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69 Cards in this Set

  • Front
  • Back
Alteration in GI Function
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)
Liver Functions
-Manufacture, storage, transformation and secretion of a number of substances involved in metabolism
-Waste Disposal Plant
*See handout*
Hepatic Disorders
Clinical Manifestations reflect alterations in normal liver function
Major Hepatic Disorders:
-Infectious and inflammatory conditions
-Structural abnormalities
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**
Types of Cirrhosis: Alcoholic Cirrhosis
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
Types of Cirrhosis: Post necrotic cirrhosis
Post necrotic cirrhosis
-complication of viral, toxic or idiopathic (autoimmune)hepatitis
-broad bands of scar tissue form within the liver
Types of Cirrhosis: Biliary Cirrhosis
Biliary Cirrhosis
-associated with chronic biliary obstruction and infection
-diffuse fibrosis of liver with jaundice as a main feature
Types of Cirrhosis: Cardiac Cirrhosis
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
*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
Clinical Manifestations/Early
-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
Clinical Manifestations/Late
*skin lesions-spider angiomas, Palmar erythema
*Hematologic Problems
-coagulation disorders: epitaxis, petechiae, easy bruising, gingival bleeding, heavy menstrual bleeding
Clinical Manifestations/Late
*Endocrine Disturbances
-Men-Gynecomastia, loss of axillary & pubic hair, testicular atrophy, impotence
-Younger women: amenorrhea
-Older women: vaginal bleeding
*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**
Major Complications
**Portal Hypertension & Esophageal Varices**
*Peripheral Edema & Ascites
*Hepatic Encephalopathy
*Hepatorenal Syndrome
Portal Hypertension
*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
Esophageal Varices
*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
Peripheral Edema & Ascites
*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
Hepatic Encephalopathy
*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
Hepatic Encephalopathy
Main breakdown of protein metabolism = ammonia
Increased ammonia levels = mental status changes
Clinical Manifestations/Hepatic Encephalopathy
*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)
*Fetor-hepaticus-musty, sweet odor of patients breath
Hepatorenal Syndrome (HRS)
*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)
Diagnostic Studies (KNOW NORMAL VALUES)
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
Diagnostic Studies
*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**
Treatments: Medical
-Maximize liver function
-**Rest: decreases metabolic demand of liver**
-Prevent infection
-Control complications
-Pharmacological treatments
Treatments: Surgical
-No surgical treatment for cirrhosis
-Surgical treatment is aimed at treating complications
-liver transplant
Treatment Ascites
*Focus - NA restriction, diuretics, fluid removal
*SPA - Salt poor albumin
*Diruetics-aldactone:K sparing, loop diuretic (lasix: K wasting)
*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
Treatment/Esophageal Varices
**GOAL: Avoid bleeding and hemorrhage
-Avoid ETOH, ASA, irritating foods
-Control coughing
-B-blockers (Inderal)decrease cardiac output
-Octreotide (growth hormone)
-Vasopressin in conjunction with Nitroglycerin
-Vitamin K
-H2 receptor blockers decrease acidity
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
Medication for Bleeding Varices
**Octreotide treatment of choice**
*Vasopressin in conjunction with Nitroglycerin
*Beta Blockers (Inderal)
*Vitamin K
*H2 receptor blockers decrease HCL
Balloon Tamponade for Bleeding Varices
*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
Shunting for Varices
*Tranjugular intrahepatic portosystemic shunt (TIPS) bypasses liver
*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
Treatment/Hepatic Encephalopathy
**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
-Neomycin (PO decreases bacterial flora in intestine decreases ammonia
-Avoid constipation (straining)
-Remove blood from the GI tract
Nutritional Therapy
*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
Health Promotion/Acute Intervention
*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
Health Promotion/Home Care
**GOAL: maintain highest level of wellness possible
-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
Liver Transplantation
*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
Post-op care/Liver transplant
*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
Nursing Process: Nursing Dx/Cirrhosis
-Altered nutrition...less
-Impaired skin integrity
-Ineffective breathing
-Ineffective airway clearance
-Activity intolerance
-Body image disturbance
*Risk and PC
-Risk for...
Ineffective management of therapeutic regime
Portal HTN & esophageal varices
Hepatic encephalopathy
Renal Failure
*Inflammation of the liver and necrosis of the hepatic cells
*Non infectious causes
-Drugs & chemicals (table 38-6)
Infectious causes
-Bacteria & Viruses
*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
*Inflammation of hepatocytes (functional cells of liver)
*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)
Clinical Manifestations
*Preicteric Phase
*Icteric Phase
*Posticteric Phase
Preicteric Phase
(before jaundice)
*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
*skin rashes
*GI symptoms N/V
*Weight loss
*RUQ discomfort
*Decreased sense of smell
Icteric Phase (jaundice phase)
*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**
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)
Variations in Manifestations
*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
Diagnostic Tests
*Table 42-5
*Serologic Tests
-Specific antibody or antigen markers for HAV, HBV, HCV, and HDV
-Liver biopsy
*Handout page 6
*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
*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
Hepatitis A
*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**
Hepatitis A
*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
Hepatitis B
*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
Hepatitis B
*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
Hepatitis C
*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
Hepatitis C
*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
Hepatitis D
*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
Hepatitis E
*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
Hepatitis G
*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
*Rest (promotes cell regeneration, decreases metabolic demand on the liver)
*Comfort measures to relieve Pruritis, H/A, arthralgias
*Avoidance of hepatotoxins for 1 year during recovery
*Prevention of spread
Treatment/Chronic Hepatitis B
*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
Treatment/Chronic Hepatitis C
*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
Emotions Associated with Hepatitis C Treatment
Prevention/Hepatitis A
*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**
-combined HAV & HBV vaccine
-requires 3 doses (0-1-6 months)
-given to high risk individuals
*Personal and environmental hygiene, good sanitation, **hand washing**
Prevention/Hepatitis B
*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
*Use of disposable needles/syringes
*Hand washing
*Avoid sharing tooth brushes/razors
*Blood, tissue, and organ screening
Prevention/Hepatitis C
*No products available
*Several vaccines in development
*Screening blood, organ, tissue donors
*Modify high risk behavior
*Use of disposable needles/syringes
*Hand washing
*Avoid sharing toothbrushes/razors
Nursing Process: Role
-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)
Nursing Interventions/Evaluation
*Nursing Intervention
-See Handout
*Expected Outcomes
-See Handout
Health Promotion/Home Care
**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)
*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