Quiz 4 - LR Flashcards
(27 cards)
Fulminant LR Dz - mc cause
acetomenaphen overdose
half of the pts dx w LR dz … dt?
next mc?
hep C
- then alcohol
- non-alc fatty lr dz
- hep B
5 general responses of the LR to problems
- degeneration, accumulation
- necrosis, apoptosis
- inflammation
- regeneration
- fibrosis
Necrosis & Apoptosis
eti?
histo?
- usu acute process of toxins
- necrosis: for staining - cells are paler - balloon
then shrink down - “inclusion body” = councilman body… hepatocytes apoptose, coalesce, and shrink to make eosinophilic staning cells w fragmented nuclei … usu assoc w hep C or viral infx
what substances can accumulate in LR
Cu
Fe
Fat
degeneration & intracellular accumulation
eti?
histo?
reversible?
- dt toxic or immunologic insult
- “ballooning degeneration”
- yes
Inflammation
eti?
histo?
- dt direct toxic or ischemic cell necrosis or damage dt cytotoxic lymphocytes esp during a viral infx
- lymphocytes in LR are there… but then activated… see w dark blue purple staining
- pale LR
Chronic Hepatitis
- genetic dz like hemochromatosis
or wilson’s dz (copper accum); alpha 1 antitrypsin enzyme xu - helps to reform damaged tissue - Hep C
- Hep D
- hepatoxins like tylenol
infx in pregnant women -> fulminant hepatic necrosis w 15-25% fatality OTHERWISE, self-limiting
Hep E
- 4-26 wk incubation; can remain in blood; also in body fluids (but not stool)
- primary risk: transfusions, blood products, dialysis, needle-sticks, IV drug abuse, sex
- vertical transmission in endemic places
- more at risk for CA; so this can become chronic; also, co-infx w D; also can be fulminant
Hep B
benign, self-limiting, incubation of 2-6 wks; rarely causes fulminant
Hep A
major cause of LR dz worldwide
- inoculations, blood transfusions // 60% cases IV drug // sex ~15%
- cirrhosis in ~20% of pts w chronic HCV infx
Hep C
chronic hep eti
- genetic dz like hemochromatosis
or wilson’s dz (copper accum); alpha 1 antitrypsin enzyme xu - helps to reform damaged tissue - Hep C
- Hep D
- hepatotoxins like tylenol «_space;acute LR failure mc cause
“ground glass” appearance - parenchymal cell w hazy staining - seen in?
chronic Hep B
50% of cases (acetaminophen)
12% dt Hep B
18% uknown
Fulminant Hepatitis
Fulminant Hepatitis
gross appearance
- necrotic areas look muddy red, mushy, blotchy bile staining // shrinks to ~500g
- pt survival >1wk —> regeneration in what?
fulminant hepatitis
Alcohol/Acetaminophen Injury
alcohol decreases metabolism of methionine —> decreased GSH // cytochrome P-450 increases break down of alcohol AND increases acetaminophin —> NAPQI
alcoholic LR dz 3 forms
Hepatic Steatosis, Alcoholic Hepatitis, Cirrhosis
Hepatic Steatosis histo
- swelling, necrosis, ballooning, mb mild deposition of iron and Kupffer cells
show up in many forms of hepatitis - hepatocytes accum. keratin/proteins which are visible as eosinophilic cytoplasmic inclusions - (seen in alc. lr dz, NASH, primary biliary cirrhosis, Wilson’s, hepatocellular tumors)
Mallory Bodies
what also accumulates in alcoholic hepatitis?
WBCs - neutro, lympho, m0
what happens to the LR with chronic hepatitis over time?
cirrhosis! slowly - fatty, yellow-tan, enlarged - then fibrosis and shrinks, non-fatty, brownish green (at least 1-2 yrs)
- fibrosing begins around portal tract, then extends thru sinusoids - regenerative activity creates “micronodules” which leads to a lumpy bumpy appearance
—> eventually mixed micronodular and macronodular pattern —> ischemic necrosis, fibrous obliteration creates tough, pale scar tissue
- green dt bile stasis
fibrous changes usu begin where?
around the portal triad
