I. Look for the answers to the following questions.

1. What have epidemiologic studies demonstrated?

2. What are morphological lesions of-both hepatitis a and b?

3. Is hepatic cell degeneration a manifestation of liver cell damage?

Why has subacute hepatic necrosis a poor prognostic significance?diseases of the liver

4. How is viral hepatitis classified?

5. What has been demonstrated by recent epidemiologic studies?

CIRRHOSIS

^irrhosis is a generic term that includes all forms of chronic diffuse liver disease characterized by significant loss of liver cells, collapse and fibrosis of the supporting reticulin network with distortion of the vascu­lar bed, and nodular regeneration of the remaining liver cell masses^ The basic causative element of this complex lesion is diffuse liver cell death; the network of scars, the regenerating cell masses, and the changes in hepatic circulation develop secondarily. Less constant pathologic features of most types of cirrhosis include intralobular or portal inflammation, focal or widespread bile stasis, and proliferation of ductular cells.

The morphologic elements of cirrhosis often have dramatic clinical counterparts ^Progressive loss of liver cells may produce jaundice, ascites and edema, central nervous system dysfunction, cachexia, and death - the syndrome of hepatic insufficiency^The advancing fibrosis leads to dis­tortion of the intrahepatic vasculature, which in turn contributes to the development of portal venous hypertension with resultant esophageal and gastric varices and splenomegaly. Nodular regeneration often leads to dis­tortion of liver shape and compression of intrahepatic venous and lym­phatic radicles which may result in ascites and portal hypertension. No clinical, etiologic, or morphologic classification of cirrhosis is satisfacto­ry at present^blinical signs and symptoms may not reflect accurately the extent and precise nature of the cirrhosis process; the causes of types of cirrhosis remain uncertain or unknown; pathologic patterns may repre­sent nonspecific hepatic responses to many different forms, of liver „cell injury Jlowever, in slP^o'f these it is¹ p6ssit>fff to ^ate^o^ze^ f

most cases of cirrhosis clinically, ^ШЩсіиaS^l^g^morphologic or efev logic terms when possibleaMost types of cirrhosis can be classified as ІЩ/С lows: (1) Laennec's, (2) postnecrotic, (3) biliary (either primary or sec­ondary), (4) hemochromatosis, (5) cardiac or congestive, or (б)гюагё and nonspecific cirrhosis.)

flMen are^affected modff^equentW^an women, but thjslsex сііШг- ence has d£p^e&secT years as drinking liaBii^^li^ve

changed in many Western countries» Although the a^Jerfge age of onset

percent of cases are discovered ii^Kte^ffiy^at laparotomy or ^Йріу!^ 188

Typically, however, after 5 to 15 years of alcoholic essive liver dysfunction, fluid /фЩугі, and SajrS.^Dver a nerbd of weeks or months, the, pati; sirig' v^KJt^s^and fatigability^anore: dice, intermittent^® ei sign of disease, but ^

strual irregularity or an megaly, and ascites. rss&^of body ha pura, er^Ding of the fingers, and diffuse' Ьурегр a^^lnonbut leg^n^ortant clinical signs.

snaking <%irs is frequent in patients with active disease. ft-bU^C

Jaundice and other signs of hepatic, dysfunction may ^subside with therapy,^J>ut continued alcoholic jspccess and poor dietary ЬзШ^ lead to further of hepatic decompensation. Acute of alco­

holic liver dmtfmb mav, follow j^mMc/ea drinking frfiks. Fever, nausea and vomiting, and ascites may

occur іЩІШщШ asslLc^wnwith wm^pr^dlrver cell loss ai^-inf lamina­tion. ^Although some patients die during the acute exa.certjfatlo^ most r&cw^mter several weeks. A few patients experience one or more tran­sient episodes of cholestatic jaundice during the course of alcoholic liver disease. Clinical and І^огд feory studies may ЩхЩеіС the^diagnosis of mechanical biliary liver biopsy ana the response to con­

weak and chronica

servative therapy usully sJ^^Txhe diagnosis of intrahepatic chole^ta^,, ^

Over a period from 1 to 5 years, the cirrhotic patient becomes eitiaciS

scites and signs of portal hyperten-

jaimdiced.

sion become Incre^ingTy prominenTJ^ost^patients with advanced cir sis die in hepatic coma, often oy hemorrhage from

varices or intercurrent infection J^mteymd chronic pancreatitis and pep­tic ulceration greater frequency in cirrhotic-patients than in normal subjects. Gram-negative bacteremia acute bactenal peritonitis, and hepatoma are uncommon complications.