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Liver, gallbladder, and biliary tract and pancreas pathology - PowerPoint PPT Presentation

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Liver, gallbladder, and biliary tract and pancreas pathology. Liver- lobule/ acinus. Lobule,acinus. Prometheus. Liver function. The liver is the largest internal organ of the body, which is supplied by the portal vein and hepatic artery

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Liver gallbladder and biliary tract and pancreas pathology

Liver, gallbladder, and biliary tract and pancreas pathology

Liver function
Liver function

  • The liver is the largest internal organ of the body, which is supplied by the portal vein and hepatic artery

  • The liver functions as an important regulator of protein synthesis, glucose and lipid metabolism, and bile production

Clinical manifestations of liver disease
Clinical manifestations of liver disease

  • Hepatic failure: clinical findings include:






    spider angiomas



    weight loss

    muscle wasting

Clinical manifestations of liver disease1
Clinical manifestations of liver disease

Complications of hepatic failure include

  • Coagulopathy

  • hepatic encephalopathy

  • hepatorenal syndrome

  • Hepatopulmonary syndrome

Hepatic encephalopathy
Hepatic encephalopathy

  • Hepatic encephalopathy is defined as a spectrum of neuropsychiatric abnormalities in patients with acute or chronic liver dysfunction

  • Hepatic encephalopathy is characterized by personality changes, intellectual impairment, and a depressed level of consciousness.

  • Clinical findings include: altered mental status, seizures, hyperreflexia, rigidity, asterixis

Hepatic encephalopathy1
Hepatic encephalopathy

  • This occurs due to astrocyte dysfunction and brain edema

  • Excessive ammonia reaches the brain via the bloodstream. Note: portosystemic shunt plays a vital role in diverting blood from the diseased liver to systemic circulation

Hepatorenal syndrome
Hepatorenal syndrome

  • Hepatorenal syndrome is the development of renal failure and in the presence of severe liver disease

  • Multiple mechanisms are involved; namely, increased renal vascular resistance and decreased peripheral resistance.

  • This leads to lowered renal blood flow, reduced GFR and urinary output- increased BUN/S. creatinine

  • Other causes of renal failure must be ruled out

Hepatopulmonary syndrome
Hepatopulmonary syndrome

  • (HPS)

  • clinical triad of chronic liver disease, hypoxemia, and intra-pulmonary vascular dilations (IVPD)8

  • The possible causes of hypoxemia are:

  • ventilation perfusion mismatch (the predominant cause), because of lack of uniform blood flow in the presence of stable alveolar ventilation; limitation of oxygen diffusion

  • ("diffusion-perfusion" defect), which occurs because there is inadequate time for oxygen exchange at the alveolo-capillary junction due to rapid flow of blood in the dilated vessels; and shunting of blood from pulmonary arteries to pulmonary veins.

Hepatopulmonary syndrome1
Hepatopulmonary syndrome

  • Enhanced production of nitric oxide (NO) by the lung appears to be the key mediator.

  • Most patients respond to oxygen therapy

  • liver transplantation is the only curative treatment.


  • Cirrhosis represents the final pathway of many chronic liver diseases

  • Cirrhosis is the ninth leading cause of death in the U.S.

  • The most common causes of cirrhosis include:

    alcohol (most common)

    viral hepatitis

    autoimmune hepatitis

    biliary tract disease


    alpha -1 antitrypsin deficiency

    Wilson disease


  • Cirrhosis is characterized by fibrosis and the conversion of normal liver architecture into abnormal nodules (diffuse involvement of the liver)

  • Collagen deposition causes vascular changes to take place, which prevent the exchange of proteins between plasma and hepatocytes

    Note: loss of microvilli also affect transport between the two sites

Pathogenesis of cirrhosis1
Pathogenesis of cirrhosis

  • The central pathogenic processes in cirrhosis are:

  • Death of hepatocytes,

  • Extracellular matrix (ECM) deposition,

  • And vascular reorganization.

  • The vascular architecture of the liver is disrupted by the parenchymal damage and scarring, with the formation of new vascular channels.

Pathogenesis of cirrhosis2
Pathogenesis of cirrhosis

  • The predominant mechanism of fibrosis is the proliferation of hepatic stellate cells and their activation into highly fibrogenic cells,

  • Other cell types, such as portal fibroblasts, fibrocytes, and cells derived from epithelium-mesenchymal transitions may also produce collagen.

  • Proliferation of hepatic stellate cells and their activation into myofibroblasts is initiated by increase in the expression of platelet-derived growth factor receptor β (PDGFR-β) in the stellate cells.

Pathogenesis of cirrhosis3
Pathogenesis of cirrhosis

The stimuli for stellate cell activation may originate :

  • chronic inflammation, with production of inflammatory cytokines such as tumor necrosis factor (TNF), lymphotoxin, and interleukin 1β (IL-1β), and lipid peroxidation products;

  • Cytokine and chemokine production by Kupffer cells, endothelial cells, hepatocytes, and bile duct epithelial cells;

  • Disruption of the ECM

  • Direct stimulation of stellate cells by toxins.

Pathogenesis of cirrhosis4
Pathogenesis of cirrhosis

  • The surviving hepatocytes are stimulated to regenerate and proliferate as spherical nodules within the confines of the fibrous septa.

  • The net outcome is a fibrotic, nodular liver in which delivery of blood to hepatocytes is severely compromised, as is the ability of hepatocytes to secrete substances into plasma.

  • Obliteration of biliary channels may lead to jaundice


  • Clinical findings:

    asymptomatic mainly

    symptoms include: anorexia, weight loss, weakness

  • Complications: overt or progressive hepatic failure

    portal hypertension hepatocellular carcinoma

Portal hypertension
Portal hypertension

  • Portal hypertension may be defined as a portal pressure gradient of 12 mm Hg or greater

  • Causes of portal hypertension:


    Intra-hepatic- especially cirrhosis

    Post hepatic

Portal hypertension1
Portal hypertension


  • Obstructive thrombosis,

  • Narrowing of the portal vein before it ramifies within the liver,

  • Massive splenomegaly with increased splenic vein blood flow.


  • Cirrhosis-Most cases

  • schistosomiasis, massive fatty change, diffuse fibrosinggranulomatous disease such as sarcoidosis, and diseases affecting the portal microcirculation such as nodular regenerative hyperplasia .

Portal hypertension2
Portal hypertension


  • Severe right-sided heart failure,

  • Constrictive pericarditis,

  • Hepatic vein outflow obstruction


  • Clinical marker of defect in metabolism and/or excretion of bilirubin.

  • Yellow discoloration of sclera, skin, mucous membranes due to deposition of bile pigment

  • Clinically detected with serum bilirubin >2-2.5mg/dl

  • There are two types of classifications:

  • Conjugated vs. unconjugated

  • Prehepatic/intrahepatic/posthepatic



  • The breakdown product of Hb from injured RBCs and other heme containing proteins.

  • Produced by reticuloendothelial system

  • Released to plasma bound to albumin

  • Hepatocytes conjugate the bilirubin and excrete it through bile channels into the small intestine

Unconjugated vs conjugated bilirubinemia
Unconjugated vs. conjugated bilirubinemia


  •  production exceeds ability of liver to conjugate

    Examples include:

  • Hemolytic anemias-Rh incompatibility/ ABO incompatibility

  • Bleeding

  • Hepatitis/cirrhosis

  • Physiologic jaundice of newborn

  • Hereditary -Gilbert and Crigler syndromes

  • Conjugated

  • Can produce but not excrete

    Examples include:

  • Biliary tract disease-PSC/PBC

  • Hereditary- Dubin-Johnson syndrome/Rotor syndrome

  • Biliary tract obstruction

  • Cirrhosis/ hepatitis

Prehepatic hemolytic jaundice
Prehepatic (hemolytic) jaundice

  • Results from excess production of bilirubin (beyond the livers ability to conjugate it) following hemolysis

  • High plasma concentrations of unconjugatedbilirubin (normal concentration ~0.5 mg/dL)

Intrahepatic jaundice
Intrahepatic jaundice

  • Impaired uptake, conjugation, or secretion of bilirubin

  • Reflects a generalized liver (hepatocyte) dysfunction

  • In this case, hyperbilirubinemia is usually accompanied by other abnormalities in biochemical markers of liver function

Posthepatic jaundice
Posthepatic jaundice

  • Caused by an obstruction of the biliary tree

  • Plasma bilirubin is conjugated, and other biliary metabolites, such as bile acids accumulate in the plasma

  • Characterized by pale colored stools (absence of fecal bilirubin or urobilin), and dark urine (increased conjugated bilirubin)

  • In a complete obstruction, urobilin is absent from the urine

Jaundice con t
Jaundice con’t

  • Clinical and diagnostic findings:

    Note: cholestasis may be present in cases of impaired bile flow, which may present as pruritus

Congenital hyperbilirubinemia syndromes
Congenital hyperbilirubinemia syndromes

  • Conjugated

  • Dubin-Johnson

  • Rotor

  • Canalicular transport deficiency-MRP2.(Multidrug resistant protein 2)

  • Unconjugated

  • Crigler-Najar 1 and 2

  • Gilberts

    UGT –uridine diphosphate glucuronyl transferase deficiency