NCM 116 PRELIMS

NCM 116 PRELIMS

Week 1: Care of Clients with Problems with Nutrition and Gastrointestinal System

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Functions of the Gastrointestinal (GI) System:

  1. Process food substances.

  2. Absorb the products of digestion into the blood.

  3. Excrete unabsorbed materials.

  4. Provide an environment for microorganisms to synthesize nutrients, such as Vitamin K.

Anatomy and Physiology of the Gastrointestinal (GI) System:

  • Mouth:

    • Contains lips, cheeks, palate, tongue, teeth, salivary glands, muscles, and maxillary bones.

    • Saliva contains the enzyme amylase (ptyalin), which aids in digestion.

  • Esophagus:

    • Collapsible muscular tube about 10 inches (25 cm) long.

    • Carries food from the pharynx to the stomach.

  • Stomach:

    • Contains cardia, fundus, and pylorus.

    • Mucous glands in the mucosa prevent autodigestion by providing an alkaline protective covering.

    • The lower esophageal (cardiac) sphincter prevents reflux of gastric contents into the esophagus.

    • The pyloric sphincter regulates the rate of stomach emptying into the small intestine.

    • Hydrochloric acid (HCl) kills microorganisms, breaks food into small particles, and provides a chemical environment that facilitates gastric enzyme activation.

    • Pepsin is the chief coenzyme of gastric juice, converting proteins into proteoses and peptones.

    • Intrinsic factor from parietal cells is necessary for the absorption of vitamin B12.

    • Gastrin controls gastric acidity.

  • Small Intestine:

    • Divided into three parts: duodenum, jejunum, and ileum.

    • Majority of the digestive process is completed in the duodenum; absorption occurs primarily in the small intestine.

    • Nutrient and water movement from the lumen of the small intestine into blood capillaries and lacteals in the villi occurs by active transport, osmosis, and diffusion.

  • Large Intestine:

    • Divided into cecum, colon, rectum, and anus; colon divided into ascending, transverse, descending, and sigmoid sections.

    • Absorbs water and eliminates wastes.

    • Intestinal bacteria play a vital role in synthesizing some B vitamins and vitamin K.

Risk Factors Associated with the Gastrointestinal System:

  • Allergic reactions to food or medications.

  • Cardiac, respiratory, and endocrine disorders leading to slowed GI movement or constipation.

  • Chronic alcohol use.

  • Chronic high stress levels.

  • Chronic laxative use.

  • Chronic use of aspirin or NSAIDs.

  • Diabetes mellitus predisposing to oral Candida infections or other GI disorders.

  • Family history of GI disorders.

  • Long-term GI conditions like ulcerative colitis, which may predispose to colorectal cancer.

  • Neurological disorders impairing movement, particularly with chewing and swallowing.

  • Previous abdominal surgery or trauma leading to adhesions.

  • Tobacco use.

Assessment of the Gastrointestinal System:

1. Health History

  • Questions about abdominal pain, dyspepsia, gas, nausea, vomiting, diarrhea, constipation, fecal incontinence, jaundice, and prior GI diseases.

2. Common Symptoms

  • Pain:

    • Abdominal pain varies based on the cause; affected by meals, activity, and defecation patterns.

  • Dyspepsia:

    • Upper abdominal discomfort related to eating, symptoms include bloating, fullness, and heartburn; common triggers include fatty or highly seasoned foods.

  • Intestinal Gas:

    • Results in belching or flatulence, often linked to food intolerance or gallbladder disease.

  • Nausea and Vomiting:

    • Caused by various factors (e.g., GI motility issues, CNS disorders, toxins); vomiting serves as a protective mechanism to expel harmful substances.

  • Bowel Habit Changes:

    • Diarrhea and constipation may indicate colonic dysfunction; stool characteristics (e.g., blood, mucus, color changes) can provide diagnostic clues.

3. Past Health, Family, and Social History

  • Includes oral hygiene, dental care, diet, alcohol and tobacco use, medication history, and previous GI procedures or surgeries. Nutritional status assessed through history and lab tests. Psychosocial and cultural factors also considered.

Physical Examination:

  • Pharynx:

    • Use a tongue blade for visualization; assess tonsils, uvula, and posterior pharynx for color, symmetry, and abnormalities.

  • Abdomen:

    • Positioning: Patient supine with slightly flexed knees.

    • Assessment Steps:

    • Inspection: Observe for skin changes, contour, symmetry, bulging, distension, or peristalsis.

    • Auscultation: Conduct before percussion and palpation.

    • Percussion: Evaluate organ size, masses, and presence of air or fluid (Tympani vs. dullness).

    • Palpation: Identify tenderness, resistance, or masses (light for surface, deep for organs).

Diagnostic Evaluation:

  1. GI Diagnostic Studies:

    • Confirm, rule out, stage, or diagnose various diseases including cancer; discuss the diagnosis with the patient and provide resource materials.

  2. Common Modalities:

    • Tests performed on an outpatient basis; preparation may involve clear liquid diet, fasting, bowel preparation, laxatives/enemas, and contrast agents.

  3. Serum Laboratory Studies:

    • Initial tests: CBC, metabolic panel, clotting times, liver function tests, etc.; specific tests like CEA (carcinoembryonic antigen), CA 19-9, and alpha-fetoprotein for colorectal and hepatocellular carcinomas.

  4. Stool Tests:

    • Examine consistency, color, and occult blood.

  5. Breath Tests:

    • Hydrogen breath test for carbohydrate absorption and bacterial overgrowth; urea breath test for H. pylori detection.

  6. Abdominal Imaging:

    • Ultrasound, MRI, CT scan.

  7. Endoscopic Procedures:

    • Endoscopy, proctoscopy.

Disturbances in Ingestion

1. Gastroesophageal Reflux Disease (GERD)

  • Defined as the backflow of gastric and duodenal contents into the esophagus.

  • Causes:

    • Incompetent lower esophageal sphincter (LES), pyloric stenosis, motility disorder.

  • Risk Factors:

    1. Nicotine

    2. High-fat foods

    3. Beta-adrenergic agents

    4. Xanthine derivatives (Theophylline, Caffeine)

    5. Ganglionic stimulants

    6. Elevated estrogen/progesterone levels

  • Key Pathophysiological Processes:

    1. LES Dysfunction: Transient relaxation or hypotension of the LES.

    2. Reflux Mechanisms: Flow of gastric contents into the esophagus.

    3. Mucosal Injury: Acid-induced damage and inflammation of the esophageal lining.

    4. Compensatory Mechanisms: Saliva and esophageal peristalsis attempt to neutralize and clear acid but may be overwhelmed.

  • Clinical Manifestations:

    1. Heartburn, epigastric pain

    2. Dyspepsia (indigestion)

    3. Nausea, regurgitation

    4. Pain and difficulty swallowing

    5. Hypersalivation

  • Factors contributing to LES dysfunction include:

    1. Transient LES Relaxations: Triggered by gastric distention or meals.

    2. Hypotension of the LES: Lower baseline pressure of the LES, reducing its barrier function.

    3. Hiatal Hernia: Part of the stomach pushes through the diaphragm disrupting LES function.

    4. Increased Intra-abdominal Pressure: Conditions like obesity, pregnancy can increase abdominal pressure.

Diagnostics:

  1. Upper GI Tract Study (Barium Swallow):

    • Examination of the upper GI tract under fluoroscopy after client drinks barium sulfate.

    • Pre-procedure: Withhold food and fluids for 8 hours prior.

    • Post-procedure:

    1. A laxative may be prescribed.

    2. Instruct client to increase oral fluid intake to help pass barium.

    3. Monitor stools for passage of barium (stools will appear chalky-white for 24-72 hours post-procedure).

Interventions:

  1. Instruct client to eat a low-fat diet, avoiding coffee, tobacco, beer, milk, peppermint, spearmint, and carbonated beverages.

  2. Avoid eating/drinking 2 hours before bedtime.

  3. Maintain normal body weight.

  4. Avoid tight-fitting clothes.

  5. Elevate head of the bed on 6 to 8 inches.

  6. Drugs:

    • H2 receptor antagonists

    • Proton pump inhibitors

    • Antacids

    • Prokinetic agents

    • Alginates

  7. Surgical Intervention:

    • Nissen fundoplication: Wrapping a portion of the gastric fundus around the sphincter area of the esophagus.

2. Achalasia

  • Absent or ineffective peristalsis of the distal esophagus; failure of the sphincter to relax in response to swallowing.

  • Most common in those over 40 years of age.

  • Clinical Manifestations:

    1. Difficulty swallowing (dysphagia)

    2. Sensation of food sticking in the lower esophagus

    3. Chest pain and heartburn

    4. Regurgitation to relieve discomfort

    5. Nocturnal Aspiration: Risk of aspiration pneumonia during sleep.

  • Pathophysiology:

    • Impaired relaxation of the LES due to loss of inhibitory neurons in the esophageal wall.

    • Loss of peristalsis leads to food stasis and progressive esophageal dilation.

Diagnostic Evaluation:

  1. Esophageal Manometry: Gold standard test; findings include increased LES resting pressure, incomplete LES relaxation, and absence of normal peristalsis.

  2. Barium Swallow (Esophagram): Classic "bird-beak" appearance: Dilated esophagus tapering to a narrow LES.

  3. Endoscopy: to exclude malignancy.

  4. Imaging: CT or endoscopic ultrasound may also be needed.

Interventions:

  1. Instruct client to eat slowly and drink fluids with meals.

  2. Temporary measures: Ca-channel blockers/nitrates for LES pressure relief.

  3. Botulinum Toxin Injection: Inhibits acetylcholine release causing relaxation; effective short-term.

  4. Endoscopic Management:

    • Pneumatic dilation.

    • Peroral Endoscopic Myotomy (POEM).

  5. Surgical Interventions:

    • Esophagomyotomy: Separation of esophageal muscle fibers to relieve lower esophageal stricture.

    • Heller Myotomy: Cutting of LES muscle for easier food passage.

3. Hiatal Hernia (Diaphragmatic Hernia)

  • Opening in the diaphragm where the esophagus passes becomes enlarged, allowing part of the upper stomach into the thorax.

  • Types:

    • Sliding (Type I): Protrusion of the esophagogastric junction into the thoracic cavity.

    • Paraesophageal (Type II): Protrusion of a portion of the stomach alongside the esophagus.

  • Clinical Manifestations:

    1. Heartburn

    2. Dysphagia

    3. Sense of fullness or chest pain after eating (paraesophageal)

    4. Abdominal pain, nausea, and vomiting.

Diagnosis:

  1. Barium Swallow Study: Visualizes the herniated portion.

  2. Upper Endoscopy (EGD): Visualizes esophagus and stomach for inflammation, ulcers, or herniation.

  3. Esophageal Manometry: Measures motility and sphincter function.

  4. 24-Hour pH Monitoring: Assesses acid reflux severity.

Interventions:

  1. Relieve pain with antacids.

  2. Client should remain upright before and after eating for 1-2 hours.

  3. Small frequent feedings to avoid gastric distention.

  4. Instruct client to eat slowly and chew food thoroughly.

  5. Avoid foods and drinks that decrease LES pressure (high-fat, carbonated beverages).

  6. Drugs:

    • Antacids, antiemetics, H2 antagonists, prokinetic agents, proton-pump inhibitors.

  7. Surgical Treatment:

    • Indicated for severe symptoms or complications.

    • Types:

    1. Nissen Fundoplication

    2. Paraesophageal Hernia Repair

    3. Mesh Reinforcement to prevent recurrence.

Disturbances in Digestion

1. Peptic Ulcer Disease (PUD)

  • May refer to gastric, duodenal, or esophageal ulcer based on location.

  • Defined as an excavation in the mucosal wall of the stomach, pylorus, duodenum, or esophagus.

  • Occurs mainly in individuals aged 40-60; prevalence decreased due to proton pump inhibitors but remains significant.

  • Predisposing Factors:

    1. Stress

    2. Smoking

    3. NSAIDs, alcohol, corticosteroids

    4. History of gastritis

    5. Family history of gastric ulcers

    6. H. pylori infection

  • Complications: Hemorrhage, perforation, pyloric obstruction.

Pathophysiology:

  1. Protective Mechanisms: Mucosal barrier, bicarbonate secretion, adequate blood flow.

  2. Aggressive Factors: Gastric acid, pepsin, H. pylori infection, NSAID use.

  3. Mechanism of Ulceration: Imbalance leads to mucosal erosion and ulcer formation.

Clinical Manifestations:

  • Duodenal Ulcer:

    • Age: 30-60; Male: Female = 2-3:1; Hypersecretion of HCl.

    • Symptoms: Pain occurs 2-3 hours after a meal, often awakens at night; relieved by food; less likely to hemorrhage.

  • Gastric Ulcer:

    • Age: Usually 50 and over; Male: Female = 1:1; Normal to hyposecretion of HCl.

    • Symptoms: Pain occurs 1/2 to 1 hour after a meal; vomiting common; hemorrhage more likely than duodenal ulcer.

  • Diagnostics:

    1. Barium swallow.

    2. Endoscopy (Esophagogastroduodenoscopy).

    • Tissue specimens can be obtained.

Interventions:

  1. Relieve pain with antacids as prescribed.

  2. Encourage Healthy Lifestyle:

    • Avoid: Fatty foods, coffee, spices, alcohol, large quantities of milk.

    • Quit smoking.

  3. Medication Overview:

    • Antacids: Neutralize HCl (e.g., aluminum hydroxide, calcium carbonate).

    • H2 Receptor Antagonists: Reduce HCl secretion (e.g., ranitidine, famotidine).

    • Cytoprotective Drug: Coats ulcers and enhances prostaglandin synthesis (Carafate).

    • Prostaglandin Analogue: Suppresses acid secretion (Cytotec).

    • Proton-pump Inhibitors: Suppress gastric acid secretion (e.g., omeprazole).

    • Anticholinergics: Reduce gastric motility and HCl secretion (e.g., atropine).

    • H. pylori Treatment: Use of antimicrobials (e.g., amoxicillin, clarithromycin).

Surgical Interventions:

  1. Vagotomy: Severing vagus nerve to decrease gastric acid.

  2. Pyloroplasty: Enlarges outlet and relaxes muscle.

  3. Billroth I: Removes lower stomach portion, anastomoses to duodenum.

  4. Billroth II: Anterior anastomosis to jejunum; issues with dumping syndrome possible.

Post-operative Interventions:

  1. Monitor vital signs.

  2. Place in Fowler’s position.

  3. Administer IV fluids for hydration.

  4. Maintain NPO until peristalsis returns and progress diet as prescribed.

  5. Monitor for postoperative complications: hemorrhage, dumping syndrome, diarrhea, hypoglycemia, vitamin B12 deficiency.

2. Gastritis

  • Inflammation of the gastric mucosa; can be acute or chronic.

  • Acute Gastritis Causes:

    • Contaminated food, irritating foods, NSAIDs, alcohol, bile reflux, radiation.

    • Clinical Manifestations:

    1. Abdominal discomfort

    2. Nausea, vomiting

    3. Headache, hiccups, reflux

  • Chronic Gastritis Causes:

    • Resulting from benign ulcers, H. pylori, autoimmune diseases, dietary factors.

    • Clinical Manifestations:

    1. Anorexia, nausea, belching

    2. Heartburn after eating, sour taste in mouth, vitamin B12 deficiency.

Diagnostics:

  1. Upper GI x-ray, endoscopy, histologic examination of tissue specimen.

Interventions:

  1. Acute Gastritis Management:

    • Refrain from food/alcohol until symptoms subside; when tolerating, recommend non-irritating diet.

  2. Chronic Gastritis Management:

    • Modify diet, promote rest, reduce stress, avoid irritants; may treat H. pylori with drug combinations.

  3. Monitor for hemorrhagic gastritis and hypotension.

3. Peritonitis

  • Inflammation of the peritoneum, often caused by gastrointestinal conditions.

  • Common Causes: Ruptured appendicitis, perforated PUD, diverticulitis.

Clinical Manifestations:

  1. Diffuse pain becoming localized.

  2. Abdominal tenderness and rigidity.

  3. Nausea, vomiting, diminished peristalsis.

  4. Signs of early shock.

Diagnostics:

  1. Elevated WBC, abdominal x-ray, ultrasound, CT scan, peritoneal aspiration/culture.

Interventions:

  1. Monitor vital signs and intake/output.

  2. Insert NG tube.

  3. Client side position with knees flexed.

  4. Deep breathing exercises to prevent complications.

  5. Peritoneal lavage with warm saline.

  6. Insert drainage tubes for exudates removal.

  7. Fluids and antibiotics as needed.

  8. Administer Total Parenteral Nutrition (TPN) as ordered.

Disturbances in Absorption and Intestinal Motility

1. Inflammatory Bowel Disease (IBD)

  • Refers to chronic GI inflammatory disorders: Crohn’s disease and ulcerative colitis. Cause unknown, theories suggest environmental triggers.

Pathophysiology:

  1. Immune dysregulation leads to chronic inflammation.

  2. Crohn’s Disease: Affects any GI tract part, involves all bowel wall layers (transmural); commonly ileum and colon.

  3. Ulcerative Colitis: Confined to the colon/rectum, affects mucosal/submucosal layers.

Comparative Differences:

  • Characteristics of IBD:

    • Crohn's Disease:

      • Course: Prolonged, variable with exacerbations/remissions.

      • Pathology: Early with transmural thickening and deep granulomas.

    • Ulcerative Colitis:

      • Course: Exacerbations/remissions.

      • Pathology: Mucosal ulceration with minute lesions.

Diagnostic Studies:

  1. Barium series, sigmoidoscopy, colonoscopy.

Interventions:

  1. Various drug therapies (antibiotics, corticosteroids).

  2. Surgical indications (refractory disease, toxic megacolon). Total colectomy may be curative.

2. Diverticulosis and Diverticulitis

  • Diverticulum: Saclike herniation of bowel lining.

  • Diverticulosis: Presence of multiple diverticula without symptoms.

  • Diverticulitis: Infection/inflammation in diverticula leads to symptoms.

Pathophysiology:

  • Diverticulosis: Weakness in bowel wall forms diverticula, often asymptomatic.

  • Diverticulitis: Infection due to trapped fecal matter leads to complications.

Clinical Manifestations:

  1. Bowel irregularity, cramps, narrow stools, abdominal pain in left lower quadrant, fever.

Diagnostics:

  1. CT scan with contrast for diverticulitis.

Interventions:

  1. Bed rest, NPO or clear liquids during acute phase.

  2. Gradual reintroduction of fiber-containing diet.

  3. Monitor for perforation and other complications.

3. Malabsorption Syndrome

  • Inability to absorb major vitamins and nutrients; conditions causing malabsorption include mucosal, infectious diseases and luminal disorders.

Pathophysiology:

  • Normal Absorption Process: Occurs mainly in the small intestine with the help of enzymes and bile acids.

Clinical Manifestations:

  1. Diarrhea, bulky foul-smelling stools (steatorrhea), abdominal pain, weakness.

  2. Vitamins and minerals deficiencies (e.g., easy bruising, anemia, osteoporosis).

Diagnostics:

  1. History and physical exams, laboratory tests (CBC, serum vitamin/mineral levels).

  2. Imaging studies (abdominal ultrasound, CT), endoscopic procedures.

Interventions:

  1. Avoid dietary substances that worsen malabsorption; supplement lost nutrients.

  2. Manage primary causes medically or surgically.

4. Intussusception

  • Telescoping of one bowel portion into another leading to obstruction and ischemia.

Pathophysiology:

  • Compression of blood vessels leading to potential necrosis.

Clinical Manifestations:

  1. Currant jelly stools, colicky pain, tender abdomen.

Interventions:

  1. Monitor for shock/perforation.

  2. Hydrostatic reduction using barium enema; IV fluids and NGT decompression as needed.

  3. Surgery if non-surgical methods fail.

5. Hirschsprung’s Disease (Aganglionic Megacolon)

  • Congenital condition with the absence of ganglionic innervation in the bowel, typically the sigmoid colon.

Pathophysiology:

  • Absence of nerve cells leads to functional obstruction and proximal bowel dilation.

Clinical Manifestations:

  1. Chronic constipation and abnormal bowel patterns (ribbon-like stools).

Diagnostics:

  1. Clinical history, imaging (X-ray, contrast enema), definitive testing via rectal biopsy.

Interventions:

  • Surgical Intervention: Pull-through procedure to remove aganglionic segment, possibly with temporary ostomy.

Disturbances in Elimination

1. Hemorrhoids

  • Dilated veins of the anal canal; internal, external, or prolapsed.

Pathophysiology:

  • Caused by portal hypertension, irritation, and increased vascular pressure.

Clinical Manifestations:

  1. Constipation, anal pain, bleeding with defecation, itchiness.

Interventions:

  1. Cold packs, sitz baths, topical anesthetics as prescribed.

  2. High-fiber diet, fluids to promote movement without straining.

  3. Surgical options: hemorrhoidectomy, sclerotherapy, band ligation, circular stapling.