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LIVER CIRRHOSIS

INTRODUCTION

Cirrhosis
caused

by

is extensive scarring of the liver, usually


a chronic irreversible reaction to hepatic

inflammation and necrosis

The disease typically develops insidiously and has a


prolonged, destructive course.
The most common causes for cirrhosis in the United
States are alcoholic liver disease and Hepatitis C.
Worldwide, hepatitis B is the leading cause.
Cirrhosis is a slowly progressing disease in which
healthy liver tissue is replaced with scar tissue, eventually
preventing the liver from functioning properly. The scar
tissue blocks the flow of blood through the liver and slows
the processing of nutrients, hormones, drugs, and
naturally produced toxins. It also slows the production of
proteins and other substances made by the liver.

ANATOMY AND
PHYSIOLOGY

The LIVER weighs about 3 pounds and is the


largest solid organ in the body. It performs
many important functions, such as:
Carbohydrate metabolism
Lipid metabolism
Protein metabolism
Processing of drugs and hormones
Excretion of bilirubin
Synthesis of bile salts
Storage of certain vitamins (A, B12, D, E, K)
and minerals (iron and copper)
Phagocytosis
Activation of vitamin D.

PATHOPHYSIOLOGY

CHRONIC ALCOHOLISM
TOXINS FROM ALCOHOL:
RELEASE OF ACETYLDEHYDE
DAMAGE HEPATOCYTES

NECROSIS OF
HEPATOCYTES

FIBROSIS

DECREASE
IVER FUNCTION

LIVER CELLS
REGENERATE
IN ABNORMAL
PATTERN

AST, ALT,
ALKALINE,
PHOSPHATAS
E, GGT

OBSTRUCTION
IN BLOOD FLOW
PORTAL
HYPERTENSION

LIVER CELLS
REGENERATE
IN ABNORMAL
PATTERN
LIVER CELLS
LOADED WITH FAT

ENLARGEMENT

IRRITATES THE
GLISSON CAPSULE

PAI
N

DECREASE LIVER
FUNCTION

INCREASE GLYCOGENESIS,
DECREASE GLYCOGENOLYSIS,
GLUCOGENESIS

ALTERED GLUCOSE
METABOLISM

DECREASE ENERGY

DECREASE LIVER
FUNCTION

DECREASE PRODUCTION
OF ALBUMIN

DECREASE COLLOIDAL
OSMOTIC PRESSURE

EDEMA,
ASCITES

DECREASE LIVER
FUNCTION
DECREASE METABOLISM OF STEROID HORMONE

ESTROGEN,
PROGESTERONE,
TESTOSTERONE

MALE

ALDOSTERONE

FEMALE

LOSS OF MALE LOSS OF FEMALE


CHARACTERISTICSCHARACTERISTICS
&
&
DEVELOPMENT OFDEVELOPMENT OF
SOME FEMININE
SOME MALE
CHARACTERISTICSCHARACTERISTICS

Na & WATER INCREASE K+


RETENTION& H+ EXCRETIO

ALKALOSIS
EDEMA,
ASCITES

HYPOKALEMIA

DECREASE LIVER
FUNCTION
DECREASE PROTEIN SYNTHESIS
(IN GENERAL)

ALTERED IMMUNE FUNCTION


& ALTERED HEALING

SUSCEPTIBILITY
TO INFECTION

DECREASE LIVER
FUNCTION

DECREASE PRODUCTION OF
CLOTTING FACTORS

ALTERED CLOTTING STUDIES

BLEEDING TENDENCIES

BLOOD LOSS

ANEMIA

DECREASE LIVER
FUNCTION
DECREASE METABOLISM OF AMMONIA
INCREASE AMMONIA LEVELS
HEPATIC ENCEPHALOPATHY

CHANGES IN COORDINATION,
MEMORY, ORIENTATION

COMA
DEATH

ASTERIXIS, FETOR HEPATICUS

DECREASE LIVER
FUNCTION

DECREASE METABOLISM
DRUGS

DRUG TOXICITY

DECREASE LIVER
FUNCTION
OBSTRUCTION OF BILE FLOW

DECREASE FAT DECREASE


ABSORPTION BILIRUBIN
IN GIT
DECREASE VIT K
ABSORPTION BILIRUBIN
IN FECES

ECREASE CLOTTING
FACTORS CLAY-COLORED

BLEEDING/ANEMIA

FECES

BILE REABSORBED
IN THE BLOOD

BILE SALTS IN
JAUNDICE
SKIN

INCREASE
BILE IN
KIDNEY

PRURITUS

DARKCOLORED
URINE

DECREASE LIVER
FUNCTION
DECREASE STORES OF
VITAMINS & MINERALS

DECREASE RBC
PRODUCTION

ANEMIA

DECREASE ENERGY
PRODUCTION

ETIOLOGY

ALCOHOL
VIRAL HEPATITIS
AUTOIMMUNE HEPATITIS
STEATOHEPATITIS
DRUGS AND TOXINS
BILIARY DISEASE
METABOLIC/GENETIC CAUSES
CARDIOVASCULAR DISEASE

CLINICAL
MANIFESTATIONS

NEUROLOGIC FINDINGS
Asterixis
Paresthesias of feet
Peripheral nerve degeneration
Portal-systemic encephalopathy
Reversal of sleep-awake pattern
Sensory disturbance
GASTROINTESTINAL (GI) FINDINGS
Abdominal pain
Anorexia
Ascites
Clay-colored stools
Diarrhea
Esophageal varices
Fetor hepaticus
Gallstones

Gastritis
Gastrointestinal bleeding
Hemorrhoidal varices
Hepatomegaly
Hiatal hernia
Hyperslenism
Malnutrition
Nausea
Small nodular liver
Vomiting

RENAL FINDINGS
Hepatorenal syndrome
Increase urine bilirubin
ENDOCRINE FINDINGS
Increased aldosterone
Increased antidiuretic hormone
Increased circulating estrogens
Increased glucocorticoids
Gynecomastia
IMMUNE SYSTEM DISTURBANCES
Increased susceptibilityof infection
Leukopenia
CADIOVASCULAR FINDINGA
Cardiac dysrhythmias
Development of callateral circulation

Fatigue
Hyperkinetik circulation
Peripheral edema
Portal hypertension
Spider angiomas
PULMONARY FINDINGS
Dyspnea
Hydrothorax
Hyperventilation
Hypoxemia
HEMATOLOGIC FINDINGS
Anemia
Disseminated intravascular
coagulation
Impaired coagulation

Splenomegaly
Thrombocytopenia
DERMATOLOGIC FINDINGS
Axillary and pubric hair changes
Caput medusae
Ecchymosis
Increased skin pigmentation
Jaundice
Palmar erythema
Pruritus
Spider angiomas
FLUID AND ELECTROLYTE
DISTORBANCES
Ascites
Decreased effective blood volume
Dilutional hyponatremia or

Hypernatremia
Hypocalcemia
Hypokalemia
Peripheral edema
Water retention

ASSESSMENT OF
ABNORMAL LABORATORY
FINDINGS IN LIVER
DISEASE

SERUM ENZYMES
Elevated serum aspartate Hepatic
cell destruction
aminotransferase (AST) hepatitis (most specific indicator)
Elevated serum alanine
Hepatic cell destruction,
amino-tranferase(ALT)
hepatitis
Elevated lactate dehy- Hepatic cell destruction
drogenase(LDH)
Elevated serum alkalineObstructive jaundice, hepatic
phosphatase
metastasis
BILIRUBIN
Elevated serum total
Hepatic cell disease
Elevated serum direct Hepatitis, liver metastasis
conjugated bilirubin
Elevated serum indirect Cirrhosis
unconjugated billrubin
Elevated urine billrubin Hepatocellular obstruction, viral
or toxic liver disease

Eleveted urine urobilinogen Hepatic dysfunction


Decreased fecal urobilinogen Obstructive liver disease
SERUM PROTEINS
Increased serum total Acute liver disease
protein
Decreased serum total Chronic liver disease
protein
Decreased serum albumin Severe liver disease
Elevated serum globulin
Immune response to liver disease
OTHER TESTS
Elevated serum ammonia Advanced liver disease or portalsystemic encephalopathy(PSE)
Prolonged prothrombin Hepatic cell damage and synthesis
time(PT) or INR
of prothrombin

INTERVENTION
ACTIVITIES

FLUID/ELECTROLYTE MANAGEMENT
Obtain laboratory specimens for monitoring of altered fluid and
electrolyte levels(e.g. Hct, BUN, protein, sodium, and potassium
levels) as appropriate.
Keep an accurate record of intake and output.
Weigh client daily and monitor trends.
Monitor for signs and symptoms of fluid retention.
Monitor vital signs, as appropriate.
Administer prescribed supplemental electrolytes, as appropriate.
BLEEDING PRECAUTIONS
Monitor the client closely for hemorrhage
Monitor for signs and symptoms of persistent bleeding
Monitor coagulation studies, including prothrombin time (PT),
partial
thromboplastin time (PTT), fibrinogen, fibrin degradation/split
products,
and platelet counts, as appropriate.

Monitor orthostatic vital signs, including blood pressure.


Use electric razor, instead of straight-edge, for shaving.
Use soft toothbrush or toothettes for oral care.
Avoid injections (IV, IM, or SC), as appropriate.
Protect the client from trauma, which may cause bleeding.

NEUROLOGIC MONITORING
Monitor level of consciousness.
Monitor level of orientation.
Monitor recent memory, attention span, past memory,
mood, affect, and behaviors.
Monitor vital signs: temperature, blood pressure, pulse, and
respirations.

DIET THERAPY

Consume a diet that adheres to the


guidelines set by your physician,
nurse, or dietitian.
If you have excessive fluid in your
abdomen, follow the low-sodium diet
prescribed for you.
Eat small, frequent meals that are
nutritionally well balanced.
Include in your diet daily supplemental
liquids and a multivitamin; low-protein
supplements are available if needed.

DRUG THERAPY

Take the diuretics or preventive beta blocker


prescribed for you. If you experience muscle
weakness, irregular heartbeat, or lightheadedness, contact your health care
provider right away.
Take the medication prescribed for you that
helps prevent gastrointestinal bleeding.
Take the lactulose syrup as prescribed to
maintain three to five bowel movements
every day.
Do not take any other medication unless
specifically prescribed by your health care
provider.

ALCOHOL ABSTINENCE

Do not consume any alcohol.


Seek support services for help if needed.