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GI USMLE

QuestionAnswer
etiology of colon cancer adenocarcinoma
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
MC place of met for colon cancer liver (as w all GI cancers)
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
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
grading colon cancer duke's criteria: A=mucosa, B=past mucosa w/o LN, C=regional LN, D=mets
tx colon cancer measure CEA, then surgical resxn; colon stage C: also give 5FU+leucovirin; rectal if B2 or C give 5FU +radiation
when use radiation in colon cancer only rectal, not colon
how/when use CEA to monitor recurrence colon cancer, when do recurrences occur check CEA q3-6mos, 90% recurrences occur within 3yrs
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
MC location of colon polyps rectosigmoid
cxns of diverticulosis v diverticulitis diverticulosis: painless bldg, diverticulitis; diverticulitis: obstruction, abscess, fistula
risks of diverticulosis (3) low fiber, fam hx, incrsd age
MC location of diverticulosis sigmoid colon
sympt of diverticulosis (usu asx) vague LLQ discomfort, may have painless bldg that usu stops spont (no tx nec)
dx for diverticulosis ba enema
tx for diverticulosis hi fiber diet or psyllium (has mucilage)
sympt of diverticulitis F, LLQ pain, incrsd WBC
dx for diverticulitis CT scan w contrast--not ba enema or colonoscopy bc risk of perf
tx for diverticulitis IV fluids and Abx, NPO, mild episodes can be outpatient; if sympt persist 3-4d or recurrence need surgery
angiodyspl of colon is due to what etiol? Is assoc w what cardiac defect? AVM, assoc w AV stenosis
how does angiodysp of colon present? In whom? Dx, tx? presents as lower GI bldg in pt>60, dx colonoscopy, tx: stops spont
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
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
presentation, tx of arterial thrombus acute mesenteric isch more gradual present in pts w CAD, PVD; tx: papaverine during arteriography
presentation, tx of nonocclusive acute mesenteric isch pts w low CO, critically ill, elderly; tx: papaverine during arteriography
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
clinical features of acute mesenteric isch abd pain >> physical findings
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
what Rx should be avoided in acute mesenteric isch vasopressors, they make isch worse
what metabolic derangement may be seen in acute mesenteric isch lactic acidosis
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
dx and tx for chronic mesenteric isch dx: mesenteric arteriography; tx: revasc surgery
what's Ogilvie's syndrome? signs/sympt of large bowel obstruction, but no evidence of mechanical obstruction
what's Ogilvie's syndrome assoc w? recent surgery or trauma, sepsis, malig, Rx (narcotics, psych, antichol)
tx for Ogilvie's syndrome? start w gentle enemas & NG suction, then colonoscopic decompression [stop Rx if that's suspected]
when is immed colonoscopic decompression called for in Ogilvie's syndrome if colon diam >10cm (bowel rupture risk)
etiol of pseudomem colitis C dif overgrowth after Abx
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]
clinical present of pseudomem colitis? Cxns? profuse, watery diarrhea, crampy Abd pain; risk: toxic megacolon
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
tx pseudomem colitis discont Abx, start metronidazole (but not in preg or kids; back up is vanc); cholestryramine can help w diarrhea
after pseudomem colitis has been tx, when might it recur 2-8wks after discont Abx
MC location of colonic volvulus sigmoid colon (same as location colonic polyps), but also can occur in cecum
clinical present of colonic volvulus acute onset colicky abd pain, constipation w abd distension; anorexia N/V
tx for 2 types of colonic volvulus 1) sigmoid: decompress w sigmoidoscopy, elective resxn; 2) cecal: emergent resxn
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
what would barium enema show for colonic volvulus bird's beak at location of volvulus
when should barium enema NOT be used in colonic volvulus work up if suspect strangulation
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)
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
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
top 2 causes of liver cirrhosis 1=EtOH, 2=chronic hep,
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
metabolic/genetic causes of liver cirrhosis hemochromatosis, Wilson's, alpha-anti trypsin defic
Rx causing liver cirrhosis (2) acetaminophen and methotrexate
classic clinical signs of liver cirrhosis ascites, varices, gynecomastia, palmar erythema, spider angioma, hemorrhoids
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
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
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
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
long term tx for varices in liver cirrhosis beta blockers to prevent rebleeding
pathophysiol and clinical findings of ascites in liver cirrhosis due to portal HTN and hypoalbumin; abd distension, shifting dullness, fluid wave
indications for parecentesis; what in parecentesis indicates portal HTN new onset, worsening ascites, or r/o SBP; serum:ascites albumin >1.1= portal HTN
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
differential ascites (6) cirrhosis/portal HTN, CHF, CRF, TB peritonitis, cancer, hypoalbumin
gold standard for liver cirrhosis liver bx
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
describe hepatorenal syndrome, lab findings, tx from renal hypoperfusion; incrsd BUN, Cr, decrsd Na and U_Na, hypotension, oliguria; tx: liver transplant
clinical findings of spont bac peritonitis ascites + abd pain, F, vomit, rebound tenderness
dx of spont bac peritonitis paracentesis WBC>500, PMN>250, +cultures [E Coli (MC), Kleb, S Pneu, but also culture - SBP]
tx of spont bac peritonitis Abx, repeat parecentesis 2-3d to see decrsd PMN (<250)
lab findings of coag in liver cirrhosis, tx incrsd PT (+/- PTT), doesn't correct w K, tx: FFP
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
tx of Wilson's (2) 1) penicillamine, 2) Zn prevents Cu uptake [can be used in presympt or preg, or w penicillamine]
what do the deposits in hemochromo consist of ferritin and hemosiderin
AD or AR: Wilsons? Hemochromo? Alpha-anti trypsin defic all AR
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)
lab iron values in hemochromo incrsd Fe, incrsd ferritin, incrsd transferrin, decrsd TIBC
dx of hemochromo liver bx is reqd
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
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)
2 MC benign liver tumor 1) liver (cavernous) hemangioma, 2) cholangiosarcoma
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
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
hepatocellular carcinoma clinical findings other than chronic liver dz painful hepatomegaly, also look for paraneoplastic syndromes (ie incrsd RBC, plts, Ca++, carcinoid)
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
% of liver cancer resectable 10%
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
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
organism and location of liver hydatid cysts Echino granulosus or multilocularis; in R lobe
types of liver abscess and organisms 1) pyogenic: E Coli, Kleb, Proteus, Enteroccoc and anaerobes; 2) amebic: Entamoeba histolytica
clinical present of liver amebic abscess F, RUQ pain, N/V, hepatosplenomegaly, diarrhea
dx and tx of liver abscess pyogenic US, CT w incrsd LFTs, tx: IV Abx and percut drainage
dx and tx of liver amebic abscess dx: Ig G enzyme immunoassay [E Histolytica stool Ag test is not sensitive]; tx: IV metronidazole
presentation and risks for Budd Chiari occlusion hepatic veins, usu gradual course; causes: hypercoag, polycythemia and myloprolifer, preg, chronic inflamm
dx and tx of Budd Chiari dx: hepatic venography; tx: balloon angioplasty w stent in IVC portocaval shunts
at what bilirubin level is juandice usu visible t_bili >2
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
where is the defect for direct hyperbili? Indirect hyperbili? indirect (unconjug)=defect before hepatic uptake; direct (conjug)=defect after hepatic uptake
LFTs indicating cholestasis v hepatocellular dz cholestasis: incrsd incrsd AlkP, incrsd ALT/AST; hepatocellular: nml or sl incrsd AlkP, incrsd incrsd ALT/AST
ALT or AST more specific to liver ALT is more sensitive and specific to liver dz, AST found elsewhere
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)
notes on AlkP levels wrt liver dz not liver specific, but GGT is; incrsd when bile obstructed
Rx that can cause acute hep acetaminophen, INH, methyldopa, TB meds (rifampin, pyrazinamide), tetracycline
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)
causes of black and brown (pigmented) gallstones black=in GB, hemolysis or EtOH cirrhosis; brown=ducts seen in biliary tract infxn
causes of cholesterol stones obesity, DM, hyperlipid; mltpl preg, OCP; Crohn's, ileal resxn, CF; native american; incrsd age; cirrhosis
classic cholelithiasis sympt RUQ/epigastric pain, classically after eating and at night; pain can go to R subscapula (Boas' sign)
complications of cholelithiasis cholecystitis, choledocholithiasis, gallstone ileus
dx of cholelithiasis, tx RUQ US good sensitivity and specificity for stones >2mm; if recurrent bouts then elective cholecystectomy
pathophysiol of acute cholecystitis obstruction of cystic duct (not infxn) causes inflamm of GB wall (pain persists several days vs. biliary colic)
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
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
abbrev for HIDA and describe HIDA for acute cholecystitis HIDA=hepatoiminodiacetic acid; if HIDA after 4 hrs GB not visualized then acute cholecystitis
tx for acute cholecystitis hydration, NPO, IV Abx and pain meds; surgery 1st 24-48hrs in most pts w sympt gallstones
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)
primary v 2ry stone in choledocholithiasis 1ry=arises in CBD, usu pigmented; 2ry=arises in GB (95%, usu chol or mixed)
dx of choledocholithiasis need ERCP, (RUQ US not sensitive)
tx choledocholithiasis ERCP w sphincterotomy, stone extraction, stent placement
pathophys and causes of cholangitis infxn of biliary tract 2ry to obstruction; 60% stones, other:pancreatic and biliary cancers, strictures from abd surg…
clinical findings of cholangitis Charcots's triad (~60%): RUQ pain, jaundice, F; Reynold's pentad: Charcots + septic shock and altered mental status **emergency!!!
labs cholangitis incrsd bili, incrsd WBC, mild incrs ALT/AST
dx of cholangitis RUQ US initial study (but not sensitive for stones in CBD)
tx cholangitis start IV fluids and Abx, once afebrile 48hrs do ERCP/PTC to decompress
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
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
etiology and pt population for GB cancer adenocarcinoma in elderly
clinical presentation of GB cancer jaundice, biliary colic, wgt loss, RUQ mass, if palp GB advanced dz
risks for GB cancer gallstones, cholecystenteric fistula, porcelin GB
how tx porcelin GB prophylactically remove (50% develop cancer)
tx GB cancer, px resxn (+/- wedge resxn of liver and LN); poor px bc presents late
bead like strictures/dilations on ERCP/PTC indicates 1ry sclerosing cholangitis
1ry sclerosing cholangitis assoc w ulcerative colitis
tx of 1ry sclerosing cholangitis no curative, can give cholestyramine for pruritus [sequesters bile acid in GI to prevent reabsorb]
location of problem for 1ry biliary cirrhosis intrahep ducts
1ry biliary cirrhosis assoc w scleroderma (seen in young women w autoimmune dzs)
clinical present of 1ry biliary cirrhosis pruritus early, jaundice late, xanthoma and xanthelasmata, osteoporosis, portal HTN, RUQ discomfort, fatigue
lab of 1ry biliary cirrhosis cholestatic LFT (incrsd alkP), incrsd chol HDL, incrsd immunoglob M, anti-mitochondrial Abs
dx of 1ry biliary cirrhosis liver bx
tx of 1ry biliary cirrhosis sympt (pruritus, osteoporosis), also ursodeoxycholic acid slows progression [can do liver transplant]
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)
risk for cholangiosarcinoma MC 1ry scl cholangitis, also UC, choledochal cysts, clonorhic sinensis infxn Hong Kong
clinical picture of cholangiosarcinoma, dx clinical=obstructive jaundice, dx=ERCP/PTC +/- stent placement to relieve obstruct if unresectable
px cholangiosarcinoma very poor, since most are not resectable
MC pts with choledochal cyst, worst cxn more common in women, worst complication is cholangiocarcinoma
dx and tx of choledochal cysts dx: US, ERCP is definitive, tx: resxn with biliary enteric anastamosis
what hormone causes relax of sphincter of Oddi and cxn of GB CCK
how dx biliary dyskinesia; tx HIDA: once GB filled w contrast, give CCK and calculate EF; tx: cholecystectomy or endo sphincterotomy
clinical present of biliary diskinesia recurrent bil colic w/o stones
causes of bile duct stricture iatrogenic, reccurent choledocholith, chronic pancreatitis, 1ry scl chol
cxns of bile duct stricture 2ry bil cirrhosis, liver abscess, asc cholangitis
tx bile duct stricture endostent
pathogen of acute appendicitis 60% hyperplasia of lymphoid, 35% fecolith
peak incidence acute appendicitis, highest risk of perf peak incidence teens-mid20's, highest rate perf in infants and elderly (and delay >24hrs)
clinical present of acute appendicitis pain: epigastric to umbilicus to RLQ w rebound tenderness, low F; anorexia***; N/V
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
dx of acute appendicitis clinical, no imaging nec [if uncertain: CT (98-100% sensitive), US (90% sensitive)]
characteristics of carcinoid syndrome flushing, sweating, wheezing, diarrhea, abd pain, heart valve dysfxn
causes of acute pancreatitis (6), MC for kids EtOH (40%), gallstones (40%), ERCP (10%), viral (mumps, coxB), Rx, scorpion bites; in kids: blunt trauma
clinical present of acute pancreatitis epigastric pain (50% radiate to back), worse supine and after meals, N/V, anorexia; low F, hypotension, incrsd WBC
signs of hemorr acute pancreatitis ecchymoses following fascial planes--Grey Turner's sign, Cullen's sign, Fox's sign
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)
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]
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
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
causes of chronic pancreatitis almost all EtOH (80%)
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
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
cxns of chronic pancreatitis narcotic abuse, DM, malab/steatorrhea (late) B12 defic, pseudocyst, pan cancer
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)
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
describe pt population and anatomy of pan cancer MC in elderly, more common in AA; pan head (75%), pan body (20%), tail
risks for pan cancer **smoking, chronic pan, DM, heavy EtOH, chemicals (benzidine, naphythylamine-both also assoc bladder cancer)
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)
dx of pan cancer; tumor mrkrs ERCP; CA 19-9 & CEA (CA 19-9 much more sensitive and specific)
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
causes of upper GI bldg (5) PUD (duo ulcer 25%, gastric ulcer 20%, gastritis 25%), esophag varices 10%, Mallory Weiss, aortoenteric fistula, neoplasm
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
what does coffee grounds emesis suggest upper GI bleed, but slower rate
causes of lower GI bleeding (5) diverticulosis (40%--MC for pts <60), angiodyspl (40%, MC for pts >60), IBD, polyps, colon cancer
how dx small GI bleeding; how might present dx by excluding upper GI and colon bleeding; can present as either melena or hematochezia
causes of dark stools other than melena (5) Bismuth (bismuth subsalicylate is Pepto-bismol and kaopectate anti-diarrheal), Fe, spinach, charcoal, licorice
how does BUN: Cr help dx GI bleeding BUN:Cr is incrsd in upper GI bleeds if nml renal fxn
how is NG tube aspirate useful for dx GI bleeding can tell upper GI bleeding, but doesn't catch duo bleeding
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
tx of upper GI bldg EGD w coag, if bleeding cont may need surgical intervention
tx of lower GI bldg colonoscopy-polyp excision and laser/cautery, arteriography can inject vasoconstrict
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)
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
risks for squamos cell cancer of esophag EtOH, smoking, nitrosamines, betel nuts, achalasia, Plummer-Vinson
risks for adeno esophag cancer GERD and Barretts
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
clinical present of esophag cancer MC: dysphagia, 2nd MC: wgt loss, also odynophagia (late, suggesting extra esophag involvement)
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)
tx esophag cancer usu palliation bc often adv dz; chemo and radiation before surgery prolongs survival; I and IIA surgery can be curative
pathophysiol of achalasia LES doesn't relax completely w swallowing
cause of achalasia usu idiopathic, no. 2 stomach adeno (but Chagas impt world wide)
clinical present of achalasia dysphagia of solids=liquids (unlike esophag cancer); may aspriate bc of regurg
type of dysphagia seen in esophag cancer solids first, then liquids
cxns of achalasia esophag cancer (SCC), so surveillance esophagoscopy
dx achalasia mannometry showing 1) incomplete relax of LES, 2) aperistalsis of esophag
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
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)
describe pathophys and dx of diffuse esophag spasm LES nml, several sections of esophag contract at once (by mannometry)
clinical present of diffuse esophag spasm non-cardiac chest pain, dysphagia (but w/o regurg)
corkscrew esophag indicates? diffuse esophag spasm (v birds beak of achalasia)
tx of diffuse esophag spasm nitrates and CCB (decrs amplit of cxns), TCA may help sympt
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
cxns of sliding esophag hiatal hernia GERD, reflux esophagitis, Barrettes/cancer, aspiration
dx of esophag hiatal hernia Ba upper GI + upper endo
tx of esophag hiatal hernias 1)sliding: antacids, sm meals, elevate head after eat, may need Niessens fundoplication in 15%; 2) paraeso: sx
differentiate Mallory Weiss Tears and Boerhaaves Mallory Weiss=mucosal tear at GEJ; Boerhaaves=transmural esophag perf
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
cxns of Pulmmer Vinson syndrome risk of SCC or oral, esophag
tx of Plummer Vinson esophag dilation, tx of anemia
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
what is Shatzki's ring assoc w digestion of toxic agents, acids, bases (alkali are worse bc full thickness liquefactive necrosis)
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)
tx for ea type of esophag diverticuli (3) [for ea treat underlying motility dz, diverticulotomy is 2ry] Zenkers-cricopharyngmyotomy; traction-none, asx; epiphrenic-esophagomyotomy
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)
dx esophag perf contrast esophagram using Gatrografin
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
clinical present of Zenkers diverticul dysphagia, regurg, halitosis, chronic cough
cxns of Shatzki stricture and esophag cancer
define Hamman's sign crunching sound as heart beats ag air filled spaces in context of esophag perf
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
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
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
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
tx of PUD--pt care/preventative no NSAIDs or ASA, no EtOH or smoking, no eating before bed
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
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
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
a specific ex of triple therapy for H Pylori amoxicillin, clarithromycin, omeprazole (PPI)
causes of acute gastritis NSAIDs/ASA, H Pylori, EtOH, heavy smoking or caffeine, extreme stress (shock, sepsis, burn)
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
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
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
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
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
name some of the named mets for gastric cancer (5) Krukengerg (ovary), Blumer (rectum), Sister Mary Joseph (periumbil), Virchow (supraclavicular), Irish (L axillary)
closed v open loop small bowel obstruct, and why impt differentiation closed=lumen occluded at 2 pts, can compromise blood supply
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
causes of small bowel obstruction 1=adhesion, 2=incarcerated hernia, also malignancy, Crohns, SMA syndrome
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)
metabolic changes seen in sm bowel obstruct usu low K low Cl metabolic alk and hypovol from vomitting
causes of large bowel obstruct volvulus, adhesions, hernias, ***MC: colon cancer
define paralytic ileus decrsd or absent peristalsis w/o mech obstruction
causes of paralytic ileus Rx (narcotic, anti chol), post op abd sx, spinal cord, shock, metabolic (low K), peritonitis
dx of paralytic ileus abd radio shows uniform gas, failure to pass contrast beyond a point is dx
tx of paralytic ileus usu resolves over time, IV fluids, correct K, NG suction if nec or long tube if persists
clinical present of celiac sprue; bx abd distension, bloating, diarrhea; small bowel bx shows flattened villi
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
cryst abscess of PMN indicates which IBD UC
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
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)
how tell EtOH hep by labs AST > 2x ALT
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
Created by: ehstephns on 2010-12-12



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