Cirrhosis
Definition-Cirrhosis is the diffuse disea se involving following characteristics• necrosis of liver cells causing liver failu re and death, • fibrosis involving central vein and port al regions, • regenerative nodules due to entrapped parenchymal hepatocytes, • distortion of normal architecture of live r, • diffuse involvement of whole liver.
• Histologically, the pattern of cirrhosis characterized by irregularly sized nod ules separated by broad scars is kno wn as postnecrotic cirrhosis.
Classification
1) Etiological classification • Alcohol cirrhosis (60-70%) • Viral hepatitis (10%) • Biliary hepatitis (5-10%) • Primary hemochromatosis (5%) • Cryptogenic cirrhosis (10-15%) • Wilson’s disease • α1-antitrypsin deficiency
• Other causes-cirrhosis due to pharm aceutical drugs (acetaminophen, α-m ethyldopa), autoimmune hepatitis, h epatotoxins ( carbon tetrachloride, m ushroom poisoning) 2) Morphological classification • Micronodular • Macronodular • Mixed
Morphology
Gross 1. Size/appearance/weight•. At first cirrhotic liver is yellow-tan, fa tty, and enlarged, weighing >2 kg. •. Over years - transformed into a brow n, shrunken, non-fatty organ, someti mes weighing ‹1 kg.
2) Diffuse surface nodularity â&#x20AC;˘ Regenerative activity of parenchymal hepatocytes generates uniformly siz ed nodules (<0.3 cm in diameter)-m icronodular cirrhosis. â&#x20AC;˘ Nodularity becomes more prominent; scattered larger nodules create a "ho bnail" appearance on surface of livermacronodular cirrhosis (Fig).
â&#x20AC;˘ As fibrous septa dissect and surroun d nodules, liver becomes more fibrot ic, loses fat, and shrinks progressivel y. 3) Cut section â&#x20AC;˘ Parenchyma is divided into rounded nodules separated by bands of fibrou s tissue.
Fig: Cirrhosis with characteristic diffuse nod ularity of surface. Greenish tint of some nod ules is due to bile stasis.
Microscopic features â&#x20AC;˘ Initially developing fibrous septa are delicate and extend through sinusoid s from central vein to portal regions as well as from portal tract to portal tract.
• Residual regenerating parenchymal i slands are engulfed by wider bands o f fibrous tissue, and liver is converte d into a mixed micronodular and mac ronodular pattern (Fig). • Ischemic necrosis and fibrous obliter ation of nodules create tough, pale s car tissue (“Laennec cirrhosis”).
â&#x20AC;˘ Bile stasis often develops. â&#x20AC;˘ Mallory bodies are rarely present.
Microscopic view shows nodules of var ying sizes entrapped in blue-staining fi brous tissue.
Complications
• Complications of portal hypertensionedema and ascites, splenomegaly, es ophageal variceal bleeding • Malnutrition • Jaundice • Infections • Hepatic failure • Hepatic encephalopathy
â&#x20AC;˘ In end-stage alcoholics, causes of de ath are(1) hepatic coma, (2) massive gastrointestinal hemorrha ge, (3) intercurrent infection (to which the se patients are predisposed),
(4) hepatorenal syndrome following a bout of alcoholic hepatitis, and (5) hepatocellular carcinoma (risk in al coholic cirrhosis 1-6% of cases annu ally).