AH1 Exam 3 Liver Flashcards
When does jaundice occur?
when Bilirubin is 3X normal
(0.2-1.2mg/dL)X3=2-3mg/dL
Hep A
fecal/oral
crowded conditions, poor personal hygiene, poor sanitation, contaminated food, milk, water, and shellfish.
Infected food handlers, sexual contact, IV drug users
*most infectious during 2weeks PRIOR to symptom onset and infectious through 1-2 weeks AFTER start of symptoms
RNA virus
Hep B
blood/blood products, sex, perinatal
infectious for 4-6 months BEFORE and AFTER symptoms appear
DNA virus
Hep C
blood/blood products, high risk sex, perinatal
infectious 1-2 weeks BEFORE symptoms appear and throughout clinical course
RNA
good chance infection will be chronic**
Hep D
must have HBV first
blood is infectious at all stages of HDV infection
called a delta virus; RNA
Hep E
fecal/oral; contaminated water supply in developing countries
hepatitis A IgM
indicates acute HAV
hepatitis A IgG
indicates past HAV infection and provides lifelong immunity
can live on a dry surface for 7 days and is much more infective than HIV!
HBV
rash, angioedema, arthritis, fever, malaise
clinical manifestations of activated circulating complement due to antigen-antibody binding from hepatitis that may cause secondary glomerulonephritis and vasculitis
malaise, anorexia, fatigue, nausea, occasional vomiting, and RUQ discomfort
acute hepatitis lasts 1-4 mos
malaise, easy fatiguability, hepatomegaly, myalgias and/or arthralgias, elevated AST/ALT
HBsAG > 6 mos
chronic hepatitis
HBeAg
indicates high infectivity; present in acute infection HBV
Anti-HBe
indicates previous infection HBV
HBcAg
ongoing HBV infection
HBsAg, anti HBc IgM are positive
acute HBV infection
Why should ppl with hepatitis rest?
rest reduces the metabolic demands on the liver and promotes cell regeneration. exercise causes protein breakdown which will further elevate ammonia. Liver tissue is destroyed with Hepatitis. Ret and adequate nutrition are necessary for regeneration of the liver tissue
Drug therapy for hepatitis
Chronic HBV alpha interferon (Intron A) Pegylated alpha-interferon (PEG-Intron, Pegasys) Lamivudine (Epivur) Adefovir (Hepsera) Entecavir (Baraclude) telbivudine (Tyzeka) tenofovir (Viread)
Chronic HCV
PEG-Intron or Pegasys
ribavirin (Rebetol, Copegus)
why cant phenothiazines be used for pts with hepatitis?
cholestatic and hepatotoxic
what herb may hep with hepatitis?
milk thistle-may lower blood glucose and interfere with P450 enzyme system
What does alpha interferon do?
binds to receptors on host cell membrane and blocks viral entry into cells, viral protein synthesis, assembly, and release
Whats the difference between Intron A and PEG-Intron or Pegasys?
Intron A has a short half life so it must be given SC 3xweek
Pegylated interferons last longer, give just once weekly, plus clinical responses are better due to higher doses lasting in the serum
What does a nurse need to know about alpha interferon drug therapy?
patients receiving alpha interferon should have blood counts and a liver panel performed q4-6weeks
suppress viral replication by inhibiting viral DNA synthesis; reduce viral load, decrease liver damage, and decrease liver enzymes
Nucleoside and Nucleotide Analogs (Epivir, Hepsera, Baraclude, Tyzeka, Viread)
loss of HGeAb
seroconversion and pt may be able to DC nucleoside and nucleotide analog therapy
Why isnt lamuvide (Epivir) used as first line treatment?
resistance develops
arthralgia/myalgia, asthenia (loss of strength), fatigue, HA, fever, nausea, anorexia
depression or irritability, hair thinning, insomnia, itching/dry skin, diarrhea, weight loss, injection site rxn
SE alpha Interferon
hemolytic anemia, anorexia, cough, dyspnea, insomnia, pruritis, rash, teratogenicity
SE ribavirin (PO BID)
nephrotoxic drugs
Hepsera and Viread
cyclosporine, aminoglycoside, vancomycin too!
hepatoxoic drugs
Fluothane, INH, Chlorothiazide, methotrexate, methyldopa
blockage of bile flow
cholestasis
splenomegaly, large collateral veins, ascites, HTN, gastric and esophageal varices
portal htn
Why do liver pts develop edema and ascites?
liver makes albumin-without albumin, colloidal oncotic pressure is low, and fluid leaves vasculature to go to third space
hyperaldosteronism (damaged hepatocytes cant metabolize aldosterone)–> increased sodium resorption and excessive potassium secretion (hypokalemia happens)
hepatic encephalopathy drug therapy
reduce ammonia with lactulose give antibiotics (neomycin, flagyl, cancomycin, rifaximin) to decrease bacteria in GI tract bc by product of bacterial action on protein in the feces results in ammonia production
conservative therapy for cirrhosis
rest, b vitamins, avoid alcohol, NSAIDs, Acataminophen
how to treat ascites?
low sodium diet, diuretics, paracentesis, peritoneovenous shunt
why give beta blockers to hepatic patients?
to reduce portal HTN
why give vasopressin to hepatic patients?
hemostatis and control bleeding of esophageal varices
Why give vit K to hepatic patients?
correct clotting abnormalities
Why give H2 blockers to hepatic patients?
decrease gastric acidity
Why give PPIs to hepatic patients?
decrease gastric acidity
anemia, thrombocytopenia, leukopenia, decreased serum albumin, decreased potassium, abnormal LFTs, increased INR, decreased platelets, ammonia, bilirubin, abnormal abdominal UA and liver-spleen scan
possible diagnostic findings in cirrhosis
what may relieve pruritis?
Cholestyramine (Questran) or hydroxyzine (Atarax)
baking soda bath
lotion with calamine
antihistamines
paracentesis nursing considerations
have pt void urine before paracentesis to avoid bladder puncture
pt in high fowlers
after paracentesis, monitor for hypovolemia and electrolyte imbalances and check for dressing bleeding/leakage
cardiac dysrhythmias, hypotension, tachycardia, generalized muscle weakness
hypokalemia
muscle cramping, weakness, lethargy, confusion
water excess
Cirrhosis: imbalanced nutrition: less than body requirements
r/t anorexia, impaired utilization and storage of nutrients, nausea, loss of nutrients from vomiting
Cirrhosis: Impaired Skin Integrity
r/t peripheral edema, ascites, pruritis
Cirrhosis: Dysfunctional family processes
r/t abuse of alcohol and inadequate coping skills
Cirrhosis: excess fluid volume
r/t portal HTN hyperaldosteronism
Cirrhosis: potential complication: Hemorrhage
r/t bleeding tendency secondary to altered clotting factors and rupture of esophageal or gastric varices
Cirrhosis: potential complication: Hepatic Encephalopathy
r/t increased serum levels of ammonia due to inability of liver to convert accumulating ammonia to urea for renal excretion
why is rest important for hepatic patients?
exercise produces ammonia as a by-product of protein metabolism
clay colored stools
obstructive jaundice (no bilirubin in stools)
pruritis is a common problem with jaundice in this phase
acute infection of hep a
a patient with hepatitis B is being discharged in 2 days. In the discharge teaching plan the nurse should include instructions to
a. avoid alcohol for the first 3 weeks
b. use a condom during sexual intercourse
c. have family members get an injection of immunoglobulin
d. follow a low-protein, moderate carb, moderate fat diet
b. use a condom during sexual intercourse
fetor hepaticus
fruity or musty breath resultant of liver’s inability to metabolize and detoxify mercaptan (derived from methionine)
dark urine
bilirubin in urine–> jaundice
what to do if an esophageal varices ruptures?
insert esophagogastric balloon tamponade (or sclerotherapy or portal systemic shunts)
vasopressors, vit K, coagulation factors, blood transfusion
elevated bilirubin, AST, ALT, alkaline phosphatase, PT and ammonia
decreased Hbg, Bct, electrolytes, albumin
cirrhosis lab findings
cirrhosis nutritional considerations
may need to restrict fluid to 1500mL/day (edema/ascites) encourage high biologic protein low sodium low potassium low fat high carb
hepatits nutritional consideration
high calorie, high carb, mod proteins and fats
Laennec’s Cirrhosis
cirrhosis due to alcoholism or malnutrition
cachexia
a general type of wasting of the body due to malnutrition often seen in cirrhosis
Nursing Considerations Liver biopsy
percutaneous liver biospy is performed by inserting a needle through the abdominal wall into the liver to obtain a tissue sample. Position pt on right side post procedure to compress the liver against the chest wall to decrease risk of bleeding and bile leakage.
Nursing consideration for paracentesis
involves the removal of peritoneal fluid for evaluation or to drain excess peritoneal fluid (ascites). Prior to procedure, have the client void to reduce the risk of accidentally rupturing bladder. after procedure, monitor client for peritonitis and peritoneal bleeding
Nursing consideration for hepatic angiography
catheterization of the hepatic vasculature allows injection of a contrast medium and visualization of the vascular supply of the liver. Vessel pressures can also be measured to assess the degree of portal hypertension. After the procedure, assess VS and insertion site frequently and client should remain on bedrest 24-48 hours.
tests that reflect clotting time will be prolonged bc the diseased liver produces less clotting factors. also, the intestine absorbes less vit K bc the liver is producing less of the bile that is necessary for vit K absorption
APTT, PT/INR
what occurs during an endoscopic sclerotherapy?
an endoscope is placed into the patient’s mouth and is passed down the esophagus. Varices are visualized. A chemical solution is injected into the varices to sclerose and harden the area. This helps to prevent bleeding from the varices.
how does GI hemorrhage precipitate hepatic encephalopathy?
increases ammonia in GI tract
how does constipation precipitate hepatic encephalopathy?
increase in ammonia from bacterial action on feces
how does hypokalemia precipitate hepatic encephalopathy?
potassium ions are needed by brain to metabolized ammonia
how does hypovolemia precipitate hepatic encephalopathy?
increase in blood ammonia by causing hepatic hypoxia, impairment of cerebral, hepatic, and renal fxn due to decreased blood flow
how does infection precipitate hepatic encephalopathy?
increase in catabolism, increase in cerebral sensitivity to toxins
how does metabolic alkalosis precipitate hepatic encephalopathy?
facilitation of transport of ammonia across BBB, increase in renal production of ammonia
how does paracentesis precipitate hepatic encephalopathy?
loss of sodium and potassium ions decrease in blood volume
how does dehydration precipitate hepatic encephalopathy?
potentiation of ammonia toxicity
how does increased metabolism precipitate hepatic encephalopathy?
increased workload of liver
how does uremia (renal failure) precipitate hepatic encephalopathy?
retention of nitrogenous metabolites