUD, what do | if possible switch to acetominophen, if need to stay on NSAIDs, put them on misoprosol
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|
||||
| what's triple therapy for H Pylori (generally)? What's quad therapy? | triple=PPI+2Abx for 2 wks; quad=PPI, bismuth, 2Abx for 1 wk
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|
||||
| a specific ex of triple therapy for H Pylori | amoxicillin, clarithromycin, omeprazole (PPI)
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|
||||
| causes of acute gastritis | NSAIDs/ASA, H Pylori, EtOH, heavy smoking or caffeine, extreme stress (shock, sepsis, burn)
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|
||||
| tx of acute gastritis | if no red flags tx empiric acid suppression and discont any NSAIDs; if doesn't respond 4-8 wks do upper GI, US (stones), and dx H Pylori
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|
||||
| types of chronic gastritis, incl %, location, causes, and risks | A (10%): fundus, auto Abs to parietal cells and IF assoc w pernicious anemia and thyroiditis, risk gastric cancer; B(90%): antrum, NSAID or H Pylori, incrsd risk PUD and gastric cancer
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|
||||
| dx of chronic gastritis | upper GI endo w bx, test H Pylori
🗑
|
||||
| types of gastric cancer (2) and risks | 1) intestinal type, from gastric mucosal cells, risks: nitrites, salts, H Pylori, chronic gastritis; 2) diffuse: poorly difftd, risks unknown but not H Pylori or chronic gastritis
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|
||||
| morphologies of gastric cancer (4) | ulcerative, polypoid, superficial spreading (most favorable px), linitis plastica leather bottle infiltrates early through all layers, stomach wall is thick and rigid, poor px
🗑
|
||||
| part of world gastric cancer MC | Japan, very rare in US
🗑
|
||||
| risks for gastric cancer (8) | gastritis, adenamatous gastric polyps, H Pylori, pern anemia, preserved foods (w salts, nitrites, smoked fish), Menetrier, postantrectomy (s/p Billroth II), blood type A
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|
||||
| tx gastric cancer | resxn w wide (>5cm) margins and extended LN dissection, +/- chemo
🗑
|
||||
| Krukengergs tumor | gastric cancer met to ovary
🗑
|
||||
| Blumer's shelf | gastric cancer rectum met, palp on DRE
🗑
|
||||
| Sister Mary joseph nodule | gastric cancer met periumbilical LN
🗑
|
||||
| Virchow's node | gastric cancer met to supraclaviular LN
🗑
|
||||
| Irish's node | gastric cancer met to left axillary
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|
||||
| name some of the named mets for gastric cancer (5) | Krukengerg (ovary), Blumer (rectum), Sister Mary Joseph (periumbil), Virchow (supraclavicular), Irish (L axillary)
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|
||||
| closed v open loop small bowel obstruct, and why impt differentiation | closed=lumen occluded at 2 pts, can compromise blood supply
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|
||||
| diffs in clin presentation of prox v distal small bowel obstruct | prox=freq vomit, severe pain, min abd distension; distal=vomit less freq, abd distension
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|
||||
| causes of small bowel obstruction | 1=adhesion, 2=incarcerated hernia, also malignancy, Crohns, SMA syndrome
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|
||||
| tx of small bowel obstruct | if incomplete obstruct and no F, incrsd WBC, or peritoneal signs: IV fluids, correct K (usu low), Abx, NG tube to decompress stomach; otherwise surgery (resect as nec and lyse adhesions)
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|
||||
| metabolic changes seen in sm bowel obstruct | usu low K low Cl metabolic alk and hypovol from vomitting
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|
||||
| causes of large bowel obstruct | volvulus, adhesions, hernias, ***MC: colon cancer
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|
||||
| define paralytic ileus | decrsd or absent peristalsis w/o mech obstruction
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|
||||
| causes of paralytic ileus | Rx (narcotic, anti chol), post op abd sx, spinal cord, shock, metabolic (low K), peritonitis
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|
||||
| dx of paralytic ileus | abd radio shows uniform gas, failure to pass contrast beyond a point is dx
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|
||||
| tx of paralytic ileus | usu resolves over time, IV fluids, correct K, NG suction if nec or long tube if persists
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|
||||
| clinical present of celiac sprue; bx | abd distension, bloating, diarrhea; small bowel bx shows flattened villi
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|
||||
| differential in general presentation of UC v Crohns | UC is usu bloody diarrhea, F and wgt loss only in more severe; Crohns diarrhea usu w/o blood and F and malaise common, along w wgt loss and malabsorb
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|
||||
| cryst abscess of PMN indicates which IBD | UC
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|
||||
| location of UC and Crohns in GI | Crohns anywhere in GI but MC terminal ileum, UC always involves rectum +/- colon (no skip lesions)
🗑
|
||||
| extra GI findings more common in Crohns | skin: erythema nodosum, gallstones and kidney stones
🗑
|
||||
| extra GI findings more common in UC | skin: pyoderma gangrenosum, arthritis: ankyl spondylitis, sclerosing cholangitis
🗑
|
||||
| extra GI findings seen in both UC and Crohns | eyes: episcleritis and uveitis, arthritis: migrating monoarticular, sacroilitis, hypercoag, ITP, osteoporosis
🗑
|
||||
| which extra GI findings in IBD often parallel bowel severity | episcleritis, monoarticular arthritis, skin
🗑
|
||||
| dx of IBD | endoscopy, r/o infxs causes of diarrhea
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|
||||
| cxns of Crohns | fistula, SBO (MC need for sx), gallstones, kidney stones, malabsorb, aphthous ulcers lips, gingiva, buccal mucosa
🗑
|
||||
| cxns of UC | colon cancer, sclerosing cholangitis, cholangiosarcoma, toxic megacolon, Fe defic anemia and lytes (diarrhea)
🗑
|
||||
| tx of IBD | acute exacerb: systemic steroids; sulfsalazine if colon is involved in Crohns and for all UC; +/- immunosuppressive; sx: only for cxns in Crohns but can be curative for UC
🗑
|
||||
| 2 types of hemorrhoids and where occur, which vessels | external-inferior hemorrhoidal plexus veins distal to dentate line (sensate);internal-superior rectal plexus submucosal ceins above dentate (insensate)
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| how tell EtOH hep by labs | AST > 2x ALT
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|
||||
| Hep A: transmission, longterm sequelae, lab diagnosis | foodborn; no longterm sequelae; IgM HAV +
🗑
|
||||
| Hep E: transmission, longterm sequelae | food/water transmission; no chronic infxn **but often fatal pregnant women
🗑
|
||||
| Hep B: transmission, longterm sequelae | needles, sex, perinatal; chronic hep B can lead to cirrhosis and hepatocellular cancer
🗑
|
||||
| Hep C transmission, longterm sequelae | blood to blood transmission, cirrosis, liver cancer
🗑
|
||||
| which Hep have vaccines | Hep A, B (not C)
🗑
|
||||
| which Hep requires another Hep to infect a person | Hep D needs Hep B +
🗑
|
||||
| which Hep assoc w urticaria and polyarteritis nodosa | Hep B
🗑
|
||||
| which Hep assoc w mebranoprolifer glomerulonephritis | Hep C
🗑
|
||||
| which Hep assoc w cirrhosis and cancer | Hep B, C, D
🗑
|
||||
| which Hep can cause chronic hepatitis | Hep B, C, D
🗑
|
||||
| Hep C Ab indicates what | only history of infxn, need to test RNA to see if current infxn [or HB sAb=resolved]
🗑
|
||||
| define the difft Hep B Abs and significance | HepB sAg=unresolved, HB sAb=immune/resolved, HBcAb=new infxn, HBeAg=infectivity
🗑
|
||||
| what Ab look for to determine chronic Hep B | HepB sAg
🗑
|
||||
| what Ab indicates new HepB infxn | HepB cAb
🗑
|
||||
| how treat chronic Hep B | interferon, lamivudine, adefovir
🗑
|
||||
| what can you give to pt exposed to Hep B | Hep IgG
🗑
|
||||
| what Rx can cause hepatitis | TB meds (rifampin, INH, pyrazinamide), acetaminophen, tetracycline, methyldopa
🗑
|
||||
| how treat chronic Hep C | peginterferon, ribavirin (v. interferon and lamivudine for Hep B)
🗑
|
||||
| name hereditary forms of hep | Wilson's (copper in liver); hemochromatosis, alpha anti-trypsin defic; Budd Chiari (occlusion IVC or hepatic veins)
🗑
|
||||
| describe Budd Chiari--pathophysiol, sequelae, assoc | occlusion of IVC or hep veins leads to congested liver; assoc w polycythemic vera, preg, and hepato cell cancer
🗑
|
||||
| describe alpha anti-trypsin defic--pathophysiol, clinical picture | misfolding protein in hepatocells' ER, decrsd elastic in lungs--> emphysema and PAS + globules in liver; clinical=cirrhosis+emphysema
🗑
|
||||
| treatment of hemochromatosis | (aka bronze DM) phlebotomy and deferoxamine
🗑
|
||||
| path signs of Wilsons | Copper in basal ganglia, Kaysar Fleischer rings in eyes
🗑
|
||||
| pathophysiol of Wilsons | copper in basal ganglia leads to hepatolenticular defen, copper in liver leads to cirrhosis
🗑
|
||||
| lab values for Wilsons, treatment | decrsd ceruloplasmin, tx w penicillamine
🗑
|
||||
| clinical features of hemochromatosis | cirrhosis of liver, bronzed skin (bronzed DM), DM due to pancreatic islet cell failure, cardiomyopathy, arthritis (Fe deposition in joints)
🗑
|
||||
| define Dubin Johnson; what findings? | problem excreting bilirubin; have benign black liver and elevated conjugated bilirubin w/o incsrd liver enz
🗑
|
||||
| define Rotor's syndrome; what findings? | problem excreting bilirubin; have benign black liver and elevated conjugated bilirubin w/o incsrd liver enz
🗑
|
||||
| what are lab findings indicating cholestasis? | incrsd alk P and bilirubin (+/- incrsd ALT, AST)
🗑
|
||||
| what can caused incrsd unconjugated bili? | 1) overproduction (hemolytic anemia), 2) defective conjugation (Gilbert, Crigler-Najar)
🗑
|
||||
| define Gilbert's syndrome; what findings? | asympt, stress-induced problem conjugating bili (decrsd UDP glucuronyltrxs); incrsd (isolated) unconjug bili
🗑
|
||||
| define Crigler-Najar's syndrome; what findings? | problem UDP glucuronyltrxs conjugating bili; type I die in first yrs, type II not as bad, tx phenobarbital
🗑
|
||||
| does unconjugated or conjugated bili appear in the urine | conjugated
🗑
|
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ehstephns
Popular Midwifery sets