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140 Cards in this Set

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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