Nursing(Degree) · First Year · NUR101
Anatomy and Physiology
Anatomy and Physiology is one of the most important foundation courses for nursing students in Zambia. This course helps you understand how the human body is structured and how it functions, from major organs to body systems such as the nervous, cardiovascular, respiratory, and digestive …
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Anatomy and Physiology is one of the most important foundation courses for nursing students in Zambia. This course helps you understand how the human body is structured and how it functions, from major organs to body systems such as the nervous, cardiovascular, respiratory, and digestive systems. A strong grasp of this subject is essential for exams set by nursing schools and regulatory bodies in Zambia. At 25schools, we simplify complex anatomy concepts using exam-focused questions, diagrams, and clear explanations designed for nursing exams. Whether you are preparing for tests, assignments, or final examinations, this course builds the clinical understanding every successful nurse needs. Start studying with 25schools today and gain the confidence to excel in anatomy and physiology exams.
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Topic 217Coming soon
Esophageal Cancer: Squamous vs Adenocarcinoma
Esophageal cancer is the SIXTH LEADING CAUSE OF CANCER DEATH worldwide, with TWO MAIN HISTOLOGIC TYPES: SQUAMOUS CELL CARCINOMA (SCC) and ADENOCARCINOMA (AC). For Zambian students, SCC is the DOMINANT TYPE (80-90%), with HIGH INCIDENCE in parts of Africa (esophageal cancer belt). EPIDEMIOLOGY: SCC: Sub-Saharan Africa, Asia, Middle East. Risk factors: TOBACCO, ALCOHOL (synergistic), hot beverages, nutritional deficiencies, HPV (controversial), achalasia, caustic injury, Plummer-Vinson, tylosis. ADENOCARCINOMA: Western, white, male. Risk factors: GERD, BARRETT'S ESOPHAGUS, obesity, smoking. CLINICAL: LATE PRESENTATION (80% incurable at diagnosis). PROGRESSIVE DYSPHAGIA (solids → liquids). ODYNOPHAGIA, weight loss (profound). HOARSENESS (recurrent laryngeal nerve), cough, aspiration (tracheoesophageal fistula), haematemesis. DIAGNOSIS: BARIUM SWALLOW: 'rat's tail' or 'apple core' stricture. ENDOSCOPY: mass, stricture, ulcer. BIOPSY: tissue diagnosis, histology (SCC vs AC). EUS: T stage (depth of invasion). CT CHEST/ABDOMEN: N stage (nodes), M stage (liver, lung, distant). PET-CT: equivocal metastases. STAGING: TNM (8th edition). MANAGEMENT: LOCALIZED DISEASE (T1-T2, N0): SURGICAL RESECTION (ESOPHAGECTOMY, Ivor Lewis, McKeown, transhiatal). ENDOSCOPIC THERAPY (T1a, HGD): EMR, ablation (selected). LOCALLY ADVANCED (T3-T4, N+): NEOADJUVANT CHEMORADIATION (CROSS regimen: carboplatin/paclitaxel + 41.4Gy) → SURGERY. DEFINITIVE CHEMORADIATION (non-surgical candidate). METASTATIC (M1): PALLIATIVE CHEMOTHERAPY (fluorouracil/cisplatin, FOLFOX), IMMUNOTHERAPY (pembrolizumab, nivolumab—PD-L1+), targeted therapy (HER2+, trastuzumab). PALLIATION: DYSPHAGIA: SELF-EXPANDING METAL STENT (SEMS), RADIOTHERAPY, laser ablation. PAIN, nutrition, psychosocial. Prognosis: POOR. 5-year survival: localized: 40-50%, locally advanced: 20-30%, metastatic: <5%. SCC: better prognosis than AC? similar stage. Zambian context: ESOPHAGEAL CANCER IS COMMON, especially in certain regions (Eastern, Lusaka?). SCC >90%. LATE PRESENTATION is the norm (dysphagia to liquids, weight loss). ENDOSCOPY available tertiary. CT available. SURGICAL RESECTION (esophagectomy) available (Lusaka, Ndola—specialized centres, high morbidity/mortality). NEOADJUVANT CHEMORADIATION: limited availability (radiotherapy, chemotherapy). PALLIATIVE STENTING: SEMS available, expensive. PALLIATIVE RADIOTHERAPY: available (Lusaka, Cancer Hospital). CHEMOTHERAPY: fluorouracil, cisplatin, paclitaxel available. IMMUNOTHERAPY NOT AVAILABLE. Prevention: tobacco/alcohol cessation, dietary modification. Focus: EARLY DETECTION? Symptomatic = late. Palliation of dysphagia (stenting, radiotherapy) is essential.
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Topic 218Coming soon
Achalasia
Achalasia is a rare, chronic, progressive esophageal motility disorder characterized by INADEQUATE LOWER ESOPHAGEAL SPHINCTER (LES) RELAXATION and LOSS OF ESOPHAGEAL PERISTALSIS. For Zambian students, it is a key differential diagnosis for DYSPHAGIA (solids and liquids) and should not be mistaken for malignancy. PATHOPHYSIOLOGY: Idiopathic. Autoimmune? Viral trigger? → inflammatory destruction of inhibitory neurons (nitric oxide, VIP) in the MYENTERIC PLEXUS → unopposed cholinergic excitation → LES APERISTALSIS, FAILED RELAXATION, esophageal dilatation. TYPES (Chicago Classification): Type I (classic): minimal pressurization. Type II: panesophageal pressurization (best prognosis). Type III: spastic (premature, spastic contractions, worst prognosis). CLINICAL: INSIDIOUS ONSET, PROGRESSIVE DYSPHAGIA to BOTH SOLIDS AND LIQUIDS (90%). REGURGITATION of undigested food (nocturnal, aspiration, cough). CHEST PAIN (10-20%). HEARTBURN (misdiagnosed as GERD). WEIGHT LOSS. BARIUM SWALLOW: DILATED ESOPHAGUS, AIR-FLUID LEVEL, SMOOTH TAPERING at GEJ ('bird-beak' or 'rat-tail' appearance). DELAYED barium emptying. ENDOSCOPY: MANDATORY to EXCLUDE PSEUDOACHALASIA (malignancy at GEJ). Tight LES with 'pop' on passage, dilated esophagus, retained food/fluid. NORMAL MUCOSA. ESOPHAGEAL MANOMETRY: GOLD STANDARD for diagnosis. High-resolution manometry (HRM) shows: INCOMPLETE LES RELAXATION (integrated relaxation pressure, IRP >15mmHg), APERISTALSIS (failed peristalsis). Chicago Classification subtypes I, II, III. MANAGEMENT: GOAL: RELIEVE LES OBSTRUCTION (palliative, does NOT restore peristalsis). GRADED PNEUMATIC DILATION: endoscopic, balloon dilation of LES. Effective (60-80%). Perforation risk (2-5%). Repeatable. LAPAROSCOPIC HELLER MYOTOMY with PARTIAL FUNDOPLICATION (Dor, Toupet): SURGICAL, longitudinal myotomy of LES. Highly effective (85-95%). Durable. PERORAL ENDOSCOPIC MYOTOMY (POEM): NOTES procedure, endoscopic myotomy. No fundoplication, higher GERD. Effective. BOTULINUM TOXIN INJECTION: endoscopic, temporary (3-6 months). For high-risk surgical patients, bridge. PHARMACOLOGIC: nitrates, calcium channel blockers—POOR efficacy, side effects. PROGNOSIS: Excellent symptom control with treatment. Persistent risk of ASPIRATION (nocturnal regurgitation), ESOPHAGEAL SCC (10-20 fold increased risk, surveillance? controversial). Zambian context: ACHALASIA IS RARE, underdiagnosed. BARIUM SWALLOW is widely available, diagnostic. ENDOSCOPY available tertiary. MANOMETRY NOT AVAILABLE. PNEUMATIC DILATION available? Endoscopy with CRE balloon dilation (off-label) may be performed. HELLER MYOTOMY available (tertiary surgical centres). POEM NOT AVAILABLE. BOTULINUM TOXIN available? Cost. Treatment pathway: Suspect (dysphagia solids + liquids, regurgitation, weight loss). Barium swallow (bird-beak). Endoscopy (exclude cancer). Refer for surgery (Heller myotomy).
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Topic 219Coming soon
Esophageal Webs and Rings
Esophageal webs and rings are thin, membranous, or muscular structures causing luminal narrowing and intermittent dysphagia. For Zambian students, Schatzki ring is COMMON, Plummer-Vinson syndrome (PVS, Paterson-Brown-Kelly) is RARE but important—associated with IRON DEFICIENCY and POSTCRICOID DYSPHAGIA, plus increased risk of ESOPHAGEAL SCC. SCHATZKI RING: Type B (mucosal) ring, at squamocolumnar junction (SCJ, Z-line). PATHOLOGY: benign, thin (<4mm), diaphragmatic. CLINICAL: INTERMITTENT, NON-PROGRESSIVE DYSPHAGIA to solids. Bolus obstruction (steakhouse syndrome). ENDOSCOPY: concentric, smooth, narrow lumen at SCJ. BARIUM SWALLOW: 'B' ring, well-defined, <13mm diameter = symptomatic. MANAGEMENT: SYMPTOMATIC: ENDOSCOPIC DILATION (bougie, balloon). Effective, durable. Recurrence common. ESOPHAGEAL WEB: THIN, MEMBRANOUS, eccentric, in CERVICAL ESOPHAGUS (postcricoid, proximal). PLUMMER-VINSON SYNDROME (PVS): TRIAD: CERVICAL DYSPHAGIA (intermittent), IRON DEFICIENCY ANAEMIA, ESOPHAGEAL WEB (postcricoid). PATHOPHYSIOLOGY: chronic iron deficiency → mucosal atrophy, web formation. Demographics: middle-aged women. COMPLICATION: INCREASED RISK OF ESOPHAGEAL SCC (hypopharynx, cervical esophagus). DIAGNOSIS: clinical, barium swallow (thin, anterior web), endoscopy, iron studies. MANAGEMENT: IRON REPLACEMENT (oral, IV). Resolves dysphagia, web, cancer risk? May regress web. ENDOSCOPIC DILATION if web persists. SURVEILLANCE: no consensus, high index suspicion for malignancy. OTHER: EOSINOPHILIC ESOPHAGITIS (rings, furrows) - see topic. MUSCULAR RING (Type A): uncommon, at proximal stomach (muscular), smooth. Prognosis: Schatzki: excellent, recurrent. PVS: excellent with iron therapy. Malignant risk persists. Zambian context: SCHATZKI RING is COMMON, likely underdiagnosed cause of intermittent dysphagia. BARIUM SWALLOW is diagnostic, widely available. Dilation available. PVS is RARE. Consider in middle-aged woman with dysphagia, koilonychia, glossitis, anaemia. IRON deficiency is common in Zambia (nutritional, hookworm, menorrhagia). IRON replacement is accessible. Dilation available. Malignancy risk: counsel, endoscopy if refractory/progressive symptoms.
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Esophageal Diverticula
Esophageal diverticula are outpouchings of one or more layers of the esophageal wall, classified by location: PHARYNGOESOPHAGEAL (ZENKER'S DIVERTICULUM, most common), MIDE SOPHAGEAL (TRACTION, usually benign), and EPIPHRENIC (PULSION, above LES). For Zambian students, Zenker's diverticulum is the most clinically relevant. ZENKER'S DIVERTICULUM: PATHOPHYSIOLOGY: Pulsion diverticulum through KILLIAN'S DEHISCENCE (between inferior pharyngeal constrictor and cricopharyngeus). Incoordination, cricopharyngeal spasm, increased hypopharyngeal pressure. TRUE DIVERTICULUM (mucosa, submucosa). CLINICAL: OLDER (>70y). CERVICAL DYSPHAGIA (progressive). REGURGITATION of undigested food (hours after meals), HALITOSIS, ASPIRATION (nocturnal cough, pneumonia), neck mass (compressible, gurgling—BOYCE'S SIGN). BARIUM SWALLOW: DIAGNOSTIC. Contrast fills diverticulum posterior to cervical esophagus, retention. ENDOSCOPY: caution (perforation risk), identify diverticulum, exclude malignancy. MANAGEMENT: SYMPTOMATIC: ENDOSCOPIC SEPTOTOMY (DOHLMAN'S PROCEDURE): division of common wall between diverticulum and esophagus (rigid or flexible endoscopy). OPEN SURGERY: CRICOPHARYNGEAL MYOTOMY + DIVERTICULECTOMY (or diverticulopexy). ASYMPTOMATIC: NO TREATMENT. MIDE SOPHAGEAL DIVERTICULUM: Pulsion? Traction (mediastinal granulomatous disease: TB, histoplasmosis). Often ASYMPTOMATIC. Treatment: underlying disease, rare surgery. EPIPHRENIC DIVERTICULUM: Associated with ESOPHAGEAL MOTILITY DISORDER (achalasia, DES). Distal 10cm. Symptoms: dysphagia, regurgitation, chest pain. Management: TREAT MOTILITY DISORDER (myotomy, diverticulectomy). Prognosis: Zenker's: excellent after treatment. Aspiration risk. Recurrence 5-10%. Zambian context: ZENKER'S is RARE but underdiagnosed. Consider in elderly with chronic dysphagia, regurgitation, aspiration. BARIUM SWALLOW is diagnostic, widely available. ENDOSCOPIC SEPTOTOMY (flexible) is available (tertiary endoscopy centres). SURGERY available. Mide esophageal diverticulum: consider TB (endemic). Treat TB, diverticulum usually requires no intervention.
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Topic 221Coming soon
Caustic Esophageal Injury
Caustic ingestion is a devastating medical emergency, causing severe, often irreversible injury to the esophagus and stomach. For Zambian students, this is a CRITICAL, TIME-SENSITIVE PRESENTATION, particularly in children (accidental) and adults (suicidal). Alkali (NaOH, drain cleaner) > Acid. PATHOPHYSIOLOGY: ALKALI: LIQUEFACTIVE NECROSIS, deep penetration, thrombosis, severe esophageal injury (stricture, perforation). ACID: COAGULATIVE NECROSIS, eschar limits depth, more gastric injury. CLINICAL: ORAL PAIN, DYSPHAGIA, ODYNOPHAGIA, HYPERSALIVATION, VOMITING. STRIDOR, HOARSENESS (laryngeal edema, airway emergency). CHEST PAIN, ABDOMINAL PAIN, PERITONITIS (perforation). SHOCK. PHARYNGEAL/ORAL BURNS (absence does NOT exclude esophageal injury). DIAGNOSIS: HISTORY: agent, quantity, intentional vs accidental. AIRWAY ASSESSMENT: IMMEDIATE. ENDOSCOPY: MANDATORY, within 24-48 hours (earlier = high perforation risk). ZARGAR'S CLASSIFICATION: Grade 0: normal. Grade 1: edema, erythema. Grade 2a: friability, hemorrhage, superficial ulceration. Grade 2b: 2a + deep, circumferential ulceration. Grade 3a: small, scattered necrosis. Grade 3b: extensive necrosis. GRADES 2B, 3 = HIGH RISK STRICTURE, PERFORATION. CONTRAST CT: suspected perforation (pneumomediastinum, pneumoperitoneum). MANAGEMENT: AIRWAY FIRST. INTUBATION if stridor, respiratory distress, deep burns. NO NEUTRALIZATION (heat, emesis). NPO. IV FLUIDS. IV PPI (stress ulcer prophylaxis, gastric protection). CORTICOSTEROIDS: CONTROVERSIAL, NOT ROUTINE. May be considered in grade 2b (prevent stricture). ANTIBIOTICS: NOT ROUTINE. Perforation, infection—broad-spectrum. EARLY NUTRITION: NG tube placement (endoscopic or fluoroscopic guidance) for enteral feeding in severe injuries (2b,3). DELAYED COMPLICATIONS: ESOPHAGEAL STRICTURE (most common, 2b,3). Dysphagia develops 2-8 weeks post-injury. MANAGEMENT: ENDOSCOPIC DILATION (serial, bougie, balloon). REFRACTORY STRICTURE: SURGICAL ESOPHAGECTOMY/GASTRIC PULL-UP or COLONIC INTERPOSITION. ESOPHAGEAL SCC: LONG-TERM RISK (>20 years). Surveillance? ESOPHAGECTOMY often eliminates risk. Prognosis: Grade 1-2a: excellent, no stricture. Grade 2b-3: high morbidity, mortality (perforation, mediastinitis), chronic dysphagia, repeated dilations, surgery. Zambian context: CAUSTIC INGESTION OCCURS. Agents: household bleach (sodium hypochlorite—milder), battery acid, drain cleaners. CHILDREN: accidental, limited volume, often mild. ADULTS: intentional, large volume, severe injury, psychiatric comorbidity. ENDOSCOPY available tertiary. STRICTURE DILATION available. ESOPHAGECTOMY/COLONIC INTERPOSITION available (specialized centres). PREVENTION: public education, childproof containers, mental health support. Focus: EARLY ENDOSCOPY, GRADE SEVERITY, AGGRESSIVE DILATION (if stricture), SURGERY (if refractory).
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Topic 222Coming soon
Mallory-Weiss Syndrome
Mallory-Weiss syndrome (MWS) is a NON-PENETRATING MUCOSAL TEAR at the gastroesophageal junction or gastric cardia, caused by forceful retching, vomiting, or straining. For Zambian students, MWS is a COMMON CAUSE of UPPER GI BLEEDING (5-15%), usually SELF-LIMITED, benign. PATHOPHYSIOLOGY: Sudden, marked increase in intra-abdominal pressure against a closed glottis → transmural pressure gradient → mucosal laceration at GEJ. PRECIPITANTS: alcohol binge (most common), hyperemesis gravidarum, coughing, straining, blunt abdominal trauma, iatrogenic (endoscopy). CLINICAL: CLASSIC TRIAD: VOMITING/RETCHING → HAEMATEMESIS (fresh red blood, small-to-moderate volume). Epigastric pain. Bleeding usually SELF-LIMITED (80-90% stop spontaneously). Haemodynamic instability: 10-15%. DIAGNOSIS: ENDOSCOPY: LINEAR, VERTICAL MUCOSAL TEAR at GEJ (usually <2cm), often single, with or without stigmata of bleeding (active oozing, visible vessel, adherent clot). Stomach and duodenum: normal. MANAGEMENT: SUPPORTIVE: IV fluids, antiemetics, PPI (if concomitant ulcer). TRANSFUSION: restrictive (Hb <7g/dL). ENDOSCOPIC THERAPY: INDICATED for active bleeding, visible vessel, adherent clot. THERAPIES: EPINEPHRINE INJECTION, THERMAL COAGULATION (heater probe, APC), HEMOCLIPS (endoclips)—highly effective. ANGIOGRAPHY/EMBOLIZATION: refractory, inaccessible. SURGERY: oversewing of tear (RARE). Prognosis: EXCELLENT. Rebleeding <5%. Mortality <1% (haemodynamic instability, comorbidities). Zambian context: MWS is COMMON (alcohol use prevalent). ENDOSCOPY available tertiary. Endoscopic therapy (epinephrine, hemoclips) available. Focus: RESUSCITATION, DIAGNOSIS (endoscopy), ENDOSCOPIC HEMOSTASIS if actively bleeding. Distinguish from VARICEAL BLEED (different management). Prevention: alcohol moderation, antiemetics.
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Topic 223Coming soon
Boerhaave Syndrome
Boerhaave syndrome is a LIFE-THREATENING, FULL-THICKNESS PERFORATION of the esophagus, caused by a sudden, massive increase in intraesophageal pressure (forceful vomiting). It is a SURGICAL EMERGENCY with HIGH MORTALITY (20-50%) if not promptly diagnosed and treated. For Zambian students, Boerhaave is a RARE but CATASTROPHIC DIAGNOSIS, frequently missed, and requires URGENT SURGICAL REFERRAL. PATHOPHYSIOLOGY: Barogenic rupture. Forceful vomiting against closed cricopharyngeus → transmural tear. LOCATION: LEFT POSTEROLATERAL WALL of DISTAL ESOPHAGUS (75-90%). Mediastinal contamination (gastric contents, bacteria, air) → chemical mediastinitis → necrotizing infection, sepsis, multi-organ failure. CLINICAL: CLASSIC TRIAD (Mackler's triad): VOMITING, LOWER THORACIC PAIN, SUBCUTANEOUS EMPHYSEMA (neck, chest). ONSET: severe, sudden, retrosternal or epigastric pain (radiating to back), following retching/vomiting. DYSPNOEA, CYANOSIS, SHOCK. HAMMAN'S SIGN: mediastinal crunch (pneumomediastinum). PLEURAL EFFUSION (left > right, reactive, then infected). DIAGNOSIS: CLINICAL SUSPICION IS PARAMOUNT. CHEST X-RAY: pneumomediastinum, subcutaneous emphysema, left pleural effusion, pneumothorax (20%). WATER-SOLUBLE CONTRAST ESOPHAGRAM (Gastrografin): EXTRAVASATION of contrast from distal esophagus—DIAGNOSTIC. CT CHEST: esophageal wall defect, mediastinal air/fluid, pleural effusion. ENDOSCOPY: AVOID (may extend perforation, insufflation). Use only if high suspicion, negative imaging, and therapeutic intervention planned (stent). MANAGEMENT: EMERGENCY SURGERY is DEFINITIVE. PRINCIPLES: RESUSCITATION (IV fluids, broad-spectrum IV antibiotics (cover Gram-negatives, anaerobes, Candida), vasopressors). SURGICAL REPAIR: PRIMARY CLOSURE (two-layer), with buttress (pleural flap, intercostal muscle). WIDE DRAINAGE (mediastinum, pleural). Gastrostomy, feeding jejunostomy. ENDOSCOPIC STENTING (covered metal stent) in SELECTED PATIENTS (early diagnosis, contained perforation, high surgical risk). EXCLUSION: T-tube drainage, esophagectomy (severe, late presentation). Prognosis: TIME IS SURVIVAL. Diagnosis <24h: mortality 25%. >24h: mortality 50-70%. Zambian context: BOERHAAVE IS RARE, ALMOST CERTAINLY UNDERDIAGNOSED (missed as MI, pancreatitis, perforated ulcer). Think Boerhaave in patient with vomiting, severe chest/abdominal pain, subcutaneous emphysema, shock. CXR is widely available—pneumomediastinum, effusion. WATER-SOLUBLE CONTRAST SWALLOW available (fluoroscopy). CT available tertiary. SURGERY available (tertiary, cardiothoracic/general surgery). Mortality is high. This is a SURGICAL EMERGENCY—DO NOT DELAY.
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Topic 224Coming soon
Peptic Ulcer Disease: Pathophysiology and Clinical Spectrum
Peptic ulcer disease (PUD) refers to mucosal defects in the stomach (gastric ulcer, GU) or proximal duodenum (duodenal ulcer, DU) that extend through the muscularis mucosae. For Zambian students, PUD is EXTREMELY COMMON, with Helicobacter pylori as the dominant etiology. NSAID use is increasing. MASTERY OF PUD PATHOPHYSIOLOGY, CLINICAL PRESENTATION, DIAGNOSIS, AND COMPLICATION MANAGEMENT IS ESSENTIAL. PATHOPHYSIOLOGY: ULCERATION RESULTS FROM IMBALANCE BETWEEN AGGRESSIVE FACTORS (acid, pepsin, H. pylori, NSAIDs) and DEFENSIVE FACTORS (mucus, bicarbonate, blood flow, prostaglandins, epithelial restitution). H. PYLORI: Gram-negative, urease-producing, colonizes gastric mucosa. Causes DU (95%) and GU (70%). Mechanisms: urease (ammonia), cytotoxins (VacA, CagA), inflammation (IL-8, neutrophils) → gastritis, hypergastrinaemia, increased acid (DU), or impaired mucosal defence (GU). NSAIDs: inhibit cyclooxygenase (COX-1, COX-2) → reduced prostaglandin synthesis → impaired mucosal blood flow, mucus secretion, bicarbonate, epithelial proliferation. Direct topical injury. RISK FACTORS: H. pylori, NSAIDs/aspirin, smoking, severe physiological stress (ICU, burns, head injury—Cushing's ulcer), Zollinger-Ellison syndrome (gastrinoma, rare). CLINICAL: EPIGASTRIC PAIN is the hallmark. DU: PAIN 2-5 HOURS AFTER MEALS, relieved by food/antacids, nocturnal pain (wakes patient). GU: PAIN IMMEDIATELY AFTER MEALS, food may worsen pain. Both: nausea, bloating, early satiety. ATYPICAL: asymptomatic (elderly, NSAID users) → PRESENT WITH COMPLICATION. PHYSICAL EXAM: epigastric tenderness. COMPLICATIONS: BLEEDING (20%): haematemesis, melaena, haemodynamic instability—most common complication. PERFORATION (5%): sudden, severe, generalized abdominal pain, peritonitis, rigidity, rebound, FREE AIR under diaphragm (CXR, erect). PENETRATION: into pancreas (back pain), liver, biliary tree. GASTRIC OUTLET OBSTRUCTION (2%): recurrent vomiting, early satiety, weight loss, succussion splash. DIAGNOSIS: ENDOSCOPY is GOLD STANDARD. Indications: ALARM SYMPTOMS (dysphagia, weight loss, GI bleeding, anaemia, persistent vomiting, age >50, family history gastric cancer). GU requires BIOPSIES (6-8) to exclude MALIGNANCY (gastric adenocarcinoma). DU: malignancy rare, biopsies not routine. H. PYLORI TESTING: Endoscopic: RAPID UREASE TEST (CLO test, sensitivity/specificity >95%), histology (Giemsa), culture. NON-INVASIVE: UREA BREATH TEST (gold standard non-invasive), STOOL ANTIGEN TEST. SEROLOGY: IgG antibodies (past infection, not active), limited utility. BARIUM SWALLOW: double-contrast, niche, radiating folds. Not first-line. MANAGEMENT: GOALS: SYMPTOM RELIEF, ULCER HEALING, ERADICATE H. PYLORI (if present), PREVENT RECURRENCE, MANAGE COMPLICATIONS. H. PYLORI-ASSOCIATED: ERADICATION THERAPY. TRIPLE THERAPY (FIRST-LINE, if clarithromycin resistance <15%): PPI (standard dose, BID) + AMOXICILLIN (1g BID) + CLARITHROMYCIN (500mg BID) x 14 days. BISMUTH QUADRUPLE THERAPY (FIRST-LINE, if clarithromycin resistance high, penicillin allergy): PPI + BISMUTH SUBSALICYLATE (524mg QID) + METRONIDAZOLE (250-500mg QID) + TETRACYCLINE (500mg QID) x 10-14 days. CONCOMITANT THERAPY: PPI + AMOXICILLIN + CLARITHROMYCIN + METRONIDAZOLE x 10-14d. TEST OF CURE: Urea breath test or stool antigen, ≥4 weeks after antibiotics, ≥2 weeks after PPI. NSAID-ASSOCIATED: DISCONTINUE NSAID/aspirin if possible. PPI THERAPY x 4-8 weeks (GU: 8 weeks, DU: 4 weeks). If NSAID/aspirin MUST be continued: PPI CO-THERAPY indefinitely. IDIOPATHIC: PPI x 4-8 weeks. REFRACTORY ULCER: reassess H. pylori (eradication failure, reinfection), NSAID use, gastrinoma (fasting gastrin, gastric pH). SURGERY: NOW RARE. Indications: REFRACTORY to medical therapy (uncommon), COMPLICATIONS (perforation, obstruction, bleeding not controlled endoscopically). PROCEDURES: VAGOTOMY + ANTRECTOMY, VAGOTOMY + DRAINAGE (pyloroplasty), HIGHLY SELECTIVE VAGOTOMY (no drainage). COMPLICATION MANAGEMENT: BLEEDING: resuscitation, endoscopy (epinephrine, clips, thermal coagulation, fibrin glue), high-dose PPI (IV bolus + infusion), repeat endoscopy, angioembolization, surgery. PERFORATION: SURGERY (omentopexy, Graham patch), IV antibiotics, PPI. OBSTRUCTION: endoscopic balloon dilation, PPI, H. pylori eradication, surgery (if refractory). Prognosis: EXCELLENT with H. pylori eradication (<5% recurrence). NSAID ulcer: recurs if NSAID continued without PPI (60-80%). Zambian context: PUD IS COMMON. H. pylori prevalence is HIGH (70-80% of population). ENDOSCOPY available tertiary. RAPID UREASE TEST may be limited. HISTOLOGY available. UREA BREATH TEST, STOOL ANTIGEN limited. SEROLOGY (IgG) widely available—poor positive predictive value (past infection). EMPIRIC H. PYLORI ERADICATION in high-risk populations? Not standard. TRIPLE THERAPY (PPI/amoxicillin/clarithromycin): amoxicillin and clarithromycin widely available? Yes. CLARITHROMYCIN RESISTANCE: increasing, unknown local rates. BISMUTH QUADRUPLE: tetracycline, metronidazole available. Bismuth (Pepto-Bismol) may not be available; can use bismuth subcitrate (if available) or omit. PPI: omeprazole widely available. NSAID use: increasing. Focus: ENDOSCOPY for alarm symptoms, biopsy for GU (exclude cancer), H. pylori eradication, PPI for NSAID ulcers, manage complications.
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Topic 225Coming soon
Helicobacter pylori: Diagnosis and Management
Helicobacter pylori is a Gram-negative, microaerophilic, spiral-shaped bacterium that colonizes the human gastric mucosa, affecting over 50% of the world's population. For Zambian students, H. pylori is a MAJOR PUBLIC HEALTH PROBLEM, with prevalence exceeding 70-80% in many African populations. It is the PRIMARY CAUSE of PEPTIC ULCER DISEASE and GASTRIC ADENOCARCINOMA (WHO Group I carcinogen), and is associated with MALT LYMPHOMA. MASTERY OF H. PYLORI DIAGNOSIS AND ERADICATION IS LIFE-SAVING. PATHOPHYSIOLOGY: Transmission: faecal-oral, oral-oral. Colonizes gastric antrum, produces UREASE (converts urea to ammonia, buffers gastric acid). Virulence factors: CagA (cytotoxin-associated gene A, injects into epithelial cells, more severe disease), VacA (vacuolating cytotoxin). Chronic inflammation (neutrophils, lymphocytes, macrophages) → atrophic gastritis → intestinal metaplasia → dysplasia → GASTRIC ADENOCARCINOMA (intestinal type). Also: MUCOSA-ASSOCIATED LYMPHOID TISSUE (MALT) LYMPHOMA (low-grade B-cell). CLINICAL: Asymptomatic (most). Peptic ulcer disease (DU 95%, GU 70%). Non-ulcer dyspepsia (NUD, 30% of infected). Gastric adenocarcinoma. MALT lymphoma (remits with eradication in 70-80%). Iron deficiency anaemia (chronic gastritis, blood loss, impaired iron absorption). Immune thrombocytopenic purpura (ITP). Vitamin B12 deficiency. DIAGNOSIS: INDICATIONS FOR TESTING: Active PUD, history of PUD (never tested), gastric MALT lymphoma, atrophic gastritis, post-gastric cancer resection, first-degree relative of gastric cancer patient, patient preference (dyspepsia), ITP, iron deficiency (unexplained), long-term PPI therapy (controversial). TEST-AND-TREAT: dyspepsia, age <50, no alarm symptoms. NON-INVASIVE: UREA BREATH TEST (UBT): Gold standard non-invasive. Sensitivity/specificity >95%. Requires PPI cessation 2 weeks, antibiotics/bismuth 4 weeks. STOOL ANTIGEN TEST (SAT): Monoclonal antibody, similar accuracy to UBT, convenient. SEROLOGY: IgG antibodies. POSITIVE = PAST OR CURRENT INFECTION. NOT USEFUL for diagnosis of active infection (cannot confirm eradication). Rapid, inexpensive. LIMITED UTILITY. INVASIVE (ENDOSCOPY): RAPID UREASE TEST (CLOtest): biopsy, color change (urease activity). Sensitivity 90-95%, specificity >95%. Rapid, inexpensive. HISTOLOGY: biopsy, special stains (Giemsa, Warthin-Starry). GOLD STANDARD for diagnosis. CULTURE: antibiotic susceptibility testing (clarithromycin, metronidazole, levofloxacin, tetracycline, amoxicillin). MOLECULAR: PCR (clarithromycin resistance, stool). MANAGEMENT: ERADICATION THERAPY. INDICATIONS: PUD, gastric MALT lymphoma, atrophic gastritis, post-gastric cancer resection, first-degree relative gastric cancer, patient preference. Increasing ANTIBIOTIC RESISTANCE is a GLOBAL PROBLEM. Clarithromycin resistance >15% in many regions (including Africa). Metronidazole resistance >40%. Amoxicillin, tetracycline resistance RARE. FIRST-LINE THERAPY (LOCAL CLARITHROMYCIN RESISTANCE <15%): TRIPLE THERAPY: PPI (standard dose BID) + AMOXICILLIN (1g BID) + CLARITHROMYCIN (500mg BID) x 14 days. FIRST-LINE THERAPY (LOCAL CLARITHROMYCIN RESISTANCE >15% OR PENICILLIN ALLERGY): BISMUTH QUADRUPLE THERAPY: PPI + BISMUTH SUBSALICYLATE (524mg QID) + METRONIDAZOLE (250-500mg QID) + TETRACYCLINE (500mg QID) x 10-14 days. CONCOMITANT THERAPY (no bismuth): PPI + AMOXICILLIN + CLARITHROMYCIN + METRONIDAZOLE x 10-14 days. LEVOFLOXACIN TRIPLE: PPI + AMOXICILLIN + LEVOFLOXACIN x 10-14 days (second-line, reserve). SEQUENTIAL THERAPY: PPI + amoxicillin x 5d → PPI + clarithromycin + metronidazole x 5d (10d total). HYBRID THERAPY: PPI + amoxicillin x 7d → PPI + amoxicillin + clarithromycin + metronidazole x 7d (14d total). SECOND-LINE THERAPY (after failure): BISMUTH QUADRUPLE (if not used first-line), LEVOFLOXACIN TRIPLE, RIFABUTIN TRIPLE (Rifabutin + amoxicillin + PPI). THIRD-LINE: CULTURE AND SUSCEPTIBILITY TESTING. ADHERENCE IS CRITICAL. TEST OF CURE: UBT or SAT, ≥4 weeks after antibiotics, ≥2 weeks after PPI. MANDATORY for PUD, MALT lymphoma, gastric cancer prevention. NON-ULCER DYSPEPSIA: test-and-treat may improve symptoms (20-30% response). Prevention: Improved sanitation, hygiene. No vaccine. Zambian context: H. pylori PREVALENCE IS VERY HIGH. Most infected are asymptomatic. CLARITHROMYCIN RESISTANCE: unknown, but likely >15% (widespread antibiotic use). METRONIDAZOLE RESISTANCE: high. BISMUTH: availability? Bismuth subcitrate may be available. TETRACYCLINE: available. UBT: limited availability. STOOL ANTIGEN: limited. SEROLOGY: widely available, but NOT USEFUL for active diagnosis (only for epidemiology). ENDOSCOPY/RAPID UREASE TEST/HISTOLOGY: available tertiary. ERADICATION REGIMEN: Bismuth quadruple may be preferable first-line (avoid clarithromycin resistance). If bismuth unavailable: TRIPLE THERAPY (PPI/amoxicillin/clarithromycin) 14d. If failure: METRONIDAZOLE/ TETRACYCLINE/BISMUTH (quadruple) or LEVOFLOXACIN triple. Adherence counselling. TEST OF CURE: often not performed (cost). Reinfection rate in Africa: high? (unsafe water, crowding). Focus: TREAT SYMPTOMATIC PATIENTS (PUD, dyspepsia with risk factors), CONFIRM ERADICATION (if resources allow).