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Flashcards in Liver Pathology Deck (44)
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Normal liver size?



Functional unit

Have three zones
1, 2 and 3
Based around terminal hepatic vein(central vein)


anatomical component

Hepatic Lobule


Porta Hepatis

Main entry point into the liver.
A fissure where the Bile Duct, Hepatic portal vein and Proper hepatic artery enter/exit


Purpose of zones? Other names for zones are?

Pathologists can describe changes specific to each zone, which helps clinicians to identify/ diagnose the disease
1 = periportal
2 = mid-zonal
3 = centrilobular


What are the Four general features of Hepatic disease

1: the patterns of hepatic injury
2: hepatic failure
3: cirrhosis (distinct to liver)
4: portal hypertension


#1 Patterns of hepatic injury are?

5 general responses (limited # of responses)
1) Degeneration and intracellular accumulation (fat-steatosis, or bilirubin-cholestasis)

2) Necrosis and apoptosis (consequence of toxins/drugs)

3) Inflammation (hepatitis)
(viral, infection, autoimmune issues)
4) Regeneration

5) Fibrosis (leads to cirrhosis > portal hypertension)


#2 Hepatic Failure

relatively unncommon
-Sudden and massive destruction OR endpoint of chronic damage
- Only seen when loss ~80-90%
- Decompensation associated with increased demand (infection, GI bleeding, sepsis) triggered by 'co-morbidity' so the liver has less ability to compensate and HF will occur at


Clinical Features of Hepatic Failure

Failure of normal function:
-Jaundice (failure to metabolise bilirubin)
-Hypoalbuminaemia (low albumin > peripheral edema)
-Elevated Ammonia (not removed/detox. leads to neurological dysfunction)
-Bleeding (decreased coagulation factors)


Paracetamol in excessive dosage is? What would you see with this?


-Hepatocellular necrosis (loss of normal hepatocyte structure) near hepatic /central vein
-Normal anatomy/tissue around portal triad



a chronic disease of the liver marked by degeneration of cells, inflammation, and fibrous thickening of tissue. It is typically a result of alcoholism or hepatitis.


Physical features of Cirrhosis

Bridging Fibrous Septae: link portal tracts

Parenchymal Nodules: Proliferating hepatocytes encircled by fibrosis
-micronodules less then 3mm
-macronodules upto a few cm

Disruption of entire architecture
-vascular architecture > shunts that avoid HPV and HA blood bypasses
-progressive fibrosis


What mediates Cirrhosis

A number of inflammatory Cytokines (particularly Kupffer cells, also know as alveolar macrophages in lungs).

Activated Kupffer cell releases inflamm. CK release > fibrosis , changes in BVs
These all cause damage to normal hepatocytes (necrosis and apoptosis)
and initiate an inflammatory response (from fibrosis)



Complications of Cirrhosis

1) Impairment of Normal Hepatic Function- synthetic/detoxification fuunction

2) Impairment of Normal blood pressures/flow in the portal vein (those with chronic liver disease > portal hypertension)


What is portal hypertension?

Increased resistance to portal blood flow, due to increase in the blood pressure within a system of veins called the portal venous system leading to eventual reversal of blood flow


Causes of Portal Hypertension

Prehepatic: Obstructive Thrombosis (block in PV)
Post Hepatic : Severe right sided heart failure (rised r.side pressure)
Intrahepatic: Cirrhosis (90% cases)


Consequences of Portal hypertension

1)Porto-systemic Shunts: lead to
-Congestive Splenomegaly (big spleen)
-Eosophageal varices (loss of blood)
-Varices around umbilicus

And due to failure of liver to do normal function
2) Ascites
3)Hepatic encephalopathy (neurodegeneration)



accumulation of fluid in abdomen due to increased PV pressure, often with decreased serum albumin levels


Portosystemic Shunts

Bypasses where systemic and portal circulation share capillary beds


Viral Hepatitis

1) Hepatitis A, B, C (these most common 90-95%), D and E
2) Cytomegalovirus (herpes virus in immuno-suppressed patients)
3) Epstein-Barr Virus (glandular fever)


Hepatitis A

-Benign self-limited disease
-Incubation period= 2-6 weeks
- DOESN'T cause chronic hepatitis or cirrhosis (usual for it to progress)
-infection of hepatocytes due to poor hygiene
-by person-person, faecal/oral transmission
- asymptomatic or mild febrile illness +/- jaundice
-May have some hepatocellular damagemild elevated liver enzyme levels


Hepatitis B and C can develop to

chronic Hepatitis > cirrhosis > hepatocellular carcinoma)


Hepatitis B

-big global issue (350mill carriers)
- spread via body fluids
- can result in acute hepatitis with resolution OR damage and chronic hepatitis due to the bodies immunological response to infection
-CH > cirrhosis


Draw flow diagram of Hep B outcomes pg 163



Hepatitis C

New Treatment

-Major Cause of Liver Disease
-vaccinations and blood transfusion
-acute infec. usually undetected
-Majority is CHRONIC DISEASE > (can havefibrosis > cirrhosis > Hep.carcinoma)
->20% will develop cirrhosis 5-10 years post infection

New Hep C antiviral treatment now available


Autoimmune Hepatitis

Chronic Progressive Hepatitis
Body is tricked immunologically to create an immune response against itself (self-antigens).

-genetic predisposition
-ass. with other autoimmune diseases
-presense of auto antibodies


What would you see?
How can you treat?

(AI hepatitis)

You will see an inflammatory infiltrate with lymphocytes and plasma cells

Treat via immunosuppresion


Drug and Toxin-induced Liver insults are classified as?

Predictable Hepatotoxins: act in dose-dependant matter and occur in most individuals eg paracetamol

Unpredictable Hepatotoxins


Hepatotoxins can act

1) directly cell toxic
(to hepatocytes)
2) Act through hepatic conversion to an active toxin or activate immune mechanisms


Drug and toxin-induced liver insults patterns of injury are?
What are the most common cause for acute and chronic

Varies from: Cholestasis, hepatocellular necrosis, Fatty liver disease, fibrosis, granulomas, neoplasms

Acute liver failure: paracetamol
Chronic Liver damage: alcohol