Cirrhosis concept map PDF

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Disease: Cirrhosis: -

End-stage of liver disease: Extensive degeneration and destruction of the liver cells; resulting in the replacement of liver tissue by fibrosis Usually develops after decades of chronic liver disease

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Etiology: -

Any chronic liver disease Most common cuases: HCV, alcohol induced liver disease, nutrition related to extreme dieting, malabsorption, and obesity Environmental factors Genetics Chronic inflammation and cell necrosis from hepatitis can result in progressive fibrosis leading to cirrhosis Chronic hepatitis+ alcohol ingestion = acceleration in liver damage Biliary causes: PBC and PSC (other concept map) The regeneration of hepatocytes Is disorganized, resulting in abnormal blood vessel and bile duct architecture Lobules of irregular size impede blood flow Results in poor cellular nutrition and hypoxia of the liver which leads to decreased function

Cardiac cirrhosis: -

Spectrum of hepatic derangements that result from long standing, severe, right-sided heart failure Caused hepatic venous congestion, parenchymal damage, necrosis of liver cells, and fibrosis over time. Treatment: manage pts underlying heart failure

S/S: Early: - Few symptoms - Fatigue - Enlarged liver - Blood tests may show normal liver function Late: Jaundice: -

from decreased ability to conjugate and excrete bilirubin into small intestine Overgrowth of connective tissue compressive biliary ducts lading to obstruction Increased bilirubin in vascular system and jaundice occurs

Skin Lesions: -

Spider angiomas: small dilated blood vessels with a brght red center point and spider like branches Occur in nose, cheeks, upper trunk, neck, and shoulders Palmar erythema Both are due to an increase in circulating estrogen as a result of the damaged livers inability to metabolize steroid hormones

Hematologic problems: - Thrombocytopenia - Leukopenia - Anemia - Coagulation disorders - Thought to be the result pf splenomegaly that results from backup of blood from the portal vein into the spleen resulting in an increase of removal of blood cells in circulation - Coagulation probs result from liver inability to produce PT and there clotting factors - Manifestation of clotting probs: epistaxis, purpura,petechia, easy bruising, gingival bleeding, heavy period Endocrine probs: -

Gynecomastia: benign growth of the glandular tissue of the male breast Liver plays role in metabolizing of hormones Loss of axillary an pubic hair Testicular atrophy Impotence with loss of libido due to increased estrogen levels Amenorrhea: absence of a period Vaginal bleeding in older women Altered aldosterone function Hyperaldosteronism with sodium and water retention and potassium loss

Peripheral neuropathy: -

Common in alcoholic cirrhosis Might be due to dietary deficiency of thiamine, folic acid, colbamine Can resulting in sensory and motor symptoms with sensory symptoms predominating.

Complications: -

No obvious complications: compensate cirrhosis

Portal hypertension: -

Increased venous pressure in portal circulation, splenomegaly, large collateral veins, ascites, and gastric esophageal varices Collateral circulation: body developing alternate circulatory pathways; collateral channels commonly form in lower esophagus, anterior abd wall, parietal peritoneum, and rectum Varicosities(distended veins) develop in areas where collateral ans systemic circulation communicate resulting in esophageal and gastric varices, Capur medusae(ring of varices around umbilicus) and hemorrhoids

Varices: -

Esophageal: Complex of tortuous, enlarged veins at the lower end of the esophagus. Gastric: Located in upper portion of the stomach Varices do not tolerate high pressure and bleed easily May present with melena and hematemesis Esophageal varices are the most life-threatening complication of cirrhosis and are a medical emergency

Ascites and peripheral edema: Peripheral edema: -

Occurs in lower extremities and presacral area Can occur before, concurrently with, or after ascites develop Results from decreased colloidal and oncotic pressure from impaired liver synthesis of albumin and increased portcaval pressure from portal hypertension

Ascites: -

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Accumulation of serous fluid in the peritoneal or abd cavity Can occur with portal hypertension which causes proteins to shift from blood vessels to lymph space Can occur with hypoalbuminemia resulting from livers decreased ability ton synthesize albumin Can also occur with hyperaldosteronism, which occurs when the hormone aldosterone is metabolized by damaged hepatocytes; retention of sodium and ADH lead to additional water retention Edema decreases intravascular volume which decreases renal blood flow and glomerular filtration S/S: abd distention, weight gain, increased abd pressure, hypokalemia due to hyperaldosteronism or diuretics Puts pts at risk for spontaneous bacterial peritonitis (SBP); common after variceal hemorrhage

Hepatic Encephalopathy: (table 43-11 and 43-12) Neuropsychiatric manifestation of liver disease Etiology: neurotoxic effects of ammonia, abnormal neurotransmission, astrocyte swelling, inflammatory cytokines Liver damage or blood being shunted past the liver, ammonia is unable to be converted to urea Ammonia crosses te BBB and causes neurotoxic manifestations Can occur after placement of transjugular intrhepaticportisystemic shunt(TIPS) s/s: changes in mental and neuro responsiveness, impaired consciousness, inappropriate behavior(ranging from sleep disturbances, trouble concentrating, to deep coma), asterixis(flapping tremors),hyperventilation, hypothermia, tongue fasciculations, grimacing, grasping reflexes, apraxia, fetor hepaticus asterixis: asked to hold the arms and hands out stretched out, the pts is unable to hold this position and does a series of rapid flexion and extension movements of the hands changes may occur: -

Due to an increase in ammonia in response to bleeding varices or infection Gradually as blood ammonia levels slowly increase

Apraxia: inability to construct simple figures Fetor hepaticus: musty, sweet odor of the pts breath due to accumulation of digestive by-products that the liver is unable to degrade Hepatorenal Syndrome: type of renal failure with azotemia, oliguria, and intractable ascites kidneys have no structural abnormality etiology is complex final common pathway is likely to be portal hypertension with liver decompensation, resulting in splanchic and systemic vasodilation and decreased arterial blood volume; as a result, renal vasoconstriction occurs and renal failure follows renal failure can be reversed by liver transplantation in a pt with cirrhosis, hepatorenal syndrome frequently follows diuretic therapy, GI hemorrhage, or paracentesis

Dx (Cirrhosis): -

Elevated liver enzyme levels Normal AST and ALT levels may be normal due to death and loss of hepatocytes at end stage Decreased serum protein and albumin Increased serum bilirubin and globulin levels Prolonged PTT Alterations in metabolism indicated by decreased cholesterol level Ultrasound not reliable dx test Liver biopsy is gold standard test

Interprofessional care:43-13 Slow progression of cirrhosis Prevent and treat any complications Ascites: -

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Sodium restriction; limit intake 2g/day; if severe 250-500mg/day; low sodium intake and subsequent problems associated with malnutrition Diuretics Fluid removal; fluid restriction if severe ascites develops Assess fluid and electrolyte imbalance Albumin infusion may be used to help maintain intravascular and volume and urine output by increasing plasma colloid oncotic pressure Diuretic therapy: spironolactone(aldactone); antagonist of aldosterone and potassium sparing Other diuretics: amiloride(midamor), triamterene(dyrenium); high potency loop diuretic such as furosemide(lasix) is frequently used in combination with a potassium-sparing drug Tolvaptan(Samsca) is a vasopressin-receptor antagonist is used to correct hyponatremia, which is often seen in pts with cirrhosis; causes an increase inn water excretion, resulting in an increasing serum sodium concentration. Paracentesis: sterile procedure in which a catheter is used to drain fluid from the abd cavity; can be used to diagnose or relive pain, pressure, or difficulty breathing; reserved for pt who does not respond to diuretic therapy; temporary measure due to rapid re-accumulation of fluid TIPS also used to alleviate ascites in pt who does nor respond to diuretics; not really used anymore due to high complications

Esophageal and Gastric varices: -

Prevent bleeding and rupture Decrease portal pressure Should avoid alcohol, aspirin, NSAIDs All pts with cirrhosis should have an upper endoscopy(esophagogastroduodenoscopy) to screen for varices

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Generally started on a nonselective beta blocker(nadolol or propanolol(pg 991)) to reduce incidence of bleeding, decrease high portal pressure which decreases the risk for rupture First step is to stabilize pt and manage airway IV therapy and blood transfusion Drug therapy and endoscopic therapy Drugs: sandostatin or vasopressin(pg 991) IV administration of octreotide or vasopressin produces vasoconstriction of the splanchic arterial blood bed, decreases portal blood flow, and decreases portal hypertension Endoscopy, band litigation sclerotherapy of varices may be used to prevent rebleeding

Endoscopic Variceal Litigation: placing a small rubber band around the base of the varix(enlarged vein) Sclerotherapy: involves injection of a sclerosing solution into a swollen veins thrugh an injection needle that is placed through the endoscope Balloon Tamponade:

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Used when acute esophageal or gastric varices cannot be controlled with intial endoscopy Controls bleeding by mechanical suppression of varices Safety: label each lumen to avoid confusion; secure tube to prevent movement that could occlude airway; deflate balloons for 5 min every 8-12 hrs per institutional policy to prevent necrosis

Other supportive measures: -

Plasma infusion Packed RBC infusion Vit K Proton pump inhibitor(Pantoprazole) Lactulose and rifaximin(xifaxan) may be administered to prevent hepatic encephalopathy from breakdown of blood and the release of ammonia in the intestine Antibiotics to prevent bacterial infection

Long term: -

N on selective beta blockers Repeated band litigation of varices Portosystemic shunts for recurrent bleeding

Shunting procedures: Some can divert portal blood flow while allowing adequate liver perfusion Most commonly used surgical shunts are the portacaval shunt and the distal splenorenal shunt

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Transjugular intrahepatic portosystemic shunt: TIPS Non surgical procedure in which a tract(shunt) between the systemic an portal venous systems is created to redirect portal blood flow The wall of the hepatic vein is punctured and the catheter is directed to the portal vein Reduces portal venous pressure and decompresses varices and controls bleeding Does not interfere with future liver transplantation Increases risk of hepatic encephalopathy and stenosis of the stent Contraindicated in pts with severe hepatic encephalopathy, hepatocellular carcinoma, severe hepatorenal syndrome, and portal vein thrombosis

Hepatic encephalopathy: Goal is reduce ammonia formation Lactulose is a drug that traps ammonia in the gut; can be given orally, as an enema, of through an NG tube Laxative effect of lactulose expels ammonia from colon Antibiotics such as rifaximin can also be given, particularly to pts who do not respond to lactulose Constipation needs to be prevented and regular bowel movements are needed to prevent ammonia build up

Treatment precipitating causes: -

Lowering dietary protein intake Preventing and controlling GI bleeds If bleeding occurs, promptly from GI tract to decrease protein accumulation in the gut

Drug therapy for cirrhosis: -

No specific drug therapy Drugs for complications of cirrhosis: 43-14

Nutritional therapy: -

Cirrhosis w/0 complications: high cal(3000 cal/day) with high carb content and moderate to low levels of fat Protein restriction may be needed after a severe flare up of symptoms Malnutrition more serious complication than hepatic Encephalopathy Pt with alcoholic cirrhosis frequently has protein calorie malnutrition; oral supplements may be needed Parenteral or enteral nutrition therapy may be required although rarely used Pt with ascites and edema are put on a low sodium diet

Nursing assessment: 43-15

Nursing implementation: Health promotion: risk factors such as alcoholism, malnutrition, viral; hepatitis, biliary obstruction, obesity, right sided HF; prevention and early treatment Abstaining from alcohol Proper nutrition Early detection and treatment of viral hepatitis

Acute care: -

Preserve pt strength/ resting while maintaining muscle strength and tone Prevent pneumonia, thromboembolic problems, and pressure ulcers Manage anorexia, N/V, pressure from ascites, and poor eating habits; help pt receive adequate nutrition Oral hygiene before meals to help increase appetite Offer small meal and in between snacks to help with appetite Monitor and assess pt status Manage and treat pt symptoms such as pruritus (pg 994) Keep ts nails short and clean and encourage them to scratch with their knuckles Note color of urine and stools and assess for normalization When jaundice is present stool may be gray or tan and urine can be dark brown I&O Measure girth Measure weight Before paracentesis have pt void to prevent puncturing of bladder Have pt sit on side of bed or in high fowlers position Check electrolyte imbalance Check for hypovolemia Check/ monitor BP and HR Check dressings for bleeding or leaking Put pt in semi-fowlers or fowler’s position to increase respirator efficiency for pts with dyspnea; use pillows to support arms or chest Use special mattresses, a turn schedule, ROM exercise to help prevent ulcer formation Cough a deep breathing exercise to help prevent respiratory probs If pt is on diuretics, monitor serum sodium, potassium, chloride, bicarbonate levels Monitors renal function Routinely check diuretic dosage

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Observe for hyper or hypokalemia that may manifest by cardiac dysrhythmias, hypotension, tachycardia, generalized muscle weakness, hyponatremia (manifested by muscle cramping, weakness, lethargy, and confusion Observe for bleeding tendencies, anemia, and increased susceptibility to infection Assess pt response to altered body image

Bleeding varices: -

Observe for signs of bleeding If hematemesis occurs, call HCP and be ready to movr pt to endoscopy and assist with equipment to control bleeding Pt may be admitted to ICU Balloon tamponade may be used for pts who have bleeding that is unresponsive to band litigation or sclerotherapy Sphygmomanometer is used to measure and maintain desired pressure 20-40 mm Hg; position is verified by x-ray Monitor for complications or erosion of the esophagus, regurgitation and aspiration of gastric contents Monitor for occlusion of airway and causing asphyxiation If balloon breaks or deflates, it will slip upward and causing an obstruction in the airway Keep scissors at bedside Minimize regurgitation by oral and pharyngeal suctioning (pt can’t swallow saliva due to balloon) and by keeping pt is semi fowlers position Provide emesis basin and tissues Do frequent oral and nasal care to relieve taste from blood and irritation from mouth breathing

Hepatic Encephalopathy: -

Reduce formation of ammonia Reduce danger of fall risks and airway obstruction (main one eing confusion) Assess level of responsiveness, sensory and motor abnormalities, fluid and electrolyte imbalances, acid base imbalances, response to treatment measures Assess neuro status including exact description of pt behavior at least every 2 hours Minimize constipation to reduce ammonia accumulation as meds will cause defecation to release ammonia Give meds, laxatives, and enemas as ordered Encourage fluid intake if not contraindicated GI bleeding can worsen Assess pt for lactulose for diarrhea and excessive fluid and electrolyte losses

Ambulatory care: - Proper diet - Rest - Avoidance of hepatotoxic OTC drugs such as acetaminophen in hihg doses - Abstinence from alcohol - Monitor for symptoms and complications secondary to cirrhosis - Pt and care giver teaching (43-16)...