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Esophageal Varices: The most common manifestation of portal hypertension.

Distended, torturous collateral veins in the lower esophagus due to prolonged ↑ increased portal pressure.


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Can Rupture  (Via coughing, sneezing, vomiting, etc) = Medical Emergency Goal: avoidance and control of bleeding Drug Therapy

β-adrenergic blockers (propranolol Inderol) ○ Nitroglycerin: may ↓BP and contribute to renal failure ○ Vitamin K Therapeutic Management ○ What is the number one priority with esophageal hemorrhage? Airway!

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Octreotide (Sandostatin): block gastric secretions, ↓ portal pressure Vasopressin

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What is the number two priority? Hemodynamic status  Vital signs  IV Therapy  Blood products Sclerotherapy: injection of a sclerosing agent to produce inflammation and scarring, shrinking the lumen of the vessel (clot & shrink). Ligation of varices: as effective as sclerosing, fewer side effects, more difficult during hemorrhage Balloon tampenade (Sengstaken-Blakemore tube): Controls hemorrhage by mechanical compression; Inserted by physician.  Gastric & esophageal tubes


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3 lumen: 2 for the balloons, 1 for gastric aspiration High risk of re-bleed after deflation May buy time for more effective therapy Nursing Actions: Check for integrity prior to insertion, assist MD in securing tube and traction, keep surgical scissors at bedside (for immediate deflation d/t respiratory distress) • Check patency of the balloons ○ Deflate q 8-12 hours • NG suction to prevent: ○ Aspiration pneumonia

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Encephalopathy – how? Digestion of blood ↑ammonia leading to encephalopathy

Shunt- transjugular intrahepatic portosystemic shunt (TIPS)

sodium and water retention. Medication management (d/c all nephrotoxic and hepatoxic drugs). Causes: Complication of hepatic failure.  – Patient Education Between systemic and portal venous systems to redirect blood blood jugular→sup. Massive GI bleeding. Esophageal and Gastric Varices. Hemocult stools (Look for blood). Transjugular Intrahepatic Portosystemic Shunt. or Idiopathic S/S: Oliguria. eat small frequent nutritionally balanced meals. GI Bleeding. don’t take meds that are not prescribed. May not have identified precipitating event./inf. ascites. hyponatemia. no EOTH. Malnutrition – – – – – – . takes meds as prescribed. Plasma volume expansion. Hepatic encephalopathy. Usually associated with advanced liver disease thus jaundice. Portal Hypertension. increased BUN. Hepatorenal syndrome: Advanced liver disease with functional renal failure with oliguria. PT/INR TX: Systemic vasoconstrictors. creatinine levels are present. Elevated urine osmolality. Vasoconstrictors. Liver transplant Nursing Care: Adequate assessment (IOs. low sodium diet (If retaining fluid). vena cava→heptatic vein→portal vein→stents placed ○ Adherence to dietary guidelines. GI bleeding can occur. Skin care and Protection from infection. Decreased urine sodium. hypotension and peripheral vasodilation – – – Usually associated with alcoholic cirrhosis or fulminant hepatitis Renal failure is NOT caused by renal disease but by systemic arterial vasodilation Usually due to sudden ↓ BP usually due to hemorrhage or liver failure. decreased urine osmolality and hypotension (> 100 mm Hg). monitor electrolytes). Complications: Ascites. include supplement drinks and multivitamin. Chemistry for LFTs. Daily weights. Excessive use of diuretics to treat ascites. Diagnostics: Elevated BUN+ Elevated Creatinine = Kidney failure. Serum ammonia level. Hepatitis panels.

– Due to hyperammonemia ○ Ammonia is a by product of amino acid catabolism ○ Ammonia is converted to urea by the liver and excreted in the kidneys ○ When blood is shunted. Hyperventilation. systemic ammonia levels rise ○ Ammonia is a powerful neurotoxin that crosses the blood brain barrier Clinical manifestations of ↑ ammonia: Lethargy → coma. Impaired judgment.Hepatic Encephalopathy: Neuropsychiatric disorder that results in an altered level of consciousness due to a build up of toxic chemicals in the brain from the normal flora of the gut. Hyperactive reflexes. Euphoria. Confusion. Irritability. nitrogenous substances and ammonia) that is produced Bowel cleansing Control GI bleed. reflexes. sensory and motor abnormalities. Apathy. Depression. + Babinski Clinical Manifestation of Impending Coma: Disorientation. Asterixis: jerking. remove blood from GI tract – Nursing Care: Assess neuro status frequently (Assess LOC. Insomnia. F&E (may have severe diarrhea with lactulose to aid in ammonia reduction. Agitation. Memory loss. rhythmic tremors. acid-base balance). Grimacing & grasping reflexes Managmement: Reduce ammonia ○ Protein restriction – – – ○ ○ ○ Lactulose & Neomycin: Lactulose and Neomycin sterilize the GI tract to reduce the amount of waste products (i. Slow. Emotional labiality. Hypothermia. deep respirations. Slow and slurred speech. Apraxia: inability to execute complex/coordinated movements. Administer medications as prescribed to reduce incidence. Hiccups.e. Yawning/drowsiness. motor coordination. or the liver is unable to handle the load. Notify MD of .

↑ liver enzymes. physical assessment. Patient states understanding of nutritional needs. Patient states understanding of abstinence from alcohol. liver enzymes. Fulminant liver failure: Encephalopathy occurs within eight weeks of the first symptoms. Avoid constipation (bacterial action in the bowel) and straining (rupture of hemorrhoids. Lots of fluids and high carb diet because liver is not storing or synthesizing glucose. ↑ PT. sulfa. INH. vital signs. Drugs (acetaminophen & ETOH. Encephalopathy. – – – – Causes: Viral hepatitis (HBV. – . HCV). other GI bleed). halothane. NSAIDs) Clinical Manifestations: jaundice.changes in ammonia levels. home care needs ○ Diagnosis: Impaired Cognition. HAV. and electrolyte abnormalities early. signs of bleeding. Alteration in Nutrition ○ Potential Complication: Bleeding Evaluation: Liver enzymes are stable. nutritional status. ↑ bilirubin TX: supportive care. liver transplant Nursing Care ○ Assessment: Neurological function.

600 new cases & 14.000 deaths ○ High percentage of patients have liver cirrhosis ○ Often associated with chronic liver diseases ○ Males – Metastatic carcinoma is more common .Liver Cancer – Primary liver cancer is rare ○ 16.

Worse when lying down. Most often middle-aged. ↑ Serum lipase & urinary amylase. Kaposi’s sarcoma – – PathoPhysiology: Auto digestion (Cellular injury activates enzyme action in the pancreas) ○ ○ Normally: trypsinogen → (enterokinase) →trypsin (in the intestines) Acute pancreatitis. Shock from hemorrhage into pancreas or toxemia Diagnostics: Serum amylase > 200. Position changes. May be life threatening – Common Causes: Alcoholism. Men > women. Trauma. Gall bladder disease. Abdominal tenderness & guarding. Dyspnea & crackles with pulmonary involvement. Hypotension. but causes spasm of the sphincter of Oddi) Antispasmodics: avoid atropine with paralytic ileus . (Trypsin activates other enzymes as well) S/S: Abdominal pain (Due to distention of the pancreas. Severe LUQ or epigastric. radiates to the back. Jaundice. Fever. Intravascular damage from Trypsin may cause: Grey Turner sign (ecchymoses on flank) and/ or Cullen’s sign (bluish periumbilical discoloration). Tachycardia. Duodenal ulcer. Nausea & vomiting. spinal flexion for relief. ↑ serum glucose. Aggravated by eating. ↑ LFTs. ↑ alk phosphatase. ↓ serum calcium. Unrelieved by vomiting. obstructed biliary tract). peritoneal irritation. Viral infection.Acute Pancreatitis: Acute inflammation of the pancreas. ileus. hyperlipidem Nursing and collaborative care: ○ – – ○ Relieve pain (Demerol or Dilaudid)   Demerol (meperedine HCl): less spasm of smooth muscle (Morphine has a longer half-life. Distention. trypsin is present in the pancreas. ↓ or absent bowel sounds. Leukocytosis.

pain. ↑temp. albumin Electrolyte balance: Ringers lactate CVP: Assessment of fluid status NG to suction. progress to j-tube. failure  Electrolyte status: ↓ chloride. oral care. no caffeine or alcohol  J-tube or TPN if deficits are severe Patient education Nursing Care:  Vital signs: ↓BP. dialysis Treat underlying process Nutrition  NPO to ↓ pancreatic secretion  ↑ carbohydrates (least stimulating to pancreas)  Limit fats & rich stimulating foods  Bland.○ Smooth muscle relaxers: Nitroglycerin. ↑ carbs Medications ○ Antacids (H2-receptor antagonists): Tagamet. then to bland. renal failure. blood glucose Collaborative Care: Glucose checks with sliding scale insulin. ↑RR → resp. calcium  Comfort measures: N&V. papaverine Prevent shock     ○ Vasoactive medications: Dopamine (Intropin) ↓ pancreatic secretions  NPO    Volume replacement: Plasma. Vitamin supplements (especially fat soluble) . • • Antispasmodics: Dicyclomine. TPN. potassium. sodium. restlessness. Pro-Banthine  ○ ○ ○ ○  ○ Assessments for complications: Paralytic ileus. mental status changes. dextran. Zantac Prevent infection  Prophylactic antibiotics: to prevent bacterial growth in necrotic pancreatic tissue Remove exudates: peritoneal lavage.

Gemcitabine . Chemotherapy: 5-FU.Pancreatic Cancer: Adenocarcinomas – S/S related to chronic pancreatitis – – Poor prognosis → Related to location of tumor TX: Whipple’s procedure. Radiation therapy.