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