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28 Cards in this Set
- Front
- Back
Liver lobule |
3 portal zones at the verticies with a central vein at the center and lobule cells angling out to the portal zone blood is going toward the central vein
bile however drains towards the portal zone in the cannaliculi |
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Sinusoids |
throughout the liver, rows of liver cells called plates with many vascular components called sinusoids |
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Viral hepatitis |
acute
fulminant = extensive necrosis
chronic and persistant viral hep |
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Hepatitis type |
Type A; portal inflammation acidophil bodies and usually is self limiting
Type B; ground glass hepatocytes, full of virus, interfacd hepatitis, T cells around hepatocytes
Type C; fatty change with lymphoid follicles |
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Morpho changes in liver injury |
Cell death; the type location
Regeneration
Intracellular accumulations
inflammation
fibrosis |
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Acute hep |
portal lymphocytic inflammation, with degeneration
lymphocytes can also move to around the hepatocvyte and sinusoids
typical of type A; acidophiclic bodies, councilman bodies = yellow fever
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HBV infection and Type B |
ground glass = frosted look
liver cells are granular and contain abundant virus |
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Hep B Viral Infection |
symptomatic acute hepatitis can leads to chronic and in rare cases become hepatocellular carcinomas |
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Viral Hep C |
acute infection leading to chronic or sometimes fulminant hep, can lead to cirrhosis and carcinoma |
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Interface or piecemeal hep C |
briding necrosis leading to fibrosis between the central vein and portal tract
results in an interface around the portal and central vein zones |
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Chronic/persistant hep |
interfance hepatitis and piecemeal necrosis
multi/binucleated hepatocytes and regeneration |
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Chronic hep diseases |
hep B/C
autoimmune hep
primary biliary cirrhosis
Wilson's disease
hemochromatosis |
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Autoimmune lupoid hep |
young females
associated with other autoimune diseases
ANA positive and anti SM antibodies (smooth muscle)
anti microsomal antibodies
elevated gamma globulins
indolent course or more acute diseaes
chronic hep may develop plasma cells prominent
can progress to cirrhosis |
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Autoimmune lupoid hep present |
piecemeal necorssis and plasma cells |
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Causes of cirrhosis |
Alcoholism and NAFLD Drugs Hep Shistosomiasis Wilsons HFE
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Hepatic cirrhosis |
probably irreversible in general
liver cell damage
regeneration formation of nodules; trapped liver cell foci enclosed by fibrosis
fibrosis briding
disruption and reorganization of vascular structure leads to increased portal hypertension |
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Pathogenesis of cirrhosis |
stellate cells (HSC) stim by growth factors PDGF
change from Vit A storing sells on the liver plate to myofibroblasts, which result in migration proliferation and secrete mediators that increase the depo of collagen I and III in the space of DISSE (space between plates and sinusoids)
Follws the liver plates and connects the fibrotic bridging between the two zones
Activated Kupfer cells damage hepatocytess (macros)
Result: scar liver cell death, nodulare regneration and vascular reorganation |
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Consequences of cirrhosis |
fibrosis chokes off the sinsoids and leads to necrosis due to decreased blood flow
PORTAL hyper
portal-systemic shunts
impaired portal blood flow
hepatic faulure portal hepatic shunts |
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ALD |
persistant exposure to large quantities of alcohol making it become steatous which can persist to cirrhosis |
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Fatty liver |
symptom of a disease
has many causes |
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acute course of alcoholic hepatitis after binge drinking |
polys around necrotic cells and mallory bodies in hepatocytes |
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NAFLD |
fairly common
men and women eqaul
usually are symptomatic, non drinkers or low alcohol intake people
obese, diabetic, dylipidemia coronary artery disease hypertension increased liver enzymes GGT |
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NASH |
intermediate of NAFLD
perivenular pathology is conspicuous
apop inflamm mallory bod |
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Primary biliary cirrhosis |
chronic progressive autoimmune disease
Women 6:1
peak onset 40-50
insidious; pruritus, faitgue, jaundice, xanthomas late |
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PBC |
elevated serum IgM
anti-mitochondiral Abs against PDH complex
elevated alkaline phos, cholesterol earl
elevated bilirubin late
bile duct destruction and infiltration by lymphocytes on viewing |
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PBC histo |
portal zones are infiltrated by lymphocytes plasma cells and eosinophils which are attacking the bile ducts
chronic perisitant hepatitis picuture may be pressent wiht lose of bile ducts
granulomas sometimes present |
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Cholestasis |
can be obstructive or non obstructive
bile pigment in hepatocytes; lysosomes wiht bile
bile plugs in canaliculi, sepsis, drugs
bile duct proliferation
bile lakes in long standing disease; free bile between disrupted cells |
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Early extrahepatic obstruction |
bile duct proliferation, portal inflammation with polys and portal edema
think gallstones |