Seminar on Cirrhosis of Liver

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    Introduction

    The liver is an important organ in the body. It performs many critical functions, two of

    which are producing substances required by the body. Cirrhosis is a complication of many liver

    diseases that is characterized by abnormal structure and function of the liver. The diseases that lead

    to cirrhosis do so because they injure and kill liver cells, and the inflammation

    Definition

    Cirrhosis is a chronic disease characterized by replacement of normal liver tissue

    with diffuse fibrosis that disrupts the structure and function of the liver.

    types

    Cirrhosis of the liver, is divided into three types: alcoholic, post necrotic ,biliary cirrhosis

    Aicoholic cirrhosis

    In this type the scar tissue characteristically surround the portal areas .This is most

    commonly caused by chronic alcoholism and is the most common type of cirrhosis

    post necrotic cirrhosis

    In this type there are broad band of scar tissue .This is late result of previous bout of acute

    viral hepatitis

    Biliary cirrhosis

    In this type scarring occurs in the liver around the bile duct. This type of cirrhosis usually

    results from chronic biliary obstruction and infection

    Causes

    - Alcohol- Chronic viral hepatitis ( hepatitis B or hepatitis C )- Inherited (genetic) disorders

    * abnormal accumulation of iron (hemochromatosis)

    * abnormal accumulation of copper (Wilson's disease)

    * psychiatric disturbances and other neurological

    - Autoimmune hepatitis

    The abnormal immune activity in autoimmune hepatitis causes progressive

    inflammation and destruction of liver cells (hepatocytes), leading ultimately to cirrhosis. more

    commonly seen in women.

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    - Less common causes of cirrhosis include unusual reactions to some drugs and prolonged

    exposure to toxins.

    -exposure to chemicals ( carbon tetrachloride,chlorinated naphthalene,arsenic,phosphorus )

    Pathophysiology

    Due to causes

    Tissue necrosis in the liver cells

    Destroyed liver cells gradually replaced by scar tissues

    Residual normal tissue and regenerating liver tissue may

    Project from the constricted areas and giving like hobnail appearance

    Cirrhosis of liver

    Clinical manifestaions

    The severity of manifestation helps to catagorize the disorder as two 1) compensated

    cirrhosis, 2)decompensated cirrhosis

    For compensated liver cirrhosis

    - Intermittent mild fever- Palmar erythema( reddened palms )- Unexplained epistaxis- Ankle edema- Vague morning indigestion- Abdominal pain- Spleno megaly

    For decompensated liver cirrhosis

    - Ascites

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    PORTAL HYPERTENSION (RESISTANCE TO BLOOD FLOW

    se leakage of leakage of plasma vasocongestion development of

    Plasma in liver out of vasculature within intestinal collateral venous

    Lymphatic and in to liver tissue vasculature vessels

    production of persistence of

    Liver lymph leakage of plasma transudation of amine neuro-

    (high protein) from liver tissue into plasma in to transmitters

    Abdominal cavity Abdominal cavity

    Dilation of lymph redistribution

    Channels draining of blood fow

    liver (reduced renal perfusion)

    leakage of lymph in to production of

    abdominal cavity ASCITES

    aldosterone

    leakage of

    osmotic gradient between plasma out sodium and water retetion

    lymph and extracellular of vascular space

    fluidfluid leakage

    in to abdominal cavity intravascular oncotic pressure

    albumin production

    Hepatocyte dysfunction metabolism of aldosterone

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    - Jaundice

    - Weakness- Weight loss- Continuous mild fever- Clubbing of fingers- Purpura (due to decreased platelet count)- epistaxis- hypotension- white nails

    other signs and symptoms

    - liver enlargement- portal obstruction

    ( All blood from digestive organs is collected in portal veins and carried to

    liver .Because a cirrhotic liver does not allow free blood passage , blood backs up in

    to spleen and GI tract .)

    - infection and peritonitis- gastro intestinal varices or haemorrhoids- mental detoriation and cognitive function

    Assessment and Diagnostic Methods

    * Liver function tests

    - Serum alkaline phosphatase,

    Aspartate aminotransferase [AST]

    Serum glutamic oxaloacetic transaminase (SGOT),

    Alanine aminotransferase [ALT] [serum glutamic pyruvic transaminase (SGPT)],

    Serum cholinesterase,

    Bilirubin,

    *prolonged Prothrombin time,

    *Ultrasound scanning-(to messure density of parenchymalcells and scar tissue )

    *CT scan

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    *MRI

    *Radioisotopic liver scans

    * ABGs, biopsy

    Management

    The management of the patient with cirrhosis of liver is usually based on the

    presenting symptoms.

    Medical management

    * Antacid or h2antagonist are used to decrease gastric distress and minimize the

    possibility of GI bleeding.

    * vitamins and nutritional supplements promote healing of damaged liver cells and

    improvethe patients general nutritional status

    * Potassium sparing diuretics such as spironolactone( aldactone) or triamterene

    (dyrenium) are used to decrease ascites

    * An adequate diet and avoidance of alcohol are essential

    *colchicine ,an anti-inflammatory agent used to treat the symptoms of gout for

    moderate cirrhosis

    Nursing Management

    * Promoting Rest

    Position bed for maximal respiratory efficiency; provide oxygen if needed.

    Initiate efforts to prevent respiratory, circulatory, and vascular disturbances.

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    Encourage patient to increase activity gradually and plan rest with activity and mild

    exercise.

    * Improving Nutritional Status

    Provide a nutritious, high-protein diet supplemented by B-complex vitamins and

    others, including A, C, and K.

    Encourage patient to eat: Provide small, frequent meals, consider patient preferences,

    and provide protein supplements, if indicated.

    Provide nutrients by feeding tube or total PN if needed.

    Provide patients who have fatty stools (steatorrhea) with water-soluble forms of fat-

    soluble vitamins A, D, and E, and give folic acid and iron to prevent anemia.

    Provide a low-protein diet temporarily if patient shows signs of impending or

    advancing coma; restrict sodium if needed.

    * Providing Skin Care

    Change patients position frequently.

    Avoid using irritating soaps and adhesive tape.

    Provide lotion to soothe irritated skin; take measures to prevent patient from

    scratching the skin.

    * Reducing Risk of Injury

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    Use padded side rails if patient becomes agitated or restless.

    Orient to time, place, and procedures to minimize agitation.

    Instruct patient to ask for assistance to get out of bed.

    Carefully evaluate any injury because of the possibility of internal bleeding.

    Provide safety measures to prevent injury or cuts (electric razor, soft toothbrush).

    Apply pressure to venipuncture sites to minimize bleeding.

    * Monitoring and Managing Complications

    Monitor for bleeding and hemorrhage.

    Monitor the patients mental status closely and report changes so that treatment of

    encephalopathy can be initiated promptly.

    Carefully monitor serum electrolyte levels are and correct if abnormal.

    Administer oxygen if oxygen desaturation occurs; monitor for fever or abdominal pain,

    which may signal the onset of bacterial peritonitis or other infection.

    Assess cardiovascular and respiratory status; administer diuretics, implementfluid

    restrictions, and enhance patient positioning, if needed.

    Monitor intake and output, daily weight changes, changes in abdominal girth, and

    edema formation.

    Monitor for nocturia and, later, for oliguria, because these states indicate increasing

    severity of liver dysfunction.

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    * follow up care

    Prepare for discharge by providing dietary instruction, including exclusion of alcohol.

    Refer to Alcoholics Anonymous, psychiatric care, counseling, or spiritual advisor if

    indicated.

    Continue sodium restriction; stress avoidance of raw shellfish.

    Provide written instructions, teaching, support, and reinforcement to patient and

    family.

    Encourage rest and probably a change in lifestyle (adequate,well-balanced diet and

    elimination of alcohol).

    Instruct family about symptoms of impending encephalopathy and possibility of

    bleeding tendencies and infection.

    Offer support and encouragement to the patient and provide positive feedback when

    the patient experiences successes.

    Refer patient to home care nurse, and assist in transition from hospital to home.

    Nursing Diagnosis

    imbalanced nutrition less than body requirements related toAnorexia,nausea/vomiting, indigestion, ascites/Abnormal bowel function

    impaired skin integrity related toPoor skin turgor, skeletal prominence,presence of edema, ascites

    ineffective Breathing Pattern related to Intra-abdominal fluid collection(ascites)or Decreased lung expansion, accumulated secretions

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    High risk for Injury related toaltered clotting factors (decreased production of prothrombin, fibrinogen,

    and factors VIII, IX, and X; impaired vitamin K absorption; and release of

    thromboplastin)

    or

    Portal hypertension

    Knowledge Deficit related to disease condition