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    Cirrhosis

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    Yani
    The document discusses cirrhosis, including its pathophysiology, types, signs and symptoms, diagnostic testing, complications, and treatment approaches. Cirrhosis results from chronic liver damage and scarring that disrupts the liver's normal structure and blood flow, potentially leading to complications like ascites, variceal bleeding, hepatic encephalopathy, and liver failure if not properly managed. Treatment focuses on managing complications, restricting dietary sodium and proteins, administering medications, and potentially using procedures or surgery to relieve pressure in the portal system.

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    Cirrhosis

    Uploaded by

    Yani
    11K views54 pages
    The document discusses cirrhosis, including its pathophysiology, types, signs and symptoms, diagnostic testing, complications, and treatment approaches. Cirrhosis results from chronic liver damage and scarring that disrupts the liver's normal structure and blood flow, potentially leading to complications like ascites, variceal bleeding, hepatic encephalopathy, and liver failure if not properly managed. Treatment focuses on managing complications, restricting dietary sodium and proteins, administering medications, and potentially using procedures or surgery to relieve pressure in the portal system.

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    The document discusses cirrhosis, including its pathophysiology, types, signs and symptoms, diagnostic testing, complications, and treatment approaches. Cirrhosis results from chronic liver damage and scarring that disrupts the liver's normal structure and blood flow, potentially leading to complications like ascites, variceal bleeding, hepatic encephalopathy, and liver failure if not properly managed. Treatment focuses on managing complications, restricting dietary sodium and proteins, administering medications, and potentially using procedures or surgery to relieve pressure in the portal system.

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    11K views54 pages

    Cirrhosis

    Uploaded by

    Yani
    The document discusses cirrhosis, including its pathophysiology, types, signs and symptoms, diagnostic testing, complications, and treatment approaches. Cirrhosis results from chronic liver damage and scarring that disrupts the liver's normal structure and blood flow, potentially leading to complications like ascites, variceal bleeding, hepatic encephalopathy, and liver failure if not properly managed. Treatment focuses on managing complications, restricting dietary sodium and proteins, administering medications, and potentially using procedures or surgery to relieve pressure in the portal system.

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    of 54
    At a glance
    Powered by AI
    Cirrhosis is a chronic, progressive liver disease caused by fibrosis and scarring of the liver. It has many potential causes and complications.

    The main types of cirrhosis mentioned are Laennec's (alcoholic), postnecrotic, biliary, and cardiac cirrhosis.

    Common signs and symptoms include abdominal pain, jaundice, edema, ascites, varices, and portal hypertension.

    Cirrhosis

    Juke R Saketi
    Internal Medicine Department,
    Gastroenterology Hepatology Subdivision,
    Medical Faculty Padjadjaran University/
    Hasan Sadikin Hospital Bandung
    Pathophysiology
    • Slow, insidious, progressive, chronic
    • Fibrous bands replace normal liver
    structure
    • Cell degeneration occurs
    • Liver attempts to regenerate cells but cells
    are abnormal and disorganized
    • Causes abnormal blood and lymph flow
    • Results in more fibrous tissue formation
    Normal Liver
    Incidence of Cirrhosis

    • Tenth leading cause of death in US


    • At least 25,000 deaths annually
    • Higher death rates for men than women
    –  mortality in African Americans and
    Hispanics
    Types of Cirrhosis
    • Laennec’s
    (alcoholic)

    • Postnecrotic

    • Biliary

    • Cardiac
    Laennec’s Cirrhosis
    • Most common type of cirrhosis
    • Also called alcoholic or portal
    • Alcohol causes inflammation to liver
    cells
    • Leads to fatty deposits and
    hepatomegaly
    • Scarring formed and liver cells
    destroyed
    • Malnutrition and more alcohol accelerate
    the damage
    Postnecrotic Cirrhosis
    • Caused by viral hepatitis or
    hepatotoxins
    • Scar tissue destroys liver
    lobes
    • Liver initially enlarges but
    then shrinks in size
    • 10 – 30% of all cirrhoses
    Biliary Cirrhosis
    • Caused by chronic biliary
    obstruction or stasis of bile,
    biliary inflammation, or hepatic
    fibrosis
    • Excessive bile leads to liver cell
    destruction and formation of
    nodules in the lobes
    • 5 – 10% of all cirrhoses
    Cardiac Cirrhosis

    • Seen with right sided heart failure


    • Liver is engorged with venous
    blood
    • Becomes enlarged, edematous,
    and dark
    • Venous congestion results in
    anoxia
    • Cell necrosis results
    Diagnostic Data

    •  AST, ALT, LDH, Alk phos


    •  bilirubin, ammonia,
    •  coagulation studies
    • Serum protein levels depend on
    disease
    –  with acute liver disease
    –  with chronic liver disease
    More Diagnostics

    • Abdominal x-ray
    • Upper GI series
    • Angiography
    • Abdominal CT
    • EGD
    • Liver biopsy
    • Nuclear scan
    Signs and Symptoms
    • Neurological
    Asterixis Paraesthesias
    LOC Sensory
    disturbances
    Behavorial changes Cognitive
    changes
    Skin
    Spider angiomas Palmar erythma
    Jaundice Pruitis
     hair production caput medusa
     pigmentation Bruising
    White Nails
    Caput Medusae
    Spider Angiomas
    Palmar Erythema
    More Signs and Symptoms
    • GI
    Abdominal pain Anorexia
    Ascites Diarrhea
    Clay colored stools Fetor hepaticus
    Gastritis GI bleeding
    N/V Varices
    Malnutrition
    “White Nails”
    More Signs and Symptoms

    • Cardiovascular
    Dysrhythmias Portal
    hypertension
    Collateral circulation Fatigue
    Peripheral edema
    • Endocrine
    Gynecomastia Amenorrhea
     aldosterone, ADH, estrogens,
    glucocorticoids
    More Signs and Symptoms
    • Respiratory
    Dyspnea Hypoxia

    • Blood
    Anemia DIC
    Thrombocytopenia 
    WBCs
    Hypokalemia Hypocalcemia
    Hypo/Hypernatremia
    Hypomagnesia
    More Signs and Symptoms

    • Immune
     Susceptibility to infections
    Leukopenia
    Renal
     Urinary output
    Complications
    • Portal hypertension
    – Ascites
    – Varices
    • Coagulation defects
    • Jaundice
    • PSE (portal systemic
    encephalopathy)
    • Hepatorenal syndrome
    Portal Hypertension
    • Increased pressure within the portal
    vein
    • Results in obstruction of blood flow
    through the portal vein
    – Blood tries to find new ways around
    obstructed area = collateral circulation
    • Causes venous distention in entire GI
    tract
    Ascites
    • Accumulation of plasma in the peritoneal
    cavity
    – Caused by increased pressure forcing fluid out of
    intravascular space into cavity
    – Plasma contains albumin so circulating proteins
    decreased
    –  serum osmotic pressure
    – Intravascular fluid depletion stimulates kidney to
    conserve sodium and water =  hydrostatic
    pressure and creates more ascites
    Ascites
    Varices
    • Occur anywhere in the GI tract
    especially
    – Esophageal
    Hemorrhoids
    • Bleeding esphageal varices
    – Caused by thin walled veins
    that are irritated, distended and
    eventually rupture
    Chemical irritants
    Mechanical trauma
    Esophagus pressure
     Prone to hemorrhage – medical
    emergency
    Esophageal Varices
    Coagulation Defects

    • Susceptible to bleeding
    • Bruises easily
    • Does not clot
    – Esophageal varices
    bleeding
    Jaundice
    • Due to hepatocellular destruction or
    hepatic obstruction
    – Hepatocellular – cannot metabolize
    bilirubin so it builds up
    – Obstruction – clogs bile ducts so excretion
    is not possible
    Jaundice
    PSE
    • Also known as
    hepatic coma
    • Seen in end stage
    hepatic failure
    • Can be insidious or
    rapid onset
    depending on the
    severity of liver
    disease
    • Caused by impaired
    ammonia
    metabolism
    PSE Continued
    • Usually protein breaks down into
    ammonia in GI tract, then ammonia into
    urea --- excreted by the kidneys
    • Liver cannot convert ammonia into urea
    – Results in  serum ammonia levels
    – Toxic to the central nervous system
    PSE Continued

    • Other factors that


    add to PSE:
    High protein diet
    Infection
    Hypovolemia
    Constipation
    GI bleeding
    Medications
    Stages of PSE
    • #1 - Prodomal – very
    subtle changes
    – Personality/behavior
    changes
    – Impaired
    thinking/concentratio
    n
    – Emotional highs and
    lows
    – Fatigue, drowsiness
    – Slurred or slow
    speech
    – Sleep pattern
    disturbance
    Stages of PSE
    • #2 – Impending
    – Continued mental
    deterioration
    – Confusion
    • Disoriented
    – Asterixis
    Stages of PSE
    • #3 – Stuporuous
    – Marked mental
    confusion
    – Drowsy but
    arousable
    – Abnormal EEG
    – Muscle twitching
    – Hyperreflexia
    – Continued
    asterixis
    Stages of PSE
    • #4 – Comatose (85%
    mortality rate)
    – Unresponsive
    – Responds to painful
    stimuli only
    – No asterixis
    – Positive Babinski’s sign
    – Muscle rigidity
    – Fetor hepaticus
    – Seizures
    Hepatorenal Syndrome
    • A primary cause of death with hepatic
    failure/cirrhosis
    • Kidneys cannot excrete ammonia and
    bilirubin
    – Results in acute tubular necrosis
    • Signs/symptoms
    Sudden  urinary output
     BUN, Cr, urine osmolarity  Urine Na
    Treatment
    • Diet
    –  Sodium (< 2 grams)
    – Carbohydrate, moderate fats
    –  Protein
    • Unless PSE present then  protein
    – Fluid restriction (total of ≤ 1500cc/day)
    – Vitamin supplements
    Treatment Continued
    • Medications
    – Diuretics
    – Electrolyte replacement
    – Antacids
    • Must be low sodium –
    Riopan
    – Lactulose
    • Facilitates evaculation of
    ammonia
    – Neomycin
    • Eliminates intestinal flora =
     protein breakdown
    – Levadopa
    • For PSE – repairs damaged
    neurotransmitters
    More Treatments
    • Ascites control
    – Paracentesis
    – Shunts
    • Le Veen Shunt - drains ascites fluid
    into superior vena cava
    • Denver Shunt – subcutaneous pump
    that is manually compressed
    – Post op care: same as with any
    abdominal surgery, watch for
    fluid volume overload and
    bleeding disorders, measure
    abdominal girth every shift
    Le Veen Shunt
    More Treatments
    • Hemorrhage from varices
    – Esophagogastric balloon tamponade
    • Sengstaken-Blakemore tube – balloon inflates in
    esophagus and puts pressure on varices
    – Blood transfusions
    – Medications
    • Beta blockers to decrease HR and BP
    • Pitressin (vasopressin) IV or into superior
    mesenteric artery (via endoscopy)
    – Sclerotherapy
    • Sclerosing agents injected into varices during EGD
    – Transjugular intrahepatic portal systemic shunt (TIPS)
    • Shunt between portal and hepatic vein to 
    pressure =  bleeding
    – Other portal system shunts – poor prognosis
    Sclerosing Procedure
    Blakemore Tube
    Another Blakemore Tube
    More Treatments
    • PSE
    – Low protein diet
    • May need TPN
    – Control GI bleeding
    – Medications
    – Neuro checks
    – Look for signs and symptoms of
    the stages of PSE
    Home Care
    • Diet
    –  calories, vitamins, protein
    (unless PSE)
    –  sodium
    • Medications
    – Diurectics
    – Antacids, H2-receptor
    antagonists
    – No OTC medications
    • No alcohol consumption
    •  activity – rest periods
    • Home care equipment
    Evaluation Outcomes
    • Patient will
    –  in ascites
    – Electrolytes WNL
    – B/P WNL
    – No bleeding or
    complications from
    bleeding
    – PSE managed
    immediatley
    – Optimal quality of life

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