RC

Upper Gastrointestinal Problems – Comprehensive Study Notes

Nausea and Vomiting

  • Definitions

    • Nausea – Subjective, unpleasant sensation of discomfort in the epigastrium that creates a conscious desire to vomit.
    • Vomiting (emesis) – Forceful ejection of partially digested food and gastric secretions from the upper GI tract (mouth and sometimes nose).
  • Etiology (multifactorial)

    • GI disorders or infection, CNS disorders, cardiovascular problems, pregnancy, endocrine or metabolic disorders, side-effects of drugs/chemotherapy/anesthetics, psychologic factors, motion sickness.
  • Pathophysiology

    • Irritating stimuli (GI tract, kidneys, heart, brain) → afferent pathways → medulla (vomiting center) → vomiting reflex.
    • Chemoreceptor Trigger Zone (CTZ) in brainstem detects drugs, toxins, motion.
    • Activates Autonomic Nervous System (ANS)
      • Sympathetic (SNS) – tachycardia, tachypnea, diaphoresis.
      • Parasympathetic (PNS) – relaxes LES, increases gastric motility, increases saliva.
  • Interprofessional Management

    • Identify and treat cause/complications, provide symptom relief.
    • Pharmacologic classes: anticholinergics, antihistamines, cannabinoids, corticosteroids, 5-HT3 antagonists, phenothiazines, prokinetics, Substance-P/neurokinin-1 antagonists.
  • Clinical Manifestations

    • Anorexia, weight loss.
    • Prolonged N/V → fluid & electrolyte imbalance, metabolic acidosis/alkalosis, ↓ plasma volume, circulatory failure.
  • Nursing Assessment

    • Subjective: health history, current meds, surgeries.
    • Functional health patterns: nutritional–metabolic, activity–exercise, cognitive–perceptual, coping–stress.
    • Objective: general appearance, skin, GI, urinary output, lab/diagnostics.
    • Characterize emesis:
    • Partially digested → gastric outlet obstruction/delayed emptying.
    • Fecal odor + bile → obstruction below pylorus.
    • Pure bile → obstruction below ampulla of Vater.
    • Bright-red blood → active bleeding (Mallory-Weiss tear, varices, ulcer, cancer).
    • Coffee-ground → gastric bleeding (blood acted on by HCl).
    • Note if vomiting, regurgitation, or projectile.
  • Common Nursing Diagnoses

    • Nausea.
    • Deficient fluid volume.
    • Imbalanced nutrition: less than body requirements.
  • Planning Goals

    • Minimal/no N/V, normal electrolytes & hydration, normal fluid/nutrient intake patterns.
  • Implementation (Acute Care)

    • NPO → clear liquids → advance diet as tolerated (high-carb, low-fat, bland, small frequent meals).
    • IV fluids, monitor I&O, vital signs, assess for dehydration.
    • NG tube (NGT) if severe/prolonged to decompress stomach.
    • Aspiration precautions, environmental comfort.
    • Patient teaching (medication adherence, triggers, non-pharm options: acupressure, ginger, peppermint).
  • Evaluation

    • Desired outcomes: no/limited N/V, labs WNL, adequate intake.
    • Gerontology – ↑ risk of dehydration/aspiration, sensitivity to antiemetics (confusion, falls).

Gastroesophageal Reflux Disease (GERD)

  • Definition – Chronic syndrome of mucosal damage caused by reflux of stomach acid and/or bile into the lower esophagus.

  • Pathophysiology

    • Reflux overwhelms esophageal defense → inflammation.
    • Main factor: incompetent LES.
    • LES pressure ↓ by certain foods/drugs, obesity, smoking, hiatal hernia.
  • Clinical Manifestations

    • Heartburn (pyrosis) – most common symptom; burning, tight sensation beneath lower sternum → throat/jaw; relieved by antacids.
    • Dyspepsia (upper-abd pain/discomfort), regurgitation of hot/sour fluid.
    • Respiratory: wheeze, cough, dyspnea, hoarseness, sore throat, choking, hypersalivation, nocturnal symptoms.
  • Complications

    • Esophagitis → ulcerations, scar tissue, stricture, dysphagia.
    • Barrett’s esophagus (BE) – replacement of normal squamous epithelium with columnar epithelium (premalignant).
    • Respiratory: cough, bronchospasm, laryngospasm; aspiration into respiratory system → asthma, chronic bronchitis, pneumonia.
    • Dental erosion.
  • Diagnostics

    • Often clinical; response to therapy.
    • Upper GI endoscopy + biopsy/cytology (gold standard for complications).
    • Barium swallow, esophageal manometry, 24-hr pH monitoring, radionuclide studies.
  • Management

    • Lifestyle: low-fat/small meals, avoid alcohol/caffeine, stop smoking, upright 2-3 h post-meal, no late meals, elevate HOB 10–15\text{ cm}, weight reduction.
    • Drug Therapy
    • Proton pump inhibitors (PPIs) – ↓ HCl, heal esophagitis, ↓ strictures; take before first meal; long-term risks: ↓ bone density, kidney dz, \text{B}_{12}/Mg deficiency, dementia.
    • Histamine (\text{H}_2) receptor blockers – ↓ HCl; onset \approx1 h, duration \le12 h.
    • Prokinetics (e.g., metoclopramide) – ↑ gastric emptying; CNS & extrapyramidal SE.
    • Antacids – quick, short relief; caution with Na^+/Mg^{2+} load & drug interactions.
    • Others: cholinergics, cytoprotectives, alginate-based.
    • Surgical (refractory/complicated): Nissen or Toupet fundoplication; LINX magnetic ring (no MRI).
    • Endoscopic: EMR for dysplasia, radiofrequency ablation.
  • Gerontology

    • ↑ incidence; polypharmacy (nitrates, CCBs, antidepressants ↓ LES; NSAIDs/K^+ cause esophagitis).
    • Presentation may be severe bleed or aspiration.

Hiatal Hernia

  • Definition – Herniation of stomach into esophagus through diaphragmatic hiatus; aka esophageal hernia or diaphragmatic hernia.

  • Types

    • Sliding – gastroesophageal junction & part of stomach slide into thorax when supine, return when upright (most common).
    • Rolling (paraesophageal) – fundus & greater curvature roll alongside esophagus; risk of strangulation.
  • Etiology

    • Structural weakness (diaphragm, esophagogastric opening) + ↑ intra-abdominal pressure (obesity, pregnancy, ascites, heavy lifting, tumors).
  • Clinical Manifestations (similar to GERD)

    • Heartburn, dyspepsia, regurgitation, respiratory symptoms, chest pain.
  • Complications – GERD, esophagitis, ulcers, hemorrhage, stenosis, strangulation, aspiration.

  • Diagnostics – Barium swallow, endoscopy.

  • Management

    • Conservative: eliminate triggers, ↓ intra-abdominal pressure (weight loss, no tight clothes, avoid lifting/straining).
    • Surgical: herniotomy, herniorrhaphy, fundoplication, gastropexy.

Peptic Ulcer Disease (PUD)

  • Definition – Erosion of GI mucosa from the digestive action of \text{HCl} acid and pepsin.

    • Sites: lower esophagus, stomach, duodenum, post-gastrojejunostomy.
    • Acute – superficial, minimal inflammation; Chronic – muscular wall erosion, fibrous tissue, long duration.
    • Classified by location (gastric vs duodenal).
  • Gastric Ulcers

    • Usually in antrum; more common in women >50 yr; higher obstruction & mortality rates.
    • Risk factors: H. pylori, NSAIDs, bile reflux.
  • Duodenal Ulcers

    • 1–2 cm below pylorus; peak age 35{-}45 yr.
    • Etiology: H. pylori, high acid secretion.
    • High-risk groups: COPD, cirrhosis, chronic pancreatitis, hyperparathyroidism, Zollinger-Ellison syndrome, CRF.
  • Major Risk Factors

    • H. pylori – \approx80\% gastric, \approx90\% duodenal ulcers; CagA strain more virulent; oral-oral/fecal-oral; ↑ prevalence in Black & Hispanic populations; produces urease → alkalinizes environment.
    • Medications – NSAIDs (synergy with corticosteroids or anticoagulants).
    • Lifestyle – alcohol, smoking, caffeine, psychological stress.
  • Clinical Manifestations

    • Gastric – burning/gaseous epigastric pain 1{-}2 h after meals; food may worsen; perforation may be first sign.
    • Duodenal – burning/cramp-like midepigastric/back pain 2{-}5 h after meals; pain may awaken at night, relieved with food/antacid.
    • Other: bloating, N/V, early satiety; silent in older adults/NSAID users.
  • Diagnostics

    • Endoscopy (EGD) – gold standard; biopsy for H. pylori urease & malignancy; repeat in 3{-}6 mo to confirm healing.
    • Non-invasive H. pylori: serology, stool antigen, urea breath.
    • Barium contrast, fasting serum gastrin, secretin stimulation (Z-E syndrome).
    • Labs: CBC (anemia), liver enzymes, serum amylase, stool occult blood.
  • Interprofessional Management

    • Goals – ↓ gastric acidity, enhance mucosal defense, eradicate H. pylori, prevent complications.
    • Conservative: rest, stop smoking/alcohol, stress manage, dietary modification (individualize), no NSAIDs/aspirin unless protected with PPI/H2/misoprostol.
    • Drug Therapy
    • PPIs (most potent acid suppression).
    • Antibiotics for H. pylori: triple/quadruple regimen x14 d (e.g., PPI + amoxicillin + clarithromycin; PCN-allergy → metronidazole).
    • Bismuth ± tetracycline/ metronidazole.
    • H2 blockers, antacids, sucralfate (cytoprotective; give 1–2 h before/after antacids; binds cimetidine, digoxin, warfarin, phenytoin, tetracycline).
    • Misoprostol, tricyclics, anticholinergics as adjuncts.
    • Nutrition: avoid foods causing distress/irritation, avoid caffeine & alcohol, six small meals if symptomatic.
    • Surgery (rare) – for intractable disease or complications.
  • Major Complications (emergent)

    • Hemorrhage – most common; duodenal ulcers.
    • Perforation – most lethal; sudden severe pain radiating to back/shoulders, rigid abdomen, absent BS, shallow RR, weak pulse; untreated → bacterial peritonitis in 6{-}12 h.
    • Management: NGT, IV fluids/blood, broad antibiotics, pain control, prep for OR if large.
    • Gastric Outlet Obstruction – edema, spasm, scar at pylorus.
    • S/S: distention, pain worsening end of day, visible dilation, projectile vomiting, belching, anorexia.
    • Treatment: NGT decompression, PPI/H2, fluid-electrolyte replacement, balloon dilation or surgery.
  • Nursing Process

    • Common Diagnoses: Acute pain, Deficient fluid volume, Ineffective health management.
    • Goals: regimen adherence, pain control, no complications, healed ulcer, lifestyle changes.
    • Acute care: NPO, NGT, IV fluids, VS, labs, gastric aspirate (pH, blood), manage anxiety & pain.
    • Monitor for complications (VS, NG output, abdominal assessment).
    • Ambulatory: education on diet, lifestyle, meds, stress, follow-up; report bleeding or pain recurrence.
  • Gerontology

    • ↑ morbidity/mortality; NSAID use for arthritis common; first sign may be GI bleed or ↓ Hct.

Gastritis

  • Definition – Inflammation of gastric mucosa (acute or chronic, diffuse or localized).

  • Pathophysiology – Breakdown of gastric mucosal barrier → \text{HCl} & pepsin back-diffuse → edema, capillary damage, plasma loss, possible hemorrhage.

  • Causes

    • Drugs – NSAIDs (risk ↑ if female, >60 yr, PUD history, anticoagulants, corticosteroids), corticosteroids, digitalis, bisphosphonates (alendronate).
    • Diet – excessive alcohol, spicy/irritant foods.
    • InfectionH. pylori, other bacteria/virus/fungus.
    • Environment – radiation, smoking.
    • Diseases/Disorders – autoimmune gastritis, burns, Crohn’s, hiatal hernia, stress, bile reflux, renal failure, sepsis, shock.
    • Other – endoscopy, NGT, psychological stress.
  • Clinical Manifestations

    • Acute – anorexia, N/V, epigastric tenderness, hemorrhage (esp. with alcohol); self-limiting.
    • Chronic – similar or asymptomatic; may develop pernicious anemia (loss of intrinsic factor).
  • Diagnostics

    • History (drugs, alcohol), symptoms.
    • Endoscopy + biopsy.
    • H. pylori testing.
    • CBC (anemia), stool occult blood, antibodies to parietal cells & intrinsic factor.
  • Management

    • Acute
    • Identify & remove cause; NPO → clear liquids → advance diet.
    • Rest, antiemetics, IV fluids; monitor dehydration.
    • Severe: NGT for lavage/decompression; monitor bleeding (VS, guaiac).
    • Drugs: PPIs or H2 blockers.
    • Chronic
    • Eliminate cause (H. pylori → antibiotics; stop alcohol/NSAIDs).
    • Lifelong \text{cobalamin} for pernicious anemia.
    • Lifestyle: no smoking, six small non-irritating meals/day, medication adherence.