GI Tract: Liver Flashcards
Cells types in the liver:
- Hepatocytes (able to regenerate)
- Kupffer cells (macrophages, able to phagocytose)
- Stellate cells (synthetic cells that can be activated to make collagen creating scare tissue and fibrosis)
Portal tract contain:
The bile duct, the lymphatics, the hepatic artery and the portal vein.
Xanthoma:
Cholesterol deposits on the skin (around the eyes, creases of the hands)
Jaundice: Potential causes
- Obstruction outside of the liver (tumors, inflammation, gallstones, biliary atresia)
- Bilirubin is conjugated (water soluble)
- Liver is excreting it in the bile duct
- The bilirubin stays in the liver. It will be absorbed in the blood because it is water soluble
Biliary Atresia:
- Blockage of the ducts from the liver to the intestine
- Pigment is not able to get into the intestine, stools are white.
- The urine is a dark colour due to the bilirubin entering in the blood stream and kidney filter this blood.
Hemolytic Jaundice:
With hemolysis, the ability to transport and breakdown conversion system to conjugate the bilirubine is impaired
(excess of unconjugated bilirubin in the blood)
Gilbert’s Syndrome:
- Mutation in the promoter region UGT gene –> Reduced transcription of glucoryl transferase. (the enzyme is not missing, just less in quantity)
- The enzyme will eventually catch up with the excess amount of bilirubin and things will go back to normal
Neonatal Jaundice:
- Enzymes in the newborn liver are less able to conjugate bilirubin, lower levels of albumin, increased RBC lysis –> So increase unconjugated bilirubin in the circulation
- The BBB is incomplete in newborn, the bilirubin can cross it and concentrates itself in the basal ganglia causing neuronal degeneration (Kernicterus)
- Tx: phototherapy (photoconversion of bilirubin into a form that the newborn are able to excrete)
Nonalcoholic fatty liver disease (NAFLD) is
- Most common liver disease in both adult and children worldwide
- Due to increase amount of fats and fructose in the diet, there is impairment of the intestinal barrier –> bacterial endotoxins can get through–> inflammation of the liver
- Adipokines are released by the excess of fat cells going to the liver. Kupffer and Stellate cells respond by recognizing the pathogen (TLR4) causing fibrosis leading to impairment of the liver.
Steatosis:
lipid accumulation in the liver
Steatohepatitis:
Lipid accumulation in the liver with inflammation
Disbyosis is:
- The different types of microorganisms that make up the microbiome is abnormal. Feature of obesity.
- Increase permeability of the intestine where bacteria can tranlocate releasing toxins into the liver. Increase inflammation.
Alcoholic Liver Disease:
- Damage due to ethanol and acetaldehyde
- Increase lipid synthesis in the liver, causing fatty liver and block lipid utilization in the liver.
- Induce intestinal permeability and intestinal inflamation.
- Stimulates the Kupffer cells which release cytokine and free radicals.
- Activation of fibroblast (by the Stellate cells) –>fibrosis.
- Death of hepatocytes via apoptosis and necrosis.
Hepatic encephalopathy:
- Brain damage and intellectual disturbances related to liver disease
- Liver do not metabolize adequatly the exogenous compounds, those compounds will travel through the blood to the brain. (bypass the liver if obstruction)
Hepatitis A (HAV):
- Contamination food
- The virus crosses the intestinal barrier, get into the blood, to the liver, reproduces itself, new particles get into the stool and it is shed into the stool.
- Sympotoms disappear after a few weeks once the antibodies are made.
Hepatitis B (HBV):
- Able to reproduce itself, and it reproduces these extra little particles that consist of only the surface antigen in either finalments long oval) or spheres (circles)
- Attaches to the receptors on the surface of the hepatocyte, reproduce itself, is transmitted through blood, serum, and wound exudate (high concentration)
- moderate concentration of HBV: in the semen, vaginal fluid and saliva.
- 35% symptomatic acute hepatitis; 65% have subclinical infection (recovery)–> 10% will develop chronic hepatitis
Hepatitis C (HCV):
- many subtype, most common in Canada, type 1
- Distinguishing feature of HCV: take different shapes and size to latches onto lipoprotein (help protect the HCV), becoming a lipoviroparticle.
- Lipoviroparticle binds to the cells by recognizing CD81 and scavenger receptor (SRB1) on the surface of the hepatocyte.
- It hijacks the hapatocytes synthesis of lipoproteins.
Hepatitis D (HDV):
-HDV needs HBV’s surface envelope, will coats itself in the HBV surface antigen. Both will begin to reproduce themselves and released into the blood.
Hepatitis E (HEV):
- No chronic state, same as hepatitis A.
- Acute illeness can progress to fulminant hepatitis in pregnant women and lead to death of the mother and fetus.
