Medical Surgical Charts | Cheat Sheet Nursing

Cirrhosis

Incidence and Prevalence

Cirrhosis combined with liver disease are a major concern cause of death in the US

o3.2 million Americans have Hep C, 1 in 7 have Hep B

Cirrhosis Pathology & Etiology

Irreversible damage to liver mostly due to chronic inflammation – developing slowly (gradual onset)

Causes fibrotic bands of connective tissue leading to changes in liver’s anatomy

oLiver becomes nodular leading to blockages & impending the function of the liver

Early on the liver becomes enlarged and firm eventually shrinking as the disease progresses

Can be caused by Hepatitis (B&D specifically), nonalcoholic fatty liver disease & chronic alcohol abuse; women

develop cirrhosis easier than men if r/t alcohol

Types of Cirrhosis

Post-necrotic cirrhosis – caused by viral hepatitis, drugs, toxins

Laenne’s/ alcoholic cirrhosis – caused by chronic alcohol consumption

Biliary/ cholestatic cirrhosis – caused by chronic biliary obstruction (change in anatomy) or autoimmune disease

Complications of Cirrhosis

Compensated cirrhosis – liver is able to maintain essential function without major symptoms despite liver being

scarred (can be asymptomatic for a very long time)

Uncompensated cirrhosis – patient has s/s of liver failure and function of liver is impaired

Portal hypertension

oIncreased pressure in portal vein from blockage or increased resistance

oBlood will backflow into spleen leading to splenomegaly (enlargement of the spleen)

oVeins in stomach, esophagus, intestine, abdomen, rectum become enlarged

oPortal HTN can lead to ascites, hemorrhoids & esophageal varices which could cause bleeding (med emergency)

Ascites (see peripheral edema first & then ascites)

oCollection of free fluid in peritoneal cavity form portal HTN

oPatient may show s/s of edema and hypovolemia at the same time

Fluid has high concentration of plasma protein reducing amount in circulating plasma

Failing liver cannot produce enough albumin leading to decreased osmotic pressure (hypovolemia comes

into place)

Leads to “third spacing” (hard to treat)

oMassive ascites will become its own positive pathway by activating the renin-angiotensin system leading to water

& Na+ retention increasing vascular volume & worsening the ascites

Esophageal varices

oResults from portal HTN

oBlood backtracks from pressure to esophageal & gastric veins

oVessels become enlarged & fragile potentially leading to bleeding

oBleeding esophageal varices are a medical emergency causes hypovolemia from severe blood loss, compromised

airway

oSome patients may have no obvious signs of bleeding – leading to LOC due to hypovolemia/ hemorrhagic shock

oBleeding can be abrupt (hematemesis) or slow leading to chronic blood loss (+ occult stool) black, tarry stool

Splenomegaly

oResulting from portal HTN

oEnlarged spleen will destroy platelets leading to thrombocytopenia & increased risk for bleeding esp when they

are in end stage liver failure

oThrombocytopenia is usually the first sign that a patient has liver failure (incidental or not) or developing

bruising, bleeding gums when they brush their teeth

Biliary obstruction

oJaundice can be caused by 2 mechanisms:

Hepatocellular jaundice: caused by liver’s inability to eliminate bilirubin effectively

Intrahepatic obstructive: bilirubin is unable to be excreted due to edema, fibrosis, scarring of hepatic bile

channels & bile ducts

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Cirrhosis Incidence and Prevalence  Cirrhosis combined with liver disease are a major concern cause of death in the US o 3.2 million Americans have Hep C, 1 in 7 have Hep B Cirrhosis Pathology & Etiology  Irreversible damage to liver mostly due to chronic inflammation – developing slowly (gradual onset)  Causes fibrotic bands of connective tissue leading to changes in liver’s anatomy o Liver becomes nodular leading to blockages & impending the function of the liver  Early on the liver becomes enlarged and firm eventually shrinking as the disease progresses  Can be caused by Hepatitis (B&D specifically), nonalcoholic fatty liver disease & chronic alcohol abuse; women develop cirrhosis easier than men if r/t alcohol Types of Cirrhosis  Post-necrotic cirrhosis – caused by viral hepatitis, drugs, toxins  Laenne’s/ alcoholic cirrhosis – caused by chronic alcohol consumption  Biliary/ cholestatic cirrhosis – caused by chronic biliary obstruction (change in anatomy) or autoimmune disease Complications of Cirrhosis  Compensated cirrhosis – liver is able to maintain essential function without major symptoms despite liver being scarred (can be asymptomatic for a very long time)  Uncompensated cirrhosis – patient has s/s of liver failure and function of liver is impaired  Portal hypertension o Increased pressure in portal vein from blockage or increased resistance o Blood will backflow into spleen leading to splenomegaly (enlargement of the spleen) o Veins in stomach, esophagus, intestine, abdomen, rectum become enlarged o Portal HTN can lead to ascites, hemorrhoids & esophageal varices which could cause bleeding (med emergency)  Ascites (see peripheral edema first & then ascites) o Collection of free fluid in peritoneal cavity form portal HTN o Patient may show s/s of edema and hypovolemia at the same time  Fluid has high concentration of plasma protein reducing amount in circulating plasma  Failing liver cannot produce enough albumin leading to decreased osmotic pressure (hypovolemia comes into place)  Leads to “third spacing” (hard to treat) o Massive ascites will become its own positive pathway by activating the renin-angiotensin system leading to water & Na+ retention increasing vascular volume & worsening the ascites  Esophageal varices o Results from portal HTN o Blood backtracks from pressure to esophageal & gastric veins o Vessels become enlarged & fragile potentially leading to bleeding o Bleeding esophageal varices are a medical emergency causes hypovolemia from severe blood loss, compromised airway o Some patients may have no obvious signs of bleeding – leading to LOC due to hypovolemia/ hemorrhagic shock o Bleeding can be abrupt (hematemesis) or slow leading to chronic blood loss (+ occult stool) black, tarry stool  Splenomegaly o Resulting from portal HTN o Enlarged spleen will destroy platelets leading to thrombocytopenia & increased risk for bleeding esp when they are in end stage liver failure o Thrombocytopenia is usually the first sign that a patient has liver failure (incidental or not) or developing bruising, bleeding gums when they brush their teeth  Biliary obstruction o Jaundice can be caused by 2 mechanisms:  Hepatocellular jaundice: caused by liver’s inability to eliminate bilirubin effectively  Intrahepatic obstructive: bilirubin is unable to be excreted due to edema, fibrosis, scarring of hepatic bile channels & bile ducts

o Pruritis is common sign of elevated bilirubin & jaundice o Bile production is reduced due to failing liver preventing absorption of fat soluble vitamins: vitamin K leading to increased clotting times & bruising also affects vitamins ADEK  Hepatic encephalopathy o Exact cause of mechanism is unknown o Causes cognitive changes in the patient o Patient may experience mood changes, sleep disturbances, mental status changes, speech problems o May be reversible, if not caught can lead to altered LOC & eventually coma o Patient with chronic liver disease will display a slow onset of s/s o Patients with acute liver dysfunction will develop symptoms quickly o Has 4 stages – patient can fluctuate between 4 stages as disease progresses o Many patients will have elevated NH3 (ammonia), elevated NH3 causes confusion o Can also be caused by: High protein diet, infections, hypovolemia, hypokalemia, constipation, GI bleeding, drugs can cause or worsen H.E.  Hepatorenal syndrome see with advanced liver failure/ cirrhosis; now it’s affecting the kidneys o Often cause of death in patients with liver failure typically occurring after worsening GI bleeding or hepatic encephalopathy o Decreased urinary flow <500 mL/day o Elevated BUN/Cr o Decreased Na+ excretion in urine  SBP & hepatopulmonary syndrome (less common) o Spontaneous bacterial peritonitis: bacteria from bowel infect ascitic fluid in peritoneal cavity – patients may have s/s of infection, belly tenderness/pain o Hepatopulmonary syndrome is due to excessive volume from ascites leading to dyspnea from decreased thoracic expansion from increased intra-abdominal pressure caused by fluid Assessment (IMPT**) 1. Ascites, 2. Check NH3, 3. Bleeding (does not stop)  Take detailed history specifically about alcohol, illicit drug use, exposure to herbal preparations and toxins o All exposures are important regardless of length of time since exposure  Take detailed sexual history  Ask the patient if they have gotten any new tattoos, been in incarcerated, in the military, healthcare worker, police  If the patient is currently sober following substance dependence or ETOH abuse, ask them how long they have been in recovery  Many patients would have been exposed to what caused the liver failure many years in the pasts  Early in the disease process s/s are vague and non-specific: o Fatigue, changes in weight, anorexia, vomiting, pain in the abdomen, liver tenderness Anorexia caused by patients not eating a lot because their GI symptoms is moving a lot slower, might become constipated  Late stage cirrhosis: o GI bleeding – nose bleed, hemorrhoids o Jaundice – pruritus (itchy skin) o Ascites o Spontaneous bruising: petechiae, ecchymoses o Warm/red palms o Spider angiomas on cheeks, nose, upper thorax, shoulders o Dependent edema o Fat soluble vitamin deficiency: ADEK  Alcohol withdrawal symptoms (develop symptoms from 6 hrs of last drink)  Fetor hepaticus: distinct odor of liver disease – fruity/musty  Amenorrhea  Men may have testicular atrophy, gynecomastia, impotence  Neurologic changes: hallucinations, confusion, anxiety, delusions  Asterixis: tremor (hand flapping)- can start mild  Psychosocial deterioration: life altering illness affecting patient and family, can have frequent hospitalizations o Substance abuse is present may continue despite worsening of illness

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