Skip this Video
Download Presentation
Liver, gallbladder, and biliary tract and pancreas pathology

Loading in 2 Seconds...

play fullscreen
1 / 40

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

  • Uploaded on

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

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about 'Liver, gallbladder, and biliary tract and pancreas pathology' - meadow

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
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