Liver Pathology

Front 1

Liver lobule

Back 1

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

Front 2

Sinusoids

Back 2

throughout the liver, rows of liver cells called plates with many vascular components called sinusoids

Front 3

Viral hepatitis

Back 3

acute

fulminant = extensive necrosis

chronic and persistant viral hep

Front 4

Hepatitis type

Back 4

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

Front 5

Morpho changes in liver injury

Back 5

Cell death; the type location

Regeneration

Intracellular accumulations

inflammation

fibrosis

Front 6

Acute hep

Back 6

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

Front 7

HBV infection and Type B

Back 7

ground glass = frosted look

liver cells are granular and contain abundant virus

Front 8

Hep B Viral Infection

Back 8

symptomatic acute hepatitis can leads to chronic and in rare cases become hepatocellular carcinomas

Front 9

Viral Hep C

Back 9

acute infection leading to chronic or sometimes fulminant hep, can lead to cirrhosis and carcinoma

Front 10

Interface or piecemeal hep C

Back 10

briding necrosis leading to fibrosis between the central vein and portal tract

results in an interface around the portal and central vein zones

Front 11

Chronic/persistant hep

Back 11

interfance hepatitis and piecemeal necrosis

multi/binucleated hepatocytes and regeneration

Front 12

Chronic hep diseases

Back 12

hep B/C

autoimmune hep

primary biliary cirrhosis

Wilson's disease

hemochromatosis

Front 13

Autoimmune lupoid hep

Back 13

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

Front 14

Autoimmune lupoid hep present

Back 14

piecemeal necorssis and plasma cells

Front 15

Causes of cirrhosis

Back 15

Alcoholism and NAFLD

Drugs

Hep

Shistosomiasis

Wilsons

HFE

Front 16

Hepatic cirrhosis

Back 16

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

Front 17

Pathogenesis of cirrhosis

Back 17

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

Front 18

Consequences of cirrhosis

Back 18

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

Front 19

ALD

Back 19

persistant exposure to large quantities of alcohol making it become steatous which can persist to cirrhosis

Front 20

Fatty liver

Back 20

symptom of a disease

has many causes

Front 21

acute course of alcoholic hepatitis after binge drinking

Back 21

polys around necrotic cells and mallory bodies in hepatocytes

Front 22

NAFLD

Back 22

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

Front 23

NASH

Back 23

intermediate of NAFLD

perivenular pathology is conspicuous

apop

inflamm

mallory bod

Front 24

Primary biliary cirrhosis

Back 24

chronic progressive autoimmune disease

Women 6:1

peak onset 40-50

insidious; pruritus, faitgue, jaundice, xanthomas late

Front 25

PBC

Back 25

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

Front 26

PBC histo

Back 26

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

Front 27

Cholestasis

Back 27

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

Front 28

Early extrahepatic obstruction

Back 28

bile duct proliferation, portal inflammation with polys and portal edema

think gallstones