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69 Cards in this Set
- Front
- Back
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Alteration in GI Function
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Cirrhosis
Hepatitis |
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Liver
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Largest internal organ of the body
Consists of two lobes Functional units of the liver are lobules Contain hepatocytes Lined with Kupffer's cells -phagocytic activity (remove viruses) |
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Liver Functions
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-Manufacture, storage, transformation and secretion of a number of substances involved in metabolism
-Waste Disposal Plant *See handout* |
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Hepatic Disorders
Clinical Manifestations reflect alterations in normal liver function |
Major Hepatic Disorders:
-Infectious and inflammatory conditions -Structural abnormalities -Trauma -Neoplasms |
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Cirrhosis
Chronic progressive disease of extensive degeneration and destruction of liver cells |
9th leading cause of death in U.S.
4th leading cause of death in 34-54 year olds Two times more common in men **Excessive alcohol intake is single most common cause** |
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Types of Cirrhosis: Alcoholic Cirrhosis
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Alcoholic cirrhosis
-associated with alcohol abuse -accumulation of fat in liver cells -potentially reversible, if alcohol abuse continues, leads to widespread scar formation -Protein malnutrition and alcohol are toxic to the hepatocytes |
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Types of Cirrhosis: Post necrotic cirrhosis
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Post necrotic cirrhosis
-complication of viral, toxic or idiopathic (autoimmune)hepatitis -broad bands of scar tissue form within the liver |
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Types of Cirrhosis: Biliary Cirrhosis
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Biliary Cirrhosis
-associated with chronic biliary obstruction and infection -diffuse fibrosis of liver with jaundice as a main feature |
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Types of Cirrhosis: Cardiac Cirrhosis
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Cardiac Cirrhosis
-secondary to long-standing, severe right-sided heart failure in patients with cor pulmonale, constrictive pericarditis, and tricuspid insufficiency **right-sided heart failure venous return impeded=portal hypertension |
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Etiology
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*20-30% of people with chronic hep C and 10-20% of people with chronic hep B will develop cirrhosis
*Some have a predisposition to cirrhosis, regardless of dietary or alcohol intake |
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Clinical Manifestations/Early
(KNOW THIS SLIDE) |
-fever
-spleenomegaly -hepatomegaly -slight weight loss -GI disturbances: anorexia, dyspepsia (fullness), flatus, N/V, change in bowel habits -abdominal pain or "heavy" feeling in RUQ -liver responsible for CHO, Fat, & Protein metabolism = reason for a change in bowel habits |
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Clinical Manifestations/Late
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*jaundice
*pruritis *skin lesions-spider angiomas, Palmar erythema *Hematologic Problems -thrombocytopenia -leukopenia -anemia -coagulation disorders: epitaxis, petechiae, easy bruising, gingival bleeding, heavy menstrual bleeding |
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Clinical Manifestations/Late
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*Endocrine Disturbances
-Men-Gynecomastia, loss of axillary & pubic hair, testicular atrophy, impotence -Younger women: amenorrhea -Older women: vaginal bleeding -Hyperaldosteronism *Peripheral Neuropathy -common alcoholic cirrhosis -secondary to dietary deficiency of thiamine, folic acid, vitamin B12 -sensory symptoms dominate **liver can't break down testosterone and estrogen** |
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Major Complications
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**Portal Hypertension & Esophageal Varices**
*Peripheral Edema & Ascites *Hepatic Encephalopathy *Hepatorenal Syndrome |
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Portal Hypertension
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*Normal blood flow through the liver becomes obstructed from scarring & compression on portal and hepatic veins and destruction of sinusoids (capillaries)
*Characterized by increased venous pressure in the portal circulation, spleenomegaly, large collateral veins, ascites, systemic HTN, and esophageal varices **vascular congestion throughout the portal system. Blood settles in the esophagus |
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Esophageal Varices
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*Tortuous, enlarged, swollen veins at lower end of esophagus
*Occurs in 2/3 to 3/4 patients with cirrhosis *Bleeding varices are most life-threatening complication of cirrhosis *30-50% die within 6 weeks of 1st esophageal bleed |
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Peripheral Edema & Ascites
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*Edema is the result of decreased colloidal osmotic pressure due to decreased albumin and increased pressure from portal hypertension
*Ankle, presacral edema, anasarca (whole body edema) *Ascites is the accumulation of serous fluid in the peritoneal or abdominal cavity *Results from increase B/P in liver, decreased albumin, & hyperaldosteronism *Client exhibits signs of intravascular dehydration **decreased albumin = ascites, fluid waves and straie on abdomen** -low u.o. -low B/P -fluid leaks out of vessels into spaces |
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Hepatic Encephalopathy
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*Hepatic Encephalopathy occurs as a result of ammonia entering the systemic circulation without liver detoxification
*Liver unable to convert ammonia to urea for kidneys to excrete *high mortality rate |
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Hepatic Encephalopathy
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Main breakdown of protein metabolism = ammonia
Increased ammonia levels = mental status changes |
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Clinical Manifestations/Hepatic Encephalopathy
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*Change in mental status/neuro status
-lethargy, deep coma, confusion, insomnia, slurred/slow speech, hyperactive reflexes, hiccups, agitation -asterixis (liver flap)involuntary movements flapping tremors of arms/hands -apraxia inability to construct simple figures (sequential things) *Hyperventilation *Hypothermia *Fetor-hepaticus-musty, sweet odor of patients breath |
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Hepatorenal Syndrome (HRS)
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*Portal HTN leads to splanchnic (internal organs)vasodilation and decreased arterial blood volume
*Renal vasoconstriction occurs and leads to renal failure *Renal failure can be reversed by liver transplantation *HRS frequently follows diuretic therapy (because of decreased circulating volume),GI hemorrhage, or paracentesis (remove fluid, no albumin fluid accumulates) |
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Diagnostic Studies (KNOW NORMAL VALUES)
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Liver Function Tests: LFT's
-Elevated serum enzymes (ALT/SGPT, AST/SGOT) -Elevated uncongugated bilirubin -Elevated serum ammonia -Prolonged prothrombin time -Decreased total serum proteins and serum albumin -Decreased cholesterol |
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Diagnostic Studies
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*Liver biopsy
-definitive diagnosis -identifies liver cell changes and alterations in lobular structure **Post-bed rest for 24 hours, lay on right side (operative side for 6-8 hours, DSD** |
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Treatments: Medical
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-Maximize liver function
-**Rest: decreases metabolic demand of liver** -Prevent infection -Control complications -Pharmacological treatments |
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Treatments: Surgical
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-No surgical treatment for cirrhosis
-Surgical treatment is aimed at treating complications -liver transplant |
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Treatment Ascites
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*Focus - NA restriction, diuretics, fluid removal
*SPA - Salt poor albumin *Diruetics-aldactone:K sparing, loop diuretic (lasix: K wasting) *Bedrest *HOB elevated semi fowlers *Paracentesis-needle puncture of abdominal cavity to remove ascitic fluid, temporary, done for symptom management *Peritoneovenous Shunt - surgical procedure that provides continuous reinfusion of ascitic fluid into the venous system |
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Treatment/Esophageal Varices
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**GOAL: Avoid bleeding and hemorrhage
-Avoid ETOH, ASA, irritating foods -?NPO -Control coughing -B-blockers (Inderal)decrease cardiac output -Octreotide (growth hormone) -Vasopressin in conjunction with Nitroglycerin -Vitamin K -H2 receptor blockers decrease acidity |
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Management of Bleeding Varices
(Massive hemorrhage) |
-Airway management/intubation
-Blood products-FFP, PRBS, PLTS -Diagonosis by endoscopic exam ASAP -Sclerotherapy or banding of varices -Ligation of varices -Shunt therapy -Balloon tamponade -Medications |
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Medication for Bleeding Varices
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**Octreotide treatment of choice**
*Vasopressin in conjunction with Nitroglycerin *Beta Blockers (Inderal) *Vitamin K *H2 receptor blockers decrease HCL |
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Balloon Tamponade for Bleeding Varices
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*Used for esophageal, gastric variceal hemorrhage or both
*Minnesota or Sengstaken-Blakemore tube *2 balloons - gastric and esophageal, 3rd port for gastric or esophageal aspiration *When inflated, provides mechanical compression of the varices *Gastric balloon anchors tube in position & applies pressure to any bleeding gastric varices |
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Shunting for Varices
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*Tranjugular intrahepatic portosystemic shunt (TIPS) bypasses liver
*Non-surgical *Shunt between systemic & portal venous system is created *Catheter inserted thru jugular vein, threaded thru superior & inferior vena cava into hepatic vein into the portal vein *Decreases portal venous pressure, decompresses varices, thus controlling bleeding |
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Treatment/Hepatic Encephalopathy
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**GOAL: Reduce ammonia formation**
*Protein restricted diet (ammonia is a by-product of protein metabolism, liver unable to break protein down therefore ammonia forms) *Decrease ammonia formation in intestines -Lactulose -Neomycin (PO decreases bacterial flora in intestine decreases ammonia -Avoid constipation (straining) -Remove blood from the GI tract |
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Nutritional Therapy
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*Cirrhosis without complications - high cals, modified fat, protein depends on degree of liver damage & potential for encephalopathy
*Hepatic encephalopathy - very low or no protein diet *Alcoholic cirrhosis - patients have protein-calorie malnutrition-Hepatic aid-contain AA metabolized by muscles *Ascites/edema - low NA diet |
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Health Promotion/Acute Intervention
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*Rest:decreases metabolic demand of liver, promotes liver regeneration
*Measures to prevent pneumonia, DVT, pressure ulcers *Oral hygiene before meals *Small frequent meals *Assess for jaundice *Assess for pruritis & treat *Accurate I&O *Prevent constipation (avoid straining) *Daily weights *Daily abdominal girths *Semi fowlers/fowlers for dyspnea *Monitor electrolytes and acid base *Bleeding precautions *Assess neuro/mental status *Assess for S&S of altered body image |
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Health Promotion/Home Care
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**GOAL: maintain highest level of wellness possible
*Teach: -symptoms of complications -importance of follow-up care -avoid high risk activities for viral hep -avoid hepatic toxins (ETOH, tylenol, ASA) *Adequate rest *Bleeding/Infection precautions *Written explanations for fluid & diet restrictions *Community support/AA |
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Liver Transplantation
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*May be considered for recurring hepatic encephalopathy and end-stage disease
*Depends on the cause and other systemic medical problems **Liver disease r/t chronic viral hepatitis is the leading indicator for liver transplantation** (dry for 1 year, eligible for liver transplant) Major post-op complication -- rejection & infection, post transplant drugs can cause renal failure, work & financial issues |
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Post-op care/Liver transplant
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*Monitor for hemorrhage
*Assess neuro status *Prevent pulmonary complications and other complications from immobility *Monitor fluid & electrolytes *Monitor for S&S of infection *Assess & measure drainage from JP, NGT, T tube *Emotional support & teaching |
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Nursing Process: Nursing Dx/Cirrhosis
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*Actual
-Altered nutrition...less -Impaired skin integrity -Ineffective breathing -Ineffective airway clearance -Activity intolerance -Body image disturbance *Risk and PC -Risk for... Injury Ineffective management of therapeutic regime Infection *PC Hemorrhage Portal HTN & esophageal varices Hepatic encephalopathy Renal Failure |
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Hepatitis
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*Inflammation of the liver and necrosis of the hepatic cells
*Non infectious causes -Drugs & chemicals (table 38-6) -Autoimmune Infectious causes -Bacteria & Viruses |
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Hepatitis
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*HCV accounts for 45% of all chronic Hepatitis
*HCV most common liver disease in US *40% of HIV clients have HCV (IV Drug Abuse) *20-30% of pts with HCV progress to cirrhosis within 20 years *Estimated 4 million infected with HCV-50% unaware of infection *152,000 cases of HAV occur annually in US *estimated 80,000 new cases of HBV annually in US |
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Pathophysiology
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*Inflammation of hepatocytes (functional cells of liver)
*Damage *Necrosis *Liver damage is mediated by cytokines that cause lysis of infected hepatocytes *Proliferation and enlargement of Kupffer cells *Inflammation of periportan areas can interrupt bile flow and cause cholestasis (from liver to small intestine) |
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Clinical Manifestations
KNOW THIS SLIDE |
*Preicteric Phase
*Icteric Phase *Posticteric Phase |
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Preicteric Phase
(before jaundice) KNOW THIS SLIDE |
*Lasts 1-3 weeks
*Flu-like symptoms-arthritis, fever, malaise *Smokers may have distaste for ciagarettes *Hepto and spleenomegaly *Elevated liver enzymes and urine bilirubin *angioedema *skin rashes *lymphadenopathy *GI symptoms N/V *Weight loss *RUQ discomfort *Decreased sense of smell |
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Icteric Phase (jaundice phase)
KNOW THIS SLIDE |
*Lasts 2-4 weeks
*Jaundice (sclera) *Dark urine *Light, clay colored stool *Steatorrhea (fatty stools) *Tenderness and fullness RUQ *Pruritis (if bile stasis) *Elevated LFT's including direct bilirubin (conjugated) *GI symptoms remain *Some fatique **When jaundice occurs, fever usually subsides** |
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Posticteric Phase
(after jaundice) |
*Lasts weeks to months (avg. 2-4 months)
*jaundice recedes *stool and urine return to normal color *CC: fatigue & malaise *LFT's return to normal *Serum antibodies rise *Hepatomegaly remains for several weeks *Spleenomegaly subsides **Relapses may occur, and disappearance of jaundice does not mean the patient has fully recovered** **Can take up to 1 year for full recovery** **need follow-up for 1 year, need to avoid hepato toxins for 1 year or relapse may occur (tylenol, ASA, ETOH) |
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Variations in Manifestations
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*Hepatitis A - onset more acute, symptoms usually mild, flu like
*Hepatitis B - onset is more insidious, symptoms more severe, fewer GI symptoms *Hepatitis C - majority are asymptomatic & mild **HCV and to a lesser extent HBV can persist and induce chronic liver disease |
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Diagnostic Tests
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*LFT's
*Table 42-5 *Serologic Tests -Specific antibody or antigen markers for HAV, HBV, HCV, and HDV -Liver biopsy *Handout page 6 |
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Sequelae/Complications
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*Chronic hepatitis
-75-85% of HCV -10% of HBV -Persistence of HBsAG for longer than 6 months = chronic HBV -More likely to develop in infants born to infected moms, children <5 yrs., and patients with an altered immune response *Fulminant Hepatitis -Severe, massive necrosis leading to liver failure and death -Most common cause HBV, particularly HBV accompanied by HDV -Less frequently with HAV and HCV -Drugs 2nd most common cause -Tx may involve transplantation |
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Sequelae/Complications
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*Cirrhosis (20%)
-HBV - 10% -HCV -20-30% will develop cirrhosis **prognosis of HCV has greatly increased the need for liver transplants** -Risk factors for progression to cirrhosis: male, heavy ETOH, excess iron deposits in liver, steatorrhea, obesity, DM |
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Hepatitis A
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*Transmitted through fecal to oral route
*Contaminated food and water *Up to 50% of people in US are infected before adulthood *Poor hygiene, crowds, poor sanitary conditions *Transmitted between family members, day care centers, institutionalized clients *Transmitted by persons who have undetectable, sub clinical infections **you recover and then you are immune** |
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Hepatitis A
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*Anti-HAV IgM indicates acute Hepatitis
*Anti-HAV IgG indicates past infection and provides lifelong immunity *No chronic carrier state for HAV *See Table 42-2 page 1106 *Handout page 6 |
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Hepatitis B
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*One of the most serious forms
*Transmitted through parenteral/permucosal exposure to blood or body fluids **Primarily sexual transmission** *Healthcare workers are at high risk *HBV can live on a dry surface for at least 7 days **Much more infectious than HIV |
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Hepatitis B
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*Three antigens -HBsAG & HBcAG-current or chronic infection
-HBeAG - acute, highly infectious *2-10% become carriers and can transmit the disease *10% chronic infection **Persistence of HBsAG in the serum for 6-12 months after infection indicates carrier state *Presence of HBsAB or anti-HBS indicates immunity from past infection or HBV vaccine |
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Hepatitis C
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*Transmitted through parenteral/permucosal exposure to blood or body fluids
*Prevalent and underreported in US *Progresses to chronic hepatitis(75-85%)-cirrhosis(20-30%)-death *Most common indication for a liver transplant |
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Hepatitis C
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*60% - IV drug use
*20% - sexual transmission *10% - occupational exposure, hemodialysis, perinatal transmission *10% cannot identify source *Anti-HCV-acute or chronic infection *Reliable antibody test for HCV was not widely available before 1992 *Unlike Hep A & B - antibodies to Hep C are not protective & may be indicator of chronic disease |
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Hepatitis D
CANNOT EXIST ALONE |
*Appears only with HBV infection - delta virus can't survive on its own
*Chronic HBV carriers at risk *High mortality rate - patients with HBV-HDV coinfection may have more acute disease & greater chance of Fulminant Hepatitis (2-20%) *Transmitted percutaneously/parenterally like HBV *Risk of transmission via sexual activity is less *Anti-HDV IgM - current infection *Anti-HDV IgG - past infection |
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Hepatitis E
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*Transmitted through fecal to oral route
*Rare in US *Seen primarily in developing countries **Acute infection that does not progress to chronic hepatitis** *10-20% mortality rate in pregnant women *Most common drinking contaminated water* *No serologic tests to dx HEV infection in US, only in research labs *Travelers should avoid raw foods, use pure H2O supply (boil), and use effective hand hygiene |
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Hepatitis G
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*Transmitted through parenteral/permucosal exposure to blood or body fluids
*Has been found as a co-infection in people with HCV *Diagnosed by detection of hep G RNA in blood or liver tissue *Some develop chronic hepatitis *Recently recognized *NO VACCINE* |
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Treatment
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*Rest (promotes cell regeneration, decreases metabolic demand on the liver)
*Nutrition *Antiemetics *Comfort measures to relieve Pruritis, H/A, arthralgias *Avoidance of hepatotoxins for 1 year during recovery *Prevention of spread |
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Treatment/Chronic Hepatitis B
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*Focus is to decrease the viral load and decrease the rate of disease progression
-Lamivudene (taken orally for a year) *Lamivudene plus HBV immunoglobin for patients who have had a transplant for HBV *Interferon - 4 month course - decreases cirrhosis and hepatocellular cancer *Multiple side effects (table 42-7)Interferon can cause debilitating life-threatening depression *Hepsera(2002) slow progression of Hep B inhibits the virus from replicating |
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Treatment/Chronic Hepatitis C
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*Drug therapy to decrease the viral load & decrease the progression & promote seroconversion (no Anti-HCV detected in serum)
*Interferon (50% will relapse in 6 months) **Interferon plus Ribavirin decrease rate of viral replication |
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Emotions Associated with Hepatitis C Treatment
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*Frustration
*Anger *Fear *Sadness |
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Prevention/Hepatitis A
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*Hepatitis A vaccine
*Immune globin (IG) -used before or after exposure **provides 6-8 weeks of passive immunity** **can be given 1-2 weeks after exposure** *Twinrix -combined HAV & HBV vaccine -requires 3 doses (0-1-6 months) -given to high risk individuals *Personal and environmental hygiene, good sanitation, **hand washing** |
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Prevention/Hepatitis B
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*Hepatitis B vaccine
-3 doses (0-1-6 months) -95% effective *Post exposure - vaccine plus Hep B immunoglobin (HBIG)Need immunoglobin w/in 24 hrs. of needle stick *Modify high risk behavior *Gloves *Use of disposable needles/syringes *Condoms *Hand washing *Avoid sharing tooth brushes/razors *Blood, tissue, and organ screening |
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Prevention/Hepatitis C
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*No products available
*Several vaccines in development *Screening blood, organ, tissue donors *Modify high risk behavior *Gloves *Use of disposable needles/syringes *Condoms *Hand washing *Avoid sharing toothbrushes/razors |
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Nursing Process: Role
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*Assessment
-Physiological integrity -Safe & effective care environment -Psychosocial integrity *Nursing Dx -Activity intolerance -Impaired Comfort: pruritis -Impaired skin integrity -Body image disturbance -Risk for ineffective management of therapeutic regime (high risk behavior) |
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Nursing Interventions/Evaluation
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*Nursing Intervention
-See Handout *Expected Outcomes -See Handout |
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Health Promotion/Home Care
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**Rest
*Nutrition **Regular follow-ups for a year *Monitor for S&S of bleeding *Monitor for S&S of encephalopathy *Prevention measures *Measures to prevent transmission *Avoid ETOH 1 year *Side effects of meds *How to administer interferon (SC/IM) |
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Research
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*Famvir & Cytovene investigational drugs for chronic HBV
*Telbivudine new, once-a-day, oral treatment for chronic HBV *Research on effect of antiviral drugs or IG for chronic HCV *Serology test for HEV |
