Exam (elaborations)
NR 325 Exam 3 Panc, Chole, Hep_Cirr, Cancers (1).
NR 325 Exam 3 Panc, Chole, Hep_Cirr, Cancers (1).
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NR 325 Exam 3 Panc, Chole, Hep/Cirr, CancersImmunity against infection
Factory for proteins and cholesterol
Excretes waste via bile
Excretes bile for fat digestion
Regulates blood clotting
Clears blood of drugs, chemicals, and alcohol
Converts excess glucose to starch for storage - ANS-Function of the Liver
Inflamed liver tissue leads to damaged liver tissue. The liver can regenerate in acute infection
and resume normal appearance and function. - ANS-Viral Hepatitis Acute Infection
Lasts at least 6 months and may persist for years. Continued inflammation slowly destroys the
liver, leading to cirrhosis, liver failure, or liver cancer. - ANS-Viral Hepatitis Chronic Infection
-Lasts 1 to 4 months
-Period of maximal infectivity
-CM: malaise, fatigue, anorexia, weight loss, nausea with occasional vomiting, jaundice,
pruritus, hepatomegaly, abdominal pain in RUQ, dark frothy urine (from protein and bilirubin),
and clay colored stool - ANS-Acute Viral Hepatitis Acute Phase: Icteric Phase
-Lasts 2 to 4 months
-Begins as jaundice disappears
-Gradually recovering, relapses may occur
-Major Complaints: easily fatigued, malaise, activity intolerance - ANS-Acute Viral Hepatitis
Convalescence Phase: Post-Icteric Phase
Most patients recover completely with no complications - ANS-Acute Viral Hepatitis Recovery
Phase
-Liver enzymes: increases ALT and GGT
-Increased alkaline phosphate
-Decreased proteins
-Increased bilirubin (indirect or unconjugated bilirubin)
-Increased urinary bilirubin
-Prolonged prothrombin time
-Decreased blood glucose level - ANS-Hepatitis Diagnostic Studies
-Alternate periods of activity and rest: less metabolic demand on the liver and more cell
regeneration
-Eat a well balanced diet, low fat, high CHO, high protein foods
,-Take a B-complex vitamin supplement: helps regenerate liver tissues
-Avoid alcohol - ANS-Hepatitis General Home Care Management
-Transmitted fecal-to-oral route between family members, institutionalized people, and children
in day care centers
-Risk Factors: poor hygiene, improper handling of foods, crowded situations, poor sanitary
conditions
-No ongoing, long-term disease process, no chronic carrier state
-Infection induces life-long immunity, no recurrence - ANS-Hepatitis A (HAV)
-Pre-exposure prophylaxis: provides passive immunity for 1-2 months
-Post-expsoure prophylaxis: get within 2 weeks, decreases severity of the illness - ANS-Immune
Globulin (IG) Injection
-Mild Case: home care, usually self-limited, utilized general home care management guidelines,
family members must wash hands frequently
-Severe Case: medical intervention/management, bed rest, enteric/contact precautions are
needed - ANS-Management of Hepatitis A
-Through direct contact with blood or body fluids of infected person
-Unprotected sexual activity with an infected person
-Needle sharing among IV drug users
-Being pierced/tattooed with contaminated instruments
-Passed onto a baby during childbirth if the mother is infected - ANS-Hepatitis B (HBV)
Transmission
-Immunization is the most effective method, routine vaccination are 3 doses at 0, 1, 6 months
-Nonimmunized adults are given Hep B Immune Globulin (HBIG) within 24 hours of exposure,
and started on the vaccine - ANS-Hepatitis B Prevention
Mild cases usually resolve on their own, a severe case will need medical treatment to restore
F&E - ANS-Hepatitis B Management of Acute Infection
-Drug therapy is needed
-Pegylated interferon: long-acting weekly subq injection, may cause flu-like symptoms
-Nucleoside and nucleotide analogs are give PO, may cause nephrotoxicity so monitor
creatinine and daily weight - ANS-Hepatitis Management of Chronic Infection
-Transmitted by blood-to-blood contact
-IV drug use is the most common mode of transmission
-Asymptomatic in the acute stage
-Most common causes of chronic liver disease, cirrhosis, and liver transplantation -
ANS-Hepatitis C (HCV)
, -Acute Infection: self-care, rest, increase fluid intake to 2500 mL per day, no alcohol intake
-Chronic Infection: drug therapy pegylated interferon subq injection and ribavirin PO BID is
needed - ANS-Management of Hepatitis C
-Irreversible, chronic, prolonged, destructive, degenerative liver disease
-Irreversible reaction to long-standing liver inflammation and necrosis
-Usually develops insidiously
-Has a disorganized cell regenerative process, new fibrous connective tissue distorts normal
structure and impedes blood flow, l/t poor cellular nutrition and hypoxia
-Scar tissue replaces damaged liver cells
-Liver is unable to make many proteins needed for the body (like coagulation) - ANS-Cirrhosis
-Excess alcohol: 32-45%
-Persistant hep C infection: 25%
-Mould toxins (aflatoxins)
-Non-alcoholic fatty liver disease - ANS-Cirrhosis Risk Factors
-Portal vein collects blood from the intestines, spleen, and stomach and channels it into the liver
-All the veins in the GI tract go to the liver, there is a complete veinous and arterial system in the
liver. If it is in intense vascular pressure, portal hypertension can occur. When liver cells
degenerate they can't adequately perfuse, circulation backs up.
-Varicose veins occur in the esophagus and GI tract, and are prone to bleeding. Clotting factors
normally made in the liver are not made because of the cirrhosis, so if the varicose veins bleed
the patient will bleed to death - ANS-Hepatic Circulation
Extensive scarring from cirrhosis leads to obstruction of the portal blood flow. Obstruction least
increase of pressure in the portal vein, causing portal HTN. Portal HTN is classified as pressure
>9mm Hg - ANS-Portal Hypertension
The damage cirrhosis causes to the liver leads to a lack of protein production, which leads to
fluid accumulation in tissue space. Massive accumulation of fluid from lack of protein and no
oncotic pressure causes peripheral edema, pleural effusion, and ascites. - ANS-Decreased
Capillary Oncotic Pressure
Hepatic encephalopathy, peripheral neuropathy, asterixis, anorexia, dyspepsia, nausea,
vomiting, change in BM, dull abdominal pain, esophageal and gastric varices, hemorrhoidal
varices, congestive gastritis, amonorrhea, testicular atrophy, gynecomastia, impotence,
jaundice, spider angioma, purpura, petechiae, anemia, thrombocytopenia, leukopenia,
coagulation disorder, splenomegaly, hypokalemia, hyponatremia, hypoalbuminemia, fluid
retention, peripheral edema, and ascites. - ANS-Cirrhosis Clinical Manifestations
-Increased AST, ALT, and alkaline phosphotase
-Increased prothrombin time
-Increased bilirubin
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