LIVER CIRRHOSIS - chronic, progressive disease - characterized by widespread fibrosis (scarring) and nodule formation - caused by alteration in the

normal flow of blood, bile and hepatic metabolites - major clinical problems: o portal hypertension o decreased liver function 4 Major types of cirrhosis: 1. Alcoholic (Laennecs cirrhosis, micronodular or portal) o associated with alcohol abuse o presence of scarring & collagen tissue deposits regenerating nodules are very small o normal lobular structure is destroyed o Tx: supportive 2. Postnecrotic ( macronodular or toxin-induced) o most common type o more common in women o massive loss of liver cells,with irregular patterns of regenerating cells o associated with hepatitis B and C, post intoxication with industrial chemical associated o liver is small and nodular o TX: supportive 3. Biliary bile flow is decreased with concurrent cell damage to hepatocytes around bile duct damage associated with chronic stasis of bile in intrahepatic ducts autoimmune process implicated Tx: Ursodiol, relieve mechanical obstruction and treat symptoms 4. Cardiac o chronic liver disease associated with severe right-sided long term heart failure o Tx: treat chronic heart failure Etiology and Risk factors: - Drugs (acetaminophen, isoniazid & methotrexate) - genetic predisposition - hypersensitivity to alcohol - poor nutritional state - viral hepatitis - bile duct obstruction - Alcohol ingestion - right sided heart failure - valvular disease - Wilsons disease

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Pathophysiology:
Liver insult Alcohol ingestion Viral hepatitis Exposure to toxins Hepatocyte damage WBC Liver inflammation Fatigue, nausea

pain fever vomiting

Bleeding tendencies

Vitamin K absorption

anorexia Alteration in blood and lymph flow Alteration in blood and lymph flow Liver necrosis liver failure androgen & estrogen Detoxification testicular atrophy palmar erythema spider angiomas Gynecomastia loss of body hair menstrual changes bilirubin metabolism &/or biliary tree damage or obstruction Conjugated & unconjugated Hyperbilirubinemi a Jaundice bile in GIT urobilinogen dark clay urine colored sto ols Liver fibrosis & scarring Portal hypertension ascites edema Esophageal varices hemorrhoids Superficial abdominal varices Splenomegaly Anemia thrombocytope nia Leukopenia Bleeding and Delayed wound healing Infection

ADH & aldosterone detoxification edema

metabolism of protein & carbohydrate fat metabolism Hypoglycemia, malnutrition Decreased plasma proteins Ascites, edema

Liver failure
Inability to metabolize Ammonia to urea hepatic encephalopathy increased serum ammonia Asterixis alteration in sleep Foul breath confusion to respiratory acidosis

Death hepatic coma

Clinical Manifestations: early findings: - Hepatomegaly - vascular changes - advanced cases: o ascites o GIT bleeding o Splenomegaly o Internal hemorrhoids o Infection o Encephalopathy o Renal failure Diagnostic exams: - liver enzyme determination - CBC - PT, PTT - Liver biopsy Medical Management: - Monitor for complications o Ascites o Bleeding esophageal varices o Hepatic encephalopathy o Renal failure - Maximize liver function o Provide nutritious diet o Vitamin supplements o Adequate rest
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o Corticosteroids Treat the underlying cause o Avoid alcohol o Remove obstruction Prevent infection

Nursing management: - Ineffective Tissue perfusion related to bleeding tendencies & varices o Monitor for hemorrhage o Prevent hemorrhage o Provide client teaching - Imbalanced Nutrition: Less Than Body requirement o Modify diet o Provide vitamin supplements - Activity Intolerance - Risk for Injury 1.
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2. 3.
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Complications of Cirrhosis: Portal hypertension persistent increase in blood pressure in the portal venous system due to increase resistance or obstruction of blood flow. most common cause: cirrhosis Clinical manifestations: caput medusa enlarged, palpable spleen internal hemorrhoids bruits ascites Diagnostic exam: o Laparotomy o liver scanning o splenoportography o abdominal angiography o liver biopsy Complications: dilatation of the superior rectal veins, abdominal wall veins & esophagogastric veins. Hepatic encephalopathy

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Medical management: Control hemorrhage Sclerotherapy Transjugular intrahepatic portosystemic shunt (TIPS) reserved for individuals who considered poor surgical risks or wh0 fail endoscopic or medical management Administration of vasopressin Beta adrenergic Blocking agents Balloon tamponade tamponade Nursing Management: Ineffective Tissue Perfusion Avoid straining maneuvers that increase intraabdominal or intrathoracic pressure Avoid rough foods that may traumatize the esophagus and spicy foods that may irritate the mucosa Acute Confusion related to portosystemic encephalopathy and hepatic coma Monitor level of consciousness Assess client for the development of Asterixis Protect from injury Surgical management: A. Endoscopic band Ligation - varices are ligated and strangulated with small elastic O rings B. Portosystemic Shunt - anastomosing of high-pressure portal venous system to low-pressure systemic venous system. - last resort for patients who are poor surgical candidates Nursing actions: 1. assess client for excess fluid volume 2. monitor for signs of infection 3. eliminate medications that may sedate , depress the CNS or are known hepatotoxins 4. maintaining nutrition 2.

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Ascites accumulation of fluid in the peritoneal cavity as a result of the ff: portal hypertension plasma colloidal osmotic pressure sodium retention Clinical manifestations: abdominal distention
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bulging flanks downward protruding umbilicus Diagnostic exams: Paracentesis bdominal x-ray studies ultrasonography computed tomography scan Medical management: correct fluid and electrolyte imbalance discontinue medications that inhibit prostaglandin synthesis & impair renal prostaglandin sodium excretion paracentesis albumin diet modification moderate protein, low sodium with restriction of fluids promote effective breathing pattern potassium sparing diuretics Semi or High Fowlers position Daily measurement of abdominal girth maintain skin integrity tepid water or emollient baths use of non-alkaline soap antihistamines as prescribed Nursing management: Excess Fluid Volume and deficient Fluid volume related to fluid shift secondary to portal related hypertension, hypoalbuminemia and hyperaldosteronism restrict fluids monitor input and output administer albumin and diuretics avoid hepatotoxins monitor after paracentesis check VS assess the dressing Ineffective breathing Pattern related to increased intra-abdominal pressure on the diaphragm Impaired skin integrity 3. Hepatic encephalopathy collection of CNS disturbances secondary to the livers inability to metabolize ammonia to form urea so that it can be excreted. characterized by elevation of ammonia levels in the CSF Causes or Precipitating factors:
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decrease in hepatocellular function hypoxia infection diuretics (produce hypokalemia, alkalosis and hypovolemia) depressants: Phenobarbital, narcotics, sedatives gastrointestinal bleeding paracentesis increase protein intake constipation dehydration portosystemic and portacaval shunts Clinical manifestations: primarily neurologic and range from mental confusion to deep coma impaired concentration, memory, attention and rate of response asterixis handwriting and speech deterioration hyperventilation fetor hepaticus Stages of hepatic Encephalopathy: Stage I fatigue restlessness irritability decreased intellectual performance decreased attention span diminished short-term memory personality changes sleep pattern reversal o Stage II deterioration in handwriting deterioration Asterixis drowsiness confusion, lethargy fetor hepaticus o Stage III severe confusion inability to follow commands deep somnolence, but arousable o Coma Stage IV
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unresponsive to painful stimuli possible decorticate or decerebrate posturing possible

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- Medical and Nursing management: Identify and treat precipitating causes reduce nitrogenous waste (Ammonia) in the Blood and bacteria in colon maintain fluid volume balance BILIARY TRACT DISORDERS CHOLELITHIASIS (GALLSTONES) crystalline structures formed by concretion (hardening) or accretion (adherence of particles, accumulation) of normal or abnormal bile constituents. Incidence increases with age More common in women Risk factors: cholesterol saturation gall bladder stasis decreased contractility and emptying of the gall bladder spasm of sphincter of Oddi low fat- weight-reduction diets pregnancy spinal cord injury infection genetics Pathophysiology: Gallstone formation involves several factors: bile must become supersaturated with cholesterol or calcium the solute must precipitate from solution as solid crystals crystals must come together and fuse to form stones stones 3 types of gallstones: 1. cholesterol 2. pigment 3. mixed Clinical manifestations: pain or biliary colic jaundice nausea and vomiting history of flatulence, bloating, epigastric pain, belching intolerance to fatty foods
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Diagnostic exams: abdominal ultrasound gallbladder nuclear scanning ERCP MRCP Medical management: reduce pain administer analgesics antacids antibiotics nitroglycerine monitor fluid and electrolyte imbalance Non- Surgical approaches to eradicate stones: retrograde endoscopy enlargement of ampulla of Vater gallstone dissolution (Cholesterol-Dissolving Agents) oral administration of chenodeoxycholic cid (CDCA), chenodiol, ursodeoxycholic acid or ursodiol extracorporeal shock wave lithotripsy lithotripsy Nursing management: Acute or Chronic pain Administer pain medications Provide comfort measures quiet environment relaxation techniques (backrub) Risk for Imbalanced Fluid Volume Insert NGT Administer IV fluids and electrolytes Health teachings: maintain low fat diet maintain ideal body weight limit number of pregnancies regular coffee consumption may help to prevent symptomatic gallstone Surgical Management: Laparoscopic Cholecystectomy Treatment of choice for symptomatic gallbladder disease Contraindication: if stone is lodge in the common bile duct Complications: hemorrhage and damage to biliary tract Cholecystectomy
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 Excising the gallbladder from the posterior liver wall and ligating the cystic duct, vein and artery Indicated for patients with physique that does not allow to the gallbladder
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Nursing management: assess postoperatively assess manifestations of shock: cyanosis diaphoresis cold, clammy skin decreased BP increased pulse prevent pneumonia change position every 2 hours auscultate lungs for rhonchi, rales and diminished breath sounds plint the incision monitor fluids and electrolytes monitor urine output maintain NGT oral care every 2 hours for client in NPO status offer ice chips advance diet as tolerated patient are not allowed to have normal diet until bowel sounds are heard or after passage of flatus prevent infection ACUTE CHOLECYSTITIS - acute inflammation of the gallbladder wall - also known as acute calculous cholecystitis - common cause: obstruction of a cystic duct by a stone - common among Chinese, Jewish, Italians - Risk factors: sedentary lifestyle obesity
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Pathophysiology: Pathophysiology: o Obstruction of the cystic duct with stone venous and lymphatic drainage are impaired proliferation of bacteria occurs localized cellular irritation or infiltration areas of ischemia develop Clinical manifestations: o tenderness in the right upper quadrant and epigastrium right o nausea and vomiting o low-grade fever
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o mild jaundice o leukocytosis Diagnostic exams: o biliary ultrasonography o abnormal aminotransferase, alkaline phosphatase and bromsulfophtahalein o abdominal x-ray study o CT scan and MRI o Hepatobiliary scintigraphy(HIDA scan) o ERCP o WBC count Medical management: o antibiotics (ampicillin, cephalosporin, or aminoglycosides) Nursing management: o similar with cholelithiasis Surgical management: o Cholecystotomy (surgical drainage of the gallbladder)

III.

o o o o o o IV.

ACUTE ACALCULOUS CHOLECYSTITIS cholecystitis without stones far less common than cholelithiasis Can be triggered by the following: multiple blood transfusions Gram-negative bacterial sepsis tissue damage after burns, trauma or extensive surgery - Pathophysiology and Clinical manifestations: similar with calculous type higher incidence of gangrene and perforation - Surgical management: emergency cholecystectomy CHRONIC CHOLECYSTITIS - a sequela of acute cholecystitis - gallbladder loses its ability to concentrate bile because fibrous tissues begin to replace normal muscle and mucosal tissues - affects middle-aged, obese women - female to male ratio is 3:1 - Clinical manifestations: pain is less severe temperature is not as high
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the leukocyte count is lower o vague symptoms of indigestion, epigastric pain, fat intolerance, heartburn and flatulence - Diagnostic exam: Ultrasonography findings: cholelithiasis gall bladder wall thickening (>3mm) delayed visualization or non-visualization of the gallbladder on radionucleid scanning - Conservative management: low-fat diet weight reduction administration of anticholinergics, sedatives and antacids cholecystectomy DISORDER OF THE EXOCRINE PANCREAS PANCREATITIS inflammation of the pancreas that can result in autodigestion of the pancreas of its own enzymes may be acute or chronic Etiology and Risk factors: alcohol (ethanol) abuse cholelithiasis abdominal trauma metabolic factors hyperlipidemia hypercalcemic hypercalcemic pancreatic trauma pancreatic ischemia drugs: (anticonvulsants, thiazides, sulfonamides, valproic acid) Pathophysiology: premature activation of proteolytis and lipolytic pancreatic enzymes. Early Prognostic manifestations: Ranson/Imrie criteria At admission or diagnosis age > 55 years old leukocytosis (WBC > 16,000 mm3) Hyperglycemia Serum LDH > 400IU/L Serum AST >250 IU/L Clinical manifestations: abdominal distention and tenderness
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fever Turners sign Cullens sign Severe circulatory complications Confusion, psychosis and coma Transient hyperglycemia Diagnostic exams: serum lipase value WBC CXR Abdominal x-ray CT scan or MRI Medical management: reduce pain opioid analgesics and meperidine Morphine maintain volume status, electrolyte balance and nutritional status anticholinergics, NSAIDS, protease inhibitor maintain pancreatic rest withholding fluids and liquids by mouth temporarily TPN treat complications pancreatic abscess infected necrosis colonic or bile obstruction metabolic or renal disorders other measures: antibiotics are not routinely given calcium gluconate Nursing management: Acute pain related to inflammation of the pancreas and surrounding tissues Administer pain medication Provide comfort measures Risk for Imbalanced Fluid Volume Imbalanced Nutrition: Less than Body requirements Ineffective Breathing pattern related to abdominal distention or ascites Surgical management: subtotal pancreatectomy Whipples procedure Indications: uncertainty of diagnosis: relief of pain treatment of secondary pancreatic infection
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correction of associated biliary tract disease progressive clinical deterioration despite optimal supportive care Complications: ileus and abdominal distention distention

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