Liver

Question 1

Q39. LESIONS OF THE LIVER - REVIEW

liver = high regeneration capacity, massive functional reserve .. surgical removal up to 60% can fully regenerate within 4-6 weeks!

Answer 1

1. DEGENERATION
   - ballooning, feathery (biliary), microvesicular & macrovesicular steatosis.
2. NECROSIS
   - coagulative necrosis, apoptosis, massive, submassive, centrilobular, interface hepatitis (portal edges), bridging (in severe acute hep).
3. REGENERATION
4. INFLAMMATION - viral hepatitis
5. FIBROSIS, CIRRHOSIS
6. CONGESTION - NUTMEG liver, hepatomegaly (>1.5kg)
   - RHF –> congestion around CV –> steatosis, necrosis/atrophic changes - induration, if severe - fibrosis – hard, ‘cirrhosis’ appearance
   - LHF –> hypoperfusion, ischemic necrosis (shard demarcation)
   - Both tog –> centrilobular hemorrhagic necrosis (in centrilobular region + nutmeg liver)
7. INFARCTIONS – rare w. dual supply portal & hepatic v. causes coagulative necrosis
   - obstruction of hepatic v./CV –> Budd Chiari sy (severe centrilob congestion, hepatomegaly, necorsis, fibrosis..weight gain, ascites, abdom pain)
   - obstruction of portal v. –> pyelothrombosis (infective, suppurative thrombosis of portal v.)
   no hepatomeg, but portal HTN, risk of esophageal varices rupture..same clinical
   - obstruction of hepatic a. –> not always ischemic necrosis exc. in transplanted liver. (PAN, embolism..)
8. REYES SY. –> hepatoencephalopathy & steatosis
   infants, children following viral infection - asprin..can die due to coma/neurolog. deficits or liver failure
9. INFECTIONS:
   - ascending e.g. from duodenum - E.coli, proteus, kleb etc. or cholestasis –> cholangitis - from biliary tract –> liver abscesses.
   - hematogenic - multiple small abscesses, trauma - large solitary abscessses, subphrenic, amebic (tropics)
   - necrosis w. neutrophils
10. TOXIC INJURY - steatosis, hepatitis
    - massive necrosis (mushrooms, anaethetics, ATBs etc.) –> acute LF, may shring to 500-700g w overly large capsule…

others: LF, JAUNDICE, ALCHOLIC LIVER DISEASE, HEMOCHROMATOSIS

Question 2

Q40. HEPATIC JAUNDICE

WHAT HAPPENS IN PRE-HEPATIC JAUNDICE?

Answer 2

1. Hemolytic e.g. anemias, sickle cell, increased RBC breakdown –> high UCB in blood
2. Eventually most conjugated –> CB also high –> urobilinogen –> absorbed into blood - urobilin in urine = yellow/dark urine & to stercobilinogen –> stercobilin in feces = dark/hypercholic feces.

Question 3

WHAT HAPPENS IN HEPATIC JAUNDICE?

Answer 3

1. e.g. viral hepatitis - destruction of hepatocytes - unable to conjugate + bile duct damage - releasing CB, increase pressure, leaks into blood.
2. Both types of bilirubin in blood - can do biphasic diazo reaction (Van den Bergh reaction) to see nature of jaundice (chemical reaction: bilirubin reacts with diazotised sulphanilic acid –> purple coloured azo bilirubin; determines the amount of conjugated bilirubin in blood).
3. CB to urobilinogen –> reabsorbed into blood - urine, enterohepatic…= ???

Question 4

WHAT HAPPENS IN POST-HEPATIC JAUNDICE?

Answer 4

1. Obstruction