ACUTE AND CHRONIC HEPATITIS - DEFIRILTIORI
The term hepatitis is applied to a broad category of clinicopathological conditions that result from the damage produced by viral, toxic, pharmacological, or immune-mediated attack upon the liver. The common pathological features of hepatitis are hepatocellular necrosis, which may be focal or extensive, and inflammatory cell infiltration of the liver, which may predominate in the portal areas or extend out into the parenchyma. Clinically, the liver is enlarged and tender with or without jaundice, and laboratory evidence of hepatocellular damage is invariably found in the form of elevated transaminase levels. Independent of its cause, the clinical course of hepatitis may range from mild or inapparent to a dramatic illness with evidence of severe hepatocellular dysfunction, marked jaundice, impairment of coagulation, and disturbance of neurological function. Hepatitis is further divided into acute and chronic types on the basis of clinical and pathological criteria.
Acute hepatitis implies a condition lasting less than six months, culminating either in complete resolution of the liver damage with return to normal liver function and structure or in rapid progression of the acute injury toward extensive necrosis and a fatal outcome.
Chronic hepatitis is defined as a sustained inflammatory process in the liver lasting longer than six months.
Differentiation of acute from chronic hepatitis on histological criteria alone may be impossible. Extension of inflammatory cells beyond the limits of the portal tracts surrounding isolated nests of hepatocytes (piecemeal necrosis) and connection of portal and/or central areas of the hepatic lobules by swaths of inflammation, necrosis, and collapse of architecture (bridging necrosis) are seen in liver biopsies taken from patients with severe forms of chronic hepatitis. These features may also be seen, however, in uncomplicated acute hepatitis that will ultimately undergo complete resolution. A purely histological diagnosis of chronic hepatitis usually requires evidence of progression toward cirrhosis such as significant fibrous scarring and disruption of the hepatic lobular architecture.
- NONOBSTRUCTIVE CAUSES OF ISCHEMIC HEART DISEASE
- SPECIFIC ENTITIES - DISEASES WITH KFiOWIi ETIOLOGIES -
- DC CARDIOVERSION AND DEFIBRILLATION
- Genitourinary System
- Skin and Conjunctiva
- SPECIFIC ARRHYTHMIAS - sinus nodal rhythm disturbances
- Pulmonary Vasculitis
- THE FAMILIAL POLYPOSIS SYNDROMES
- DEFINITION
- CLASSIFICATION OF THE MALABSORPTION SYNDROMES
- CHEST WALL DISEASE
- CHRONIC RENAL FAILURE
- PHYSIOLOGY OF THE CORONARY CIRCULATION
- Differential Diagnosis and Evaluation of the Patient
- Ovarian Cancer
- DISEASES OF THE ESOPHAGUS
- GAS TRANSFER
- Therapy
- BILIRUBIN METABOLISM
- PERFUSION
- Membranoproliferative Glomerulonephritis (MPGN)
- Aspiration Pneumonia and Lung Abscess
- PULMONARY HEART DISEASE
- Urinalysis, Renal ‘Tubular Function, and Urine Flow Rate
- Vitamin Dresistant Rickets
- CLINICAL PRESENTATION
- Clinical Course, Pathogenesis, and Anatomy of Acute Tubular Necrosis
- Nephrosclerosis
- Ultrasound and Computed Tomography
- CAUSES OF PULMONARY HYPERTENSION
- SMOKING CESSATION
- CLINICAL PRESENTATION
- Other Cystic Diseases
- DIAGNOSTIC TECHNIQUES AND THEIR INDICATIONS - IMAGING PROCEDURES
- Aminoaciduria