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140 Cards in this Set
- Front
- Back
dual blood supply to liver from
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hepatic artery, portal vein
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portal tract contains
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artery, vein, bile ducts
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blood flow in liver
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central vein - hepatic vein - Vena cavae
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causes, results - viral hepatitis
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multiple causes, results: inflammation, hepatocyte necrosis
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Hep A spread desc.
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fecal - oral. contam water.
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carrier of Hep A
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usually asymptomatic, or mild symptoms
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treatment Hep A
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self limiting - 1 to 2 weeks
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Hep A serology
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Current infection IgM -maintain, past infection IgG - gone
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Hep B desc
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300M carriers, in ALL body fluids except feces
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spread of Hep B how?
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parenteral, sexual, placental
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hep B increases risk of what and how much
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hepatocellular carcinoma by 200 percent
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HepC def
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parenterally transmitted - majority of sporadic hep infections
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Hep C mainly effects
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IV drug users (40percent) - PERENTERAL spread
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Common effects Hep C
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80 carrier state, other 20 percent cirrhosis
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Hep D
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occurs with HepB
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Cause of HepD
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DEFECTIVE RNA virus - NEEDS HEPB to replicate
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Hepatitis pathogenesis
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inflamm. in portal tracts, lobules.dmg, kill hepatocytes. fibrosis.
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cirrhosis
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liver can’t regenerate. chronic dmg. leads to broad bands of fibrosis. liver broken into nodules
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effects of nodules in cirrhosis
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abnormal shunting of blood, liver cells can’t function
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6 causes cirrhosis
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infection, drugs-toxins, metabolic, autoimmune, biliary obstruction, vascular
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unknown cause cirrhosis
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cryptogenic
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2 early complications cirrhosis
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abnormal blood flow, loss of functional mass
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problems of cirrhosis bloodflow complications
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enlarged spleen, esophageal varices
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loss of functional liver mass problem
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impaired protein synth, drug deactivate, clotting probs.
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late complications cirrhosis
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hepatocellular carcinoma
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end stages cirrhosis
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hepatic encephalopathy, hemorrhage, infection
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cause of liver dmg ethanol
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alcoholic steatohepatitis
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pathology alcoholic liver dmg
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hepatocytes metabolize EtOH via enzymes, excrete acetate
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High doses alcohol cause
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o2 dependent reaction. liver overwhelmed, fatty acid processing paralyzed, fat accumulates
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3 maj. forms liver dmg.
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steatosis, hepatitis, cirrhosis
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steatosis chars
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enlarged greasy liver, large fat globs
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alcoholic hepatitis chars
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fat and inflammation
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cirrhosis chars
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chronic dmg and inflamm
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devs in 15 percent cirrhosis patients
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hepatocellular carcinoma
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amts alcohol req. to prod. dmg in liver - reversible
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short term 80gm alc
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amts alcohol req. to prod. dmg in liver -chronic
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80-160gm/day - long term cirrhosis risk
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NASH def
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non-alcoholic steato hepatitis
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NASH symptoms
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patient denies drinking, may have diabetes, obesity, hyperlipidemia, drugs
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wilsons disease
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copper buildup in liver - doesn’t metabolize properly
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wilsons disease effects
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liver, pancreas, brain. causes cirrhosis, psychosis, copper deposition in ye
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alpha one anti trypsin deficiency
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proteases aren’t stopped due to genetic disorder - effects lung, liver - cirrhosis
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excessive accum. of body iron in liver
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hemochromatosis
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causes iron deposition
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genetic or parenteral admin of iron (transfusion)
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result of excess iron deposition
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cirrhosis - iron is toxic, produces free radicals, damage
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associated diseases of excess iron
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cardiac failure, diabetes, joint problems
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risk assoc. w hemochromatosis
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hepatocellular carcinoma due to genetic dmg
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diagnosis treatment of hemochromatosis
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biopsy for iron in liver, phlebotomy treatment
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bronze diabetes
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hemocromatosis knocks out insulin production
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drug dmg to liver
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antibiotics, anti-cholesterol, etc. drugs cause bile duct dmg
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drugs which dmg hepatocytes
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acetominophen, tylenol, can lead to liver failure
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drugs which cause steatohepatitis
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steroids, estrogens
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drugs assoc. w granuloma
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sulpha drugs
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itching term
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pruritis
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excess bilirubin in blood, tissues
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cholestasis - inter or extrahepatic causes
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extra or inter hepatic cholestasis cause
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obstruction (gallstones or tumour in comm. bile duct), failure of bile secretion - hepatitis, drugs, sepsis, pruritis, jaundice
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clinical signs choleostasis
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pruritis and jaundice
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body attack epithelium of bile duct
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primary biliary cirrhosis - autoimmune disorder
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primary biliary cirrhosis effects what pop.
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mostly females - see granulomas in bile ducts
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prim. biliary cirrhosis assoc with?
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usually rheumatoid arthritis
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autoimmune dis. causing bile duct atrophy
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primary sclerosing cholangitis
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3 benign neoplasms of liver
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hepatic adenoma (birth control pills), bile duct adenoma, hemiangioma (accum. bile ducts or bl.vess.)
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most comm. malig. tumour
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HCC
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Why HCC
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metastasis from other CA, ESPEC. COLON CA
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Liver inflamm - 2 consequences
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regeneration or fibrosis
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consequence of hepato-regen
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can lead to malignancy
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pathogenesis cirrhosis
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dmg. to liver parenchyma and destruct: necrosis
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hepatic dmg begins where
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portal tracts
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steatohepatitis dmg begins where
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zone 3
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why liver regen. impaired
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too much necrosis, reticulin scaffold destroyed, hepatocytes injured, inflammation interferes, blood supp. effected, poor nutrition
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potential chemical inhibitors of liver regen.
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prolif:inhibitors or absence of regen. stimulants
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fibrosis cause
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various liver cells produce tissue - expands and forms septae around parenchyma
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blood flow chg in cirrhosis
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portal v. flow obstructed, acts like lesion, causes portal hypertension, varices, etc.
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effect of loss of functioning parenchyma
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impaired protein synth, inadequate neutralization: drugs, hormones, toxins. jaundice. clotting probs. waste metabolism probs.
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4 addtl causes cirrhosis
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infection (schistosomiasis), drugs, toxins, metabolic, autoimmune disorders
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def: peptic ulcer
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damage to FULL THICKNESS of mucosa in an area bathed by acid and pepsin
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3 causes normal acid/pepsin secretion
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cephalic (sensory), gastric distension (stim.vagus N), intestinal (alkalines in lumen).
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4 mucosa defenses against acid
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structural, mucous secretion, bicarbonate prod., prostaglandin rel.
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diff btwn. gastric vs. duodenal ulcers
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duodenal: high acid prod. gastric: low acid prod.
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4 mucosal defense inhibitors
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mucosal ischemia, bile reflux, drugs(ASA,Prednisone), smoking, alcohol
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other ulcer factors
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genetic(type O- duodenal ulcer, type A - gastric), environmental (stress, smoking, spicy food), excess gastrin prod., Helicobacteria Pylori
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location of ulcers
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duodenum, stomach antrum, distal esophagus
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3 zones of an ulcer
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superficial - fibrinopurulent exudate, necrosis. inflamed granulation. fibrotic tissue at base.
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btwn normal and ulcerative tissue
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sharp line of demarkation
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5 peptic ulcer complications
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hemorrhage, perforation, adjacent mvmt (involve pancrease etc.) obstruction, transform to malignant.
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treatment aims of ulcer
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increase resistance of mucosa, reduce acid production
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two bowel diseases known as IBD
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ulcerative colitis and crohns
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def. crohns
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chronic granulomatous inflamm. disease of bowel wall
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symptoms crohns
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abdom. pain, diarrhea, colonic bleeding, fever, malabsorption, malnutrition
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crohns pathology
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transmural, segmental, any part of GI
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percents of GI tract areas involved in crohns
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ileum, cecum 50, colon 20, sm.int 15, anorectal 15
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crohns gross features
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thickened edematous bowel wall, lumen narrowed, cobbled appearance, skip lesion
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cobbled app. of crohns due to
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nodular swelling, fibrosis, linear ulceration
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microscopic features crohns
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involves ENTIRE wall, superficial ulcers, edema, inflammation, fibrosis, non-caseating granulomas
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crohns complications
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fistulas, abscesses, obstruction, perforation
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crohns risk of intestinal CA
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three times the risk
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treatment of crohns
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none. treat symptoms only: anti-inflam, surgical resection, drain abscesses.
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clinical signs - ulcerative colitis
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intermittent, recurrent rectal bleeding, profuse bloody diarrhea, cramps, fever, anemia
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ulcerative colitis manifests extraintestinally via
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arthritis in 25 percent of cases
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diff btwn crohns and ulcerative colitis
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ulcerative is only colon, only mucosa, and continuous (not ‘skip’)
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pathology ulcerative col
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distal rectum extending proximally, continous, only mucosa, only colon
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early ulcerative colitis, gross
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red, granular, ulcerations, small ulcers coalesce with islands of intact mucosa, pseudopolyps in lumen
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early ulcerative colitis - microscopic
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congestion, edema, hemorrhage of mucosa, inflamm of lamina propria, loss of surf. epithelium, ulceration
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adv. ulcerative colitis, 2 main chgs
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mucosa thinned, atrophied, torturous branched shortened intestinal crypts
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ulcerative worse complication
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toxic megacolon
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toxic megacolon chars
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extreme dilation, thinning of colon wall, high risk of perforation, gangrene
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treatment - toxic megacolon
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emergency colectomy
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chronic ulcerative colitis
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10 yrs +, extensive colonic involvement, HIGH risk CA
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ulcerative colitis trtmt
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sub-total colectomy, anti-inflam, corticosteriods
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most esophageal tumours are
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cancer, squamous cell, 2nd most comm - adenoCA
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contributing factor to esophageal CA
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food, alcohol thru esophagus, exposure to pathogens
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most esophageal CA assoc w
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alterations to tumour supp. genes
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pathology esophag. CA
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squamous dysplasia - CA in situ
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3 types lesions in esophag CA
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polypoid fungoid masses, necrotizing ulcerated lesions, diffuse infiltrative lesions
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consequences of tumour masses in esophagus
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protrude into lumen, erode resp. tree/aorta, thicken esophagus wall, narrow lumen
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main locations tumours esophagus
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middle 50, lower 30, upper 20
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esophageal adenocarcinoma appearance
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mucin-producing glandular neoplastic epithelium
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clinical features esophageal CA
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dysphagia, weight loss, pain swallowing
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term: pain swallowing
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odyophagia
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diagnosis, trtmt esophag CA
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endoscopic biopsy, EARLY surgery. If late, bad prog.
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most tumours w/in stomach
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CA 90-95%
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2 protective environ. factors against gastric adenoCA
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increase refridgeration, decrease preservation, more fresh veg and fruit
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3 main environ. factors - gastric CA
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poor diet, (nitrates, smoking, salt) chronic gastritis, helicobacterpylori, mucosal dysplasia
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3 growth patterns
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exophytic-tumour mass protrudes, flat-depressed, excavated
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rigid thickened stomach wall
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linitis plastica - entire stomach infiltrated by CA
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clinical - early vs. late gastric CA
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asymptomatic vs. pain, weight loss, dysphagia, obstruction
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three types colonic adenomas
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tubular, villous, tubulovillous
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risks of malignancy based on
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size, architecture of polyp, severity of dysplasia
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main determinant of risk of adenoma containing CA
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polyp size
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size determinants - polyps
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less than 1cm -CA rare, more than 4cm, CA likely
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tubular adenoma, where, appearance
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anywhere in colon, slender stalk with raspberry head
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clinical features tubular adenoma
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asymptomatic, bleeding, anemia
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villous adenoma where, appearance
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mostly sigmoid, rectum. sessile, cauliflowerlike
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clinical features villous adenoma
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hypoprotein, hypokalemia
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adenoma treatment
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excision
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most large intestine tumours
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adenocarcinoma - usually at 60-70 years old
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dietary/environmental contriubting factors colorectal CA
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low veggies, high carb, protein, low vit C,A,E, low fibre intake, decreased stool bulk
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etiologic agent colorectal CA
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altered bacterial flora - conversion to carcinogens
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colorectal gross appearance
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napkin ring appearance
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clinical features colorectal CA - right side
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cecal - fatigue, weakness, anemia
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clinical features colorectal CA - left side
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occult bleeding, chgs in bowel habit, cramps lower left
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