↑
Chronic Hepatitis B HBV virus, hepadnavirus, DNA virus with DNA polymerase enzyme
Sexual, parenteral, mother to child transmission
Risk of chronic infection related to age, higher risk in younger age
Chronic infection due to viral persistence hepatic inflammation, necrosis, mitosis, regeneration
cirrhosis, cellular dysplasia HCC
Acute with 1-6 month incubation
Chronic with unspecific features, hepatic failure, most patients are iactive noncontagious carriers
5 stages of chronic hepatitis
Immune tolerant phase – HbsAg +, HBeAg +, no anti HBe, high viral load, normal or low ALT
Immune reactive phase – HbsAg + HBeAg+, no anti HBe Ab viral load, raised ALT
Inactive carrier phase – HbsAg +, HBeAg -, anti-HBeAg +, normal ALT
HBeAg negative chronic hepatitis phase – HbsAg + antiHBeAb + no HBeAg fluctuating ALT
HBsAg negative phase – only anti-HBe Ab is positive here, everything else normal
Treatment: Nucleoside/Nucleotide analogues Tenofovir, Entecavir, Telbuvudine, Lamivudine,
Adefovir, pegylated IFN-a
Hepatits B testing HBsAg – first evidence of infection, if present indicates carrier, with out anti-HBs but with anti-HBs
resolved infection or vaccination
HBcAg (core antigen) – anti HBc IgM – shows recent infection
Anti-HBc IgG – shows chronic or resolved infection
HBeAg – indicates high active replication, if anti-HBe – long term clearance
Chronic Hepatitis C RNA flavivirus, acute infection rare, parenteral transmission, vertical, almost always chronic, 20%
develop cirrhosis. Chronic Hepc – HCV infection persisting for >6 months
Liver cirrhosis 25%, extrahepatic – cryoglobulinemia, lymphoma, ITP, autoimmune haemolytic anemia
Diagnosis is via ELISA – anti-HCV antibodies, if positive do PCR
Positive PCR = active infection, negative PCR = prior infection
Transaminase with AST/ALT ratio which is >1 in chronic hepatitis
Treatment – multidrug approach – 2 direct acting antiviral agents
Ledipasvir + sofosbuvir
Sofosbuvir + Velpatasvir, IFN + ribavirin
Liver cirrhosis classified by Child-Pugh class
Autoimmune Rare form of chronic hepatitis, more in (f), associated with T1DM, coeliac, 2 types:
hepatitis Type 1 autoimmune hepatitis (80%) ANA, anti-smooth muscle AB (ASMAs) anti-SLA/LP (antisoulble
liver antigen/liver pancreas antibodies, more common in adults, 4x more common females, associated
with hashimoto, UC, celiac, RA
Type 2 autoimmune hepatitis (20%) – anti-liver-kidney micrsosomal-1 antibodies (anti-LKM1) and anti
liver cytosol antibodies (ALC-1), more common in children, 10x more common females, associated with
T1DM, hashimoto, vitiligo.
Insidious onset, widely variable presentation from nonspecific fatigue, weight loss, pain to signs of
acute liver failure – jaundice, RUQ pain, fever, hepatomeg, splenomeg
Diagnosis by ↑↑ ALT and ↑ AST, ↑GGT + ALP
ANA, ASMA, anti-SLA/MP, AMA T1 Anti-LKM, ALC-1 T2
Biopsy – lymphoplasmacytic interface hepatitis – lymphocytes, bridging or multiacinar necrosis, fibrosis
Treatment – induction prednisone + azathioprine (mycophenolate, cyclosporine, tacrolismus)
maintenance with azathioprine or prednisone
Primary Biliary Aka primary biliary cholangitis –chronic progressive autoimmune liver disease destruction of
Cirrhosis intralobular bile ducts. 9x more common in women, age 30-65, causes vanishing bile duct syndrome
(progressive destruction of intrahepatic ducts) autoimmune inflammation + destruction of small and
medium sized intrahepatic bile ducts ductopenia defective bile duct degeneration
cholestasis hepatic damage portal and periportal fibrosis cirrhosis
Presents with fatigue, pruritis, hyperpigmentation, hepatomegaly, RUQ pain, jaundice, pale stool,
xanthomas. ↑ALP GGT, bilirubin, AST/ALT normal, ↑AMA (antimitochondrial abs) ANA, ↑IgM
Stage 1 – lympcytic infiltration + granuloma, 2- bile ductopenia, fibrosis 3- bridging fibrosis 4-cirrhosis
Ursodeoxycholic acid (ursodiol) – slows progression (immunomodulator, antiapoptotic) liver
transplant. Obeticholic acid is alternative. Cholestyramine used for pruritis.
, ↑
Primary sclerosing Progressive chronic inflammation of intrahepatic and extrahepatic bile ducts associated with
cholangitis ulcerative colitis, 2x more common in men, 40yrs mean age, 90% of PSC patients have UC, HLA-B8 +
DR3. Eventually obliteration of intra + extrahepatic bile ducts biliary cirrhosis, portal HTN + liver
failure.
Signs of cholestasis jaundice, pruritis, pale stool, dark urine, fatigue, can acute cholangitis with
fever, chills RUQ pain. Later cirrhosis with HSM, portal HTN + failure
pANCA 80% ↑cholestasis – GGT, ALP, bilirubin, ↑cholesterol + IgM
MRCP multifocal strictures alternating with dilation and beading of bile ducts, ERCP also
Liver biopsy onion skin scarring + fibrosis 4 stages: 1. Inflammatory infiltration of portal triads and
degeneration of bile duct epithelium 2- periportal inflammation, fibrosis, 3- septal fibrosis, bridging
necrosis, stage 4 – biliary cirrhosis. Treatment – Ursodeoxycholic acid, tacrolismus ERCP with duct
dilation, liver transplant curative.
Wilson disease Aka hepatolenticular degeneration, autosomal recessive metabolic disorder copper accumulation in
body, due to mutations in ATP7B gene which encodes a copper transport protein decreased
incorporation of copper into ceruloplasmin increased copper, decreased serum ceruloplasmin +
increased free copper. Which is deposited into organs, mostly the liver, CNS basal ganglia, kidneys
and enterocytes. Onset is usually 5-35 years. Clinically – different degrees of liver damage, HSM, portal
HTN, pain, jaundice, ascites, hepatic encephalopathy, Kayser-Fleischer rings, parkinsonism, tremor,
dystonia, wing beating tremor, cognitive impairment. Diagnosis is via kayser Fleischer rings, increased
transaminase, decreased ceruloplasmin, increased copper, 24hr urinary copper excretion shows
increased excretion and abnormalities of basal ganglia seen MRI
Treatment – penicilliamine – chelating agent, zinc salts or trientine alternatives.
Hereditary Hereditary (primary) hemochromatosis – iron overload disease iron deposition in many organs.
Hemochromatosis This leads to hemochromatosis type 1 – gene defect is HFE on chromosome 6, HLA-A3, AR with
incomplete penetrance. The gene regulates normal iron balance so mutation accumulation. 75% no
symptoms, can be fatigue, lethargy, Hepatomegaly, cirrhosis, ↑HCC risk, diabetes, bronze skin due to
hyperpigmentation, cardiac siderosis + cardiomyopathy. Diagnosis by ↑iron, ferritin, transferrin and
liver enzymes, decreased TIBC, genetic test for confirmation, liver biopsy shows hemosiderin laden
macrophages and Prussian blue staining. Treatment is phlebotomy 1-2 times per week to remove iron.
Chelators also deferoxamine or defasirox can be used.
Non alcoholic fatty 2 types – NAFLD + NASH non alcoholic fatty liver disease, non alcoholic steatohepatitis
liver disease NAFLD – accumulation of fat in liver cells, not related to alcohol
NASH – NAFLD + chronic inflammation and hepatocyte damage
Most common in obesity, T2DM, medication induced (amiodarone, GCS, estrogen, antiretrovirals)
↑insulin resistance, ↑uptake of FFA by liver ↑fat synthesis ↑peripheral lipolysis, presents with
hepatomegaly, can cirrhosis. There is ↑transaminase with AST/ALT ratio <1 (if it goes >1 represents
progression to cirrhosis) the lipid accumulation is macro vesicular with balloon degeneration +
necrosis. Management is with weight loss, ursodeoxycholic acid. NAFLD fibrosis score and FIB-4 score
used to predict outcomes and risk of cirrhosis. Histological changes on liver biopsy: balloon
degeneration, steatosis, centrilobular, acidophil bodies, necrosis, Mallory hyaline
Alcohol related liver ALD – Range of progressive liver conditions due to chronic alcohol consumption. 3 stages:
disease Alcoholic fatty liver (reversible) Alcoholic Hepatitis, Alcoholic cirrhosis (irreversible) it occurs when
men >210g pure alcohol per week, women >140g per week. Hepatic degradation of ethanol to acetyl-
coA by alcohol dehydrogenase NADH excess increased NADH formation of G3P increased
triglyceride synthesis in liver + inflammation steatohepatitis chronic inflammation hepatic
fibrosis, sclerosis portal HTN and cirrhosis. 1. Pressure, hepatomegaly, can be reversed, usually then
declining liver function progressing to cirrhosis. D: AST>ALT but both ↑ GGT ferritin ↑ CDT
(carbohydrate deficient transferrin) ↑ macrocytic anemia. Ultrasound: hepatomegaly, cant see blood
vessels ↑echogenicity due to steatosis. On CT – decreased attenuation. Treatment is alcohol cessation,
GCS in some cases.
Alcohol acetylaldehyde (ADH) Acetyl co-A + acetate (aldehyde DH) generates NADH
Maddrey score – score calculated from PT and bilirubin prognosis – value >32 = severe liver disease
with poor prognosis. Glasgow alcoholic hepatitis score – age, WBC, urea, PT bilirubin – score >9 – poor
prognosis. Glucocorticoids – prednisolone 40mg for 28 days used in severe cases with madrey score
>32
Liver cirrhosis Cirrhosis characterized by diffuse hepatic fibrosis + nodule formation. Most often due to chronic
, ↑
hepatitis, alcohol, NAFLD, PBC + PSC also.
Liver injury causes stellate cells in space of Disse to be activated by cytokines transformation of
stellate cell into myofibroblast like cell which produces collagen, pro inflammatory cytokines and
mediators hepatic fibrosis + damage . histologically cirrhosis is:
Micronodular – small nodules <1mm macronodular – large nodules.
Can be asymptomatic or with hepatomegaly, splenomegaly, portal HTN, insufficiency, weakness,
fatigue, anorexia, vomiting, pain. Hepatomegaly common in alcoholism + hemochromatosis, atrophic
liver in many other causes e.g. viral hepatitis or autoimmune. Spider telangiectasia, pigmentation,
gynecomastia, splenomegaly, ascites, encephalopathy, dupuytrens contracture.
Once diagnosed, endoscopy for oesophageal varices should be done, repeated every 2 years. HCC
screening also. Child Pugh score + MELD score used to calculate prognosis in cirrhosis, only treatment
is transplantation.
Complications of Decompensated cirrhosis – worsening of LFT + jaundice, ascites, variceal hemorrhage, hepatic
liver cirrhosis encephalopathy. Ascites and spontaneous bacterial peritonitis, coagulopathy that does not respond to
vitamin K.
Hepatic encephalopathy – cirrhosis decreased hepatic metabolism, accumulation of neurotoxic
metabolites especially ammonia cerebral edema, ↑ intracranial pressure neurologic problems –
fatigue, altered consciousness, memory loss, slurred speech etc- treated with lactulose as it decreases
ammonia absorption in the bowel increases excretion of ammonia, rifaximin – also prevents hepatic
encephalopathy.
Hepatorenal syndrome – deterioration of kidney function can lead to kidney failure, oliguria, anuria
and hypotension with wide pulse pressure. Give albumin and norepinephrine.
Portal vein thrombosis – due to portal HTN and imbalance of coagulation factors RUQ pain,
splenomegaly, fever ascites, esophageal variceal hemorrhage and encephalopathy, treatment is with
anticoagulants or trans jugular intrahepatic portosystemic shunt.
Hepatopulmonary syndrome – hypoxemia, intrapulmonary vasodilation and portal HTN dyspnea,
platypnea (shortness of breath worse when lying) and orthodeoxia (decreased oxygen sat when
standing)
Portal HTN – when hepatic venous pressure gradient >10mmHg, risk of variceal bleeding occurs when
>12mmHg.
Child-Pugh Child Pugh score – calculated from:
classification encephalopathy (none, mild marked) = 1,2,3 points
bilirubin - <68, 68-170, >170 (PBC/PSC) or <34, 34-50, >50 = 1,2,3
albumin >35, 28-35, <28 = 1,2,3
prothrombin time <4, 4-6, >6 (secs prolonged) = 1,2,3
ascites – none, mild, marked – 1,2,3
Child A = <7, Child B = 7-9 Child C >9
Diagnostic Ascites = abnormal accumulation of fluid within peritoneal cavity, common complication of portal
algorithm in ascites hypertension, hypoalbuminemia. Clinically with progressive abdominal distension, shifting dullness and
positive fluid wave test. 1- abdominal ultrasound, shows free peritoneal fluid. 2- CT abdomen and
pelvis – free peritoneal fluid, fluid density shows type of ascites. lab studies – serum albumin for
SAAG calculation – serum ascites albumin gradient. 3- diagnostic paracentesis, ascites fluid analysis.
Transparent to yellow – uncomplicated, cloudy – infection or malignancy, bloody – trauma or
malignancy, milky – chylous ascites.
Ascites due to portal HTN SAAG >1.1, increased protein level >2.5 right heart failure, decreased
protein level <2.5 hepatic cirrhosis. If not due to portal hypertension the SAAG is <1.1 Ascites can
be classified: grade 1 mild – only seen on ultrasound. Grade 2 moderate – with moderate abdominal
distension. Grade 3 large – with marked distension.
Treatment – salt and fluid restriction, serial paracentesis, diuretics – spironolactone +/- furosemide
trans jugular intrahepatic portosystemic shunt for refractor cases. Splanchnic arterial vasodilation +
portal HTN increased capillary permeability ascites. Complications of ascites: renal failure,
hepatorenal syndrome, spontaneous bacterial peritonitis (cefotaxime or piperacillin/tazobactam)
HCC most common primary liver malignancy, leading cause of cancer mortality. More common in males,
occurs on background of cirrhosis, chronic hepatitis, often is a solitary tumor. Liver cirrhosis is present
in 80% cases, chronic hep B+C also important, chronic hep b 100 fold risk of HCC, alcohol, NAFLD,
hemochromatosis, Wilson autoimmune diseases also ↑ risk. Ingestion of foods with aflatoxin also.
Chronic Hepatitis B HBV virus, hepadnavirus, DNA virus with DNA polymerase enzyme
Sexual, parenteral, mother to child transmission
Risk of chronic infection related to age, higher risk in younger age
Chronic infection due to viral persistence hepatic inflammation, necrosis, mitosis, regeneration
cirrhosis, cellular dysplasia HCC
Acute with 1-6 month incubation
Chronic with unspecific features, hepatic failure, most patients are iactive noncontagious carriers
5 stages of chronic hepatitis
Immune tolerant phase – HbsAg +, HBeAg +, no anti HBe, high viral load, normal or low ALT
Immune reactive phase – HbsAg + HBeAg+, no anti HBe Ab viral load, raised ALT
Inactive carrier phase – HbsAg +, HBeAg -, anti-HBeAg +, normal ALT
HBeAg negative chronic hepatitis phase – HbsAg + antiHBeAb + no HBeAg fluctuating ALT
HBsAg negative phase – only anti-HBe Ab is positive here, everything else normal
Treatment: Nucleoside/Nucleotide analogues Tenofovir, Entecavir, Telbuvudine, Lamivudine,
Adefovir, pegylated IFN-a
Hepatits B testing HBsAg – first evidence of infection, if present indicates carrier, with out anti-HBs but with anti-HBs
resolved infection or vaccination
HBcAg (core antigen) – anti HBc IgM – shows recent infection
Anti-HBc IgG – shows chronic or resolved infection
HBeAg – indicates high active replication, if anti-HBe – long term clearance
Chronic Hepatitis C RNA flavivirus, acute infection rare, parenteral transmission, vertical, almost always chronic, 20%
develop cirrhosis. Chronic Hepc – HCV infection persisting for >6 months
Liver cirrhosis 25%, extrahepatic – cryoglobulinemia, lymphoma, ITP, autoimmune haemolytic anemia
Diagnosis is via ELISA – anti-HCV antibodies, if positive do PCR
Positive PCR = active infection, negative PCR = prior infection
Transaminase with AST/ALT ratio which is >1 in chronic hepatitis
Treatment – multidrug approach – 2 direct acting antiviral agents
Ledipasvir + sofosbuvir
Sofosbuvir + Velpatasvir, IFN + ribavirin
Liver cirrhosis classified by Child-Pugh class
Autoimmune Rare form of chronic hepatitis, more in (f), associated with T1DM, coeliac, 2 types:
hepatitis Type 1 autoimmune hepatitis (80%) ANA, anti-smooth muscle AB (ASMAs) anti-SLA/LP (antisoulble
liver antigen/liver pancreas antibodies, more common in adults, 4x more common females, associated
with hashimoto, UC, celiac, RA
Type 2 autoimmune hepatitis (20%) – anti-liver-kidney micrsosomal-1 antibodies (anti-LKM1) and anti
liver cytosol antibodies (ALC-1), more common in children, 10x more common females, associated with
T1DM, hashimoto, vitiligo.
Insidious onset, widely variable presentation from nonspecific fatigue, weight loss, pain to signs of
acute liver failure – jaundice, RUQ pain, fever, hepatomeg, splenomeg
Diagnosis by ↑↑ ALT and ↑ AST, ↑GGT + ALP
ANA, ASMA, anti-SLA/MP, AMA T1 Anti-LKM, ALC-1 T2
Biopsy – lymphoplasmacytic interface hepatitis – lymphocytes, bridging or multiacinar necrosis, fibrosis
Treatment – induction prednisone + azathioprine (mycophenolate, cyclosporine, tacrolismus)
maintenance with azathioprine or prednisone
Primary Biliary Aka primary biliary cholangitis –chronic progressive autoimmune liver disease destruction of
Cirrhosis intralobular bile ducts. 9x more common in women, age 30-65, causes vanishing bile duct syndrome
(progressive destruction of intrahepatic ducts) autoimmune inflammation + destruction of small and
medium sized intrahepatic bile ducts ductopenia defective bile duct degeneration
cholestasis hepatic damage portal and periportal fibrosis cirrhosis
Presents with fatigue, pruritis, hyperpigmentation, hepatomegaly, RUQ pain, jaundice, pale stool,
xanthomas. ↑ALP GGT, bilirubin, AST/ALT normal, ↑AMA (antimitochondrial abs) ANA, ↑IgM
Stage 1 – lympcytic infiltration + granuloma, 2- bile ductopenia, fibrosis 3- bridging fibrosis 4-cirrhosis
Ursodeoxycholic acid (ursodiol) – slows progression (immunomodulator, antiapoptotic) liver
transplant. Obeticholic acid is alternative. Cholestyramine used for pruritis.
, ↑
Primary sclerosing Progressive chronic inflammation of intrahepatic and extrahepatic bile ducts associated with
cholangitis ulcerative colitis, 2x more common in men, 40yrs mean age, 90% of PSC patients have UC, HLA-B8 +
DR3. Eventually obliteration of intra + extrahepatic bile ducts biliary cirrhosis, portal HTN + liver
failure.
Signs of cholestasis jaundice, pruritis, pale stool, dark urine, fatigue, can acute cholangitis with
fever, chills RUQ pain. Later cirrhosis with HSM, portal HTN + failure
pANCA 80% ↑cholestasis – GGT, ALP, bilirubin, ↑cholesterol + IgM
MRCP multifocal strictures alternating with dilation and beading of bile ducts, ERCP also
Liver biopsy onion skin scarring + fibrosis 4 stages: 1. Inflammatory infiltration of portal triads and
degeneration of bile duct epithelium 2- periportal inflammation, fibrosis, 3- septal fibrosis, bridging
necrosis, stage 4 – biliary cirrhosis. Treatment – Ursodeoxycholic acid, tacrolismus ERCP with duct
dilation, liver transplant curative.
Wilson disease Aka hepatolenticular degeneration, autosomal recessive metabolic disorder copper accumulation in
body, due to mutations in ATP7B gene which encodes a copper transport protein decreased
incorporation of copper into ceruloplasmin increased copper, decreased serum ceruloplasmin +
increased free copper. Which is deposited into organs, mostly the liver, CNS basal ganglia, kidneys
and enterocytes. Onset is usually 5-35 years. Clinically – different degrees of liver damage, HSM, portal
HTN, pain, jaundice, ascites, hepatic encephalopathy, Kayser-Fleischer rings, parkinsonism, tremor,
dystonia, wing beating tremor, cognitive impairment. Diagnosis is via kayser Fleischer rings, increased
transaminase, decreased ceruloplasmin, increased copper, 24hr urinary copper excretion shows
increased excretion and abnormalities of basal ganglia seen MRI
Treatment – penicilliamine – chelating agent, zinc salts or trientine alternatives.
Hereditary Hereditary (primary) hemochromatosis – iron overload disease iron deposition in many organs.
Hemochromatosis This leads to hemochromatosis type 1 – gene defect is HFE on chromosome 6, HLA-A3, AR with
incomplete penetrance. The gene regulates normal iron balance so mutation accumulation. 75% no
symptoms, can be fatigue, lethargy, Hepatomegaly, cirrhosis, ↑HCC risk, diabetes, bronze skin due to
hyperpigmentation, cardiac siderosis + cardiomyopathy. Diagnosis by ↑iron, ferritin, transferrin and
liver enzymes, decreased TIBC, genetic test for confirmation, liver biopsy shows hemosiderin laden
macrophages and Prussian blue staining. Treatment is phlebotomy 1-2 times per week to remove iron.
Chelators also deferoxamine or defasirox can be used.
Non alcoholic fatty 2 types – NAFLD + NASH non alcoholic fatty liver disease, non alcoholic steatohepatitis
liver disease NAFLD – accumulation of fat in liver cells, not related to alcohol
NASH – NAFLD + chronic inflammation and hepatocyte damage
Most common in obesity, T2DM, medication induced (amiodarone, GCS, estrogen, antiretrovirals)
↑insulin resistance, ↑uptake of FFA by liver ↑fat synthesis ↑peripheral lipolysis, presents with
hepatomegaly, can cirrhosis. There is ↑transaminase with AST/ALT ratio <1 (if it goes >1 represents
progression to cirrhosis) the lipid accumulation is macro vesicular with balloon degeneration +
necrosis. Management is with weight loss, ursodeoxycholic acid. NAFLD fibrosis score and FIB-4 score
used to predict outcomes and risk of cirrhosis. Histological changes on liver biopsy: balloon
degeneration, steatosis, centrilobular, acidophil bodies, necrosis, Mallory hyaline
Alcohol related liver ALD – Range of progressive liver conditions due to chronic alcohol consumption. 3 stages:
disease Alcoholic fatty liver (reversible) Alcoholic Hepatitis, Alcoholic cirrhosis (irreversible) it occurs when
men >210g pure alcohol per week, women >140g per week. Hepatic degradation of ethanol to acetyl-
coA by alcohol dehydrogenase NADH excess increased NADH formation of G3P increased
triglyceride synthesis in liver + inflammation steatohepatitis chronic inflammation hepatic
fibrosis, sclerosis portal HTN and cirrhosis. 1. Pressure, hepatomegaly, can be reversed, usually then
declining liver function progressing to cirrhosis. D: AST>ALT but both ↑ GGT ferritin ↑ CDT
(carbohydrate deficient transferrin) ↑ macrocytic anemia. Ultrasound: hepatomegaly, cant see blood
vessels ↑echogenicity due to steatosis. On CT – decreased attenuation. Treatment is alcohol cessation,
GCS in some cases.
Alcohol acetylaldehyde (ADH) Acetyl co-A + acetate (aldehyde DH) generates NADH
Maddrey score – score calculated from PT and bilirubin prognosis – value >32 = severe liver disease
with poor prognosis. Glasgow alcoholic hepatitis score – age, WBC, urea, PT bilirubin – score >9 – poor
prognosis. Glucocorticoids – prednisolone 40mg for 28 days used in severe cases with madrey score
>32
Liver cirrhosis Cirrhosis characterized by diffuse hepatic fibrosis + nodule formation. Most often due to chronic
, ↑
hepatitis, alcohol, NAFLD, PBC + PSC also.
Liver injury causes stellate cells in space of Disse to be activated by cytokines transformation of
stellate cell into myofibroblast like cell which produces collagen, pro inflammatory cytokines and
mediators hepatic fibrosis + damage . histologically cirrhosis is:
Micronodular – small nodules <1mm macronodular – large nodules.
Can be asymptomatic or with hepatomegaly, splenomegaly, portal HTN, insufficiency, weakness,
fatigue, anorexia, vomiting, pain. Hepatomegaly common in alcoholism + hemochromatosis, atrophic
liver in many other causes e.g. viral hepatitis or autoimmune. Spider telangiectasia, pigmentation,
gynecomastia, splenomegaly, ascites, encephalopathy, dupuytrens contracture.
Once diagnosed, endoscopy for oesophageal varices should be done, repeated every 2 years. HCC
screening also. Child Pugh score + MELD score used to calculate prognosis in cirrhosis, only treatment
is transplantation.
Complications of Decompensated cirrhosis – worsening of LFT + jaundice, ascites, variceal hemorrhage, hepatic
liver cirrhosis encephalopathy. Ascites and spontaneous bacterial peritonitis, coagulopathy that does not respond to
vitamin K.
Hepatic encephalopathy – cirrhosis decreased hepatic metabolism, accumulation of neurotoxic
metabolites especially ammonia cerebral edema, ↑ intracranial pressure neurologic problems –
fatigue, altered consciousness, memory loss, slurred speech etc- treated with lactulose as it decreases
ammonia absorption in the bowel increases excretion of ammonia, rifaximin – also prevents hepatic
encephalopathy.
Hepatorenal syndrome – deterioration of kidney function can lead to kidney failure, oliguria, anuria
and hypotension with wide pulse pressure. Give albumin and norepinephrine.
Portal vein thrombosis – due to portal HTN and imbalance of coagulation factors RUQ pain,
splenomegaly, fever ascites, esophageal variceal hemorrhage and encephalopathy, treatment is with
anticoagulants or trans jugular intrahepatic portosystemic shunt.
Hepatopulmonary syndrome – hypoxemia, intrapulmonary vasodilation and portal HTN dyspnea,
platypnea (shortness of breath worse when lying) and orthodeoxia (decreased oxygen sat when
standing)
Portal HTN – when hepatic venous pressure gradient >10mmHg, risk of variceal bleeding occurs when
>12mmHg.
Child-Pugh Child Pugh score – calculated from:
classification encephalopathy (none, mild marked) = 1,2,3 points
bilirubin - <68, 68-170, >170 (PBC/PSC) or <34, 34-50, >50 = 1,2,3
albumin >35, 28-35, <28 = 1,2,3
prothrombin time <4, 4-6, >6 (secs prolonged) = 1,2,3
ascites – none, mild, marked – 1,2,3
Child A = <7, Child B = 7-9 Child C >9
Diagnostic Ascites = abnormal accumulation of fluid within peritoneal cavity, common complication of portal
algorithm in ascites hypertension, hypoalbuminemia. Clinically with progressive abdominal distension, shifting dullness and
positive fluid wave test. 1- abdominal ultrasound, shows free peritoneal fluid. 2- CT abdomen and
pelvis – free peritoneal fluid, fluid density shows type of ascites. lab studies – serum albumin for
SAAG calculation – serum ascites albumin gradient. 3- diagnostic paracentesis, ascites fluid analysis.
Transparent to yellow – uncomplicated, cloudy – infection or malignancy, bloody – trauma or
malignancy, milky – chylous ascites.
Ascites due to portal HTN SAAG >1.1, increased protein level >2.5 right heart failure, decreased
protein level <2.5 hepatic cirrhosis. If not due to portal hypertension the SAAG is <1.1 Ascites can
be classified: grade 1 mild – only seen on ultrasound. Grade 2 moderate – with moderate abdominal
distension. Grade 3 large – with marked distension.
Treatment – salt and fluid restriction, serial paracentesis, diuretics – spironolactone +/- furosemide
trans jugular intrahepatic portosystemic shunt for refractor cases. Splanchnic arterial vasodilation +
portal HTN increased capillary permeability ascites. Complications of ascites: renal failure,
hepatorenal syndrome, spontaneous bacterial peritonitis (cefotaxime or piperacillin/tazobactam)
HCC most common primary liver malignancy, leading cause of cancer mortality. More common in males,
occurs on background of cirrhosis, chronic hepatitis, often is a solitary tumor. Liver cirrhosis is present
in 80% cases, chronic hep B+C also important, chronic hep b 100 fold risk of HCC, alcohol, NAFLD,
hemochromatosis, Wilson autoimmune diseases also ↑ risk. Ingestion of foods with aflatoxin also.
