NURS 2003H Chapter Notes - Chapter 46: Constipation, Abdominal Cavity, Gastric Varices
26 Jun 2018
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Viral Hepatitis CH 46 p. 1218- 1230
- Inflammation of the liver
- A, B, C, D, E and G hepatitis viruses
- Hepatitis can also be caused by drugs or alcohol, autoimmune diseases, metabolic
disorders, and genetic abnormalities.
- Viral hepatitis is a major public health concern
oMost common types in Canada is hep A, B, and C.
- The only definitive way to distinguish among the various types of viral hepatitis is by the
presence of the antigens and the subsequent development of antibodies to them.
- Person who is immune to one virus can still develop another type of viral hepatitis.
Pathophysiological Features
-Liver:
oWidespread inflammation of the liver tissue
oAcute infection liver damage is mediated by cytotoxic cytokines and natural
killer cells that cause lysis of infected hepatocytes (liver cells).
oLiver cell damage results in liver cell death.
oInflammation of the periportal areas may interrupt bile flow, causing cholestasis
(impaired flow of bile).
oLiver cells normally regenerate through cellular replication, and if no
complications occur, they should resume their normal function.
If liver cell loss is massive, cellular replication may not be possible.
-Systemic effects:
oAntigen-antibody complexes between the virus and its corresponding antibody
form a circulating immune complex in the early phases of hepatitis.
This activates the complement system
oThe clinical manifestations of this activation are rash, angioedema, arthritis, fever,
malaise, cryoglobulinemia (presence of abnormal proteins in the blood),
glomerulonephritis (inflammation of the tiny filters in your kidneys-glomeruli),
and vasculitis.
Clinical Manifestations
- Acute phase is the time of initial exposure to the virus
oMost have no symptoms
- Infections are often not known to be present and therefore not diagnosed.
- The clinical symptoms, if present, in acute infections are similar across all types of
hepatitis viruses.
oCourse of infection varies
oA and E have similar clinical course
oAcute hep A usually resolves, whereas many cases of acute hep B and C result in
lifelong infections.
-Acute Phase:
oLasts 1-4 months
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oIncubation period: symptoms are mostly GI, with nausea, vomiting, anorexia,
right upper quadrant pain, constipation, or diarreah.
oMay find food and alcohol repugnant
oSmokers will develop a distaste for cigarettes.
oMalaise, fatigue, Head ache, low-grade fever, arthralgia (joint pain), skin rashes.
oHepatomegaly, lymphadenopathy, splenomegaly
oThe acute phase is the period of maximal infectivity.
oMay be icteric (jaundice) or anicteric (no jaundice)
Jaundice happens when bilirubin diffuses into the tissues
Urine may be darker because of excretion of excess bilirubin by the
kidneys
If conjugated bilirubin cannot flow out of the liver because of obstruction
or inflammation of the bile ducts, the stools are light or clay colored.
When jaundice occurs, other symptoms decrease in severity
oPruritus (itching) sometimes accompanies the jaundice
Occurs as a result of accumulation of bile salts beneath the skin.
oThe convalescent period of the acute phase begins as jaundice id disappearing and
lasts from 2-4 months.
Major complaint is malaise and easy fatigability
Hepatomegaly (enlarged liver) remains for several weeks, but
splenomegaly subsides
-Chronic Phase:
oAlmost all cases of hep A resolve with no progression to this stage
Relapse may occur in a few patients a few months after infection
oThe disappearance of jaundice does not mean you are cured
oHep B and C infections usually result in chronic disease
oMost have no symptoms
oNonspecific symptoms: malaise, fatigue, myalgia (muscle pain), arthralgia (joint
pain), hepatomegaly
oHep B and C can progress to severe scarring of the liver (cirrhosis) and liver
failure if left untreated.
Complications
- Less than 1% mortality rate
-Fulminant hepatitis:
oAcute clinical syndrome that results in severe impairment or necrosis of liver cells
and potential liver failure.
oOnly occurs in a small number of patients
oMay develop in co-infection with HBV and HDV
oLess frequent with acute HCV and rarely occurs with acute HAV
oToxic rxns to drugs and congenital metabolic disorders may also cause death
unless liver transplantation occurs.
Diagnostic Studies
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-Viral Serological Tests:
oViral antigens and antibodies are serological markers used to diagnose the
different types of viral hepatitis.
-Serum Liver enzymes:
oHelp determine whether it is related to liver cell injury or bile duct abnormalities
oAspartate aminotransferase (AST) and alanine aminotransferase (ALT) are liver
enzymes whose levels can indicate liver cell injury.
oIn severe acute viral hep, the levels can be very high at 1000 U/L.
oElevated levels of alkaline phosphate (ALP) and y-glutamyl transpeptidase (GGT)
are usually associated with bile duct injuries
These levels rise to a lesser extent in viral hep
-Liver function tests:
oSerum albumin, serum bilirubin, and prothrombin time, which is standardized to
the international normalized ratio (INR)
oIn mild acute viral hep, serum albumin, serum bilirubin and INR remain normal
oWhen jaundice is detectable, serum bilirubin level is usually at least twice the
normal upper limit (>34 mcmol/L)
oDeteriorating liver function is demonstrated by increased INR and serum
bilirubin, and decreased serum albumin.
Cirrhosis of the Liver CH 46 p.1233-1240
- Diffuse pathological process, characterized by fibrosis (scar tissue) and concersion of
normal liver architecture to abnormal nodules.
- When the liver cells attempt to regenerate after liver injury but the regenerative process is
disorganized
- The overgrowth of new fibrous connective tissue distorts the normal lobular structure,
resulting in lobules of irregular size and shape with impeded blood flow.
- Irregular regeneration, poor cellular nutrition, and hypoxia caused by inadequate blood
flow and scar tissue result in decreased functioning of the liver.
- Cirrhosis is the final stage of liver disease, cirrhosis is reversible because of fibrosis
regression.
- 13th leading cause of death in Canada, highest between ages 40-60 and twice as common
in men than women.
Etiology
- Chronic viral hepatitis, NAFLD, and auto immune hepatitis as well as excessive alcohol
intake can cause cirrhosis
- Excessive alcohol ingestion remains one of the most common causes of cirrhosis
o Has a direct hepatotoxic effect and it causes cell necrosis and fatty infiltration in
the liver
o some argued that malnutrition is the cause that frequently coexist with chronic
ingestion of alcohol
- Environmental factors as well as genetic predisposition may also lead to the
development
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Document Summary
A, b, c, d, e and g hepatitis viruses. Hepatitis can also be caused by drugs or alcohol, autoimmune diseases, metabolic disorders, and genetic abnormalities. Viral hepatitis is a major public health concern: most common types in canada is hep a, b, and c. The only definitive way to distinguish among the various types of viral hepatitis is by the presence of the antigens and the subsequent development of antibodies to them. Person who is immune to one virus can still develop another type of viral hepatitis. If liver cell loss is massive, cellular replication may not be possible. Systemic effects: antigen-antibody complexes between the virus and its corresponding antibody form a circulating immune complex in the early phases of hepatitis. This activates the complement system: the clinical manifestations of this activation are rash, angioedema, arthritis, fever, malaise, cryoglobulinemia (presence of abnormal proteins in the blood), glomerulonephritis (inflammation of the tiny filters in your kidneys-glomeruli), and vasculitis.
