Transcript Changes in Peripheral Nervous System

GI: Liver Hepatitis
and Cirrhosis
Marnie Quick, RN, MSN, CNRN
Normal Liver
Label:
Answers from previous slide
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A. Liver
B. Hepatic vein- blood from liver
C. Hepatic artery- oxygenated blood to liver
D. Portal vein- partly O2 blood to liver
E. Common bile duct
F. Stomach
G. Cystic duct
H. Gallbladder
Liver
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Symptoms of liver
failure appear when
80% liver destroyed
Liver can regenerate
itself if adequate
nutrition and no
alcohol
Liver functions
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1. Metabolic functions
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CHO- liver removes glucose from blood, stores it as
glycogen, breaks it down to release glucose PRN
Protein- converts ammonia to urea**
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Protein (food/blood) is 1st broken down by bacteria in GI to
form ammonia. Ammonia to liver which converts to urea.
Fat- ketogenesis. (see next slide- bile)
Steriod- aldosterone metabolism (liver damage= inc
levels aldosterone causing Na & H2O retention)
2. Bile synthesis & secretionBile aids digestion/absorption fats in small intestine.
Indirect bilirubin broken down & excreted stool
3. Storage- Vitamin A, all B’s, D, E, and K
4. Regulates blood coagulation**-Forms prothrombin,
fibrinogen, heparin
If decrease Vit K & fibrinogen= increase fibrinolysis, &
decrease platelets> hemorrhage
5. Detoxification** -Rids body of endogenous waste- drugs,
bacteria, etc
6. Heat production
7. Phagocyte action- breakdown old RBC, WBC, bacteria
Hepatitis- inflammation of the liver
Etiology/pathophysiology
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Viral- most common cause
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Toxic
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Hepatitis A,B,C,D, E
Chronic- Hep B,C,D
primary cause liver damage
Fuminant- rapidly
progressive form- Hep B, D
hepatotoxins directly
damage liver
chronic alcohol abuse,
drugs- acetaminophen,
chemicals
Hepatobillary- disruption flow
bile out liver
Viral hepatitis
Hepatitis A
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Fecal-oral transmission
Contaminated food, unsanitary conditions, water,
shelfish, direct contact with infected person
Onset abrupt, flu-like symptoms before jaundice
Liver repairs itself- no chronic state
2/2/2/2 Rule: 2 doses vaccine IM to prevent;
contagious 2 wks before S&S; S&S last 2
months; post exposure dose IG-immune globulin
given IM within 2 wks of exposure
Prevent by handwashing!
Viral Hepatitis
Hepatitis B
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Blood and body fluid transmission
Health care workers*, IV drug users, multiple sex
partners, men who have sex each other, body piercing,
tattoos, exposure to blood products (hemodialysis). Freq
seen HIV. Hep B is more infectious than HIV
Incubation 6-25 wks
Risk for liver cancer, chronic & fulminant hepatitis and
becoming a chronic carrier
Vaccine 3 doses IM 4-6 wks apart
Post exposure- hep B immune globulin IM 2 doses: 1st
dose 1-7 days post exposure; 2nd 28-30 days
Viral Hepatitis:
Hepatitis C (formally non A, non B)
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Blood and body fluid transmission
IV drug users (primary); body piercing, tattoos
Worldwide cause of chronic hepatitis, cirrhosis
and liver cancer
Initial symptoms mild, nonspecific
10-20 year delay between infection and clinical
appearance of liver damage
Interferon alpha to reduce risk of chronic C with
Ribavirin (oral antiviral)
Hepatitis C
Viral Hepatitis:
Hepatitis D and E
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Hepatitis D
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Blood body fluid transmission
Transmitted with Hepatitis B
Causes acute and chronic hepatitis
Hepatitis E
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Oral-fecal transmission
Contaminated water supply in developing countries
Rare in USA
Hepatitis
Common manifestations/complications
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Incubation phase- no symptoms
Preicteric- Flu-like sym & N&V
Icteric- 5-7 days post preicteric- jaundice sclera,
skin, & mucous; pruitius; clay colored stools;
brown urine (elevated bilirubin)
Posticteric (convalescent)- serum bilirubin &
enzymes return normal; energy level inc; no pain
Complications some hepatitis- cirrhosis, liver
failure
Jaundice- Note yellow eyes
Acute and chronic hepatitis
Hepatitis:
Collaborative care
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Diagnostic tests
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ALT (specific liver); AST (liver/heart)- elevated- enzymes
released into blood liver cell damaged
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Bilirubin- elevated from impaired metabolism or obstruction
hepatobiliary ducts
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Albumin- decreased in liver damage; affects clotting
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Viral antigens & specific antibioties
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Liver biopsy- chronic hepatitis
Medications- vaccines; post exp prophylaxis
Acute hepatits treatments- BR; adeq nutrition; avoid toxic substances
as alcohol
Hepatitis:
Pertinent Nursing Problems & Interventions
Lewis 1097 Table 44-1
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Risk for infection (transmission)
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Educate:vaccines;handwashing,body fluid precaution
Report health department food handlers and child
care workers with Hepatitis A
Activity intolerance- adeq rest- maybe > 4 wks
Imbalanced nutrition-less: small,freq,calorieCHO
Ineffective therapeutic regimen management
Home care
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Educate; avoid hepatic toxins, need for follow-up
Cirrhosis of the liver:
Etiology/pathophysiology
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End stage of chronic liver disease
Functional liver tissue destroyed and replaced by
fibrous scar tissue
Metabolic functions are lost; blood and bile flow
in liver is disrupted, portal hypertension develops
Types: Alcoholic/nutritional (common); biliary
(chronic biliary obstruction); postnecrotic
(hepatitis B or C; toxic substances); cardiac
Stages of alcohol-induced liver damage
Cirrhosis
Alcoholic/nutritional cirrhosis
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Most common cause of cirrhosis with resultant
lack of nutrition
Stage 1: metabolic changes affect fatty
metabolism, fat accumulates in liver. In this stage
abstinence from alcohol could allow liver to heal
Stage 2: With continued use of alcohol,
inflammatory cells infiltrate the liver causing
necrosis, fibrosis and destruction of liver
Stage 3: regenerative nodules form liver shrinks
Cirrhosis of liver: Complication & treatment
Portal hypertension
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Fibrous connective tissue in liver disrupt blood
and bile flow. Portal and hepatic veins become
compressed.
With backup of blood have acites, splenomegaly,
peripheral edema, increase blood cell destructionanemia, low WBC and low platelets
Treatment: medication to control hypertension,
diuretics to decrease fluid retention/acites and
TIPS procedure to increase blood flow
TIPS procedure- Note shunt that will divert
blood- relieving hypertension & esophegeal
varcies
Cirrhosis: complication & treatment
Esophageal varices
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As a result of portal hypertension, veins in
esophagus, rectum and abdomen become
engorged/congested resulting in esophageal and
gastric varices (major concern- can bleed out)
60% esophageal varices occur with cirrhosis
Treat
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Medications: vasopressin (control bleeding), beta
blockers (prevent bleeding), blood replace, Vit K
Surgery: shunt (TIPS), ligation varices, banding
Sengstaken-Blakemeore tube (tamponade bleeding)
Esophageal varices
Esophageal varcies
Sengstaken Blackmore tube:
Inflate gastric balloon; Esophageal balloon; and third one to
aspirate stomach
Cirrhosis: Complications and treatment
Splenomegaly, acites and peripheral edema
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Spleen enlarges from blood shunted from portal
hypertension. Blood cells destroyed
As liver impairment of synthesis of albuium
occurs have accumulation plasma-rich fluid in
abd cavity- acites (abd distention & wt gain)
Treat acites- diuretics (aldactone), paracentesis,
diet (hi CHO, hi protein (stage?), low fat, low Na
Ascites with dilated veins
Ascites
Cirrhosis: Complications & treatment
Hepatic encephalopathy
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Protein (from food or blood in GI) is broken
down (with the aid of bacteria) in GI to ammonia
Liver then converts ammonia to urea and is
excreted by kidneys
With liver failure have accumulation of ammonia
in blood. Ammonia then enters brain and
interferes with function of brain- encephalopathy
Hepatic encephalopathy continued
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Stages:1. personality changes, irritability 2. hyper
reflexia (liver flap) violent/abusive beh 3. coma
Treat:
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Enemas decrease ammonia absorption
Lactulose- a laxative that decreases ammonia by
decreasing the bacteria in bowel that normally
converts protein to ammonia. Causes 3-4 stools/day
Neomycin- intestinal antiseptic to decrease bacteria
Decrease protein intake
Asterixis- liver flap
Liver Failure
Cirrhosis:
Therapeutic intervention
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Diagnostic tests
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Liver function test ALT, AST- not as high as
hepatitis;
CBC platelets (anemia, thrombocytopenia)
Coagulation studies (lack Vit K- prolonged PT)
Bilirubin (elevated); ammonia (elevated)
Serum albumin (hypoalbuminemia)
Abdominal ultrasound (liver size/nodular, ascitis)
Esophagoscopy- varices
Liver biopsy(p 590) not done if bleeding time
elevated
Liver biopsy
Cirrhosis
Therapeutic Interventions cont
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Medications:
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Avoid toxic drugs- sedatives, hynotics, actaminophen, and
alcohol. Drugs metabolized by the liver.
Diuretics to reduce ascites
Lactulose (laxative) and neomycin (antibiotic) to dec ammoniahepatic encephalopathy
Vit K to reduce risk bleeding
Beta-blockers to prevent esophegeal varices from rebleeding
Ferrous sulfate and folic acid to treat anemia
Antacids decrease acute gastritis
Cirrhosis:
Therapeutic interventions cont
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Dietary and fluid
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Restricted fluid/Na intake based on response to
diuretic therapy, urine output and electrolyte values
Hi calories; Hi CHO; low fat
Surgery
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Surgery to treat complications
Liver transplant (p 593)
Liver transplant
Cirrhosis:
Nursing Assessment specific to Cirrhosis
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Health history
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Current symptoms, altered bowel; excess bleeding;
abdominal distention; jaundice; pruritus; history liver
or gallbladder disease; alchohol history
Physical assessment
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VS; mental status, color skin; peripheral pulses and
edema; abd assessment; bowel sounds; abd girth;
tenderness and liver size
Cirrhosis:
Pertinent Nursing problems/Care
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Health promotion
Patient family teaching guides
Acute intervention
Ambulatory home care
Imbalance nutrition less than body reequirements
Dysfunctional family process: alcoholism
Excess fluid volume
Potential complication: hemorrhage; hepatic
encephalopathy