PATHOPHYSIOLOGY

Predisposing Factor Age: 3-18 y/o (40+) Race: Afro-American

Etiology *PICORNAVIRUS U

Precipitating Factor Poor sanitation Contaminated foods/waters Overcrowding

Ingestion of contaminated food Virus enters through the epithelium in the mouth ot gut Migrates to the liver over a period of about 2 6 weeks HAV reproduces itself by utilizing liver cells (hepatocytes & kupffer cell) ribosomes for viral replication Inflammation of the liver Disruption of the normal blood supply to the cell Hepatic necrosis Liver cells damaged Failure of damaged liver cells to detoxify an abnormal product

WBC=2.0x10 /L 9 5.0-10.0 x10 /L Neotrophils=30% 35 71 % Alters the bodys defense against bacterial invaders Immune system Invasion of opportunistic bacteria in the mouth Oral trush

Lymphocyte=90% 24 44 %

Inflammatory process: Hyperthermia Paracetamol AST=45 u/L Up to 40 u/L ALT=53 u/L Up to 41 u/L

Stretching of the liver capsule Discomfort in the upper right abdominal quadrant

Nausea

Pain in the gut

Daktarin

Release of toxins Anorexia

Increased destruction of hemoglobin & other hemoproteins Increased unconjugated bilirubin (Because bilirubin is highly insoluble in water, it must be converted into a soluble conjugate before elimination in the body)

Hemoglobin=100g/L 120 160 g/L

Albumin=13 24

BT of PRBCs

Human serum albumin

Bilirubin starts concentrating in the blood Leak in the skin, sclera, mucous membrane & other less visible tissues Tissues become oversaturated with bilirubin

Increased in the unconjugated bile salts in the blood

Water soluble conjugated excreted in the urine Dark colored urine

Feces containing little sterconilin Pale stools (Abolis)

Itching

Rashes

Urticaria

Jaundice

Scarring of liver

Continued hepatic tissues

Encelopathy

Coma

Death

Legend:

Signs and symtoms of the patient Treatment * Contributing risk factors of the pateint

Reference: Focus on Pathophysiology by Barbara L. Bullock & Reet L. Henze Medical Surgical Nursing by Brunner & Suddarth www.emedecinehealth.com