Hepatology Flashcards
LFTs measure what
Serum bilirubin(elevation means liver injury)
Aminotransferases(elevation means hepatocellular damage,hepatitic)
Alkaline phosphatase (elevation means infiltrative liver disease)
Gamma glutamyl transferase(elevation means cholestatic or obstructive)
Albumin
Aim of investigation in suspected liver disease
. Detect hepatic abnormality
. Measure severity of liver disease
. Detect pattern of LFT abnormality:whether hepatitic or obstructive
. Identify specific cause
. Investigate possible complication
Drugs that increase gamma glutamyl transferase
Barbiturates
Carbamezepine
Ethanol
Rifampicin
What is hepatic encephalopathy
Is a neuropsychiatric syndrome caused by liver disease, apathy ,inability to concentrate,delirium, disoriented,drowsiness,slurring of speech,coma
Pathophysiology of hepatic encephalopathy
Due to disturbance of brain function provoked by circulating neurotoxins that are normally metabolised by the liver.
DD of hepatic encephalopathy
. Intracranial bleed
. Drug or alcohol intoxication
. Delirium tremens or alc withdrawal
. Wernickes encephalopathy
. Primary psychiatric disorders
. Hypoglycemia
. Neurological Wilson’s disease
. Post ictal state
Factors precipitating hepatic encephalopathy
.drugs(sedatives,antideps)
.dehrydration
.portosystemic shunting
.infection
.hypokalemia
. constipation
.increased protein load(gi bleed)
Management of hepatic encephalopathy
. Lactulose(15-30 ml 3 times daily)
Produces osmotic laxative effect,reduces pH of colonic contenthereby limiting colonic ammonia absorption and promotes incorporation of nitrogen into bacteria
. Rifaximin(400mg 3 times daily)
Antibiotic,reduces bacterial content of bowel
Pathophysiology of cirrhosis
Following liver injury,stellate cells in the space of Disse are activated by cytokines produced by kupffer cells and hepatocytes. This transforms the stellate cell into a myifibriblast like cell,capable of producing collagen,pro inflammatory cytokines and tissue fibrosis
Hepatocyte loss
Distortion of normal liver architecture
Disrupts hepatic vasculature
Portosystemic shunts
Causes of cirrhosis
. Alcohol
. Chronic virla hepatitis (B or C)
. Non alc fatty liver disease
. Immune
Primary sclerosing cholangitis
. Biliary
Primary biliary cholangitis
Secondary biliary sclerosis
Cystic fibrosis
. Genetic
Haemochromatosis
Wilson’s disease
Alpha 1 antitrypsin deficiency
. Chronic venous outflow obstruction(sinusoidal obstruction syndrome,budd-chiari)
Clinical feature of cirrhosis
. Hepatomegaly
. Jaundice
. Ascites
. Circulatory changes(spider telengiectasia almar erythema,cyanosis)
. Endocrine changes(loss of libido,gynecomastia,testicular atrophy,impotence, amenorrhea)
. Haemorrhagic tendencies(bruises,purpura,epistaxis)
. Portal hypertension(splenomegaly,collateral vessels,variceal bleeding)
. Hepatic encephalopathy
. Others (pigmentation,dupuytrens contracture,clubbing)
Features of chronic liver failure
. Worsening liver function
Prolonged prothrombin time
Low albumin
. Jaundice
. Portal hypertension
. Variceal bleeding
. Hepatic encephalopathy
. Ascites
Child Pugh classification of prognosis of cirrhosis
Encephalopathy
Bilirubin
Albumin
PTT
ascites
What is portal hypertension
Normal heptic venous pressure gradient (difference between wedged hepatic venous pressure and free hepatic venous pressure) is 5-6 mm hg. Clinically significant portal hypertension is present when gradient exceeds 10 mm hg and risk of variceal bleeding increases beyond 12 mm hg
Classification of portal hypertension
. Pre hepatic pre sinusoidal
Portal vein thrombosis
Abdominal trauma during surgery
. Intrahepatic presinusoidal
Schistosomiasis
Sarcoidosis
Congenital hepatic fibrosis
. Sinusoidal
Cirrhosis
Polycystic liver disease
Metastatic malignant disease
. Intra hepatic post sinusoidal
Veno occlusive disease
. Post hepatic post sinusoidal
Budd chiari syndrome