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.
  • Infection – H. 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.