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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Solitary Rectal Ulcer Syndrome
Solitary rectal ulcer syndrome (SRUS) is a rare, benign disorder of defecation, characterized by CHRONIC CONSTIPATION, EXCESSIVE STRAINING, and a BENIGN RECTAL ULCER (or erythematous, polypoid lesion). For Zambian students, SRUS is a DIAGNOSTIC CHALLENGE, often misdiagnosed as malignancy, IBD, or infection. PATHOPHYSIOLOGY: Dysfunctional defecation, PARADOXICAL CONTRACTION (non-relaxation) of PUBORECTALIS and EXTERNAL ANAL SPHINCTER during straining → direct trauma, ischemia, mucosal prolapse → ulceration. CLINICAL: YOUNG ADULTS (30-50y), female predominance. CHRONIC CONSTIPATION, EXCESSIVE STRAINING, INCOMPLETE EVACUATION. RECTAL BLEEDING (bright red, small volume), MUCOUS DISCHARGE, TENESMUS, PERINEAL PAIN. 'SOLITARY' ULCER is solitary in 70%, multiple in 30%, located on ANTERIOR RECTAL WALL (7-10cm from anal verge). ENDOSCOPY: TYPICAL: well-demarcated, shallow ulcer, erythematous rim, white slough base. ATYPICAL: POLYPOID, NODULAR, HYPEREMIC MUCOSA (mimics neoplasia, prolapse). HISTOLOGY: PATHOGNOMONIC: FIBROMUSCULAR OBLITERATION of lamina propria (smooth muscle fibres extending between crypts), thickened muscularis mucosae, regenerative changes, NO dysplasia, NO malignancy. DIAGNOSIS: CLINICAL SUSPICION + ENDOSCOPY + BIOPSY. DEFECOGRAPHY (evacuation proctography): non-relaxing puborectalis, internal rectal prolapse, intussusception. ANORECTAL MANOMETRY: dyssynergic defecation. EXCLUDE: RECTAL CANCER (biopsy mandatory), IBD (Crohn's, UC), INFECTION (LGV, TB, amoebiasis, CMV), ISCHEMIA, NSAID-induced. MANAGEMENT: CONSERVATIVE (FIRST-LINE): HIGH-FIBRE DIET, FIBRE SUPPLEMENTS (psyllium), BOWEL RETRAINING, BIOFEEDBACK (pelvic floor physiotherapy). AVOID STRAINING. SUCRALFATE ENEMAS, 5-ASA ENEMAS, TOPICAL CORTICOSTEROIDS (limited efficacy). SURGERY: INDICATED for REFRACTORY SYMPTOMS, SEVERE PROLAPSE, COMPLICATIONS (bleeding). PROCEDURES: RECTAL PROLAPSE REPAIR (Delorme, Altemeier, rectopexy), LOCAL EXCISION (rare). Prognosis: CHRONIC, BENIGN. No malignant potential. 70% improve with conservative therapy/biofeedback. Surgery effective for prolapse. Zambian context: SRUS IS RARE, UNDERDIAGNOSED. SUSPECT in young patient with chronic constipation, straining, rectal bleeding, anterior rectal ulcer. BIOPSY is ESSENTIAL (exclude cancer, IBD, TB). HISTOLOGY (fibromuscular obliteration) is diagnostic. FIBRE SUPPLEMENTS (psyllium), BOWEL RETRAINING, BIOFEEDBACK (limited availability). SURGERY: rectal prolapse repair (available). FOCUS: CLINICAL SUSPICION, COLONOSCOPY + BIOPSY (mandatory), CONSERVATIVE MANAGEMENT, SURGERY FOR PROLAPSE. DO NOT MISDIAGNOSE AS CANCER.
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Anogenital Warts (Condyloma Acuminata)
Anogenital warts are BENIGN EPITHELIAL PROLIFERATIONS caused by HUMAN PAPILLOMAVIRUS (HPV), primarily types 6 and 11 (low-risk). For Zambian students, they are EXTREMELY COMMON, frequently presenting to surgical, dermatology, and STI clinics. They are HIGHLY INFECTIOUS and have PSYCHOSOCIAL IMPACT. PATHOPHYSIOLOGY: HPV infects basal keratinocytes via microabrasions, viral replication induces acanthosis, papillomatosis, hyperkeratosis. Transmission: sexual, autoinoculation, vertical. INCUBATION: weeks to months. CLINICAL: EXOPHYTIC, CAULIFLOWER-LIKE, FLESHY, PINK/GREY PAPULES OR NODULES. Perianal, perineum, anal canal, vulva, vagina, cervix, penis, scrotum, groin. SIZE: few mm to large masses. ASYMPTOMATIC, or PRURITUS, BLEEDING, DISCHARGE, COSMETIC CONCERN. GIANT CONDYLOMA (BUSCHKE-LOWENSTEIN TUMOUR): rare, locally aggressive, destructive, but benign (verrucous carcinoma, HPV 6/11). DIAGNOSIS: CLINICAL (visual inspection). ANOSCOPY: intra-anal warts. BIOPSY: INDICATED if atypical (pigmented, indurated, ulcerated, fixed, rapidly growing, immunosuppressed) to exclude high-grade dysplasia (HSIL) or squamous cell carcinoma (HPV 16/18). MANAGEMENT: PATIENT EDUCATION: HPV is common, transmitted sexually, condoms reduce risk, treat sexual partners (examination, not mandatory), self-resolution possible, recurrence common. NO SINGLE BEST THERAPY. PATIENT-APPLIED: PODOPHYLLOTOXIN 0.5% solution/gel (BID x3d/week, up to 4 cycles). IM IQUIMOD 5% cream (3x/week, up to 16 weeks). SINECATECHINS 15% ointment (green tea extract). PROVIDER-APPLIED: CRYOTHERAPY (liquid nitrogen, q1-2 weeks). TRICHLOROACETIC ACID (TCA) 80-90% (weekly). SURGICAL: EXCISION (scissor snip, curettage, electrocautery, laser). PODOPHYLLIN RESIN (10-25%): provider-applied, toxic, NOT recommended. INTRALESIONAL: interferon. IMMUNOSUPPRESSED (HIV): higher recurrence, treat underlying HIV, consider imiquimod, TCA, surgery. PREVENTION: HPV VACCINE (quadrivalent, 9-valent) covers HPV 6, 11, 16, 18. Highly effective for primary prevention. Prognosis: BENIGN. Recurrence rate HIGH (20-70%), regardless of therapy. Clears spontaneously in 20-30% within 6 months. HIV, immunosuppression: worse. Malignant transformation RARE (except Buschke-Lowenstein, HPV 16/18-related HSIL/cancer). Zambian context: ANOGENITAL WARTS ARE COMMON. HIGH HIV PREVALENCE (more common, severe, recurrent). DIAGNOSIS: clinical. PODOPHYLLOTOXIN: available? Imiquimod: available (expensive). CRYOTHERAPY: available (tertiary). TCA: available. SURGICAL EXCISION: widely available (surgical clinic, cautery). PODOPHYLLIN: available? HPV VACCINE: available (private sector, expensive), NOT in EPI. FOCUS: CLINICAL DIAGNOSIS, PATIENT-APPLIED THERAPY (podophyllotoxin, imiquimod) if accessible, PROVIDER-APPLIED (TCA, cryotherapy), SURGICAL EXCISION for large, refractory, or giant lesions. COUNSELLING (STI screening, condoms, HPV vaccine). HIV TESTING (recommended).
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Pruritus Ani
Pruritus ani is an INTENSE, CHRONIC ITCHING of the perianal skin, a COMMON and DISTRESSING condition. For Zambian students, it is frequently encountered but often mismanaged. PATHOPHYSIOLOGY: Idiopathic (primary) or SECONDARY to dermatologic, infectious, anorectal, or dietary causes. SECONDARY CAUSES: DERMATOLOGIC: psoriasis, atopic dermatitis, contact dermatitis (soaps, perfumes, topical anaesthetics). INFECTIOUS: PINWORMS (Enterobius vermicularis, children, nocturnal), CANDIDA (moist, satellite lesions), DERMATOPHYTES (tinea cruris), ERYTHRASMA (Corynebacterium, coral-red fluorescence), HPV (warts), HSV. ANORECTAL: hemorrhoids, fissure, fistula, prolapse, neoplasia (Paget's, Bowen's). DIETARY: caffeine, spicy foods, citrus, tomatoes, alcohol. HYGIENE: excessive cleaning (soap, scrubbing) or poor hygiene. CLINICAL: INTENSE, REFRACTORY ITCHING, worse at night, after defecation, with stress. Excoriations, lichenification, erythema, maceration. DIAGNOSIS: HISTORY and PHYSICAL EXAMINATION. IDENTIFY UNDERLYING CAUSE. STOOL TEST for pinworms (cellophane tape test). SKIN SCRAPING (KOH) for fungus. BIOPSY if atypical (persistent, unilateral, indurated, ulcerated) to exclude Paget's, Bowen's, SCC. MANAGEMENT: GENERAL MEASURES (CORNERSTONE): GENTLE CLEANSING (water only, or emollient cleanser), PAT DRY (no rubbing), AVOID SOAP, PERFUMES, WIPES. COTTON UNDERWEAR, loose clothing. DIETARY MODIFICATION: eliminate triggers (caffeine, spicy foods, citrus, tomatoes, alcohol) for 2 weeks, then reintroduce. TOPICAL: ZINC OXIDE (barrier), 1% HYDROCORTISONE cream (short-term, <2 weeks, for inflammation). AVOID topical anaesthetics (benzocaine, lidocaine—sensitizing). TREAT UNDERLYING CAUSE: anti-helminthics (pinworms), antifungals, treat anorectal disease. Prognosis: GOOD with consistent perianal hygiene and trigger avoidance. Recurrence common. Zambian context: PRURITUS ANI IS COMMON. PINWORMS (Enterobius) are prevalent in children, consider in all cases. CANDIDA: common in HIV, diabetes, antibiotic use. HYGIENE ADVICE: accessible, effective. TOPICAL STEROIDS (hydrocortisone): available. ANTIFUNGALS (clotrimazole, miconazole): available. ANTI-HELMINTHICS (albendazole, mebendazole): available. FOCUS: IDENTIFY SECONDARY CAUSES (pinworms, candida, anorectal disease), HYGIENE MEASURES, ELIMINATION DIET, SHORT-TERM TOPICAL STEROIDS.
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Fecal Incontinence
Fecal incontinence (FI) is the INVOLUNTARY LOSS OF SOLID OR LIQUID STOOL, a DEVASTATING, STIGMATIZING condition affecting quality of life. For Zambian students, FI is UNDERREPORTED and UNDERDIAGNOSED. ETIOLOGY: NORMAL STOOL CONSISTENCY + NORMAL ANAL SPHINCTER + NORMAL PELVIC FLOOR + NORMAL RECTAL SENSATION + NORMAL COGNITION/MOBILITY. Disruption of any component. COMMON CAUSES: OBSTETRIC INJURY (vaginal delivery, forceps, episiotomy, occult sphincter tear) → most common in women. IATROGENIC (anorectal surgery: fistulotomy, sphincterotomy, hemorrhoidectomy). NEUROLOGIC: diabetic neuropathy, spinal cord injury, multiple sclerosis, stroke, dementia. PELVIC FLOOR DYSFUNCTION: rectal prolapse, descending perineum syndrome. DIARRHEA (loose stool overwhelms continence). IMPACTION WITH OVERFLOW (elderly, nursing home). CLINICAL: PASSIVE INCONTINENCE (unaware, loss of solid/liquid stool) → internal sphincter dysfunction. URGENCY INCONTINENCE (unable to defer defecation) → external sphincter/pelvic floor dysfunction. SOILING (staining of underwear) → often hemorrhoids, prolapse, poor hygiene. SEVERITY: Cleveland Clinic Florida (Wexner) score. DIAGNOSIS: HISTORY (obstetric, surgical, neurological, stool consistency). PHYSICAL EXAM: perianal inspection (scarring, gaping, prolapse, dermatitis), digital rectal exam (resting tone, squeeze pressure, sensation, stool impaction). ENDOANAL ULTRASOUND: GOLD STANDARD for sphincter defects. ANORECTAL MANOMETRY: resting/squeeze pressures, sensation, compliance, rectoranal inhibitory reflex. MRI DEFECOGRAPHY: pelvic floor dysfunction, prolapse, intussusception. MANAGEMENT: CONSERVATIVE (FIRST-LINE): DIARRHEA CONTROL: antidiarrheals (LOPERAMIDE, diphenoxylate, codeine). BULKING AGENTS: psyllium (improves stool consistency). BOWEL PROGRAM: scheduled defecation, stimulated defecation (glycerin suppository). PELVIC FLOOR REHABILITATION: biofeedback, pelvic floor exercises (Kegel). PERIANAL SKIN CARE: barrier creams, cleansing. PESSARY: vaginal support for prolapse. SURGICAL: SPHINCTER REPAIR (overlapping sphincteroplasty) for defined sphincter defect (obstetric injury). SACRAL NERVE STIMULATION (SNS): neuromodulation, effective for FI without major sphincter defect. GRACILOPLASTY, ARTIFICIAL BOWEL SPHINCTER, COLOSTOMY (last resort). Prognosis: CONSERVATIVE therapy improves 60-70%. Sphincteroplasty: 50-70% good short-term, long-term outcomes decline. SNS: 80% improvement. Zambian context: FI IS UNDERDIAGNOSED. ETIOLOGIES: OBSTETRIC INJURY (common), ANORECTAL SURGERY (fistulotomy), NEUROLOGIC (diabetes, spinal TB), PROLAPSE, IMPACTION (elderly). ENDOANAL ULTRASOUND: NOT AVAILABLE. ANORECTAL MANOMETRY: NOT AVAILABLE. DIAGNOSIS: CLINICAL (history, DRE). CONSERVATIVE: LOPERAMIDE (available), PSYLLIUM (available), BIOFEEDBACK (limited). SURGERY: SPHINCTER REPAIR (overlapping sphincteroplasty) available (colorectal surgeons, limited). SACRAL NERVE STIMULATION: NOT AVAILABLE. COLOSTOMY: available. FOCUS: IDENTIFY AND TREAT REVERSIBLE CAUSES (diarrhea, impaction, prolapse), CONSERVATIVE THERAPY (loperamide, psyllium, bowel program), SPHINCTER REPAIR (if defect, surgical expertise), COLOSTOMY (severe, refractory).
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Chronic Constipation
Chronic constipation is a COMMON, SYMPTOM-BASED disorder defined by ROME IV CRITERIA: ≥2 of: straining, lumpy/hard stools, sensation of incomplete evacuation, sensation of anorectal obstruction, manual manoeuvres, <3 defecations per week, for >3 months. For Zambian students, constipation is a DAILY CLINICAL PROBLEM. SUBTYPES: NORMAL TRANSIT CONSTIPATION (most common), SLOW TRANSIT CONSTIPATION (colonic inertia), DEFECATORY DISORDERS (pelvic floor dyssynergia, obstructed defecation). ETIOLOGY: PRIMARY (FUNCTIONAL): no identifiable cause. SECONDARY: MEDICATIONS (opioids, iron, calcium channel blockers, anticholinergics), ENDOCRINE (hypothyroidism, diabetes, hypercalcaemia), NEUROLOGIC (Parkinson's, spinal cord injury, autonomic neuropathy), OBSTRUCTION (colorectal cancer, stricture, volvulus), PELVIC FLOOR DYSFUNCTION, SYSTEMIC (scleroderma). DIAGNOSIS: HISTORY (Rome IV criteria, alarm features: rectal bleeding, weight loss, family history CRC, anaemia, onset >50y). PHYSICAL EXAM: abdominal mass, digital rectal exam (pelvic floor dyssynergia, stricture, cancer, impaction). LABS: TSH, calcium, glucose. COLONOSCOPY: INDICATED for ALARM FEATURES, CRC screening, age ≥50y. ANORECTAL PHYSIOLOGY TESTING: anorectal manometry, balloon expulsion test, defecography (for suspected defecatory disorders, refractory). MANAGEMENT: CONSERVATIVE (ALL PATIENTS): DIETARY FIBRE 20-30g/day, increased fluids, regular exercise, scheduled defecation (postprandial). FIBRE SUPPLEMENTS: PSYLLIUM (ispaghula), methylcellulose. OSMOTIC LAXATIVES: POLYETHYLENE GLYCOL (PEG, macrogol), LACTULOSE, MAGNESIUM HYDROXIDE. STIMULANT LAXATIVES: BISACODYL, SENNA (short-term, rescue). SECRETAGOGUES: LUBIPROSTONE, LINACLOTIDE, PLEGOTIDE (IBS-C, chronic idiopathic constipation, unavailable). SEROTONIN AGONISTS: PRUCALOPRIDE (slow-transit constipation, unavailable). DEFECATORY DISORDERS: BIOFEEDBACK (pelvic floor retraining) is FIRST-LINE, HIGHLY EFFECTIVE. SURGERY: SUBTOTAL COLECTOMY with ILEORECTAL ANASTOMOSIS (EXTREME, selected slow-transit constipation, fails all therapy). Prognosis: MOST improve with fibre, laxatives. Biofeedback 70-80% effective. Zambian context: CHRONIC CONSTIPATION IS COMMON. DIETARY FIBRE: inadequate intake (low fruit, vegetable consumption). PSYLLIUM (ispaghula): available, inexpensive. LACTULOSE: available. BISACODYL, SENNA: available. PEG (macrogol): available (cost). COLONOSCOPY: available tertiary, limited by cost/capacity. BIOFEEDBACK: NOT AVAILABLE. PRUCALOPRIDE, LINACLOTIDE: NOT AVAILABLE. SURGERY: colectomy available, extremely rare. FOCUS: DIETARY FIBRE (counselling), PSYLLIUM, LACTULOSE, STIMULANT LAXATIVES (short-term), IDENTIFY RED FLAGS (colonoscopy), EXCLUDE SECONDARY CAUSES (hypothyroidism, drugs, cancer).
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Clostridium difficile Infection
Clostridium difficile infection (CDI) is a TOXIN-MEDIATED, antibiotic-associated diarrheal disease, the MOST COMMON CAUSE of HEALTHCARE-ASSOCIATED INFECTIOUS DIARRHEA. For Zambian students, CDI is UNDERDIAGNOSED, but likely EMERGING with increased antibiotic use, healthcare exposure, and immunocompromise (HIV, TB). PATHOPHYSIOLOGY: Disruption of normal gut microbiota (antibiotics) → C. difficile overgrowth, produces TOXIN A (enterotoxin) and TOXIN B (cytotoxin) → mucosal inflammation, necrosis, pseudomembrane formation. RISK FACTORS: ANTIBIOTICS (clindamycin, cephalosporins, fluoroquinolones, penicillins—high risk), ADVANCED AGE, HOSPITALIZATION, LONG-TERM CARE, PPI USE, CHEMOTHERAPY, IBD, IMMUNOCOMPROMISE. CLINICAL: WATERY DIARRHEA (mild to profuse), LOWER ABDOMINAL PAIN, FEVER, LEUKOCYTOSIS. SEVERE CDI: leukocytosis >15,000, elevated creatinine (>1.5x baseline), hypotension, ileus, toxic megacolon, shock. FULMINANT COLITIS: hypotension, shock, ileus, megacolon, perforation, peritonitis. DIAGNOSIS: STOOL TEST. NUCLEIC ACID AMPLIFICATION TEST (NAAT, PCR): detects toxin gene, HIGHLY SENSITIVE, does NOT distinguish colonization from active infection. TOXIN A/B ENZYME IMMUNOASSAY (EIA): detects toxin, LESS SENSITIVE (60-80%), more specific for active disease. GLUTAMATE DEHYDROGENASE (GDH) SCREEN: sensitive, requires confirmatory toxin test (two-step algorithm). ENDOSCOPY (flexible sigmoidoscopy): pseudomembranes (raised, yellow-white plaques), NOT routine, reserved for diagnostic uncertainty, suspected fulminant colitis. MANAGEMENT: INFECTION CONTROL: CONTACT PRECAUTIONS, hand hygiene (soap and water—alcohol resistant), environmental disinfection. SUPPORTIVE: IV fluids, electrolytes, AVOID ANTI-MOTILITY AGENTS (loperamide, opioids). DISCONTINUE OFFENDING ANTIBIOTIC if possible. ANTIBIOTICS: ORAL VANCOMYCIN 125mg QID x 10d is FIRST-LINE for ALL SEVERITY. METRONIDAZOLE 500mg TID x 10d (oral/IV) is INFERIOR, reserve if vancomycin unavailable. FIDAXOMICIN 200mg BID x 10d: NON-INFERIOR, lower recurrence. SEVERE CDI: VANCOMYCIN 125mg QID ORAL + IV METRONIDAZOLE. FULMINANT CDI (ileus, toxic megacolon): VANCOMYCIN via NG TUBE + IV METRONIDAZOLE, plus VANCOMYCIN RECTAL ENEMA. SURGERY: EMERGENCY SUBTOTAL COLECTOMY for fulminant colitis, perforation, necrotizing enterocolitis. RECURRENT CDI (20-30% after first episode, 40-60% after second): PULSED/VANCOMYCIN TAPER (125mg QID x10-14d, then BID x7d, then daily x7d, then q2d x2-8weeks). FIDAXOMICIN. FAECAL MICROBIOTA TRANSPLANTATION (FMT): HIGHLY EFFECTIVE (90%) for recurrent CDI, investigational. BEZ LOTOXUMAB (monoclonal anti-toxin B): reduces recurrence. PROGNOSIS: 5-10% mortality (severe CDI). Recurrence common. Zambian context: CDI IS UNDERDIAGNOSED. DIAGNOSTIC TESTING: NOT ROUTINELY AVAILABLE. NAAT/EIA: limited. Suspect CDI in: hospitalized patient, recent antibiotics, profuse watery diarrhea, leukocytosis. ENDOSCOPY: pseudomembranes (if available). MANAGEMENT: ORAL VANCOMYCIN: available (cost). METRONIDAZOLE: available, inexpensive. FIDAXOMICIN, BEZ LOTOXUMAB: NOT AVAILABLE. FMT: NOT AVAILABLE. INFECTION CONTROL: contact precautions, soap/water hand hygiene (feasible). SURGERY: colectomy available. FOCUS: CLINICAL SUSPICION (antibiotics + diarrhea), EMPIRIC THERAPY (oral vancomycin or metronidazole), DISCONTINUE OFFENDING ANTIBIOTIC, INFECTION CONTROL. CDI is an IMPORTANT EMERGING DIAGNOSIS.
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Eosinophilic Esophagitis: Diagnosis and Management
Eosinophilic esophagitis (EoE) is a chronic, TH2-mediated, antigen-driven esophageal disease characterized by symptoms of esophageal dysfunction and EOSINOPHIL-PREDOMINANT INFLAMMATION (≥15 eosinophils/HPF). For Zambian students, EoE is an EMERGING DIAGNOSIS in adults with DYSPHAGIA and FOOD IMPACTION. PATHOPHYSIOLOGY: Food antigens (milk, wheat, egg, soy, peanut, fish/shellfish) trigger Th2 response → IL-5, IL-13 → eosinophil recruitment, degranulation → edema, fibrosis, remodeling. Associated with atopy (asthma, eczema, allergic rhinitis, 50-80%). CLINICAL: ADULTS: DYSPHAGIA (90%, solid food), FOOD IMPACTION (50-60%), HEARTBURN (GERD-like, PPI-refractory). CHILDREN: feeding refusal, vomiting, abdominal pain, failure to thrive. ENDOSCOPY: RINGS (trachealization, corrugated), FURROWS (linear, vertical), EXUDATES (white plaques, eosinophilic microabscesses), CREPE PAPER MUCOSA (friable, tears with scope passage), STRICTURES (proximal, long-segment). NORMAL ENDOSCOPY in 10% (biopsy is key). HISTOLOGY: GOLD STANDARD: ≥15 eosinophils/HPF (peak count) in esophageal epithelium. Eosinophil microabscesses, superficial layering, basal zone hyperplasia, dilated intercellular spaces. DISTAL AND PROXIMAL biopsies required. DIAGNOSIS: Symptoms of esophageal dysfunction + eosinophilic infiltration (≥15 eos/HPF) + exclusion of other causes (GERD, PPI-REE, achalasia, Crohn's, parasitic, drug). PPI TRIAL: high-dose PPI for 8 weeks, then re-biopsy. PPI-RESPONSIVE ESOPHAGEAL EOSINOPHILIA (PPI-REE) is indistinguishable; some consider it EoE responsive to PPI. MANAGEMENT: DIETARY THERAPY (children, motivated adults): ELEMENTAL DIET (amino-acid based), SIX-FOOD ELIMINATION DIET (SFED: milk, wheat, egg, soy, peanut/tree nut, fish/shellfish). Reintroduction to identify triggers. PHARMACOLOGIC: TOPICAL CORTICOSTEROIDS: SWALLOWED FLUTICASONE (MDI, 880-1760 mcg/day, spray and swallow) or ORAL BUDESONIDE (viscous suspension, 1-2mg/day, mixed with thickener). Swallow, NOT inhale. No systemic absorption. DILATION: ENDOSCOPIC DILATION for strictures (high perforation risk, gradual, bougie or balloon). BIOLOGICS: DUPILUMAB (anti-IL-4/13), FDA-approved for EoE, improves dysphagia, histology. Prognosis: CHRONIC, RELAPSING. Treatment is suppressive, not curative. No malignant potential. Zambian context: EoE IS RARE but increasingly recognized. DYSPHAGIA + FOOD IMPACTION = SUSPECT. ENDOSCOPY + BIOPSIES (multiple levels) essential. PATHOLOGY: eosinophil count. PPI trial accessible. SWALLOWED FLUTICASONE: inhaler (press-and-breathe) available, off-label use. BUDESONIDE (nebuliser suspension) available. DIETARY ELIMINATION challenging. DUPILUMAB: NOT AVAILABLE. DILATION: available. HIGH INDEX OF SUSPICION.
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Oropharyngeal Dysphagia
Oropharyngeal dysphagia (transfer dysphagia) is difficulty initiating a swallow, transferring food from mouth to esophagus. For Zambian students, it is a COMMON NEUROLOGIC PRESENTATION, distinct from esophageal dysphagia. PATHOPHYSIOLOGY: Impaired oral preparatory, oral transit, or pharyngeal phase. CAUSES: NEUROLOGIC (80%): STROKE (most common), PARKINSON'S, MULTIPLE SCLEROSIS, ALS, DEMENTIA, POLIOMYELITIS, MYASTHENIA GRAVIS, BRAINSTEM TUMOUR. MUSCULAR: dermatomyositis, polymyositis, muscular dystrophies. STRUCTURAL: cricopharyngeal bar/achalasia, Zenker's diverticulum, oropharyngeal tumour (SCC), post-surgical, radiation. CLINICAL: DIFFICULTY INITIATING SWALLOW, food 'sticks' in throat, NASAL REGURGITATION, TRACHEAL ASPIRATION (coughing, choking during meals), DROOLING, POCKETING of food in buccal sulcus, WEIGHT LOSS. WET, GURGLY VOICE after swallow. PHYSICAL EXAM: cranial nerve exam (IX, X, XII), palatal elevation, gag reflex, tongue strength, voice. WATER SWALLOW TEST: observe for cough, throat clearing, voice change. DIAGNOSIS: VIDEOFLUOROSCOPIC SWALLOW STUDY (VFSS, modified barium swallow): GOLD STANDARD. Assess oral, pharyngeal, esophageal phases, aspiration, response to compensatory manoeuvres. FIBEROPTIC ENDOSCOPIC EVALUATION OF SWALLOWING (FEES): bedside, assesses pharyngeal sensation, secretions, aspiration. MANAGEMENT: TREAT UNDERLYING CAUSE (Parkinson's, myasthenia, tumour). SWALLOW THERAPY: COMPENSATORY (chin tuck, head turn, effortful swallow), POSTURAL TECHNIQUES, DIETARY MODIFICATION (thickened liquids, pureed solids). ENTERAL FEEDING (NG tube, PEG) if severe aspiration, inadequate nutrition. CRICOPHARYNGEAL MYOTOMY (for cricopharyngeal bar, Zenker's). Prognosis: DEPENDS ON ETIOLOGY. Post-stroke: 50% recover within 2 weeks. Progressive neurologic disease: worsens. Aspiration pneumonia = major morbidity, mortality. Zambian context: OROPHARYNGEAL DYSPHAGIA IS COMMON. STROKE is #1 cause. PARKINSON'S, POLIO SEQUELAE, TB MENINGITIS (basal, cranial nerve palsies), HIV (neurologic), ORAL SCC (late). DIAGNOSIS: CLINICAL (water swallow test, cranial nerve exam). VFSS: NOT AVAILABLE. FEES: NOT AVAILABLE. MANAGEMENT: DIETARY MODIFICATION (soft, pureed, thickened fluids—sorghum porridge), COMPENSATORY TECHNIQUES (chin tuck), NG TUBE FEEDING, PEG (available tertiary). SPEECH THERAPY: limited. FOCUS: CLINICAL DIAGNOSIS, ASPIRATION PREVENTION (thickened fluids, tube feeding), TREAT REVERSIBLE CAUSES (myasthenia, Parkinson's, TB), REFERRAL FOR PEG (if prolonged).
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Topic 270Coming soon
Esophageal Motility Disorders
Esophageal motility disorders are a heterogeneous group of conditions characterized by ABNORMAL ESOPHAGEAL CONTRACTILITY or RELAXATION, causing DYSPHAGIA and CHEST PAIN. For Zambian students, diagnosis is challenging as HIGH-RESOLUTION MANOMETRY (HRM) is NOT AVAILABLE; recognition relies on CLINICAL PRESENTATION and BARIUM SWALLOW. CLASSIFICATION (CHICAGO CLASSIFICATION v4.0): ACHALASIA (Type I, II, III), EGJ OUTFLOW OBSTRUCTION, ABSENT CONTRACTILITY, DISTAL ESOPHAGEAL SPASM (DES), HYPERCONTRACTILE (JACKHAMMER) ESOPHAGUS, INEFFECTIVE ESOPHAGEAL MOTILITY (IEM). ACHALASIA: see topic. EGJ OUTFLOW OBSTRUCTION: impaired EGJ relaxation with preserved peristalsis. Causes: mechanical (stricture, tumour, vascular), motility disorder. IDIOPATHIC. DISTAL ESOPHAGEAL SPASM (DES): PREMATURE CONTRACTIONS (distal latency <4.5s), NORMAL EGJ relaxation. CLINICAL: CHEST PAIN, DYSPHAGIA (intermittent). BARIUM: CORkscrew esophagus, ROSARY BEAD esophagus. MANAGEMENT: CALCIUM CHANNEL BLOCKERS, NITRATES (sublingual), BOTULINUM TOXIN, PNEUMATIC DILATION, LONG MYOTOMY (surgical, POEM). HYPERCONTRACTILE (JACKHAMMER) ESOPHAGUS: HYPERCONTRACTILE (>800 mmHg) peristalsis, NORMAL EGJ relaxation. CLINICAL: DYSPHAGIA, CHEST PAIN. MANAGEMENT: similar to DES. ABSENT CONTRACTILITY: no peristalsis, NORMAL EGJ relaxation. Rule out achalasia, scleroderma. SCLERODERMA: smooth muscle atrophy, low LES pressure, absent peristalsis, SEVERE GERD, stricture. MANAGEMENT: aggressive PPI, prokinetics (limited). INEFFECTIVE ESOPHAGEAL MOTILITY (IEM): weak or failed peristalsis (>50% ineffective swallows). Associated with GERD, connective tissue disease. CLINICAL: DYSPHAGIA (mild), GERD. MANAGEMENT: treat GERD (PPI). PROKINETICS: limited efficacy. DIAGNOSIS: BARIUM SWALLOW (solid, tablet) may show abnormalities (corkscrew, bird-beak, poor emptying). ESOPHAGOGASTRODUODENOSCOPY (EGD): exclude pseudoachalasia (malignancy), stricture. ESOPHAGEAL MANOMETRY: GOLD STANDARD. Zambian context: ESOPHAGEAL MANOMETRY IS NOT AVAILABLE. DIAGNOSIS is CLINICAL + BARIUM SWALLOW. ACHALASIA is the most common and treatable. SUSPECT DES/JACKHAMMER in patient with intermittent dysphagia and chest pain, normal barium/endoscopy. SCLERODERMA: skin thickening, Raynaud's, severe GERD, barium shows dilated esophagus, poor peristalsis. MANAGEMENT: ACHALASIA: Heller myotomy, pneumatic dilation (available). DES/JACKHAMMER: calcium channel blockers, nitrates (trial), botulinum toxin (if available). IEM: treat GERD (PPI). FOCUS: EXCLUDE ACHALASIA (barium, endoscopy), DISTINGUISH from DES/JACKHAMMER (intermittent symptoms, chest pain), MANAGE GERD aggressively in scleroderma/IEM.