Section 9.1: Nutrition, Gastrointestinal, and Metabolic/Endocrine Disorders

Gastrointestinal Disorders

Gastrointestinal (GI) and metabolic/endocrine disorders are major testing areas in the Philippine Nurse Licensure Examination (PNLE), reflecting the high prevalence of these conditions in clinical practice and the critical need for safe nursing judgment under the Philippine Nursing Act of 2002 (RA 9173).

Gastroesophageal Reflux Disease (GERD)

Gastroesophageal Reflux Disease (GERD) is a chronic digestive disease occurring when stomach acid or, occasionally, bile flows back into the food pipe (esophagus). The reflux irritates the lining of the esophagus, causing inflammation (esophagitis).

• Pathophysiology & LES Dysfunction: The primary pathophysiologic defect is the transient or permanent incompetence of the Lower Esophageal Sphincter (LES). Under normal conditions, the LES acts as a high-pressure barrier preventing gastric contents from refluxing. Factors that decrease LES pressure include obesity, pregnancy, hiatal hernia, smoking, alcohol, and certain medications (e.g., calcium channel blockers, anticholinergics).
• Clinical Manifestations: Key features include pyrosis (heartburn, burning sensation behind the sternum), dyspepsia (indigestion), regurgitation of sour or bitter liquid, hypersalivation (water brash), and dysphagia.
• Dietary and Lifestyle Modifications:
  • Meal Patterns: Instruct the client to consume small, frequent meals rather than large, heavy meals to prevent gastric distension and subsequent LES relaxation.
  • Offending Foods: Counsel the patient to avoid substances that lower LES tone or directly irritate the esophageal mucosa: caffeine (coffee, tea, sodas), chocolate, peppermint/spearmint, alcohol, nicotine, spicy foods, acidic foods (citrus fruits, tomatoes), and high-fat items.
  • Meal Timing: Advise the patient to avoid lying down or sleeping for at least 2 to 3 hours after a meal to utilize gravity in keeping gastric contents in the stomach.
• Pharmacotherapy:
  1. Antacids: Neutralize gastric acid quickly (e.g., aluminum hydroxide, magnesium hydroxide). Take 1–3 hours after meals and at bedtime.
  2. Histamine-2 (H2) Receptor Antagonists: Reduce acid secretion by blocking H2 receptors on parietal cells (e.g., famotidine, ranitidine). Take 30–60 minutes before meals.
  3. Proton Pump Inhibitors (PPIs): Most potent acid suppressors that block the $H^+/K^+$ ATPase pump (e.g., omeprazole, pantoprazole, esomeprazole). Must be taken 30 minutes before the first meal of the day on an empty stomach.
• Positioning: Instruct the client to elevate the head of the bed (HOB) by 6 to 8 inches (15 to 20 cm) using blocks under the bedposts rather than stacking pillows, which can bend the torso and increase intra-abdominal pressure.

Peptic Ulcer Disease (PUD)

Peptic Ulcer Disease involves ulcerations in the mucosal wall of the stomach (gastric ulcers) or the duodenum (duodenal ulcers).

• Etiology: The primary causative agents are Helicobacter pylori infection (a Gram-negative bacterium that colonizes the gastric mucosa) and chronic use of Nonsteroidal Anti-inflammatory Drugs (NSAIDs), which inhibit cyclooxygenase (COX-1) enzymes, thereby depleting protective prostaglandins that maintain the mucosal barrier.
• Clinical Comparison:

• Pharmacological Management:
  • H. pylori Eradication: Typically requires triple therapy (a PPI plus two antibiotics like clarithromycin and amoxicillin or metronidazole) for 10–14 days, or quadruple therapy (adding bismuth subsalicylate).
  • Mucosal Protectors: Sucralfate (creates a physical barrier over the ulcer crater; must be taken on an empty stomach 1 hour before meals and at bedtime).
• Critical Complications:
  • Perforation: The most lethal complication. Gastric or duodenal contents spill into the sterile peritoneal cavity, causing chemical and bacterial peritonitis.
    • Clinical Presentation: Sudden, severe, sharp, and excruciating epigastric pain that rapidly radiates across the entire abdomen. The patient exhibits a rigid, board-like abdomen, severe abdominal guarding, hyperactive followed by absent bowel sounds, tachypnea, tachycardia, and signs of septic/hypovolemic shock.
    • Nursing Interventions: Immediately make the patient NPO (Nothing by Mouth). Insert a nasogastric tube (NGT) to low intermittent suction to decompress the stomach and prevent further spillage. Establish large-bore IV access and administer prescribed IV fluids and broad-spectrum antibiotics. Monitor vital signs closely and prepare the client for emergency surgical intervention (laparotomy or Graham patch).

Viral Hepatitis

Hepatitis is a systemic viral infection causing widespread inflammation and necrosis of hepatic cells.

• Clinical Phases of Acute Hepatitis:
  1. Pre-icteric (Prodromal) Phase: Lasts 1 to 21 days. Highly infectious. Characterized by flu-like symptoms: severe fatigue, anorexia, nausea, vomiting, right upper quadrant (RUQ) discomfort, joint pain, and mild fever.
  2. Icteric Phase: Lasts 2 to 6 weeks. Characterized by jaundice (yellowing of sclera and skin due to bilirubin accumulation), dark (tea-colored) urine (excess bilirubin excreted by kidneys), clay-colored (acholic) stools (lack of bile flowing into the duodenum), and severe pruritus (deposition of bile salts under the skin). The liver is tender and enlarged.
  3. Post-icteric (Convalescent) Phase: Lasts weeks to months. Jaundice resolves, energy levels gradually return, and liver enzymes (alanine aminotransferase [ALT] and aspartate aminotransferase [AST]) decline toward baseline.
• Nursing Care: Promote physical rest to decrease metabolic demands on the liver. Provide a high-carbohydrate, moderate-protein, low-fat diet. Offer small, frequent meals as nausea is worse in the afternoon. Avoid hepatotoxic drugs (e.g., acetaminophen) and alcohol. Teach personal hygiene and avoid sharing personal items.

Liver Cirrhosis and Portal Hypertension

Cirrhosis is the end-stage of chronic liver disease, characterized by widespread destruction of hepatocytes, nodular regeneration, and fibrotic scarring that destroys normal liver architecture.

• Portal Hypertension: Fibrotic tissue blocks the venous flow of blood through the liver, increasing pressure in the portal venous system. This leads to splenomegaly, ascites, and collateral circulation pathways (esophageal and gastric varices, caput medusae).
• Ascites: The accumulation of serous fluid in the peritoneal cavity. It is caused by:
  1. Portal hypertension: Forces fluid out of capillary beds into the abdomen.
  2. Hypoalbuminemia: Impaired hepatic synthesis of albumin decreases intravascular oncotic pressure, causing fluid shift into the interstitium.
  3. Hyperaldosteronism: Failed hepatic clearance of aldosterone leads to excessive renal sodium and water retention.
  • Nursing Care: Assess abdominal girth daily at the level of the umbilicus, obtain daily weights, and restrict sodium and fluids. Position the client in semi-Fowler's or high-Fowler's to relieve dyspnea. Administer potassium-sparing diuretics (spironolactone) and loop diuretics (furosemide).
  • Paracentesis Support: Ensure the client voids completely before the procedure to prevent accidental needle puncture of the bladder. Position the patient upright at the edge of the bed. Monitor blood pressure and heart rate closely during and after the procedure for signs of hypovolemic shock (due to rapid fluid shift).
• Esophageal Varices: Fragile, thin-walled, distended veins in the lower esophagus. They are prone to rupture under high pressure, causing massive, life-threatening upper GI hemorrhage.
  • Nursing Care: Teach patients to avoid activities that increase portal pressure: coughing, sneezing, straining at stool (administer stool softeners), and vomiting. Avoid rough, dry, or poorly chewed food.
  • Emergency Interventions: Administer IV octreotide or vasopressin to induce splanchnic vasoconstriction and decrease portal pressure. Prepare for emergency endoscopy for band ligation or sclerotherapy. In cases of uncontrolled bleeding, assist with the insertion of a Sengstaken-Blakemore tube. This triple-lumen tube has a gastric balloon, an esophageal balloon, and a gastric suction port.
    • CRITICAL SAFETY WARNING: Always keep a pair of scissors at the bedside. If the patient develops respiratory distress or airway obstruction (which can happen if the gastric balloon ruptures and the esophageal balloon migrates upward), the nurse must immediately cut all three tubes to deflate the balloons and remove the tube.
• Hepatic Encephalopathy: A neuropsychiatric complication of advanced liver disease. It is caused by the liver's inability to convert toxic ammonia ($NH_3$)—a byproduct of protein digestion by intestinal bacteria—into urea for renal excretion. High serum ammonia levels cross the blood-brain barrier, causing cerebral edema and neurological dysfunction.
  • Clinical Manifestations: Altered mental status, confusion, drowsiness, sleep-wake reversal, asterixis (a flapping tremor of the hands when wrists are hyperextended), and fetor hepaticus (a sweet, musty, fecal odor of the breath).
  • Pharmacological Management:
    • Lactulose: The cornerstone of treatment. Lactulose is a synthetic disaccharide that is broken down by colonic bacteria into organic acids. This lowers colonic pH, converting ammonia ($NH_3$) into ammonium ($NH_4^+$), which is polar and cannot be absorbed. The ammonium is trapped in the colon and expelled.
    • Therapeutic Goal: Titrate lactulose to achieve 2 to 3 soft, loose stools per day. Monitor for side effects: dehydration, hypokalemia, and diarrhea.
    • Neomycin / Rifaximin: Non-absorbable antibiotics administered to reduce the bacterial population in the bowel, thereby decreasing ammonia production.

Appendicitis

Appendicitis is the acute inflammation of the vermiform appendix, typically caused by obstruction of the appendiceal lumen by a fecalith (hardened stool), foreign body, lymphoid hyperplasia, or parasites.

• Clinical Presentation:
  • Vague periumbilical pain that shifts over 12–24 hours to the right lower quadrant (RLQ), localizing at McBurney's Point (located midway between the anterior superior iliac spine and the umbilicus).
  • Rebound Tenderness: Pain elicited upon the sudden release of pressure applied to the abdomen.
  • Rovsing's Sign: Palpation of the left lower quadrant (LLQ) causes referred pain in the right lower quadrant (RLQ), indicating peritoneal irritation.
  • Psoas Sign: Pain elicited by extending the patient's right hip, indicating irritation of the psoas muscle.
  • Obturator Sign: Pain elicited by flexing and internally rotating the patient's right hip.
  • Low-grade fever, anorexia, nausea, and vomiting.
• Pre-operative Nursing Care:
  1. Keep the patient strictly NPO to prepare for emergency surgery.
  2. Start IV fluids as prescribed to maintain hydration and electrolyte balance.
  3. DO NOT apply heat to the abdomen (e.g., heating pads), as heat increases blood flow, promotes inflammation, and significantly increases the risk of appendix rupture.
  4. DO NOT administer laxatives or enemas, as these increase bowel motility and intraluminal pressure, which can precipitate rupture.
  5. An ice pack can be applied to the RLQ to help reduce inflammation.
  6. Avoid administering strong analgesics before diagnosis, as they can mask symptoms of rupture.
  7. Complication Warning: If the patient reports a sudden, complete cessation of abdominal pain, this is an ominous sign indicating that the appendix has ruptured. This is a medical emergency that leads to peritonitis. The nurse must immediately notify the physician, keep the patient NPO, and prepare for emergency appendectomy.

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Endocrine and Metabolic Disorders

Diabetes Mellitus (DM)

Diabetes Mellitus is a chronic, multi-system metabolic disorder characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both.

• Pathophysiology:
  • Type 1 DM: Characterized by autoimmune destruction of pancreatic beta cells, leading to an absolute deficiency of insulin. These patients are dependent on exogenous insulin for survival and are highly susceptible to Diabetic Ketoacidosis (DKA).
  • Type 2 DM: Characterized by insulin resistance (target tissues fail to respond effectively to insulin) and a relative insulin secretory defect. It is strongly linked to obesity, physical inactivity, and genetics.
• Diagnostic Criteria:
  • Glycosylated Hemoglobin (HbA1c) $\ge 6.5%$ (reflects average blood glucose over the past 120 days).
  • Fasting Blood Sugar (FBS) $\ge 126 ext{ mg/dL}$ (no caloric intake for at least 8 hours).
  • Random Blood Sugar $\ge 200 ext{ mg/dL}$ accompanied by the classic symptoms of hyperglycemia: polyuria (excessive urination), polydipsia (excessive thirst), and polyphagia (excessive hunger).
• Critical Complications: DKA vs. HHS:

• Clinical Management of DKA and HHS:
  1. Fluid Resuscitation: The primary priority. Infuse 0.9% Normal Saline (NS) at a rapid rate (1L/hour initially) to restore intravascular volume and renal perfusion. When blood glucose levels drop to approximately 250 mg/dL, the IV fluid must be switched to a dextrose-containing solution (e.g., D5% in 0.45% NS) to prevent rapid drops in blood glucose that can precipitate hypoglycemia and fatal cerebral edema.
  2. Regular Insulin Infusion: Regular insulin is the only type of insulin that can be administered intravenously. Start a continuous low-dose Regular insulin infusion (e.g., 0.1 units/kg/hour). Monitor capillary blood glucose hourly. Do not decrease blood glucose by more than 50–75 mg/dL per hour.
  3. Potassium Monitoring: Insulin acts as a key that drives glucose into cells, and it simultaneously drives potassium ($K^+$) from the extracellular fluid into the intracellular space. This causes a rapid drop in serum potassium levels.
     • Nursing Responsibility: Prior to starting insulin, check the serum potassium level. If potassium is $< 3.3 ext{ mEq/L}$, hold the insulin and notify the physician to administer potassium replacements first, as insulin will cause life-threatening hypokalemia (leading to cardiac dysrhythmias). If potassium is between 3.3 and 5.0 mEq/L, add potassium chloride (KCl) to the IV fluids as prescribed. Ensure the patient has adequate urine output ($\ge 30 ext{ mL/hour}$) before administering potassium to avoid accidental hyperkalemia.

Thyroid Disorders

The thyroid gland secretes thyroxine ($T_4$) and triiodothyronine ($T_3$), which regulate the body's basal metabolic rate.

• Hyperthyroidism (Graves' Disease):

  • Pathophysiology: An autoimmune disorder where thyroid-stimulating immunoglobulins (TSI) bind to and activate TSH receptors, causing sustained thyroid hormone overproduction.
  • Clinical Manifestations: Hypermetabolic state. Heat intolerance, weight loss despite increased appetite, tachycardia, palpitations, hand tremors, diarrhea, smooth warm skin, goiter, and exophthalmos (bulging eyes due to fat and fluid accumulation behind the orbits).
  • Thyroid Storm (Thyrotoxic Crisis): A life-threatening hypermetabolic state triggered by infection, trauma, stress, or thyroid surgery.
    • Signs: Extreme hyperthermia (fever $> 104^\circ ext{F}$ or $40^\circ ext{C}$), severe tachycardia, atrial fibrillation, severe agitation, delirium, and cardiovascular collapse.
    • Nursing Interventions: Maintain airway and oxygenation. Administer prescribed antithyroid medications (Propylthiouracil [PTU] or Methimazole) to block thyroid hormone synthesis. Administer IV beta-blockers (propranolol) to control heart rate and block peripheral conversion of T4 to T3. Administer iodine solutions (Lugol's solution or SSKI) after antithyroid drugs to inhibit hormone release. Apply cooling blankets and administer acetaminophen for fever; do not give aspirin (salicylates) as they displace thyroid hormones from binding proteins, worsening the crisis.
  • Post-Thyroidectomy Care:
    1. Airway Management: Position in semi-Fowler's to reduce neck swelling. Avoid neck extension or flexion to prevent stress on the suture line. Keep a tracheostomy tray, suction equipment, and oxygen at the bedside at all times. Monitor for laryngeal stridor (harsh, high-pitched sound indicating airway obstruction).
    2. Hypocalcemia/Tetany: Accidental damage or removal of the parathyroid glands during surgery leads to hypoparathyroidism and acute hypocalcemia. Monitor for Chvostek's sign (facial muscle twitching elicited by tapping the facial nerve in front of the ear) and Trousseau's sign (carpal spasm induced by inflating a blood pressure cuff above systolic pressure for 3 minutes). Ensure IV Calcium Gluconate is readily available at the bedside.
    3. Laryngeal Nerve Injury: Assess the patient's voice every 1–2 hours. Mild hoarseness is common, but severe hoarseness or inability to speak requires physician notification.

• Hypothyroidism (Hashimoto's Thyroiditis):

  • Pathophysiology: An autoimmune destruction of the thyroid gland, leading to insufficient thyroid hormone production and a hypometabolic state.
  • Clinical Manifestations: Cold intolerance, weight gain despite poor appetite, bradycardia, extreme fatigue, lethargy, constipation, dry thick skin, brittle hair, generalized non-pitting edema (myxedema), and forgetfulness.
  • Myxedema Coma: A life-threatening, end-stage complication of untreated or poorly managed hypothyroidism.
    • Signs: Profound hypothermia, severe hypoventilation, respiratory acidosis, bradycardia, hypotension, hyponatremia, hypoglycemia, and generalized non-pitting edema.
    • Nursing Interventions: Immediate airway support and mechanical ventilation if necessary. Administer IV levothyroxine ($T_4$) and IV liothyronine ($T_3$) as prescribed. Administer IV corticosteroids (hydrocortisone) to prevent adrenal insufficiency. Warm the patient gradually with blankets (avoid warming devices/heaters as rapid vasodilation can cause circulatory collapse). Monitor ECG and vital signs continuously.