Lecture 17 Flashcards
The Liver
Largest organ in body, right upper quadrant abdominal area, beneath the diaphragm, has a double blood supply
Function of the liver
Metabolism: Carbohydrates (glucose), protein, and fat delivered through the portal circulation
Synthesis: Plasma proteins (albumin), clotting factors, bile production
Storage: iron, vitamin B12 and other materials
Detoxification and catabolism: toxins (alcohol, drugs), hormones, ammonia (aa breakdown)
RBC/platelet maintenance and Immune surveillance (80% of Tissue Macrophages)
Portal vein
70% of blood, drains spleen and gastrointestinal tract, rich in nutrients absorbed from intestines, low in oxygen.
Hepatic artery
Rest of blood, high in oxygen, low in nutrients
What is the functional unit of the liver?
Liver lobule
Common types of liver injury
Viral infection, Fatty liver (metabolic syndrome or FLD), Toxins/ alcoholic liver disease or alcoholic hepatitis, and Leads to cirrhosis (scarring/fibrosis) of the liver and potential for cancer development
Manifestation of liver injuries
Cell necrosis or apoptosis, Fatty changes, and Mixed necrosis and fatty change
Diagnosis tests for viruses associated with hepatitis
Blood Tests - ALT (alanine aminotransferase) and AST (aspartate aminotransferase), Biliary tree - ALP (alkaline phosphatase) and GGT(gamma-glutamyl transferase) hepatocytes/biliary tree, ultrasounds (liver inflammation)
Hepatitis A (transmission and prevention)
RNA virus, Incubation period: 2 to 6 weeks, Excreted through nose, throat, stools (person-to-person or contamination)
Prevention/Treatment: Hepatitis A vaccine and Hepatitis A immune globulin: Given after exposure
Hepatitis B (transmission, Diagnosis, prevention/treatment)
ds DNAvirus, Incubation period: 6 weeks to 4 months, Transmission: Blood or body fluids (primarily sexual transmission)
Diagnosis: Antigen–antibody test results
Prevention/Treatment: Hepatitis B vaccine, Hepatitis B immune globulin: Given immediately after exposure, Antiviral drug treatment are also available (control/slow progression, not cure) – liver transplant
Hepatitis C
ssRNA virus - Incubation period: 3 to 12 weeks, Transmission: Blood and body fluids – primarily injection drug use, not as readily transmitted sexually, Diagnosis: Antigen–antibody test results, ultrasound or biopsy
Treatment: no vaccine, treated with antiviral drugs
Anti-HCV Ab
Indicates infection but does not confer immunity (only Anti-HBsAg in HepB indicates immunity)
Hepatitis D: Delta Hepatitis
Small, defective RNA virus and Only infects persons with acute or chronic hepatitis B virus (HBV) infection (uses HBsAg to produce virus coat), usually happens from sharing needles
Hepatitis E
RNA-containing virus, Transmission: Oral–fecal
and Contaminated water, No prevention of disease after exposure and no vaccine
Fatty Liver Disease + diagnosis
Caused by injury to liver that either: Increases fatty acid synthesis, Decreases oxidation of FA or impairs release of lipids from carrier proteins; Common in heavy drinkers and alcoholics and can be caused by drugs/chemicals and solvents (this is reversible if controlled)
FLD Diagnosis: Liver enzymes (AST/ALT), Ultrasound, CT/MRI, biopsy
Alcoholic Liver Disease
Refers to a group of structural and functional changes in the liver resulting from excessive alcohol consumption. Severity depends on amount and duration of alcohol consumption
3 Stages of Alcoholic liver disease
- Alcoholic fatty liver: Mildest form – reversible
- Alcoholic hepatitis: Causes degenerative changes and necrosis of liver cells (inflammation – neutrophil infiltration)
- Alcoholic cirrhosis: Most advanced, progressive, diffuse scarring leading to disturbed liver function
Mallory bodies
Irregularly shaped pink (cytokeratin filament) deposits in hepatocyte cytoplasm and are indicative of severe hepatic injury (irreparable)
Cirrhosis
Diffuse scarring of the liver from any cause with derangement of liver function. Usually caused by Alcoholic liver disease, Chronic hepatitis, and Severe liver necrosis (sometimes liver injury (drugs), autoimmune disease, and long-standing bile obstruction). Outcomes include Liver failure, Portal hypertension, Ascites, collateral circulation formation
Hepatic encephalopathy
Confusion, disorientation (decreased toxin clearance from blood – ammonia and bacterial breakdown products from gut)
Portal hypertension causes…
Ascites – collection of fluid in abdomen
Anastomoses
Circulatory bypass routes are formed to connect systemic-portal venous systems which cause blood to shunt away from high-pressure portal systems into low-pressure veins
Treatment of Cirrhosis-portal hypertension
Drugs to reduce portal hypertension (octetride), Surgical procedures (Portal-systemic anastomoses to control varices) or Trans jugular intrahepatic portosystemic shunt (TIPS), liver transplants (5 year survival rate)
Reye Syndrome
Caused from viral illness and use of Aspirin. Affects infants and children, Fatty liver with liver dysfunction, Cerebral edema with neurologic dysfunction, No specific treatment – mortality rate of 25%
Bile
Aqueous solution with various dissolved substances that is secreted continually and stored in gallbladder to act as a biological detergent; Conjugated bilirubin
Bile salts
A major constituent of bile; derivatives of cholesterol and amino acids; emulsify fat; function as detergents
Substances present in bile
Lecithin (Lipid that also functions as a detergent), Cholesterol, Water, and Minerals
Bilirubin
Bilirubin (non-iron portion of blood) is produced by the liver, from the breakdown of red blood cells in spleen and liver by resident macrophages through conjugation. It is eliminated in feces (stercobilin) and urine (urobilin)
Jaundice
Yellow discoloration of skin and sclera from accumulation of bile pigment (bilirubin) in tissues and body fluids
Hemolytic jaundice
Increased breakdown of red cells (prehepatic)
Hepatocellular jaundice
Liver injury that impairs conjugation of bilirubin and downstream elimination (hepatic)
Obstructive jaundice
Bile duct obstructed by tumor or stone that impairs delivery of bile into duodenum (post hepatic)
Primary biliary cirrhosis
Slow and progressive autoimmune disease that attacks small intrahepatic bile ducts; has no specific treatment other than a liver transplant
Secondary biliary cirrhosis
Obstruction of large extrahepatic bile ducts (Gallstone, carcinoma in pancreas, cancer from common bile duct) which causes increased pressure; Treatment includes Relieving or bypassing duct obstruction
Cholelithiasis
Formation of stones in the gallbladder – excess cholesterol; estrogen can play a role therefore higher in women than men
Factors influencing stone formation
Increased cholesterol in bile (obesity, high fat diet) and Decreased bile excretion (dieting)
Cholangitis
Bile duct obstruction/inflammation
Complications and Diagnosis of Cholelithiasis
Asymptomatic if remain in gall bladder, can cause Common duct obstruction (jaundice) and Cystic duct obstruction (no jaundice), and pancreatitis
Diagnosis: Elevated bilirubin, ALP, GGT elevated, Ultrasound, and CT
Cholecystitis + treatment
Inflammation of gallbladder due to gallstone blockage
Treatment:
Antibiotics, analgesics, Removal of stone by endoscopy (Endoscopic Retrograde CholangioPancreatography -ERCP), Cholecystectomy (removal of gall bladder), and Chenodeoxycholic acid dissolves gallstones
