Gastrointestinal 4
Complications - obstruction Management
radiation chemotherapy treatment of choice is surgery - bowel resection, colostomy
right hemicolectomy - involves ascending colon left hemicolectomy - involves descending colon abdominal-perineal resection: removal of sigmoid colon and rectum with formation of a colostomy
Nursing interventions
manage pain monitor for complications
wound infection atelectasis thrombophlebitis
maintain fluid and electrolyte balance care of ostomy
Disorders of the Liver Hepatitis
Definition/etiology - acute inflammatory disease of the liver caused by viral, bacterial, or toxic ingestion Pathophysiology
inflammation of liver, enlargement of Kupffer cells , bile stasis regeneration of cells with no residual damage types
hepatitis A
transmitted from infected food, water, milk, shellfish fecal-oral route of infection common in poor sanitation/overcrowding higher incidence in fall and winter new vaccine available
hepatitis B
blood-borne and sexually transmitted may become a carrier
hepatitis C
transmitted parenterally (post-transfusion hepatitis) and possibly fecal-oral route may become a carrier
hepatitis D
blood borne coexists with hepatitis B
hepatitis E
water borne contaminated food or water; rare in the United States
Hepatitis B
Risk factors/infection route
homosexuality iv drug use health professionals hemodialysis transmission routes
infected blood, semen, vaginal secretions or saliva must enter the body
pathophysiology
hepatitis B has three distinct antigens
HBsAg - surface antigen HBcAg - core antigen HBeAg - e antigen
damage to the hepatocytes causes inflammation and necrosis liver function decreased in proportion to damage healing takes three - four months
Findings
jaundice if liver fails to conjugate bilirubin or excrete it clay-colored stools from lack of urobilin urine is dark from urobilin excreted in urine rather than stool urine foams when shaken pruritus from bile salts excreted through skin right upper quadrant pain from edema and inflammation of liver anorexia, nausea, vomiting, malaise, weight loss prolonged bleeding from impaired absorption of vitamin K anemia from decreased RBC lifespan
Diagnostics - serologic markers of HBV
HBsAg - hepatitis B surface antigen anti-Hbc - antibodies to B core antigens elevated alanine aminotransferase (ALT previously SGPT) elevated bilirubin elevated aspartate aminotransferase (AST; previously SGOT) elevated alkaline phosphatase prolonged prothrombin time
Management - nonspecific and supportive
symptomatic treatment of pain antiemetics as needed
Nursing interventions
fatigue - provide rest periods; may require bed rest initially maintain skin integrity client will tolerate less activity nutrition needs:
increase carbohydrates and proteins; decrease fat avoid alcohol eat frequent, small meals
remedy knowledge deficit arrange for home care needs teach infection control
use disposable utensils and dishes or keep separate from others good handwashing do not share razors, toothbrush, etc.
Prevention
hepatitis B vaccine provides active immunity hepatitis B immune globulin provides passive immunity observe Standard and Enteric Precautions good handwashing
Cirrhosis
Definition/etiology - irreversible, chronic, progressive degeneration of the liver, with fibrosis and areas of nodular regeneration
types
Laennec's cirrhosis - related to alcohol abuse post-necrotic - associated with viral hepatitis or exposure to hepatotoxin biliary cirrhosis - associated with inflammation or obstruction of gallbladder or bile duct cardiac cirrhosis - associated with congestive heart failure
Pathophysiology
nodular liver with fibrosis and scar tissue destroys hepatocytes and kills tissue ( necrosis ) necrosis, nodules, and scar tissue obstruct flow of blood, lymph, and bile impaired bilirubin metabolism
Findings
weakness, fatigue, weight loss, hepatomegaly right upper quadrant pain ( illustration ) jaundice , pruritus , steatorrhea (decreased absorption of fat and fat-soluble vitamins) clay-colored stools increased bilirubin in urine, producing dark colored urine impaired aldosterone metabolism resulting in edema impaired estrogen metabolism: gynecomastia , menstrual changes, changes in distribution of body hair, vascular changes - spider angiomas , palmar erythema impaired metabolism of protein, carbohydrate, and fat
produces less plasma protein, resulting in edema and ascites produces less of proteins needed for clotting ( fibrinogen and prothrombin ) absorbs less vitamin K, resulting in prolonged bleeding liver fails to convert glycogen to glucose, resulting in hypoglycemia
Diagnostics
liver function studies - ALT, AST, alkaline phosphatase prothrombin time, CBC decreased cholesterol because liver synthesis impaired elevated serum bilirubin and urine bilirubin ERCP to examine bile duct CTscan of liver liver biopsy
Management
steroids for post-necrotic cirrhosis replace B vitamins and fat-soluble vitamins diet
increased carbohydrates protein may be restricted, depending on amount of damage and symptoms no alcohol
Nursing interventions
monitor for bleeding alteration in nutrition
2,000-3,000 calories daily low fat
provide rest periods; client will not tolerate strenuous activities remedy any knowledge deficit about cirrhosis and its therapies changes in LOC
confusion avoid sedation
impaired skin integrity, from edema and pruritus monitor fluid balance measure abdominal girth daily weigh daily measure I & O
Complications
portal hypertension ascites hepatic encephalopathy
Portal hypertension
Definition/etiology - increased pressure in the portal Pathophysiology: normal blood flow is altered producing an increased resistance to flow through the liver. Congestion in the portal system dilates veins, especially in esophagus and rectum. Findings
prominent abdominal-wall veins (caput medusa) hemorrhoids enlarged spleen anemia from increased destruction of RBCs esophageal varices and GI bleeding
Diagnostics: endoscopy
