Download Hepatic disorders_notes

Alteration in Nutrition, less than
body requirements
Hepatitis/Cirrhosis
Liver: Largest internal organ
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 Hepatic Artery

1/3 blood supply
 Portal Vein

2/3 blood supply
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Organs of the Gastrointestinal Tract
 Liver
(hepatitis, cirrhosis)
 Gallbladder
(biliary diseases)
 Pancreas
(pancreatitis, diabetes)
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Major Functions (pg 904/Table 39-4)
Review
 Metabolic

CHO, Protein, and Fat metabolism


Albumin, clotting factors
Detoxification – Ammonia (NH3) to Urea
 Bile/Bilirubin (Production/Excretion)
 Liver cells destroyed – scar tissue forms – alters
blood flow in liver – BP in GI system elevates
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Inflammatory (Hepatitis)
Disorders of Liver
 Inflammation of the liver caused by virus,
autoimmune, drugs
 Liver cell damage results in hepatic cell
necrosis.
 Viral hepatitis (A, B, C, D, E, G)
 Toxic Hepatitis (most common –
Acetaminophen, ETOH)
 Autoimmune (Wilson’s disease, PBC)
 Non-Alcoholic Fatty Liver Disease (NAFLD)
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Table 44-1
Viral Hepatitis
 Type A (HAV)



Fecal oral transmission
Onset Acute-Flu like symptoms
Hepatitis A vaccine
 Type B (HBV)

Blood and body fluid transmission (not urine, feces, breast
milk, tears, sweat)

Onset slow-symptoms more severe
Hepatitis B vaccine

 Type C (co-infection HIV)




Percutaneous transmission (needle thru skin)
Asymptomatic or mild symptoms
20% will progress to cirrhosis 20-30 years
Liver damage 15-20 years after infection
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Other causes of Hepatitis
(hepatoxicity)
 Toxic & Drug induced
 Table 39-6: Toxic agents causing liver
damage
 Wilson’s disease
 Neurological disease associated with
disorder of copper storage
 DX by brownish/red rings around corneas
 Also neuro changes such as drooling,
tremors, migraines
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Other causes of Hepatitis
 Hemochromatosis
 Iron
storage disorder
 Autoimmune hepatitis – primary biliary
cirrhosis (PBC)
 NAFLD and NASH
 hepatic
steatosis, elevated ALT
 Linked to obesity, certain drug
(steroids)
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Assessment
 History
Exposure, foreign travel, Sexual practices,
etc
 Medications/Toxic exposures
 misuse of acetaminophen, illicit drugs,
chemical exposures

 Physical Assessment Findings (table 44-2)
 Depend on phase of infection
30% of patients with acute HBV and 80% of patients with acute HCV will be
asymptomatic.
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Phases of Infections
fulminant hepatic failure
 Incubation/Prodromal



Asymptomatic to vague SX (anorexia, N/V,
malaise, fatigue, pruritis, arthralgia)
May be dx as a flu/virus gastro
Virus load can be detected
 Icteric Phase


Classic presentation of jaundice, dark urine,
clay-colored stools, rt upper quad pain
Abnormal LFTs
 Convalescent phase

Sx & jaundice resolve, LFTs return to normal
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Diagnostics - Lab values
 Elevated liver enzymes
 Serum/Urinary bilirubin
 Coagulopathy – prolonged PT/PTT
 Serum proteins (albumin) decreased
 Hepatitis panel for high-risk exposures
(consider HIV co-infection)
Hep A – one dx test for active infection
 Hep B – many DX tests for active infection
 Genotyping Hep C important in TX

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Treatment of Hepatitis
Acute and Chronic
 Well-balanced diet
 Vitamin supplements
 Rest (degree of strictness varies)
 Avoidance of alcohol intake and drugs
detoxified by the liver
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Nursing Implementation
 Acute interventions
 Rest
 Jaundice/ pruritus
 Small, frequent meals
 Ambulatory and home care




Dietary teaching (avoid ETOH) (low fat, high CHO)
Assessment for complications
Regular follow-up for 1 year after diagnosis
Medication teaching
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Collaborative Care: Drug therapy
 No specific drug therapies (acute hepatitis)
 Supportive therapy
 Antiemetics
 Watch for drugs metabolized by liver
 Vitamins
 Milk Thistle (Silymarin)
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Drug therapies: Chronic HBV & HCV
 Anti-virals: Interferon



↓ viral load
↓ liver enzyme levels
↓ rate of disease progression
 Side effects
Flu-like SX
 Anemia, anorexia
 Depression, insomnia

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Prevention/Health Promotion
 Hepatitis A
 Hepatitis B and C
 Hand washing! Food
 Screen donated blood
Washing
 Use disposable needles
 Proper personal hygiene
 Hand washing
 Immunization: HAV
 Safe sex
vaccine (2 shots,
 Avoid sharing
immunity in 30 days)
toothbrushes/razors
 Immune Globulin
 Immunization: HBV

1-2 weeks post exposure
Table 44-8: preventative
measures for Hepatitis
vaccine (3 doses, 1st @
birth/complete by 18m/o)
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Table 44-6
Plan of Care (see Moodle)
Imbalanced Nutrition: less than body requirements
r/t anorexia, N/V, metabolic problems
 Goals: maintain weight, food/fluid intake to meet
nutritional needs
Activity Intolerance r/t fatigue, weakness
 Goals: gradual increase in activity, able to
perform ADLs
Risk for impaired Liver Function r/t viral infection
 Goal: maintain adequate liver FX throughout
infectious process
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Chronic HBV, HCV
 Long-term goals
 Prevention
of cirrhosis and
hepatocellular cancer
 Not all patients respond to current
therapeutic regimens.
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Evaluation: Expected outcomes
 Adequate nutritional intake
 Increased tolerance for activity
 Verbalization of understanding of
follow-up care
 Able to explain to others methods of
transmission and methods of preventing
transmission
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Major Functions (pg 870/Table 39-4)
Review
 Metabolic

CHO, Protein, and Fat metabolism


Albumin, clotting factors
Detoxification – Ammonia (NH3) to Urea
 Management of Bilirubin (Production/Excretion)
 Liver cells destroyed – scar tissue forms – alters
blood flow in liver – BP in GI system elevates
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Cirrhosis
Pg 1018
Acute liver failure
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Continuum of Liver dysfunction
 Early S/SX of liver DX
 Pain, Fever, Anorexia (N/V)
 Fatigue
 Physical exam may reveal hepatomegaly,
lymphadenopathy, and splenomegaly.
Complications:
 Progressive S/SX
- Fulminant/acute hepatic
failure
 Jaundice
- Chronic hepatitis
 Ascites, anasarca
- Cirrhosis
 Skin Lesions/bruising
- carcinomas
 Patho Map – figure 44-5 pg 1018/Text
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Liver Dysfunction
 Bleeding


Inability to make clotting factors
Development of collateral circulation r/t portal
hypertension
 Increased serum Ammonia

Inability to convert NH3, from metabolism of
protein, to urea
 Third spacing – ascites

Inability make plasma protein (albumin)
 Other: altered drug metabolism, electrolyte
imbalances, etc
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Nursing Assessment (table 44-14)
 Past health history
Chronic alcoholism
 Viral hepatitis
 Chronic biliary
disease
 Medications

 Physical examination
 Weight loss
 Jaundice
 Abdominal distention
 Nausea/vomiting
 Altered
mentation/asterixis
 RUQ pain
 Abnormal laboratory
values
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Complications of liver failure
 Portal hypertension

Esophageal and gastric varices
 Peripheral edema and ascites (table 44-9)

Portal HTN, Hypoalbuminemia, hyperaldosteronism
 Hepatic encephalopathy (table 44-10)

Protein metabolism dysfunction produces elevated
ammonia levels (conversion of ammonia to urea)
 Hepatorenal syndrome

Kidney failure related poor circulating blood volume
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Esophageal Varices
 No special assessment findings – obvious GI
bleed,
low H & H, occult
Sengstaken-Blakemore
Tubeblood
 Goal: Avoid bleeding/hemorrhage

Avoid alcohol, aspirin, irritating foods, straining.
 Supportive measures for acute bleeds

Next slide
 Treatment Measures


Endoscopic sclerotherapy, Endoscopic ligation
Balloon tamponade (Blakemore tube) – old TX
 Shunting procedures (TIPS) (portacaval shunt)
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Treatment for acute UGI bleed
 Support ABCs, fluid resuscitation
 Drug therapy may include


Octreotide (Sandostatin)
Vasopressin (VP, Terlipressin)
 Fresh frozen plasma, Packed RBCs
 Vitamin K
 Histamine blockers, Proton pump inhibitors
 Lactulose & Neomycin – prevents hepatic
encephalopathy from increased RBC
breakdown/ammonia
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Treatment of Ascites
 High-carbohydrate, low-Na+ diet (2 g/day)
 Diuretics, albumin infusion
 Paracentesis
 Peritoneovenous shunt
Continuous reinfusion of
ascitic fluid from abdomen to
vena cava
 Complications : Thrombosis, infection,
fluid overload

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Paracentesis
 Patient Positioning – sitting upright, HOB ↑
 Empty bladder
 Complications:
Persistent leak from the puncture site, bruising
 Hypotension after a large-volume paracentesis
 Perforation of bowel, infection, Major blood
vessel laceration
 Post procedure


Position on right side to splint puncture site
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Hepatic encephalopathy
 S/SX: altered mentation, asterixis (liver
flap), fetor hepaticus,
NH3 (ammonia)
 Goal: Decrease ammonia formation
 May reduce protein in diet
 Sterilization of GI tract with antibiotics (e.g.,
neomycin)
 Lactulose (Cephulac) traps NH3 in gut.
 Cathartics/enemas
 Treatment of precipitating cause
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Nursing Dx: Liver Failure
 See Nursing Care Plan (44-2)
 Imbalanced nutrition
 Impaired skin integrity (jaundice /pruritis)
 Ineffective breathing pattern
 Excess fluid volume
 Dysfunctional family processes: Alcoholism
 Overall goals
 Relief of discomfort
 Minimal to no complications
 Return to as normal a lifestyle as possible
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Generalized Collaborative Care
 Rest, avoid further liver damage


Avoidance of alcohol, aspirin, acetaminophen,
and NSAIDs
Monitor LFTs, electrolytes
 Management of ascites


Accurate I/O, Daily weights, Abdominal girth,
extremities measurement
Nursing care r/t paracentesis
 Prevention and management of esophageal
variceal bleeding
 Management of encephalopathy
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Nutritional Treatment
 High in calories (3000 kcal/day)
↑ carbohydrate
 Moderate to low fat
 Protein restriction depends on degree of
hepatic encephalopathy
 Low-sodium diet for patient with ascites and
edema
 Between-meal nourishment, Explanation of
dietary restrictions
 Administration of B-complex vitamins, vitamin K

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Nursing Evaluation
 Maintenance of food/fluid intake to meet






needs
Maintenance of muscle tone and energy
Maintenance of skin integrity
Normalization of fluid balance
Maintenance of blood pressure and urinary
output
Reports increased ease of breathing
Experiences normal respiratory rate/rhythm
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