AACN PCCN Review. Gastrointestinal
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1 AACN PCCN Review Gastrointestinal Presenter: Carol A. Rauen, RN, MS, CCNS, CCRN, PCCN, CEN Independent Clinical Nurse Specialist & Education Consultant
2 Gastrointestinal I. INTRODUCTION PCCN Test Plan Endocrine, Heme, GI, & Renal: 18% a. Functional GI Disorders (e.g., obstruction, ileus, diabetic gastroparesis, gastroesophageal reflux, irritable bowel syndrome) b. GI Bleed Lower Upper c. GI Infections d. Hepatic Failure e. Ischemic Bowel f. Malnutrition (e.g., failure to thrive, malabsorption disorders) g. Pancreatitis Structures/Function/Digestion a. Mouth b. Esophagus c. Stomach d. Small Intestine e. Pancreas f. Gallbladder g. Liver h. Spleen i. Portal Circulation j. Mesentery Circulation k. Large Intestine l. Digestive Hormones m. Digestive Enzymes Assessment a. Inspection b. Auscultation c. Palpation d. Percussion 1
3 II. THE HEPATIC SYSTEM Liver Function a. Metabolic Factory & Waste Disposal Plant b. Carbohydrate, Fat & Protein Metabolism c. Production of Bile Salts d. Production of Clotting Factors e. Bilirubin Metabolism f. Detoxification: Nutrients, Drugs, Toxins, Bacteria, Everything g. Vitamin & Mineral Storage: h. Blood Reservoir: 10% of Total Blood Volume Liver Function Tests Test Serum Proteins Serum Ammonia Bilirubin Coagulation Studies Hepatic Enzymes Liver Function Tests Results Total Protein: g/dl Serum Albumin: g/dl Serum Globulins: g/dL Pre-Albumin: mg/dl mcg/dl Total Bilirubin: mg/dl Unconjugated Bilirubin: mg/dl Conjugated Bilirubin: mg/dl Indirectly reflect liver function o PT o PTT o INR o Bleeding Time o ACT ALP: U/L GGT o Men: 0 85 U/L o Women: 0-70 U/L AST o Men: U/L o Women: 13-35U/L ALT o Men: 10-55U/L o Women: 7-30U/L 2
4 Liver Dysfunction & Failure Pathophysiology a. Liver Tissue (cells) are Destroyed and Replaced with Fibrotic Tissue b. Functions are Altered c. Organ Changes Shape d. Vascular Flow is Obstructed e. Portal Hypertension Cirrhosis A chronic progressive liver disease where diffuse fibrotic bands of connective tissue, distort the liver s normal architecture and functional ability. The liver loses its ability to regulate fluids, metabolize waste, regulate coagulation and nutrition. a. Causes Alcoholic, Laennec's Portal, or Fatty Post Necrotic: Toxic, Nodular, or Post Hepatic Biliary: Cholangitic or Obstructive Hepatitis Widespread Inflammation of Liver Cells a. Causes Primary Viral Most Common Hepatotoxins - Toxic or Drugs Secondary Viral, Low Mortality Clinical Presentation of Liver Dysfunction Hepatic Encephalopathy The liver is unable to perform its detoxification function and toxins build up. Primarily ammonia causing altered LOC, behavior and motor abilities. Confusion Coma Agitation Unsafe Behavior Asterixis: Flap like Tremor of Hands Apraxia: Inability to Perform Purposeful Acts Elevated Ammonia Limit Protein Intake Limit Hepatotoxic Drugs Lactulose & Neomycin Safe Environment 3
5 Malnutrition The liver is unable to perform its function of carbohydrate, protein and fat metabolism. This leads to malnutrition Need to tx the Cause of Liver Failure Parenteral Nutrition Limit Protein Intake Restrict Fluids Coagulopathy The liver is unable to synthesize fibrinogen, prothrombin and factors V, VII, IX, X, XI, XIII, fibrinolytic factors and Vit. K. These are needed to maintain the ability to clot. Platelet aggregation and adhesion are also effected by liver dysfunction. Bleeding Tendencies Nonspecific Bleeding Monitor Coagulation Studies & Platelet Ct Decrease Bleeding and Bruising Risk Administer Blood Products Portal Hypertension Increased pressure in the portal vein occurs secondary to flow obstruction from inflammation, bands, or fibrotic hepatic tissue. This retrograde pressure leads to formation of varices in the esophagus, stomach and rectal vault. Caput Medusae: dilated cutaneous veins radiating from the umbilical Spider angiomas commonly seen in Cirrhosis Upper GI Bleeding Surgical Shunting TIPSS - Transjugular Intrahepatic Portosytemic Stent Shunt Treat Bleeding Treat Cause Hepatorenal Syndrome A form of pre-renal failure caused by the liver dysfunction. Mortality of liver failure is very high once renal failure develops. S&S of Renal Dysfunction 4
6 Maintain Adequate Renal Perfusion Restrict Fluids Restrict Nephrotoxic Agents Continuous Renal Replacement Therapies Ascites Fluid accumulation in the peritoneal space secondary to decreased production of albumin, decreased systemic oncotic pressure, increased hepatic lymph production and increased capillary permeability. The fluid accumulation impacts the respiratory (diaphragm) and cardiac (hemodynamic) systems primarily as well as comfort and body image. Inc. Abdominal Girth Hypotension and Tachycardia Dyspnea, Orthopnea, Tachypnea S&S of Dehydration N&V Restrict PO Fluid Diuretics (if tolerated hemodynamically) Restrict Na Respiratory Support Paracentesis Peritoneovenous Shunt Surgery Infection One of the functions of the liver cells (Kuppfer cells) is to clean the blood of bacteria. With liver failure this function is not provided and bacteria builds up (primarily gram negative bugs) in the systemic circulation increasing the risk of infection. Poor Wound Healing Increased Risk of Infection Heightened Prevention Measures Abx Therapy w Caution 5
7 III. THE PANCREAS Function a. Endocrine Functions Synthesis & Release of Hormones: o Glycogen o Insulin o Gastrin b. Exocrine Functions Pancreatic Enzymes Break Down Protein, Starch & Fat. > 2L/day Bicarbonate Raise ph c. PNS, Gastrin & Hormones Regulate Secretions Pancreatic Enzymes a. Trypsin: Aids in Protein Digestion b. Amylase: Aids in Carbohydrate Digestion c. Lipase: Aids in Fat Digestion Acute Pancreatitis Pathophysiology a. Auto Digestion Tissue Damage Fat Necrosis Vascular Damage & Hemorrhage Increased Capillary Permeability Hypotension b. Forms/Types Edematous Hemorrhagic c. Classifications Acute Pancreatitis Recurrent Acute Recurrent Chronic Chronic Pancreatitis Cause (blocked enzyme release) a. Alcoholism b. Biliary Stones c. Hyperlipidemia d. Abd Trauma e. Infection (bacterial or viral) 6
8 f. Shock g. Drugs (Most Common: Cyclosporine, Acetaminophen, Cimetidine, Steroids, Salicylates, Furosemide, Thiazides, Estrogens) Clinical Presentation a. Pain b. Low Grade Fever c. N&V d. Distended/Tender/Rigid Abd e. Guarding with Rebound Tenderness f. Jaundice g. Hypoactive Bowel Sounds h. Steatorrhea: bulky, pale, foul-smelling stools i.? Ascites j. Hypovolemic Shock k. In Necrotizing Pancreatitis Cullen s Sign: o Bluish Discoloration Umbilical Grey Turner s Sign: o Bluish Discoloration Flanks Labs Underlined labs are the MOST diagnostic a. Hypocalcemia (classic sign) b. Low Ca, Mg, K c. Hyperglycemia d. Hyperbilirubinemia e. Hypertriglyceridemia f. Increased BUN & Creatinine g. Elevated Amylase h. Elevated Lipase i. Elevated LFTs j. Elevated WBC k. Decreased H/H l.? Increased H/H Treatment Options a. Fluid Resuscitation b. Rest the Pancreas: NPO, NGT c. Pain Management d. Monitor & Replace Electrolytes e. Tx Multisystem f. Nutritional Support g. Surgery 7
9 IV. ACUTE GI HEMORRHAGE Lower GI Bleeding Not Typically Life Threatening a. Causes Diverticulitis Angiodysplasia Cancer Hemorrhoids Inflammatory Bowel Disease (Ulcerative Colitis; Crohn's Disease) Bowel Infarction Upper GI Bleeding a. Causes Peptic Ulcer Disease: Duodenal, Gastric and Stomal ulcers account for 50% bleeding episodes Gastritis or Esophagitis Esophageal Varices Mallory -Weiss Syndrome b. Clinical Presentation Hematemesis Melena PUD Distended & Tender Abd Hyperactive Bowel Sounds Hypovolemia Shock c. Assessment H & H Coags & Platelets Hemoconcentration Elevated BUN LFTs Endoscopy Angiography Raionuclide Scans d. Treatment NG Decompression/Lavage Room Temp vs Iced Fluid Resuscitation Blood Product Admin Endoscopic Sclerotherapy 8
10 Pharmacology Surgery o Vagotomy and Pyloroplasty o Oversew Ulcer or Tear o Total and Subtotal Gastric Resection o Billroth I: Vagotomy, Antrectomy, Anastomosis Stomach and Duodenum o Billroth II: Vagotomy, Antrectomy, Anastomosis Stomach and Jejunum o Whipple: Removal of the Distal 3 rd of Stomach, Entire Duodenum, Head of Pancreas, Gastrojejunotomy o Colon Resection Bleeding Esophageal Varices o TIPSS: Transjugular Intrahepatic Portosytemic Stent Shunt o Beta Blocker Decreases Pressure o Portal Caval Shunt V. DISORDERS OF THE BOWEL Bowel Infarction a. Etiology Embolic or Thrombotic Occlusion Typically from the Superior Mesenteric Artery b. Clinical Presentation Severe Epigastric Pain Rebound Tenderness Guarding & Rigidity Stimulated Sympathetic Response from Pain c. Treatment Options Angiography to Identify/Confirm Occlusion Surgery to Remove Occlusion & Dead Bowel Bowel Obstruction a. Etiology Internal Lumen Obstruction ex. Tumor External Lumen Obstruction ex. Adhesions Emboli: no blood flow Paralytic Ileus 9
11 b. Clinical Presentation Complete vs Partial Distended Edematous Bowel Fluid and Electrolytes Leaking from Bowel Elevated WBC Fever Small Intestine o Acute Pain w Sudden Onset o N & V (movement on both ends) o Wave-Like Hyperactive High Pitched Bowel Sounds o May Have Some Gas or Feces o Distention (mild) Large Intestine o Slow Onset Pain Progression Mild Severe, Lower Abd o No N & V (nothing moving) o No Stool o Low Pitched Bowel Sounds o Distention (large amount) Treatment Options o Diagnosis Obstruction by Hx, X-Ray, CT, Upper or Lower Barium Radiology Tests o Pain Management o IV Fluids o Decompress w NG, Rectal or Intestinal Tube o Abx o NPO and Time (rest the bowel) o Surgery Perforation/Peritonitis a. Etiology Gastric/Intestinal Contents Leak into Peritoneal Cavity Ulcer Perforation Diverticular Rupture Trauma Bowel Infarction b. Clinical Presentation Infection/Sepsis (all the S&S) Sudden Onset of Severe Pain Rigid Abdomen w Rebound Tenderness Hypoactive Bowel Sounds No Bowel Sounds 10
12 c. Treatment Options Surgery to Repair Cause & Clean Up ABX Fluids Tx of Sepsis Tx of MODS Functional GI Disorders a. Ileus b. Diabetic Gastroparesis c. Gastroesophageal Reflux d. Irritable Bowel Syndrome 11
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