approach to elevated liver enzymes

liver bl supply

Portal vein (70%), hepatic artery (30%).

Metabolic functions of liver

Metabolic: Glucose homeostasis, synthesis of albumin, globulins, coagulation factors, lipoproteins.

Storage function of liver

Storage: Glycogen, triglycerides, iron, copper, vitamins

Detoxification and excretory function of liver

Detoxification: Hormones, toxins, drugs, ammonia → urea, old RBC destruction.

Excretory: Bile pigments, bile salts, cholesterol.

Markers of hepatocellular damage

ALT (specific), AST (less specific, also in heart, muscle, kidney, RBCs).

Markers of cholestasis:

ALP, GGT, 5'NT, bilirubin (direct/indirect), urine/stool pigments

Markers of synthetic function

Serum albumin (↓ in chronic disease), PT/INR (↑ early in acute/chronic disease).

Inf causes of elevated liver enzymes

Infectious: HAV, HBV, HCV, HEV, EBV, CMV, HSV, bacterial abscess, parasites.

Toxins or drugs that elevate liver enzymes

Toxins/Drugs: Statins, amiodarone, antifungals, paracetamol, alcohol.

Vascular causes of elevated liver enzymes

Vascular: Shock liver, CHF, Budd-Chiari.

Heriditary causes of elevated liver enzymes

Hereditary: Hemochromatosis, Wilson's, α1-antitrypsin deficiency.

Auto immune causes of elevated liver enzymes

Autoimmune: AIH, PBC, PSC, celiac disease

Infiltrative causes of elevated liver enzymes

Infiltrative: NAFLD/NASH, sarcoidosis, amyloidosis.

Preg related causes of elevated liver enzymes

Pregnancy-related:HELLP, AFLP, cholestasis, hyperemesis gravidarum

ALT > AST

Viral hepatitis, toxins, autoimmune, metabolic.

AST > ALT:

Alcoholic liver disease (AST/ALT > 2), cirrhosis, muscle injury

chronic hepatiris

≥6 months inflammation/necrosis

causes of chronic hep

Viral (HBV, HCV), toxins, autoimmune, metabolic.

histology and assessment of chronic hep

Histology: Portal inflammation, fibrosis → cirrhosis.

Assessment: HAI/Ishak scoring (Grade = inflammation, Stage = fibrosis)

presentation of chronic hep

From asymptomatic to CLD signs ± extrahepatic features

HBV phases

Replicative: ↑ ALT/AST, high HBV DNA, +HBeAg.

Immune tolerance: High DNA, +HBeAg, normal enzymes.

Non-replicative carrier: -HBeAg, +anti-HBe, low/undetectable DNA, normal enzymes.

Reactivation possible anytime.

High risk of HCC even pre-cirrhosis

when to treat CHB

Treat if active disease or cirrhosis (regardless of ALT/DNA).

treatment plan of CHB

First-line: Entecavir, Tenofovir.

Others: PEG-IFN, lamivudine, telbivudine, adefovir (less preferred).

Often long-term or indefinite therapy.

CHC ttt

Interferon-free DAAs (e.g., Sofosbuvir + Ledipasvir, Sofosbuvir + Velpatasvir) tailored to cirrhosis status.

auto immune hepatitis types

Types I-III (ANA, SMA, LKM-1, SLA markers).

Features of auto immune hep

Features: Female predominance, jaundice, hepatosplenomegaly, extrahepatic autoimmunity.

Ttt for auto immune hep

Treat: Prednisolone ± azathioprine

DILI mech

Mechanisms: Predictable (dose-dependent) vs idiosyncratic.

DILI patterns

Patterns: Hepatitis-like (INH, halothane), cholestatic (OCP, steroids), steatosis (amiodarone), necrosis (paracetamol), granulomas (allopurinol).

Ttt for DILI

Management: Stop drug, supportive ± antidote

Fatty liver causes and risk

NAFLD/NASH: Related to obesity, DM2, metabolic syndrome.

Risks: Progression to cirrhosis, HCC.

Fatty liver diag and manag

Diagnosis: Labs (↑ ALT/AST), imaging, biopsy.

Treatment: Weight loss, metabolic control, antioxidants, under-trial drugs.

preg associated liver disease + berif explaination

Cholestasis: Itching ± jaundice in 3rd trimester, good prognosis.

HELLP: Hemolysis, ↑ LFTs, low platelets — urgent delivery.

Hyperemesis gravidarum: Severe N/V ± jaundice.

AFLP:Fulminant hepatic failure late pregnancy — terminate pregnancy