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32 Cards in this Set
- Front
- Back
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What is the hilum of the liver called?
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porta hepatis
Entry way into the liver |
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How many hepatic segments are there?
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8
4 in each functional lobe (divided at the line of the gallbladder) |
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What are the ligamentum teres and ligamentum venosum remnants of?
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teres - umbilical vein
oxygenated blood from the placenta to the liver venosum - ductus venosus L. umbilical vein to IVC - short-circuiting the liver |
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Which Cells in the liver will be mostly affected by a poison? Ischaemia?
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Poison - cells on the outer edge of the liver lobule (closest to the incoming blood from the portal vein)
Ischaemia - cells at the center of the liver lobule - near the central vein (reduced Oxygen) |
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What are the key Histological features of the liver?
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Liver lobule - central vein + portal triad at edge of lobule
bile canaliculi phagocytic cells - Kupffer cells Perisinusoidal space of Disse Also - haematopoiesis in foetus and anaemic adults |
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What enzymes convert Glucose to Glucose - 6 - phosphate and channelled into glycogen production ?
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All tissues - Hexokinase (low Vmax) - becomes saturated at levels above >5mmol - ie after meals
Liver - Glucokinase (High Vmax) - |
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What enzyme is involved in the break down of Glucose-6-phosphate to glucose?
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glucose-6-phosphatase
Controlled by GLUCAGON, and increased by ADRENALIN via SNS |
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What happens to excess CHO intake when there is sufficient glycogen synthesis?
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Excess CHO is channelled through glycolysis --> leading to long chain fatty acid formation (LCF)
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What happens to LCFAs (long chain fatty acids) when ingested?
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LCFAs are converted into TAGs and are transported to adipose tissue as VLDLs for storage
When energy demand increases - LCFAs are released from adipocytes and are degraded within the liver to give acetyl CoA -- Citric acid cycle (ATP synthesis) or converted to cholesterol or Ketone bodies |
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Nitrogen containing compounds are ingested in excess of normal requirements are also processed by the liver.
How is the Nitrogen wastes removed from the body? |
Via the urea cycle.
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Lactate is produced by RCBs and white muscle in glucose metabolism.
What happens to this lactate? |
taken up by the liver
~30% processed by oxidation to CO2 ~70% is converted to glucose |
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How are liver Biopsies obtained?
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Percutaneous biopsy - Although due to clotting abnormalities this is often difficult
Transjugular liver biopsy, autopsy, liver transplantation |
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Histopathologically what is usually evident in Acute Vs Chronic Liver Failure?
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ACUTE
Massive necrosis of hepatocytes - few or no hepatocytes inflammatory cells - lymphocytes + neutrophils' CHRONIC Cirrhosis - bands of fibrous tissue surrounding nodules of hepatocytes SPECIFIC Hep B - immunohistochemisty Hep C - fat deposits in hepatocytes with nodular portal tract infiltrates Alcoholic Liver Disease - neutrophillic inflammatory infiltrate, pericellular fibrosis, and Mallory's hyaline in hepatocytes. Haemachromatosis - Fe staining Wilson's Disease - Cu staining |
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What is the epidemiology of Chronic Hep B infection?
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afflicts 350mil people worldwide
1-2% AUS adults 10-15% of aboriginals + migrants (asia, africa, pacific islands) Untreated - 1/4 will develop severe chronic liver disease or primary liver cancer |
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Where in the body can the Hep B virus replicate?
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Mainly Liver
but also - salivary glands, pancreas, testis |
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How does Hep B cause Liver cancer - HCC?
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Integration into the host DNA
Also HB X - Oncogene - transformation |
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What makes cirrhosis development in Hep B patients much worse?
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Hep C infection
Alcohol use Toxins |
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How is HBV Transmitted?
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maternal
parenteral inoculation Sexual transmission Saliva - much lower levels of virus Cannot penetrate intact skin and is NOT infectious orally and is not present in urine or faeces unless contaminated with blood * 50-100 x more infectious than HIV and can survive outside the body for 7 days or more |
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What are the signs of Acute hepatitis in HBV infection?
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Incubation of 3 months (1-6m)
High Viraemia Immue complete symptoms - rash, arthritis often proceed liver damage. Jaundiced High HBsAg, HBV DNA in blood - also Anti-HBc, Anti-HBc IgA * the vast majority of people exposed to HBV remain asymptomatic |
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How can you prevent infection of neonates with Hep B Virus?
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Hep B vaccine + specific Hep B Ig is given to the neonate within 12 hours of birth.
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How is Hep B Treated?
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The aim of treatment in chronic hepatitis B is prolonged suppression of viral replication.This leads to reduced necroinflammation and fibrosis, and can prevent progression to liver failure and hepatocellular carcinoma.
ORAL ANTIVIRAL DRUGS - target the RNA polymerase - Entecavir, Tenofovir - Well tolerated or Weekly PEGYLATED INTERFERON injections - ADRs MONITOR 6 monthly - liver US, Serum Alpha-Foetoprotein (AFP) is recommended for those at highest risk. * Even Pt with Liver failure usually respond to antiviral therapy and transplants are rarely needed to treat HBV |
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How Do you treat HCC - Liver cancer?
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surgical resection, liver transplantation or local ablation techniques, Chemotherapy (more advanced disease)
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What do ALT and AST levels reflect and how are they helpful?
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ALT (alanine aminotransferase) + AST (aspartate aminotransferase) - Serum Aminotransferases
ALT -- released when these is damage to liver hepatocytes and the enzyme is released - Increases of >10 fold x the upper limit indicate hepatocellular necrosis (HEPATITIS) In most liver diseases ALT > AST EXCEPT - Alcoholic Liver disease (AST >10x normal) or chronic hepatitis at the stage of cirrhosis |
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What are SAP and GGT?
What are they useful for? |
SAP - Serum alkaline phosphatase (bone, intestine, placenta)
GGT - gamma-glutamyl transpeptidase Both are present on the hepatocyte membrane Raise levels - often due to cholestasis Alcohol or drug ingestion (ie anticonvulsants) can stimulate synthesis and release of GGT in the absence of Liver injury --> a process of adaptive change referred to enzyme induction. |
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Where is AST Found?
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liver, heart, skeletal muscle, kidneys, brain, and red blood cells
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What can cause an elevated ALT?
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viral hepatitis, diabetes, congestive heart failure, liver damage, bile duct problems (measure SAP), infectious mononucleosis, or myopathy (Measure CK)
Can also vary through the day, rise with stress or exercise |
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What does elevated serum bilirubin mean?
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Increased Production
Impaired Hepatic Uptake and Conjugation Impaired Secretion into Bile DISEASES Liver disease - mixed conjugated/unconjugated (due to function of secretion and conjugation) Cholestasis - conjugated hyperbilirubinaemia |
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What is the most common cause for elevated bilirubin?
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Gilbert's Syndrome
raised unconjugated bilirubin 5-10% of the population Hereditary "hyperbilirubinaemia" Reduced activity of the enzyme which conjugates bilirubin - ie difficult to remove |
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How may cholestasis cause Vit K deficiency?
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because of the resultant malabsorption of long chain fatty acids (lipid soluble vitamin)
Leads to prolonged Prothrombin time Will be corrected with parenteral Vit K |
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What is the most useful test for liver function in acute liver failure?
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Prolonged PT
This is because of the rapid turnover of clotting factors - it is not corrected with Parenteral Vit K (which would fix PT in cholestasis) |
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What happens to serum albumin and globulins in chronic liver disease?
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Albumin - usually low
Total globulins - usually raised due to dysregulation (but not usually measured) Specific globulins may indicate Dx IgG - autoimmune hepatitis IgM - primary biliary cirrhosis IgA - alcoholic liver disease |
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What liver specific tests are commonly used ?
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ALT, AST
GGT, ASP Serum Ferritin - haemachromatosis Caeruloplasmin (Cu carrying protein) - low in Wilson's disease Alpha-fetoprotein - HCC or active cirrhosis |
