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236 Cards in this Set

  • Front
  • Back
size and location of liver
largest gland in body, located Upper Right Abdomen
veins and arteries of the liver
One exit the Hepatic Vein, 1 artery the Hepatic Artery rich in O2, and the Portal Vein, where the Liver gets the nutrients from the GI tract
What are the functions of the liver per PP
Carbohydrate Metabolism
Protein metabolism
Lipid & Lipoprotein metabolism
Bile acid synthesis & excretion
bilirubin excretion
Storage
Biotransformation/detoxification and excretion of endogenous & exogenous compounds
removal of pathogens
steroid catabolism
what are the funcitons of the liver - brunners
amonia conversion
protein, fat, glucose and drug metabolism
Vitamin & iron storage
Bile formation
glycogenolysis is
glycogen into glucose
gluconeogenesis is
synthesis of glucose
glycogenesis
glycogen from glucose
synthesis of plasma proteins includes
albumin, alfa and beta globulins
(not gamma globuins)
formation of ketone bodies comes from
broken down fatty acids
hepatotoxic mes include
acetaminophen
ketoconazole (fungal)
valproic acid
T or F
the majority of blood supply to the liver, which is poor in nutrients, comes from the portal vein
False, the majority of blood supply to the liver which is rich in nutrients from the GI tract, comes from the portal vein
Carbohydrate metabolism includes
glycogenesis
glycogenolysis
gluconeogenesis
Protein metabolism includes
Synthesis amino acids
Synthesis plasma proteins
Formation of urea
lipid & lipoprotein metabolism includes
 Synthesis lipoproteins
 Breakdown of triglycerides
 Formation ketone bodies
 Synthesis of fatty acids
 Synthesis & breakdown of cholesterol
Bile acid synthesis & excretion includes
Bile formation (containing bile salts, bile pigments (bilirubin, biliverdin), cholesterol
Bile excretion—about 1 liter/day
bilirubin excretion is
(pigment from breakdown of hemoglobin)Destroyed & ingested by macrophage system of liver, spleen, marrow. Chemically changed & excreted in bile via duodenum.
storage includes
 Glucose (as glycogen)
 Vitamins A,D,E,K??, B1, B2, B12, folic acid)
 Fatty acids
 Minerals (Fe, Cu)
 Amino acids (albumin, beta globulins)
Biotransformation, detoxification, excretion of endogenous & exogenous compounds includes
 Inactivation of drugs & excretion of breakdown products
 Clearance of procoagulants, activated clotting factors, byproducts of coagulation
steroid catabolism includes
 Conjugation & excretion of gonadal steroids
 Conjugation & excretion of adrenal steroids (cortisol, aldosterone)
gerontologic considerations of the liver are
• Steady decrease in size and weight
• Decrease blood flow
• Decrease repair
• Reduced drug metabolism / clearance
• Decreased clearance Hep B antigen
• Increase progression Hep C, lower response to therapy
what is the scoop on Vit K and the liver
Vit K is absorbed and needed for prothrombin and clotting factors
what are the minerals stored in the liver
iron and copper
which type of steroids can be excreted conjugated or unconjugated
conjugated
explain protein turning into urea
use of amino acids from protein for gluconeogensis (glucose from liver) results in formation of ammonia, which turns into urea
what are causes of Chronic Liver Dysfunction ( 9th leading cause of death)
*Infectious agents—bacterial, viruses (Hepatitis B & C)
*Nutritional deficiencies— malnutrition, alcoholism
*Anoxia
*Toxins, medications
what are the different types of hepatic cirrhosis
• Alcoholic cirrhosis (#1)
• Postnecrotic cirrhosis
• Biliary cirrhosis
what is the path of cirrhosis
 Chronic degeneration of liver tissues
 Results in destruction of hepatic cells (hepatocytes)
 Formation of extensive dense fibrous scar tissue
• Scarring causes compression of blood, lymph and bile channels
• Hepatic insufficiency
Hepatic Cirrhosis can lead to
• Infection and peritonitis
• Gastrointestinal varices
• Edema
• Vitamin deficiency and anemia
what is postnecrotic cirrhosis
from previous bout of acute viral hepatitis and the broad bands of scar tissue
what is the common make up of a person who gets hepatic cirrhosis
Women, 40-60
alcoholism plays a part of cirrhosis?
major, though some nondrinkers can get it.
explain the liver in the early stages of cirrhosis
large and loaded w/fat. firm w/sharp edge on palpation, ABD pain
explain the liver in the late stages of cirrhosis
decrease in size, scar tissue contracts liver, edge is palable but nondular
Dx of Hepatic Disease includes what type of tests
PHYSICAL ASSESSMENT
Liver Function Tests
Alakaline phosphatase (ALK. PHOS)
LDH
ALT (SGPT)
AST (SGOT)
SERUM BILIRUBIN 0-0.3 mg/dL
SERUM CHOLESTEROL
ELECTROLYTES
Ammonia 40 mcg/dL
Serum Albumin 4-5.5 g/dL

DIAGNOSTIC PROCEDURES
Ultrasound of Liver
CT SCAN of Biliary Tract and Liver
LIVER SPLEEN SCAN
LIVER BIOPSY
ALP (ALK Phos) norm is
42-128
LDH norm is
under a few hundred normally
ALT (SGPT) norm is,
and a ALT of 45 is
8-20
most definitive of Hepatitis and cirrhosis
AST (SGOT) norm is
and is indicative of
5-40
damage to other organs
liver function test of ALP, ALT, AST, and LDH are called serum ......
serum aminotransferase
what 2 liver enzymes will initially elevate then return to normal when no longer able to create an inflammatory response
ALT and AST
why does Alakaline phosphatase (Alk Phos) or ALP increase in cirrhosis
usually due to biliary obstruction
what is the most definitive diagnostic procedure for ID intensity of infection and
degree of tissue damage
liver biopsy
what are nsg considerations for a liver biopsy
consent
lie on affected side after surgery
monitor BP & HR to detect bleeding.
Post op - place pt on R side with Pillow under costal margin for several hours
Caution: bleeding and bile peritonits pot op
CBCs for a pt with cirrhosis will be
will be decreased due to anemia
PT and INR in a pt with hepatic diseases will be
increased
liver's ability to synthesize fibrinogen and vitamin K–dependent clotting factors: factors II (prothrombin), V, VII, and X
manifestations of liver dysfunction incldues
Jaundice
Elevated bilirubin in blood, greater than 2.5 mg/dL
 Hepatocellular: damaged liver cells unable to clear bilirubin
 Obstructive: occlusion of bile duct; extrahepatic or intrahepatic
Jaundice is _ and found ___
Jaundice - Yellow- or green-tinged body tissues; sclera and skin due to increased serum bilirubin levels.
what is the bilirubin in blood level suppose to be under
2.mg/dL
what are the different types of Jaundice
Hemolytic, Hepatocellular, and Obstructive
Hereditary hyperbilirubineamia
what are the s/s of hepatocellular Jaundice
May appear mildly or severely ill
Lack of appetite, nausea, weight loss
Malaise, fatigue, weakness
Headache chills and fever if infectious in origin
how is hepatocellular Jaundice Dx and is it reversible
Elevated Serum bilirubin > 2.5
urine urobilinogen > 17
AST > 40
ALT > 20
May be reversible
what are the s/s of obstructive Jaundice
Dark orange-brown (foamy) urine and light clay-colored stools
Dyspepsia and intolerance of fats, impaired digestion
Pruritis
Dyspepsia
Intolerance to fatty foods
Bilirubin & Alk Phos elevated
bile stains skin, mucous membranes and sclerae
where does obstructive jaundice go
reabsorbed into the blood, due to occulsion of bile duct
what is hepatocellular jaundice from
inability to clear normal levels of bilirubin
what is hemolytic Jaundice
increase in RBC destruction, so much the liver cant conjugate it fast enough
in obstructive jaundice which liver aminotransferases are elevated
Alk Phos is elevated along with bilirubin
(AST, ALT and GGT are not significant)
what is Portal hypertension
Obstructed blood flow through the liver results in increased pressure throughout the portal venous system
what are the 3 main effects of Portal hypertension
Ascites
Varices
Splenomegaly
what is Ascites due to
Portal HTN, decrease in albumin and obstruction of hepatic Lymph Flow
what is the pathology of ascites
• Increased capillary pressure, obstructed venous blood flow
• Vasodilation in splanchnic circulation
• Aldosterone not metabolize then Na+ and water retention
• Decreased albumin synthesis , fluid to peritoneal space
what is the fluid that goes into the peritoneal cavity in Ascites
albumin (15L)
s/s of Ascites
• Increased abd girth
• Rapid wt gain
• SOB due to enlarged ABD
• Striae and distended veins
nsg considerations for Ascites
• Dx: fluid wave
• Monitor daily wt and girth
Assess for fluid in abdominal cavity by percussion for shifting dullness or by fluid wave
Monitor for potential fluid and electrolyte imbalances
what is the medical management for Ascites
 Dietary: low sodium
 Diuretics: Spironolactone, furosemide
 Bedrest promotes sodium excretion
 Admin IV of salt-poor albumin
 Paracentesis

Administration of salt-poor albumin
Transjugular intrahepatic portosystemic shunt (TIPS)
Paracentesis for Ascites is to....
is it a permanent fix?
is to relieve ascites for those at risk of difficulty breathing due to pressure. It is a temporary fix due to RAAS and increase ADH
what is the diet for ascites
low sodium diet from 2 g to 500mg. increase Milk
no fluid restriction.
Why is TIPS used in Ascities
good for those who will be getting a transplant
what type of diuretic is used with the pt with ascites
Spironolactone (Aldactone).
Tell whether the following statement is true or false.
Aldactone is most often the first therapy in patients with ascites from cirrhosis.
True. - Rationale: Spironolactone (Aldactone), an aldosterone-blocking agent, is most often the first-line therapy in patients with ascites from cirrhosis.
what are some surgical procedures for diverting portal vein
• TIPS (TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT)
• PORTACAVAL SHUNT
• H-GRAFT MESOCAVAL SHUNT
• SPLENORENAL SHUNT
what is the normal pressure gradient between the portal vein and inferior vena cava
< 12
how do you know the portal vein has increased resistance by measurement
when it is > 12mmHg between the portal vein and inferior vena cava
DO THE MATH
What happens with Portal hypertension?
Venous collateral develop from high portal system pressure to systemic veins in esophageal plexus and retroperitoneal veins
why do you get resistance to portal blood flow.
scarring, or fat deposits in liver
what are esophageal varices
Dilated, tortuous veins
Esophagus into stomach
Caused by portal hypertension
Contributing factors: increased pressure in esophagus, irritation, medications, alcohol
how serious are esophageal varices
first bleeding episode has a mortality of 30-50%
occurs in about 1/3 of pts with cirrhosis and varices
what are the manifestations from esophageal varices
Hematemesis
Melena
General deterioration mental or physical
Shock
pts with cirrhosis should undergo screening endoscopy every 2 years
what is the Dx for esophageal varices
Diagnosis: endoscopy,
Portal hypertension measurements
where will you see abnormal varicoid vessels
above the liver
what is the main nsg consideration for the endoscopy
no fluids until gag reflex
what is the Pharmacologic Tx to control bleeding in for Varices
Vasopressin (pit) - not for Coronary Artery Disea pts, the vasoconstriction may create an MI!!
Propranolo - BB to decrease Portal Pressure
Somatostatin - more effective the Pitessin. Lacks Vasoconstriction
what are some non-pharmacologic Tx to control bleeding in Varices
Esophageal balloon tamponade
Injection sclerotherapy—endoscopy
Variceal banding
Can nitroglycerin be used for Varices
Yes with Vasopressin to reduce coronary vasoconstriction.
Is the following statement True or False?
Bleeding esophageal varices result in an increase in renal perfusion.
False - Bleeding esophageal varices do not result in an increase in renal perfusion. Bleeding esophageal varices result in an decrease in renal perfusion.
Which of the following treatment modalities exert pressure directly to bleeding sites in the esophagus and stomach?
a. Injection sclerotherapy
b. Portal-systemic shunt
c. Pitressin
d. Balloon tamponade
d. Balloon tamponade
Rationale: Balloon tamponade exerts pressure directly to bleeding sites in the esophagus and stomach to treat bleeding esophageal varices.
Nsg Management for Varices includes
 Monitor for encephalopathy - emotional and cognitive status
 Parenteral nutrition
 Gastric suctioning
 Oral care
 Vitamin K
 Blood transfusions
 Decrease anxiety
what are things we should monitor for
Monitor patient condition frequently, including emotional responses and cognitive status.
Monitor for associated complications such as hepatic encephalopathy resulting form blood breakdown in the GI tract and delirium related to alcohol withdrawal.
Monitor treatments including tube care and GI suction.
what type of environment is good for pt.
Quiet clam environment and reassuring manner
Implement measures to reduce anxiety and agitation
Teaching and support of patient and family
Hepatic encephalopathy and coma occurs primary in pts with..... and .....
portal HTN and Portal Shunting
what is hepatic encephalopathy from
From Profound liver failure from accumulation of ammonia and toxic metobolites
Ammonia from bacterial digestion of dietary and blood proteins
Possible generation of endogenous benzodiazepines or opiates
what is the coma from
increased toxins, ammonia and
Advanced false or weak neurotransmitters may cause hepatic coma
What are the early manifestations of encephalopathy
minor mental & motor changes, day sleeping & insomnia @ night, hyperactive deep tendon reflexes,
Fector hepaticus,
may see Asterixis (liver flap), apraxia
what are the late manifestations of encephalopathy
DTRs disappear, flaccid, may have seizures
what is fector hepaticus
liver breath, fruity or musty
what is liver flap
tremoors
what is apraxia
flexion of the wrist, inability to draw connected stick figures/stars
what is pharmacological management of encephalopathy
Lactulose (Cephulac) - decreases colon pH by removing amonia (excreted into stool), bowel evacuation, changes fecal flora
IV glucose, vitamins, electrolytes
Neomycin - antibiotic
diruetics
Flagyl (metronidazole) same as Neomycin
what is Neomycin do
it is an antibiotic to reduce # of GI bacteria capable of converting urea to ammonia.
what is the objectives for tx of cirrhosis
• Control bleeding
• Improve nutrition
• Prevent skin breakdown
• Prevent encephalopathy
• Control fluid retention
what vitamins are for mgmt of encephalopathy
B comples, folic acid, iron
nsg care of encephalopathy
• Daily Weights
• Monitor Electrolytes, Ammonia Levels
• Assess Bowel Sounds & Measure Abdominal Girth
• Maintain Diet
• High CHO, High Calorie,LOW PROTEIN!!!!, Low Fat, as low as 500 to 800 mg NA+, Soft Diet
• Consents for Procedures, Teaching
• Monitor for signs of hepatic encephalopathy
• Routine care, including pre-op & post-op care for portal caval shunts
• Meticulous skin care
Is protein high or low in encephalopathy
low,
high CHO
low fat
Na is 500=800
what is a spider angioma
above the waist on the skin surface
Nsg considerations for assessment
Focus upon onset of symptoms and history of precipitating factors
Alcohol use/abuse
Dietary intake and nutritional status
Exposure to toxic agents and drugs
Assess mental status
Abilities to carry on ADL/IADLs, maintain a job, and maintain social relationships
Monitor for signs and symptoms related to the disease including indicators for bleeding, fluid volume changes, and lab data
nsg considerations for Diagnosis
Activity intolerance
Imbalanced nutrition
Impaired skin integrity
Risk for injury and bleeding
Complications:
Bleeding and hemorrhage
Hepatic encephalopathy
Fluid volume excess
nsg considerations for Planning
Goals may include increased participation in activities, improvement of nutritional status, improvement of skin integrity, decreased potential for injury, improvement of mental status, and absence of complications.
nsg considerations for Activity Intolerance
Goals may include increased participation in activities, improvement of nutritional status, improvement of skin integrity, decreased potential for injury, improvement of mental status, and absence of complications.
nsg considerations for Imbalanced Nutrition
I&O
Encourage patient to eat
Small frequent meals may be better tolerated
Consider patient preferences
Supplemental vitamins and minerals, especially B complex, provide water-soluble forms of fat-soluble vitamins if patient has steatorrhea
High-calorie diet, sodium restriction for ascites
Protein is modified to patient needs
Protein is restricted if patient is at risk for encephalopathy
other interventions, safety/skin
Impaired skin integrity
Frequent position changes
Gentle skin care
Measures to reduce scratching by the patient
Risk for injury
Measures to prevent falls
Measures to prevent trauma related to risk for bleeding
Careful evaluation of any injury related to potential for bleeding
what are infectious causes of Hepatitis
Viral
Bacterial
Fungal
Rickettsial
Protozoal
what are noninfectious causes of hepatitis
Metastatic Cancer
Alcoholism
Chemical or Drug Reaction
Rheumatological (lupus)
what is viral hepatitis
a systemic viral infection that causes necrosis and inflammation of liver cells with characteristic symptoms and cellular and biochemical changes. A, B, C, D, E, Hepatitis G and GB virus-C
what is nonviral hepatitis
—toxic and drug induced
which hepatitis is considered infectious hepatitis
hepatitis A
which hepatitis is considered Serum hepatitis
HBV
which hepatitis is considered post transfusion hepatitis
HCV
which hepatitis is considered Delta virus
HDv
which hepatitis is considered enteric non-A, non-B
HEV
what is the incubation and lasting time for HAV
Incubation--one month
Illness lasts 1-2 weeks
what is the incubation and lasting time for HBV
Long Incubation period 26 weeks (up to 6 months)
Early acute phase 2-3 weeks
Chronic
what is the incubation and lasting time for HCV
 Incubation 2 weeks to 6 months
 Communicable 1-2 weeks before symptoms
Chronic
what is the incubation and lasting time for HDV
 Incubation: 2-26 weeks
chronic
what is the incubation and lasting time for HEV
 Incubation 15-65 days
self limiting - non chronic
how is HAV contracted
Fecal–oral transmission
Spread primarily by poor hygiene; hand-to-mouth contact, close contact, or through food and fluids
how is HBV contracted
• Blood
• Body fluids
• Mother to baby/pregnancy & birth
• IV drug needle sharing, tatoos
• Dialysis
• Broken skin
how is HCV contracted
- The most common blood-borne infection

Transmission
needle sticks
blood transfusions
IV drug use
sexual contact
how is HDV contracted
Only persons with hepatitis B are at risk for hepatitis D.
Transmission is through blood and sexual contact.
how is HEV contracted
Transmission oral-fecal route
Resembles hepatitis A and is self-limited with an abrupt onset. No chronic form
s/s of HAV
mild flu-like symptoms, low-grade fever, anorexia, later jaundice and dark urine, indigestion and epigastric distress, enlargement of liver and spleen
Anti-HAV antibody in serum after symptoms appear
Dx of Hep A
 Diagnosis
Positive anti-HAV IgM antibody
Anti-HAV IgG
Elevated liver function tests
Stool specimen
Tx of HAV
Bed rest, high protein, low fat diet
Immune globulin within 2 weeks of exposure
Prevention of HAV
Good hand washing, safe water, and proper sewage disposal
Vaccine
Immunoglobulin for contacts to provide passive immunity
why is a pt with HAV on bed rest
to decrease metabolic demaind, will increase blood flow and regenerate liver cells
how does the dosing of the Vaccine for HAV work - how many doses
Hepatitis A vaccine: one dose protects exposed children, recommended to travelers to high-risk countries
what are the immunoglobulins for
passive immunity (not active like the vaccine). for family members prophylactic or those who are exposed within 2 weeks. Lasts 6-8 weeks only
what does anictertric mean
with out jaundice
when is the hep A antigen found in the stool
7-10 days before illness and 2-3 weeks after symptoms appear.
main consideration with HAV
HAND WASHING!!
Hep B may progress to
cirrhosis, chronic hepatitis, liver cancer, death
who is most likely to get HBV
Highest in young adults, homosexual men, heterosexuals with multiple sex partners, health care & public safety workers
300,000 cases/year
1 million carriers in U.S.
the virus Hep B has antigenic particles that elicit specific antibody markers during different stages of the disease
what are they
HBsAg (Hepatitis B Surface Antigen)--incubation or early acute phase. At 3 months, chronic or carrier state.
HBeAg (soluble antigen)--high infectivity, more likely to be chronic.
Anti-HBs (antibody to surface component of B virus)--after symptoms gone & HBsAg gone).
Anti-HBc IgM (antibody to core B antigen)--acute infection with B virus.
Anti-HBc (antibody to core B antigen)--past infection. Not protective.
if you have Anti-HBs antibody where are you in the disease
symptoms gone, and HBsAg is gone (1st one)
due to recovery of Hep B or to vaccine
if you have HBc antibody to surface component of B virus, where are you in the disease
past infection - no longer protective
if you have HBeAg (soluble) antigen, where are
you in the disease
hihly infective
if you have HBsAg surface antigen where are you in the disease process
incubation or early acute phase. At 3 months, chronic or carrier state.
if you have anti-HBc IgM antibody to core B antigen where are you in the infection
acute infection with B virus
how is HBV diagnosed
Elevated liver function tests:
Aspartate aminotransferase (AST)
Alanine aminotransferase (ALT)
Elevated Alkaline Phosphatase
Total bilirubin
s/s of HBV
are insidious and varible
Tx Meds for HBV
• Recombinant interferon
• alfa-2b (Intron-A)
o 33% remission in chronic
o 10% cured
• HB immune globulin (HBIG)
• Lamivudine (Epivir) - antiviral agent with adefovir (good for transplants)
• Adefovir (Hepsera)
Medications for chronic hepatitis type B include alpha interferon and antiviral agents:lamividine (Epivir), adefovir (Hepsera)
non pharmacologic interventions for HBV
• Bedrest
• Low protein diet
• Prevention:
• HBV vaccine
Vaccine: for persons at high risk, routine vaccination of infants. Passive immunization for those exposed. Standard precautions/infection control measures
Screening of blood and blood products
 Condom use
 Standard precautions
• Full Recovery: negative HBsAg test, Positive anti-HBs, Normal ALT (SGPT)
which Hepatitis is least likely to have S/S
Hep C
chronic carrier state frequently occurs
when is Hep C communicable
1-2 weeks before symptoms
how is Hep C transmitted
needle sticks
blood transfusions
IV drug use
sexual contact
how is Hep C diagnosed
enzyme immunoassay (EIA) - assays confirm presence of antibodies
recombinant immunoblot assay
Tx for HCV
supportive
protective barrier with sex
steroids
antiviral drugs (Ribavirin)
Interferon (Intron-A)
there is no benefit of bedrest, diet or Vit. Must have antiviral drugs and Interferon Intron-A alfa 2A
what are good teaching measures for Hep C
Prevention
Screening of blood
Prevention of needle sticks for health care workers
Measures to reduce spread of infection as with hepatitis B
Alcohol encourages the progression of the disease, so alcohol and medications that effect the liver should be avoided
what is the contradiction of Hep C meds
Ribavirin is contraindicated with Pregnancy
Hemolytic anemia may happen - stop medication
what med will help extend the interferon
+PEG will exend the interferon to taking it only once a week
what combination of meds is important in Hep C
Ribavirin an antiviral and
Interferon - Intron A alfa 2A
does HDV have a high mortality
yes, seen in Italy, middle east, Africa, south America.
 Incidence--epidemically & endemically in those high risk for HBV.
Dx of HDV
anti-HDV (antibody to HDV) indicates past of present infection.
Tx of HDV
Supportive
Recombinant interferon alfa-2b
Vaccination against HBV prevents
transmission of HDV
Transmission is through blood and sexual contact.
Symptoms and treatment are similar to hepatitis B but more likely to develop fulminant liver failure and chronic active hepatitis and cirrhosis.
Is the following statement True or False?
Only persons with hepatitis B are at risk for hepatitis D.
T - Only persons with hepatitis B are at risk for hepatitis D
what antigen is required for HDV
HBsAg, surface antigen for replication
HDV may go on to develop
fulmiant hepatitis and then progress to chronic active hepatitis and cirrhosis.
how is HEV transmitted
 Transmission oral-fecal route
Resembles hepatitis A and is self-limited with an abrupt onset. No chronic form.
rare in US
Dx of HEV
Diagnosis:
*No test
*Diagnosis made if other types ruled out.
*Research on Anti-HEV
IgM and IgG
Tx of HEV
*Supportive (as with HAV)
how is hepatitis G transmitted
Blood
risk group for Hep G
transfusion recipients - 50%
*IV drug users
*frequent co-infection with HBV or HCV
Associated with chronic liver disease
what is Hep G
 Positive-stranded RNA virus with nucleotide sequence almost identical to HCV.
Which of the following types of hepatitis is spread by poor sanitation?
a. Hepatitis C
b. Hepatitis B
c. Hepatitis A
d. Hepatitis D
c. Hepatitis A
A
Rationale: The mode of transmission of hepatitis A is through the fecal-oral route, water, food, poor sanitation, and person-to-person contact
Toxic hepatitis if from
hepatotoxins and drug induced hepatitis
 Hepatotoxins
carbon tetrachloride
phosphorus
chloroform
gold compounds
 Drug-Induced Hepatitis
isoniazid, halothane (use nitrous oxide instead for anesthesia), acetaminophen, anesthetic agents, methyldopa, antibiotics, antimetabolites
toxic hepatitis s/s
elevated temperature
persistent vomiting
clotting abnormalities
hemorrhages (under skin)
delirium, convulsions & coma
resembles viral,
Tx of toxic hepatitis
restore, maintain fluids & lytes
replace blood loss
liver transplant
rapid relief if ID early, no antidotes
what isFulminant Hepatic Failure
is usually defined as the severe impairment of hepatic functions or severe necrosis of hepatocytes in the absence of preexisting liver disease.
Fulminant Hepatic Failure is caused by
viral hepatitis
s/s of fulminant hepatic failure
 Signs & Symptoms: (60-85% mortality)
jaundice #1
anorexia
coagulation defects
renal failure
electrolyte disturbances
infection
hypoglycemia
encephalopathy, cerebral edema
Jaundice in Fulminant Hepatic Failure has three stages Highly acute, acute and subacute. When does jaundice occur in each
0-7 days = hyperacute
8-28 days = acute
28-72 days = subacute
Tx for heaptic Failure
• Bedrest
• Low protein diet
• Neomycin
• Lactulose
• Watch for slower metabolism of narcotics, toxicity

• Blood & plasma exchange
• Charcoal hemoperfusion
• Corticosteroids
• Liver transplant
• Isolation (Hepatitis A & E)
what are the stages of encephalopathy
1 plamr erythemia, normal loc , night day sleep patterns, asterixis
2 increase drowsiness,
3 everything. arousal difficult, increase deep tendon reflexes, rigidity, marked EEG
4 increase ICP, comatose, flaccidity
antidote for acetaminophen
N-acetylcysteine (NAC). It is most effective when given within 8 hours of ingesting acetaminophen.
Hepatitis Vaccines - OSHA requires:
 OSHA requires employers to offer Hep. B vaccine to at-risk employees at no cost.
Hepatitis vaccines - CDC requires
 CDC: Hep. B vaccine to infants & children entering elementary & middle school
Hep A vaccine is how often
 Hepatitis A vaccine: one dose protects exposed children, recommended to travelers to high-risk countries
Hep B vaccine is
• Recombinant form (Engerix-B or Recombivax-B)

• Plasma-derived vaccine (Heptavax-B)
how often is hep b vaccine
• 3 IM doses of 20 mcg. In deltoid for adults:
o Initial dose
o 2nd dose in one month
o 3rd dose in five months
titer for HB vaccine
Assess titer >10 SN ratio
if you have been exposed to hep b, what vaccine do you get
 With exposure—give vaccine & Hepatitis B immune globulin
Health care workers protection includes
Standard precautions

Wash hands after patient care

Hepatitis B vaccine

Hepatitis B immune globulin
patient protection of Hepatitis includes
Patient Protection
Patient education
Modes of transmission
Handwashing after toileting
Wash food
Barriers from body fluids
Vaccines

Wash equipment between patients

For those with hepatitis:
Avoid alcohol (6-12 months)
Rest periods are essential
which is active, the vaccine or the HBIG
Vaccine!!!
HBIG is passive prepared from plasma w/high titers of antiBGs.
what is liver cancer from
• Usually associated with hepatitis B and C, cig smoking, fungus (aspergillus )
• Hepatocellular carcinoma (HCC)
manifestations of live of cancer
• Pain, a dull continuous ache in RUQ, epigastrium, or back!!!!!

• Weight loss, loss of strength, anorexia, anemia may occur
• Jaundice if bile ducts occluded, ascites if obstructed portal veins
nonsurgical mgmt of liver cancer
Underlying cirrhosis, which is prevalent in patients with liver cancer, increases risks of surgery
Major effect of nonsurgical therapy may be palliative
Radiation therapy
Chemotherapy
Percutaneous biliary drainage (document blood total, color, debris) keep irrigated, don't aspirate
what markers are elevated with liver cancer
alfa fetoprotein tumor marker AFP 30-40% elevation
CEA marker
surgical mgmt of liver cancer
Treatment of choice for HCC if confined to one lobe and liver function is adequate
Liver has regenerative capacity
Types of surgery:
Lobectomy
Cryosurgery ( -196C)
Liver transplant
10% glucose 1st 48 hrs
in a lobectomy what is the cut on the R side
thoracabdominal incision

L - ABD incision
what do they use to prioritize ones level for transplant
MELD score
Model of End-Stage Liver Disease: used to prioritize one’s level by medical need
what is Orthotopic Liver Transplantation
in the same atomical location
surgical complications of transplantation
 Bleeding - lack of clotting factors
 Infection
 Rejection
who isn't considered a candidate for transplant
severe cardiac and resp disease
metastic malignant live CA
Hx of alcohol/substance abuse
diet for Transplant
increase calories, mod fat, decrease Na (ascites) or fluid restrictions if na is low
decrease protein if encephalopathy or elevated ammonia, vitamins
what might be cause of rejection
GVHD - recipients bone marrow T cells attack liver
s/s of rejection
increase HR, U R flank Pain, jaundice, lab results
teaching for transplant
immunosuppressants - DO NO miss a dose
what are some immunosuppresants
Cyclosporine
Tacrolimus
Corticosteroids
Azathioprine
Mycophenolate mofetil
Sirolimus (rapamycin)
Anti-thymocyte globulin
Muromonab-CD3 (OKT3)
adverse effects of cyclosporine
 Nephrotoxicity
 Hepatotoxicity
 Hypertension
 Hirsutism
 Gingival Hyperplasia
 Tremors
 Paresthesia
 Nausea/Vomiting
 Diarrhea
adverse effects of azathiprine (Imuran)
Bone Marrow Suppression with decreased WBC—leukopenia, thrombocytopenia, anemia, pancytopenia
Increased Risk of Infection
Hair Loss
Hepatotoxicity
Increased Risk of Neoplasm
adverse effects of prednisone
Increased Risk of Infection
Increased Appetite
GI Irritation and ulceration
Delayed Wound Healing
Increased Risk of Bleeding
Cushingnoid Face
Muscle Weakness
Emotional Distress
Cataracts
interventions for pt undergoing a liver transplantation
Preoperative nursing interventions

Postoperative nursing interventions

Patient teaching
What do the bile salts do to the skin
the synthesis and excretion of bile has bile salts that can cause puritis
How much bile is excreted in 1 day
1 liter/day
what is digoxins normal levels and doses
levels 1.8 - 2.0
dose 0.15 - .25
geriatrics - loading dose should exceed .125
what are some toxins that effect chronic liver dysfunction under etiology
mushrooms
what is the normal dose of acetaminophen
326 - 650
with lab values overall for Liver Disease, what is the normal range
under 50. If the lab is over 100 there is disease
what does a low serum albumin (norm 4-5.5) mean for hepatic disease
if you have low seum albumin, then pt may get ascites
what is the elevated bilirubin level at
> 2.5mg/dL
when you have hepatocellular Jaundice (due to damaged liver cells unable to clear bilirubin), what is the changes in the pts wt.
wt loss initially, later increase due to edema.
what does the urine of obstructive jaundice look like
deep orange and foamy
some labs to remember:
Bilirubin
liver enzymes
2.5
<50 okay, > 100 bad!
why isn't aldosterone metabolized by the liver, and then what happens, what med do you give
aldosterone isn't metaboliszed because liver function is decreased (portal HTN with increased capillary pressure and obstruction of venous blood flow) This makes increase in Na and water leading to ascites along with the decreased albumin contributing to it
Spironolactone (aldactone)
where do you measure girth
at umbilicus
what is melena
black tarry stools
what is the balloon tamponade called
Blakemore tube
when in emergencies, to control bleeding with varicies, what is used?
Esophageal balloon tamponade
when using ____ as an antibiotic for hepatic encephalopathy, how is it taken
PO, 1-3g q 6 hrs for 5 days
in a diet for hepatic encephalopathy, what does the diet contain (protein-wise)
low protein 1.5g/kg use vegetable (soy)
also Na low as 500-800, monitor electrolyte labs and call doctor on significant changes.
If a pt on Cephulac (lactulose), what do you do if ammonia is 96
norm levels 10-80
don't stop med, but call doctor!
what type of fluids will be given for encephalopathy
D50%, TPN with thiamine and vitamins will be given (Bs, folic acids, iron)
some other high risks for Hep B
tattoos, hemodialysis, blood transfusions, needle sticks, Splashes
Hep B and A vaccine is active or passive
active
Immune Globulin is active or passive
passive
Hep vaccine should be taken if you have an allergy to
bakers yeast