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Summary Pathology of the Liver and Gallbladder

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  • Course
  • Pathology (PATHO)
  • Institution
  • Poznan University Of Medical Sciences
  • Book
  • Robbins & Cotran Pathologic Basis of Disease

This document presents in a very organized and easily accessible way all the informations about diseases and pathology of the liver and gallbladder. It contains images that facilitate learning. Is has all the informations presented in Robbins and Cortan Pathologic Basis of Diseases.

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  • No
  • The liver, the gallbladder, the pancreas, the gastrointestinal tract
  • April 4, 2022
  • 20
  • 2021/2022
  • Summary

Subjects

  • pathology
  • medicine
  • disease
  • illness
  • symptoms
  • liver
  • cirrhosis
  • bile

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  • Pathology (PATHO)
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Liver & Gallbladder
GENERAL FEATURES OF LIVER DISEASE
MECHANISMS OF INJURY & REPAIR
 Reversible changes: fat accumulation and cholestasis (bilirubin accumulation)
 Irreversible changes: necrosis (following hypoxia and ischemia) and apoptosis (autoimmune
diseases, viruses, drugs, and toxins)
 Confluent necrosis: widespread death of hepatocytes
o Begins around the central vein  bridges central veins and portal tracts
 Regeneration of dead hepatocytes
o Mitotic replication of adjacent cells
o Differentiation and proliferation of stem cells in the canal of Hering (in chronic liver
diseases)  ductular reactions (duct like structures formation)
 Chronic injury  large number of hepatocytes death and collapse of the underlying reticulin 
scar formation: by the perisinusoidal hepatic stellate cells (highly fibrogenic myofibroblasts) 
cirrhosis (fibrous septae formation)



LIVER FAILURE
ACUTE LIVER FAILURE
 Live disease that produce hepatic encephalopathy within 6 months of the onset of jaundice
 Fulminant liver failure  encephalopathy within 2 weeks
 Subfulminant liver failure  encephalopathy within 3 months
 Caused by: acetaminophen overdose, hepatitis (A, B, C, D, E, autoimmune, drug-induced, fatty
liver)
 Cause massive hepatic necrosis, without scar formation (acute)

CLINICAL FEATURES
 Increased serum transaminase  decline dramatically (with loss of hepatocytes)
 Hepatomegaly  shrinkage (parenchyma destruction)
 Retention of bilirubin  jaundice (yellow discoloration of the skin), icterus (yellow discoloration
of the sclera), and cholestasis (decreased bile flow)
 Hepatic encephalopathy: rigidity, hyperreflexia, and asterixis (nonrhythmic rapid extension-
flexion of the head and extremities  flapping of the hands wen arms are extended and wrists
are dorsiflexed)
o Increased ammonia levels in blood and CNS
 Coagulopathy
o Decreased production of coagulation factors  bruising and bleeding
o Decreased metabolism of activated coagulation factors  DIC
 Intrahepatic obstruction  ascites (but causes portal hypertension in chronic liver failure)
 Hepatorenal syndrome (renal failure): sodium retention, impaired water excretion (decreased
urine output), decreased renal perfusion and GFR (by activation of renin-angiotensin axis and
sympathetic nervous system  vasoconstriction of afferent arteriole)

, o Increase blood urea nitrogen and creatinine levels

CHRONIC LIVER FAILURE & CIRRHOSIS
 Cirrhosis: associated with chronic liver failure, diffuse transformation of liver into regenerative
parenchymal nodules surrounded by fibrous bands
o Prominent ductular reactions with disease progression  bad prognosis
 Caused by: chronic hepatitis B and C, non-alcoholic fatty liver disease (NAFLD), and alcoholic liver
disease
 Disease remission  regression of fibrosis: thinner scar, fibrous septa breaks, regenerating
parenchymal nodules coalesce




Active drinker liver cirrhosis | After long-term abstinence

CLINICAL FEATURES
 Asymptomatic until advanced stage
 Jaundice, encephalopathy, and coagulopathy (similar to acute liver failure) with the addition of:
 Chronic sever jaundice  pruritus (itching): patients scratch their skin (risk of infections)
o Indication of liver transplantation
o Also seen in: cholestasis
 Portal hypertension  esophagogastric varices (causes by portosystemic shunts: blood flow
reversed from portal to systemic circulation)  hematemesis
o Also causes congestive splenomegaly  expanded red pulp  increased sequestration
 decreased platelets count
o In males: periumbilical caput medusae, hemorrhoids, testicular atrophy
o In females: oligomenorrhea, amenorrhea, sterility
 Impaired estrogen metabolism in males  hyperestrogenemia, causes
o Palmar erythema (local vasodilation) and spider angioma
o Hypogonadism (also in women) and gynecomastia
 Increased risk of hepatocellular carcinoma HCC
 Thin fibrous septa and large islands of regenerated parenchyma  NO portal hypertension
 Broad bands of fibrosis and loss of parenchyma  portal hypertension and end-stage liver
disease

ACUTE-ON-CHRONIC LIVER FAILURE
 Sudden signs of acute liver failure after years of stable and well-compensated chronic disease
 Previous cirrhosis with vascular shunting OR liver parenchyma with borderline vascular supply 
liver vulnerable of lethal insults: hepatitis D superinfection of chronic hepatitis B, resistance to
therapy of viral hepatitis, ascending bacterial cholangitis in primary sclerosing cholangitis,
development of metastatic carcinoma



INFECTIOUS DISORDERS
VIRAL HEPATITIS

, HEPATITIS A VIRUS (HAV)
 (+) RNA, picornavirus (genus: hepatovirus)
 Benign, self-limited infection, cleared by host immune response, NO carrier state
 DOES NOT cause chronic hepatitis, rarely causes fulminant hepatitis
 Incubation period: 3 – 6 weeks
 Associated with poor hygiene and sanitation
 Available vaccine
 Symptoms: fever with jaundice, and nonspecific fatigue and loss of appetite
 Transmission: oral-fecal, contaminated food (shellfish) and water
 Detected in stool (2 – 3 weeks before and 1 week after jaundice), serum, and saliva
o Transient viremia  NO blood-borne transmission




IgM appear at the onset of symptoms
Fecal shedding ends with IgM rise
IgM declines in months  IgG persist for years

HEPATITIS B VIRUS (HBV)
 Circular ds-DNA virus, hepadnaviridae
 Self-limited infection without treatment, but with risk of chronic liver disease development
 Incubation period: 2 – 26 weeks
 Transmission: perinatal (during childbirth), spread among children through breaks in skin and
mucous membranes, sexual, IV drug users, blood transfusion (HBsAg screening in donors)
 Young patients  increased risk of chronic infection
 Remains in blood during acute and chronic disease
 DNA encodes
o HBcAg: nucleocapsid core protein antigen
o HBeAg: nucleocapsid precure and core region antigen
o HBsAg: envelope glycoprotein surface antigen
o Polymerase with both polymerase and reverse transcriptase activity (against treatment)
o HBx protein: transcription activator for viral genes
 Outcomes of the disease (depends on host CD4+ and CD8+ immune response)
o Acute hepatitis with complete recovery
o Nonprogressive chronic hepatitis
o Progressive chronic disease with cirrhosis
o Fulminant hepatitis with massive necrosis
o Asymptomatic healthy carrier state
 Increased risk of HCC
 Serum markers:

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