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• 4 Causes of Jaundice are destruction of RBC (hemolytic jaundice), impaired uptake of bilirubin by liver cells (Hepatocellular
jaundice), Decreased conjugation of bilirubin (hepatocellular jaundice), Obstruction of bile flow (obstructive jaundice)
• Signs and symptoms of jaundice are the following 4. 1. Yellow skin, sclera and mucus membranes b/c bilirubin diffuses into
the tissue and stains it. 2. Dark urine b/c excess bilirubin is excreted by kidneys. 3. Light clay colored stool if bile ducts are
obstructed or inflamed and bile can’t flow to intestines. 4. Itching b/c bile salts accumulate under the skin
• Facts about jaundice – 1. Yellow is from the flow of bile into hepatic or billary ducts. 2. Bilirubin must be 3 xs normal for
jaundice to occur. 3. It is a symptom not a disease 4. Abnormal increase in bilirubin concentration occurs 5. It is first detected
in the sclera and skin
Type of Jaundice Commonly caused by Bilirubin
Hemolytic (prehepatic) what causes it happens • Blood transfusion reactions Increased breakdown of rbc causes increased
before the liver gets involved • Hereditary disorders of RBC’s such as amounts of unconjugated bilirubin in the blood
sickle cell anemia, thalasemia, (liver cannot handle the load.)
• Acquired hemolytic disorder
Hepatocellular (hepatic) it happens w/I the liver, • Hepatitis Hepatocytes cant convert so bilirubin increases.
the liver cells cant convert bili or leaks bili or both • Cirrhosis Both direct and indirect increase. Conjugated
• Hepatic carcinomas (direct) bilirubin is secreted through urine since
they are water soluble. (impaired uptake of
bilirubin by the liver
Obstructive intrahepatic (post hepatic) it is an • Swelling or fibrosis of the canalculi and Increased direct and indirect bilirubin and increased
obstructive flow of bile in the liver bowel ducts inside the liver urine bilirubin
s/s clay colored stool • Tumors
• Hepatitis
• Cirrhosis

Obstructive extrahepatic (post hepatic) it is an • d/t whatever keeps bile from getting into Increased direct and indirect bilirubin and increased
obstructive blow if bile in the biliary system the intestines urine bilirubin
s/s clay colored stool • stones caught in the CBD, biliary
strictures, schlerosing cholangitis,
carcinoma of the head of the pancreas
Hepatitis Phases
Phase Time Signs and Symptoms Misc. Facts
Acute phase Lasts 1-4 months * anorexia * nausea *fatigue * headache * • fever usually subsides
Acute infection, infected Hepatocytes are (incubation) occasional vomiting * ruq discomfort * low when jaundice occurs
lysed by cytotoxic cytokines and killer
cells, kupffer cells enlarge and proliferate grade fever * joint pain* rashes* • anorexia nausea &
this causes periportal inflammation that hepatomegaly * lymphoidenopathy * fatigue continues after
can interrupt bile flow (cholestasis splenomegaly * Jaundice * fever * enlarged jaundice sets in
tender liver • time of maximal
infectivity for hep A
Convelescent Phase Lasts 2-4 months *malaise * fatigue * hepatomegaly may • begins as jaundice
Follows acute phase continue for several weeks after disappears
(relapse may occur) • splenomegaly subsides
• disappearance of
jaundice does not mean
pt is fully recovered

Chronic Phase Some may be asymptomatic * malaise * • Almost all hep A

fatigue * myalgia * arthralgia * resolves
hepatomegly • Some hep b results in
chronic infection
• Most hep C results in
chronic infection (75%-
Chronic hep B is a risk factor
for hepatocellulcar carcinomas
Things that kill the liver:
Acetominophine, amiodarone, arseniz, azathioprine, carbamazepine, chloroform, gold compounds, halothane, isoniazil (inh), ketoconazole, mercantopurine 6, mercury,
methotrexate, nevirapine, niacin, statins, sulfonamides, thiazide diuretics, thizolidinediones
Viral Hepatitis is ABCDEG. Local is widespread liver inflammation. Liver damage comes from hepatic cell necrosis. Liver cells can
regenerate and may resume normal function if no complications occur. On a systemic level antigen – antibody complexes are formed.
These complexes activate the complement system, this can cause rashes, angioedema, arthrisit, fever, malaise (complications can
include cryoglobulinemia, glomerulonephritis, and vasculitis.
Hep. Strand How its spread Facts
Hep A • Spread through fecal/oral route from • No chronic carrier state
RNA virus contaminated food or drinking water • IGM antibody = past infection and gives lifetime immunity
• Most infectious during the incubation period
• Almost all cases resolve self
• Acute onset
• Mild flu like symptoms
• Many have no jaundice
Does not cause chronic hep.
Hep B • Unprotected sex • Can live on a dry surface for 7 days (more infectious than HIV)
DNA virus • Parenteral/premucosal ( iv needles, • Pattern of core and surface antigens and antibodies in the serum can indicate time
toothbrushes, etc.) frame of infection
• Perinatal transmission • Abs can be given by vaccination and give protection
• Can be acute, chronic, or carrier state
• Is a factor for hepatocellular carcinoma
• Onset slower than hep A
• Small number get chronic hep B
• Becomes fulminant hepatitis less often than hep D but more often than hep C
Hep C • Shared iv needles • may progress to chronic hep, fibrosis, cirrhosis, hepatocellular carcinoma
RNA virus • Blood transfusions • has caused an increased demand for liver transplants
No VACCINE! • Occupational exposure • many progress to chronic hep C
• High risk sexual behavior • most cases are asymptomatic or mild symptoms
• Hemodialysis • often leads to chronic liver disease
• perinatal • very rarely can beomce fulminant hepatitis
• No vaccine available

Hep. Strand How its spread Facts

Hep D • Injection drug users. . • Virus cannot live alone, can only survive with hep B virus
RNA virus • Sex contacts of infected people. • HBV/HDV infections together increase risk of severe disease
Delta Virus • Hemodialysis patients. • No vaccine
No vaccine • Health-care and public safety • Requires hep b to replicate
workers who have contact with • Fulminant hepatitis is more common in a person infected with hbv
infected blood. and hdv viruses.
• Infants born to infected mothers •
(very rare).

Hep E • Fecal oral route (same has hep a) • No specific test

RNA virus • Primarily in developing countries
• Serum tests can only detect igm and igg and anti hev, and serum rna
Hep G • Unprotected sex • co – exists with hbv, hcv, hiv,
RNA virus • parenteral • does not cause liver damage by itself

Fulminant hepatitis
Fulminant Hep: rare,frequently fatal form of acute hepatitis more often with hbv, F. Hepatitis nsg care: : may progress rapidly, condition can change by the hr.
esp. w/ hdv co infection. Less often w/ hcv. toxic reactions to drugs & (assess frequently. Monitor labs (lft’s and kidney function). Plan for early transfer
cogentenital metabolic disorders can also cause this liver failure. Usually causes to ICU or transplant center. (keep paper work updated), assess for renal failure
death unless liver transplant is done. Rapidly deteriorates w/ liver failure, hep secondary to liver failure
encephalopathy, necrosis of hep parenchyma, cougu –lopathy, renal failure, coma

Acute Viral Hepititis

Assessment: lab specific antigen antibody panels to diagnose viral hepatitis, hep b/c can be genotyped to give more specific therapy,
look for hepatic tenderness, hepatomegaly, splenomegaly, palpable liver. Liver biopsy not done in acute viral hep, may be doen w/
chronic hep to look for fibrosis or cirhosis

Diagnostic Findings: specific hep virus antigens/antibody panels. AST increase in acute, ALT increase in acute, GGT increase,
Alkaline phosphatase moderately increased, globulin wnl or increased, albumin wnl or decreased, serum bilirubin increased to approx
8-15mg/dl, urinary bilirubin increase, urine urobilinogen increased 2-3 days before jaundice, prothrombin time is prolonged.

• goal is to reduce metabolic demands on liver
• managed at home
• rest
• high calorie, high protein, high carb, low fat diet
• vitamin supplements
• avoid alcohol and drugs detoxified by liver
• counseling if needed

Drug therapy w/ acute viral Hep

• For Acute Hep: supportive, depending on symptoms
• Antimetics – dimenhydrinate (Dramamine), methobenzamide (tigan)
• Avoid phenothiazines for nausea – hepatotoxic, can cause cholestasis (bile stasis)
• Do not use compazine or phenergan (phenothiazines) for nausea/vomiting
• For sedative/hypnotic, may use benadry or chloral hydrate
Drug Therapy for Chronic Hep
• Chronic Hep b: goal is to reducle viral load, decrease alt and ast, reduce rate of disease progression, reduce rate of drug
resistant HBV, prevent cirrhosis & liver cancer
• Not all pt. respond to drugs currently on the market
Drug Therapy for Hep B
Drug Name Action Regimen S/E Misc. Facts
Interferon Affects viral replication cycle. *Conventional form • Flu-like
Blocks entry into cells, synthesis of given subq @ least • Depression
viral proteins and viral assembly and 3x/week • Thinning hair
release *long-acting form • Insomnia
(pegylated) given subq • Itching/dry skin
• Diarrhea
• Weight loss
• Local reaction at
injection site
Nucleoside Suppress viral replication by Other Names:
Analogs inhibiting viral DNA synthesis Epivir
Lamivudine *Not first line therapy
(Epivir) d/t possibility of
developing drug
resistance (40%)
*used for hbv and HIV
*when drug is stopped
viral level and
inflammation return to
pre treatment levels
*Monitor bun/creat
*caution w/ impaired
renal function
*some pts + antigen test
will turn – undectable
Adefovir Used in w/ lamivudine – resistant • taken for 1 yr *monitor for * decreases liver damage
(hepsera) HBV, reduces viral load, nephrotoxicity *decreases liver
* do not give to pregnant enzymes in 2/3 of pt.
women *seroconversion
*inflammation returns
when drug is stopped

Entecavir Can be used with lamivudine, *taken for 1 year * do not give to pregnant *reduces viral load,
(Baraclude) resistant hbv women * decreases liver damage
*decreases liver
enzymes in 2/3 of pt.
*inflammation returns
when drug is stopped

Telbivudine *taken orally once daily *muscle pain

(Tyzeka) *elevated creatine kinase
*upper respiratory tract