Alcohol liver disease
Here's a detailed yet simplified overview of Alcoholic Liver Disease (ALD):
1. Definition:
Alcoholic Liver Disease (ALD) refers to liver damage caused by chronic
excessive alcohol intake. It progresses through stages and can become
life-threatening if untreated.
2. Stages of ALD:
Stage Description
Fatty Liver (Steatosis) Early, reversible fat accumulation in
liver cells
Alcoholic Hepatitis Inflammation and necrosis of liver
cells;potentially life-threatening
AlcoholicCirrhosis Irreversible scarring of the liver and
loss of function
3. Causes:
"Chronic alcohol consumption (typically >40-80g/day for men, > 20-40g/
day for women)
Genetic susceptibility
Nutritional deficiencies (especially folate, thiamine)
Co-existing liver infections (like Hepatitis C)
4. Clinical Features:
Mild (Fatty Liver) Often asymptomatic, or mild
discomfort in right upper abdomen
Alcoholic Hepatitis Fever, jaundice, abdominal pain,
tender liver, nausea
Cirrhosis Ascites, variceal bleeding,
encephalopathy, spider angiomas
5. Investigations:
Blood Tests:
" ElevatedAST >ALT (typically 2:1 ratio)
oElevated bilirubin
o Increased INR, low albumin (in severe disease)
" Ultrasound: Fatty infiltration, nodular liver in cirrhosis
" Fibroscan / Liver Biopsy: To assess fibrosis or confirm diagnosis
6. Treatment:
Stage Management
All Stages Complete alcohol abstinence,
nutritional support (vitamins:
thiamine,folate, B12)
Alcoholic Hepatitis Corticosteroids (e.g., prednisolone if
MDF >32),Pentoxifylline
(alternative)
Cirrhosis Treat complications (e.g., diuretics
for ascites, lactulose for
encephalopathy); consider liver
transplant
7. Prognosis:
Fatty liver: Reversible with abstinence
" Hepatitis:Can be fatal (30-50% mortality in severe cases)
" Cirrhosis: Poor prognosis without transplant
8. Prevention:
" Limit or avoid alcohol
Regular liver function monitoring in alcohol users
"Adequate nutrition
" Early intervention and counseling
Liver cirrhosis
Here's a complete summary of Liver Cirrhosis,organized for easy reference,
especially helpful for academic, clinical, or exam use:
Liver Cirrhosis
1. Definition:
Cirrhosis is achronic, progressive liver disease characterized by fibrosis
and the formation of regenerative nodules, leading to loss of normal liver
architecture and function.
2. Causes (Etiology):
Category Examples
Alcoholic Chronic alcohol use
Viral Hepatitis B, Hepatitis C
Metabolic Non-alcoholic fatty liver disease
(NAFLD/NASH), Hemochromatosis
Autoimmune Autoimmune hepatitis, Primary
biliary cholangitis
Drug-induced Methotrexate, amiodarone
Biliary Biliary atresia, sclerosing
cholangitis
Cryptogenic Unknown cause
3. Pathophysiology:
" Chronic liver injury ’ inflammation - fibrosis disruption of liver
architecture ’ portal hypertension and liver dysfunction
4. Clinical Features:
Early (Compensated) Cirrhosis:
" Fatigue
" Anorexia
" Mild RUQ pain
Hepatomegaly
Late (Decompensated) Cirrhosis:
" Jaundice
" Ascites
"Hepatic encephalopathy (confusion, asterixis)
"Variceal bleeding (hematemesis, melena)
" Edema
Spider angiomas, palmar erythema, gynecomastia(due to estrogen
excess)
5. Complications:
" Portal hypertension
" Ascites and spontaneous bacterial peritonitis (SBP)
Esophageal varices and bleeding
"Hepatic encephalopathy
" Hepatorenal syndrome
" Hepatocellular carcinoma (HCC)
6. Investigations:
Blood Tests:
" LFTs: ‘ bilirubin, AST, ALT, ALP, ! albumin
Coagulopathy: 1 PT/INR
CBC: anemia, thrombocytopenia
" Viral markers: HBSAg, anti-HCV
Imaging:
"Ultrasound: nodular liver, splenomegaly, ascites
" Fibroscan / Elastography: fibrosis assessment
"CT/MRI: detect HCC or complications
Other:
"Endoscopy: check for varices
"Liver biopsy: gold standard butoften avoided due to risk
7. Treatment:
General Alcohol cessation, low-sodium diet,
avoid hepatotoxins
Ascites Diuretics (spironolactone t
furosemide), paracentesis
Encephalopathy Lactulose, rifaximin
Variceal Bleeding Beta-blockers (propranolol),
endoscopicband ligation
SBP Antibiotics (e.g., cefotaxime)
HCC Screening Ultrasound + AFP every 6 months
Liver Transplant Definitive treatment for end-stage
cirrhosis
8. Prognosis:
" Scored using:
Child-Pugh Score (A-C)
MELD Score (for transplant priority)
" Survival depends on stage and complications.
9. Prevention:
" Vaccinate against Hep A and B
" Avoid alcohol
" Manage obesity and diabetes
" Early treatment of hepatitis B/C
Portal Hypertension
1. Definition:
Portal Hypertension is an increase in pressure within the portal venous
system, defined as:
"Portal pressure >12 mmHg
"Or Hepatic venous pressure gradient (HVPG) >5 mmHg
2. Classification (Based on Site):
Type Location of Examples
Obstruction
Pre-hepatic Before the liver (portal Portalvein thrombosis,
vein) splenic vein thrombosis
Intra-hepatic Inside the liver Cirrhosis (most
common),
schistosomiasis,
fibrosis
Post-hepatic After the liver (hepatic Budd-Chiari syndrome,
veins, heart) right heart failure
3. Causes:
" Cirrhosis (most common)
" Portal vein thrombosis
"Schistosomiasis
" Budd-Chiarisyndrome
Congenital hepatic fibrosis
" Right heart failure
4. Clinical Features:
Key Features Explanation
Splenomegaly Due to congestion
Ascites Fluid accumulation in abdomen
Esophageal and gastric varices Collateral veins prone to rupture
Caput medusae Dilated abdominal wall veins
Hemorrhoids Rectal varices due to collateral
formation
Hepatic encephalopathy Due to portosystemic shunting and
toxins
Thrombocytopenia From hypersplenism
5. Investigations:
" Ultrasound with Doppler - enlarged portalvein, flow reversal, collaterals
"Endoscopy - varices
" CT/MRI abdomen - collaterals, liver anatomy
" HVPG measurement - to quantify portal pressure
"Blood tests - LFTs, CBC (low platelets), coagulopathy
6. Complications:
"Variceal bleeding (life-threatening)
" Ascites
"Spontaneous bacterial peritonitis (SBP)
Hepatic encephalopathy
"Hepatorenal syndrome
7. Treatment:
Acute Variceal Bleeding:
Resuscitation with fluids, blood
"|VOctreotide or Terlipressin
Endoscopic band ligation or sclerotherapy
" Antibiotics (e.g., ceftriaxone to prevent SBP)
Prevention/Chronic:
" Non-selective beta blockers (propranolol, nadolol)
" EVL (Endoscopic Variceal Ligation) for high-risk varices
"TIPS (Transjugular Intrahepatic PortosystemicShunt) for refractory cases
Ascites
1. Definition:
Ascites is the abnormal accumulation of fluid in the peritoneal cavity, often a
sign of portal hypertension or other underlying systemic diseases.
2. Causes of Ascites:
Category Common Causes
Portal Hypertension Cirrhosis (most common),
Budd-Chiari syndrome,portal vein
thrombosis
Malignancy Peritoneal carcinomatosis (e.g.
ovarian, gastric, coloncancers)
Infections Tuberculous peritonitis,
spontaneous bacterialperitonitis
(SBP)
Cardiac Congestive heart failure, constrictive
pericarditis
Renal Nephrotic syndrome
Pancreatic Pancreatic ascites due to chronic
pancreatitis or rupture of
pseudocyst
Hypoalbuminemia Severe malnutrition,protein-losing
enteropathy
3. Clinical Features:
"Abdominal distension
Shifting dullness on percussion
" Fluid thrill (in massive ascites)
" Weight gain
Dyspnea (from diaphragmatic elevation)
Umbilical hernia or eversion
4. Investigations:
Diagnostic Paracentesis:
" Appearance:Clear/straw (benign), cloudy (infection), bloody (malignancy,
TB)
" Cell count: >250 PMNs suggest SBP
" Albumin: Use SAAG (Serum-Ascites Albumin Gradient)
o SAAGe1.1 g/dL: Portal hypertension (e.g. cirrhosis, CHF)
o SAAG <1.1g/dL: TB, malignancy, pancreatitis
Other Tests:
" LFTS, renal function, CBC
" Ultrasound/CT Scan abdomen
" Cultures (if infection suspected)
" Cytology (if malignancy suspected)
5. Treatment:
General Measures:
" Sodium restriction (<2g/day)
Fluid restriction (if hyponatremia)
"Avoid alcohol (if alcohol-related liver disease)
Medical Therapy:
"Diuretics: Spironolactone (1st-line), + Furosemide if needed
" Monitor electrolytes and weight regularly
Paracentesis:
"Therapeutic large-volume paracentesis for tense ascites
" Albumin infusion (if >5L fluid removed) toprevent hypotension
Refractory Ascites:
" TIPS(Transjugular Intrahepatic Portosystemic Shunt)
" Peritoneovenous shunt (rare)
" Consider liver transplant in end-stage cirrhosis
6. Complications:
Spontaneous Bacterial Peritonitis (SBP)
Hepatorenal Syndrome
" Umbilical hernia rupture
"Pleural effusion (hepatic hydrothorax)
Hepatic encephalopathy
Here's a complete and high-yield summary of Hepatic Encephalopathy (HE) -
essential for exams, clinical understanding, or quick reference:
Hepatic Encephalopathy (HE)
1. Definition:
A neuropsychiatric syndrome caused by liver dysfunction, leading to
accumulation of neurotoxins (especially ammonia) that affect brain function.
Occurs in acute or chronic liver failure, often reversible with treatment.
2. Types:
Type Context
Type A Acute liver failure
Type B Portosystemicshunting (no liver
disease)
Type C Cirrhosis and portal hypertensi
(most common)
3. Precipitating Factors:
Category Examples
Infections SBP, pneumonia, UTI
GI Bleeding Increases nitrogen load
Electrolyte Imbalance Hypokalemia, hyponatremia
Constipation Increased ammonia absorption
Excess dietary protein Especially indecompensated
cirrhosis
Drugs Sedatives,diuretics, narcotics
TIPS Procedure Portosystemic shunting increases
risk
4. Clinical Features:
Stage Symptoms
Grade I Mild confusion, personality changes,
sleep disturbance
Grade I| Lethargy, disorientation, asterixis
(flapping tremor)
Grade III Stupor, confusion, aggressive
behavior
Grade IV Coma
Other signs: Fetor hepaticus (musty odor), slurred speech, hyperreflexia
5. Diagnosis:
"Clinical diagnosis based on mental status and signs
" Serum ammonia (not always correlating with severity but useful for
monitoring)
EEG: Triphasic waves (supportive)
" CT/MRI brain: Rule out other causes (stroke, infection)
6. Treatment:
Initial Management:
"Treat underlying cause (infection, GI bleed, electrolyte imbalance)
" Avoid sedatives
Ammonia-lowering therapy:
Drug Mechanism
Lactulose I ammoniaabsorption by acidifying
gut, causes diarrhea
Rifaximin Kills gut bacteria that produce
ammonia (add-on therapy)
Neomycin/Metronidazole (alternative antibiotics - less
preferred)
Supportive Care:
" Fluid/electrolyte correction
" Protein restriction (in acute phase), then balanced intake
Monitor GCS and vitals
Here's a concise comparison between Acute Liver Disease (ALD) and Chronic
Liver Disease (CLD):
1. Duration:
Acute Liver Disease (ALD) Chronic Liver Disease (CLD)
Develops rapidly, often within days Develops over months to years,
to weeks typically >6 months
Can be reversible if treated early Irreversible damage, may progress
to cirrhosis
2. Etiology (Causes):
Acute Liver Disease Chronic Liver Disease
Viral hepatitis (e.g., Hepatitis A, B, Chronic alcohol use, hepatitis B/C,
C), alcohol, drug toxicity (e.g., non-alcoholic fatty liver disease
acetaminophen overdose), (NAFLD), autoimmune diseases,
autoimmune hepatitis, ischemia metabolic conditions (e.g.,
hemochromatosis)
3. Clinical Features:
Acute Liver Disease Chronic Liver Disease
Rapid onset of jaundice, fatigue, Slow onset of fatigue, jaundice,
nausea, vomiting, abdominal pain, ascites, pruritus, edema, varices,
and confusion (hepatic hepatic encephalopathy
encephalopathy)
May progress to acute liver failure Features like ascites, splenomegaly,
(ALF) with coagulopathy, and variceal bleeding are common
hypoglycemia, and encephalopathy in advanced stages
4. Liver Function:
Acute Liver Disease Chronic Liver Disease
Severe dysfunction in a short Long-term gradual dysfunction: May
period: High liver enzymes (ALT, present with compensated liver
AST), jaundice, impaired synthetic failure, or decompensated disease
function (low albumin, elevated INR) with low albumin, high INR, and
cirrhosis markers
5. Pathology:
Acute Liver Disease Chronic Liver Disease
Inflammatory changes, Cirrhosis: fibrosis, regenerative
hepatocellular necrosis, sometimes nodules, and loss of liver
hepatocyte regeneration architecture
6. Treatment:
Acute Liver Disease Chronic Liver Disease
Acute management: supportive care, Chronic management: lifestyle
treat the underlying cause (e.g. modifications, treat underlying
antiviral treatment, acetaminophen condition (e.g., antivirals for
antidote), liver transplant (in severe hepatitis,alcohol cessation),
cases) manage complications (ascites,
variceal bleeding)
7. Prognosis:
Acute Liver Disease Chronic Liver Disease
Can be fatal without treatment, Progressive disease: cirrhosis and
especially in cases of acute liver complications can lead to liver
failure failure or HCC, but prognosis
depends on the underlying etiology
and stage
Key Differences:
" Acute liver disease occurs suddenly with rapid onset of symptoms,
potentially life-threatening in a short time frame.
" Chronic liver disease develops gradually, often over many years, and may
remain asymptomatic in its early stages before complications arise.
