CLINICAL AMD LABORATORY FEATURES
The presence of cirrhosis may remain undetected until autopsy. Individuals with cirrhosis who experience no symptoms and show little clinical evidence of hepatocellular dysfunction are often said to have well-compensated cirrhosis. As evidence of complications develops, particularly signs implying disturbed hepatocellular function, the clinical condition is referred to as decompensated cirrhosis. Where the disease process leading to cirrhosis primarily affects the hepatocytes, e.g., alcohol (parenchymal liver disease), evidence of failing hepatocellular function may be prominent in the clinical presentation. On the other hand, if the biliary system is primarily affected, as occurs in primary or secondary biliary - cirrhosis, the clinical features of cholestasis predominate and hepatocellular function is often well-preserved until late in the course of the disease.
It is convenient to divide the main clinical and laboratory features of cirrhosis into four categories :
1. Size and consistency of the liver.
2. Features attributable to hepatocellular dysfunction. These result from both intrinsically “sick” hepatocytes and the shunting of portal blood away from hepatocytes with consequent failure to extract toxins and metabolites.
3. Features attributable to portal hypertension.
4. Extrahepatic features related to specific diseases causing cirrhosis.
Liver size depends upon the underlying pathological process. In end-stage hepatitis B virus liver disease, the liver is often small, scarred, and shrunken. In alcoholic cirrhosis, fat infiltration may lead to marked enlargement of the liver. Impaired hepatic detoxification of estrogens, as well as disturbed hypothalamic-pituitary function,produces several cutaneous signs (often called “stigmata” of cirrhosis, e.g., spider angiomata, palmar erythema). Marked jaundice in the absence of complete bile duct obstruction is often a grave prognostic sign implying advanced hepatocellular dysfunction. Impaired hepatocellular protein synthesis leads to hypoalbuminemia and hypoprothrombinemia.
- ARTERIAL TRAUMA
- Other Glomerulonephritides
- HEMODIALYSIS AND HEMOPERFUSION IN THE TREATMENT OF DRUG OVERDOSES
- NONATHEROSCLEROTIC CAUSES OF CORONARY ARTERY OBSTRUCTION
- CARCINOMA OF THE PANCREAS - Clinical Manifestations
- MAJOR COMPLICATIONS OF CIRRHOSIS
- Important NEPHROTOXIRIS
- Clinical Manifestations
- Amyloidosis
- RESPIRATORY CONTROL CENTERS
- Minimal Change Nephropathy
- PERIPHERAL ANEURYSMS AMD FISTULAE
- GRANULOMATOUS LIVER DISEASE
- Classification or Glomerular Diseases
- CARDIAC TRAUMA
- TREATMENT AND PROGNOSIS
- MEDICAL MANAGEMENT OF ANGINA
- RISK FACTORS
- GASTROESOPHAGEAL REFLUX DISEASE
- ENVIRONMENTAL DAMAGE OF THE EXTREMITIES
- Polycystic Kidney Disease (PKD)
- Acid-Base Abnormalities
- THE AIRWAY STRUCTURE
- VARIATiT ANGINA
- OXYGEN
- Sigmoidoscopy and Colonoscopy
- Gastrointestinal Tract
- Cardiovascular
- Portal Hypertension
- Skin and Conjunctiva
- THE APPROACH TO THE PATIENT WITH GASTROINTESTINAL HEMORRHAGE
- Diagnosis
- DIAGNOSTIC TECHNIQUES AND THEIR INDICATIONS - IMAGING PROCEDURES
- CLINICAL MANIFESTATIONS OF MALABSORPTION
- Blood Chemistries