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Bett SK
 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.
 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
 Hyperbilirubinemia classified as
◦ Conjugated
◦ Unconjugated
 Also classifed as
◦ Prehepatic
◦ Hepatocellular
◦ Post hepatic
 Unconjugated hyperbilirubinemia
◦ Caused by
 Increased bilirubin production
 Hemolysis
 Decreased conjugation in the liver
 Criglar najar
 Gilbert syndrome
 Cirrhosis
 Hepatitis
 Drugs and toxins
Extra hepatic cholestasis Intrahepatic cholestasis/damage
 Gall stones
 Tumors
 Sclerosing cholangitis
 Parasitic infections
 Pancreatitis
 Strictures
 Hepatitis
 Primary biliary cirhosis
 Drugs and toxins
 Autoimmine disorders
 Dubin jonson syndrome
 Rotor syndrome
 Granulomatous diseases
 Alcohol
 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
 Bilirubin levels
 Liver enzymes
 Serum proteins
 Complete blood count
 Reticulocyte count
 Abdominal ultrasound
 Abdominal CT
 Treat underlying cause
 Cholestyramine for pruritus
 Surgery
◦ To unblock the biliary tree
 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
 Under filling theory
◦ Splanchnic sequestration of fluid
 Overflow theory
◦ Inappropriate retention of sodium and water
 Peripheral vasodilation theory
◦ Combination of above 2
 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
 Abdominal distension
 Everted umbilicus
 Respiratory distress
 positive shifting dullness
 Positive fluid thrill
 Features of underlying etiology
 Paracentesis
◦ Appearance
◦ Biochemistry
 Albumin
 amylase
◦ Micrsospy
 G-staining, Z-N staining
◦ Gene expert for TB
◦ Culture
◦ Cytology
 WBCs, malignant cells
 LFTs
◦ Liver enzymes
◦ Coagulation profile
◦ Blirubin
◦ Serum proteins
 UECs
 CBC
 Abdominal ultrasound
 Abdominal CT
 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
 Spontaneous bacterial peritonitis
 Hepato-renal syndrome
 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
 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
 Alcohol
 Chronic viral hepatitis (B or C)
 Non-alcoholic fatty liver disease
 Immune
◦ Primary sclerosing cholangitis
◦ Autoimmune liver disease
 Biliary
◦ Primary biliary cirrhosis
◦ Cystic fibrosis
 Genetic
◦ Haemochromatosis
◦ Wilson's disease
◦ α1-antitrypsin deficiency
 Cryptogenic (unknown-15%)
 Chronic venous outflow obstruction
 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
 Assymptomatic
 Upper abdominal discormfort
 Anorexia nausea vomiting, weight loss
 Weakness and fatigue
 Hepatomegally, splenomegally
 Features of portal hypertension
 Features of hepatic insufficiency
 Features portal hypertension
◦ Splenomegally
◦ Oesophageal varices
◦ Rectal varices
◦ Dilated anterior abdominal wall veins
◦ Feto-hepaticus
◦ Ascites
 Features of hepatic insufficiency
◦ Oedema and ascites
◦ Jaundice
◦ Hepatic encephalopathy
◦ Bleeding
◦ Hypoglycemia
◦ Loss of libido, hair loss
◦ Men: gynaecomastia, testicular atrophy, impotence
◦ Women: breast atrophy, irregular menses, amenorrhoea
 Other features
◦ Spider telangiectasia,
◦ Palmar erythema,
◦ Digital clubbing,
◦ Dupuytren's contracture
 Treat the underlying cause
 Avoid precipitants
 Nutritional support
 Treatment of complications
◦ Ascites
 Tapping
 Diuretics
◦ Encephalopathy
 Shunting
 Gut sterilisation; aminosidine, neomycin
◦ Variceal bleeding
 Sclerotherapy
 Nifedipine
◦ Coagulopathy
 Vitamin K
Thanks

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Disorders of the Liver.pptx

  • 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
  • 6. Extra hepatic cholestasis Intrahepatic cholestasis/damage  Gall stones  Tumors  Sclerosing cholangitis  Parasitic infections  Pancreatitis  Strictures  Hepatitis  Primary biliary cirhosis  Drugs and toxins  Autoimmine disorders  Dubin jonson syndrome  Rotor syndrome  Granulomatous diseases  Alcohol
  • 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
  • 8.  Bilirubin levels  Liver enzymes  Serum proteins  Complete blood count  Reticulocyte count  Abdominal ultrasound  Abdominal CT
  • 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
  • 14.  Abdominal distension  Everted umbilicus  Respiratory distress  positive shifting dullness  Positive fluid thrill  Features of underlying etiology
  • 15.  Paracentesis ◦ Appearance ◦ Biochemistry  Albumin  amylase ◦ Micrsospy  G-staining, Z-N staining ◦ Gene expert for TB ◦ Culture ◦ Cytology  WBCs, malignant cells
  • 16.  LFTs ◦ Liver enzymes ◦ Coagulation profile ◦ Blirubin ◦ Serum proteins  UECs  CBC  Abdominal ultrasound  Abdominal CT
  • 17.
  • 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
  • 19.  Spontaneous bacterial peritonitis  Hepato-renal syndrome
  • 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
  • 22.  Alcohol  Chronic viral hepatitis (B or C)  Non-alcoholic fatty liver disease  Immune ◦ Primary sclerosing cholangitis ◦ Autoimmune liver disease  Biliary ◦ Primary biliary cirrhosis ◦ Cystic fibrosis  Genetic ◦ Haemochromatosis ◦ Wilson's disease ◦ α1-antitrypsin deficiency  Cryptogenic (unknown-15%)  Chronic venous outflow obstruction
  • 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
  • 25.  Features portal hypertension ◦ Splenomegally ◦ Oesophageal varices ◦ Rectal varices ◦ Dilated anterior abdominal wall veins ◦ Feto-hepaticus ◦ Ascites
  • 26.  Features of hepatic insufficiency ◦ Oedema and ascites ◦ Jaundice ◦ Hepatic encephalopathy ◦ Bleeding ◦ Hypoglycemia ◦ Loss of libido, hair loss ◦ Men: gynaecomastia, testicular atrophy, impotence ◦ Women: breast atrophy, irregular menses, amenorrhoea
  • 27.  Other features ◦ Spider telangiectasia, ◦ Palmar erythema, ◦ Digital clubbing, ◦ Dupuytren's contracture
  • 28.  Treat the underlying cause  Avoid precipitants  Nutritional support  Treatment of complications ◦ Ascites  Tapping  Diuretics ◦ Encephalopathy  Shunting  Gut sterilisation; aminosidine, neomycin ◦ Variceal bleeding  Sclerotherapy  Nifedipine ◦ Coagulopathy  Vitamin K
  • 29.