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)
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.