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Liver, gallbladder, and biliary tract and pancreas pathology

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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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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:

jaundice/cholestasis

hypoalbuminemia

hyperammonemia

hypoglycemia

palmarerythema

spider angiomas

hypogonadism

gynecomastia

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
cirrhosis
  • 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

hemachromatosis

alpha -1 antitrypsin deficiency

Wilson disease

cirrhosis1
Cirrhosis
  • 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
cirrhosis2
cirrhosis
  • 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:

Pre-hepatic

Intra-hepatic- especially cirrhosis

Post hepatic

portal hypertension1
Portal hypertension

PRE-HEPATIC CAUSES

  • Obstructive thrombosis,
  • Narrowing of the portal vein before it ramifies within the liver,
  • Massive splenomegaly with increased splenic vein blood flow.

INTRA-HEPATICA CAUSES

  • 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

POST-HEPATIC CAUSES

  • Severe right-sided heart failure,
  • Constrictive pericarditis,
  • Hepatic vein outflow obstruction
jaundice
Jaundice
  • 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
jaundice1
Jaundice

Bilirubin:

  • 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

Unconjugated

  •  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

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