Liver and liver disease Flashcards
What are the functions of the liver?
- protein metabolism
- hormone and drug inactivation
- immunological function
- formation of bile
- lipid metabolism
- carbohydrate metabolism
- form coagulation factors
What are the different liver function tests?
albumin (protein synthesis)
coagulation (PT, INR)
What are the different liver biochemistry tests?
- AST (if AST>ALT = alcohol-induced hepatitis)
- ALT (if ALT>AST = viruses/non-alcoholic fatty liver disease)
- alkaline phosphatase (elevated = biliary obstruction)
- gamma glutamyltransferase(elevated = chronic viral hepatits)
- bilirubin (elevated = jaundice)
How are units of alcohol calculated?
units = strength (ABV) x volume (ml)/1000
Describe the metabolism of alcohol.
ethanol –alcohol dehydrogenase–> acetaldehyde –aldehyde dehydrogenase–> acetate
What is the result of:
- increased acetaldehyde
- increased acetate
- increased NADH
- increased acetaldehyde: uncoupling of mitochondria = reduced ATP
- increased acetate: more fatty acid production
- increased NADH: more G3P production
END RESULT: more triglycerides and reversible cell injury
What are the consequences of alcohol-induced liver damage?
- alcoholic fatty liver
- asymptomatic fat deposits in liver
- liver enzymes normal/moderately raised
- liver will be slightly enlarged and pale yellow
- microanatomy: fat deposits in hepatocytes, especially zone 3 - alcoholic hepatitis
- painful hepatomegaly
- fever
- lots of mallory bodies, neutrophils, hepatocyte swelling
- raised AST, raised ALT therefore raised AST:ALT
- raised gamma GT (alcohol causing microsomal hyperplasia)
How is alcoholic hepatitis managed?
- lifelong alcohol abstinence is vital
- steroids may help in severe cases
- supplements if liver function is permanently compromised
- encephalopathy (deficiency in ammonia removal)
- coagulopathy (deficiency in clotting factors)
What is hepatic encephalopathy? How is it diagnosed and treated?
- precipitated by sepsis, bleeding, drugs (opioids, benzodiazepines), deteriorating liver function
- presents as mild confusion –> coma
Diagnosis:
- hepatic flap
- clinical symptoms
- EEG/MRI changes
Treatment:
- lactulose
- transplantation
What is haematemesis a sign of? How is it managed?
Sign of a complication of fibrosis:
- portal HTN
- variceal bleeding from lower oesophagus
Management:
- resuscitation (blood or albumin)
- correct clotting factor abnormalities
- IV terlipressin: splanchnic vasoconstrictor
- endoscopic banding or scleropathy
- emergency portosystemic compression (sengstaken-blakemore tube)
Describe the different portosystemic shunts.
- oesophageal branch of left gastric vein anastomoses with oesophageal branch of azygos vein –> can pop if engorged with blood
- Paraumbilical vein of HPV anastomoses with superficial epigastric branch of femoral vein
- superior rectal vein of IMV anastomoses with inferior and middle rectal veins of internal pudendal vein
What is the most common chronic blood infection?
Hepatitis C
What causes hepatitis C?
drug use
unprotected sex
transfusion
What family of viruses dos hepatitis belong to?
Flavivirus family
What is the incubation period of HCV?
~2 months
Compare the acute and chronic presentation of HCV.
Acute:
- asymptomatic (85%)
- reduced appetite, reduced weight, muscle ache, nausea and fatigue
- raised AST > increased ALT
- inflammatory infiltrate (mainly CD8+ cells removing hepatocyte intracellular infection)
- councilmann bodies (apoptosis eosinophil-like hepatocytes)
Chronic:
- > 6 months
- Fatigue + mild cognitive dysfunction
- S+S:
1. palmar erythema
2. spider naevi
3. hair loss - -> if all 3 S+S = 80% chance of liver disease
4. leuchonychia
5. proximal easting
6. stretch marks
7. xanthelasma (yellowish deposit of cholesterol underneath skin) - portal triad inflammation
What is pruritis?
itching (bile irritates the skin)
What are S+S of damage to the gallbladder/cholestatic symptoms?
- pruritis
2. pale stools + dark urine
How is HCV diagnosed and managed?
Diagnosis:
- HCV IgG antibody enzyme immunoassay (ELISA) –> can’t differentiate acute, chronic or resolved
- PCR to detect HCV RNA (GOLD STANDARD)
- Liver biopsy - can assess degree of liver damage
Treatment:
- depends on serotype
- 95% cure rate (e.g. Sofosbuvir/velpatasvir)
- treatment for ~12 weeks
What can cause hepatocellular carcinoma?
- cirrhosis
- hep B+C
What are the causes of cirrhosis?
- haemachromatosis
- Wilson disease (increased copper in blood)
- alpha-1 antitrypsin deficiency
- fat
- viral hepatitis
- biliary disease
- autoimmune disease
- alcoholic/non-alcoholic fatty liver disease
What are the clinical and biochemical findings in hepatocellular carcinoma?
- nodules on free edge of liver (palpation)
- portal hypertension: backlog of blood, ascites, tender hepatomegaly, splenomegaly, hepatorenal syndrome
- reduced detoxification:
- jaundiced (bilirubin)
- mental status changes (ammonia)
- gynaecomastia, spider naevi (oestrogen) - reduced protein synthesis
- hypoalbuminaemia (exacerbate ascites)
- coagulopathy - Albumin <28g/L
- Prolonged PT
- liver biochemistry = compensated normal
- Decompensated: raised AST, ALT, ALP and gamma GT
What investigations are carried out for hepatocellular carcinoma?
- raised alpha-fetoprotein
- US or contrast CT/MRI
- -> contrast MRI = GOLD STANDARD - biopsy –> only when you can’t diagnose via MRI, want to avoid –> can help spread the cancer
How is HCC managed?
- surgery (lobe resection)/liver transplant
- percutaneous ablation (ethanol injection/US probes)
- transarterial chemoembolisation (if someone can’t have ablation)
- injection of chemotherapeutic agents (hepatic artery) and embolising agents (blocks blood supply to tumour)