2. Yellow discoloration of tissues due to accumulation of
bilirubin
Clinical jaundice occurs when bilirubin exceed 3mg/dL
Scleral tissue have higher affinity for bilirubin
It is not a diagnosis; rather etiology should be sought.
3. Bilirubin is a product of RBC breakdown
◦ Hemoglobin → heme+ globin
By heme oxygenase
◦ Heme → biliverdin + CO+ iron
By bilirubin reductase
◦ Biliverdin → bilirubin
By blrubin reductase
Bilirubin lipid soluble
◦ Bilirubin conjugated in the liver
To make it water soluble
4. Hyperbilirubinemia classified as
◦ Conjugated
◦ Unconjugated
Also classifed as
◦ Prehepatic
◦ Hepatocellular
◦ Post hepatic
5. Unconjugated hyperbilirubinemia
◦ Caused by
Increased bilirubin production
Hemolysis
Decreased conjugation in the liver
Criglar najar
Gilbert syndrome
Cirrhosis
Hepatitis
Drugs and toxins
7. Unconjugated
◦ Jaundice
◦ Normal stool and urine color
◦ Features of underlying etiology
Conjugated
◦ Jaundice
◦ Pruritus
◦ Pale stool
◦ Dark colored urine
◦ Signs of underlying etiology
◦ Steatorhoea
◦ Bleeding
9. Treat underlying cause
Cholestyramine for pruritus
Surgery
◦ To unblock the biliary tree
10. Ascites derived from the word askos than means a bag
or a sac
Accumulation of fluid within the peritoneal cavity
Small accumulation produces no symptoms
Healthy males have little or no fluid normally
Females have up to 20 ml of fluid in the peritoneal
cavity
Not a diagnosis; look for etiology
11.
12. Under filling theory
◦ Splanchnic sequestration of fluid
Overflow theory
◦ Inappropriate retention of sodium and water
Peripheral vasodilation theory
◦ Combination of above 2
13. Transudative ascites
◦ No intrinsic problem to the peritoneal membrane
◦ SAAG more than 11g/L
Exudative ascites
◦ There is an intrinsic problem to the peritoneal membrane
◦ SAAG less than 11g/L
18. Treat the cause
Sodium and fluid restriction
Diuretics
Spironolactone or amiloride
Therapeutic paracentesis (ascitic tap)
Infusion of albumin
Trans Jugular Intrahepatic Portosystemic Stent Shunt.
Peritoneo-venous shunt
20. Neuropsychiatric disorder due to liver disease
Caused by nitrogenous toxins that bypasses the liver
and reaches the CNS
This follows inability of the liver to metabolize these
toxins
Toxins implicated include ammonia, GABA, etc.
Presents with psychiatric symptoms, altered level of
conciousness, convulsion, etec.
Treatment
◦ Lactulose
◦ Rifaximin, neomycin for gut sterilization
21. Characterised by diffuse hepatic fibrosis and nodule
formation
Caused by recurrent/chronic hepatocyte damage
Normal liver tissue replaced by fibrous tissue
Occurs at any age
Significant cause of premature death
23. Chronic inflammation and hepatocyte damage
◦ Cytokines from kupfer cells transform stalete cells into
myofibroblast
◦ Myofroblast are converted to collagen
◦ Collagen together with cytokines worsen injury
Replacement of normal liver tissue by fibrous tissue
◦ Micronodular or
◦ Macronodular
Progressive loss of liver function
Portal hypertension
24. Assymptomatic
Upper abdominal discormfort
Anorexia nausea vomiting, weight loss
Weakness and fatigue
Hepatomegally, splenomegally
Features of portal hypertension
Features of hepatic insufficiency