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 271Coming soon
Gastroparesis
Gastroparesis is a chronic disorder characterized by DELAYED GASTRIC EMPTYING in the absence of mechanical obstruction, with symptoms of postprandial fullness, nausea, vomiting, and abdominal pain. For Zambian students, gastroparesis is an UNDERDIAGNOSED condition, often misattributed to dyspepsia or GERD. PATHOPHYSIOLOGY: Impaired gastric motility due to autonomic neuropathy, loss of interstitial cells of Cajal (pacemaker cells), smooth muscle dysfunction, or neuronal nitric oxide synthase deficiency. ETIOLOGY: DIABETIC (most common, type 1 > type 2, poor glycemic control, autonomic neuropathy). IDIOPATHIC (30-50%). POST-SURGICAL (vagal injury: fundoplication, esophagectomy, gastrectomy). NEUROLOGIC: Parkinson's disease, multiple sclerosis, brainstem stroke. MEDICATIONS: GLP-1 agonists, opiates, anticholinergics. CONNECTIVE TISSUE DISEASE: scleroderma, SLE. ENDOCRINE: hypothyroidism. CLINICAL: NAUSEA (90%), VOMITING (undigested food, hours after meals), POSTPRANDIAL FULLNESS (early satiety), ABDOMINAL PAIN (epigastric, bloating), WEIGHT LOSS, MALNUTRITION. BEZOAR formation (20%). PHYSICAL EXAM: epigastric distension, succussion splash (delayed). DIAGNOSIS: DELAYED GASTRIC EMPTYING STUDY: GOLD STANDARD. Scintigraphy: solid meal, % retained at 2h (>60%) and 4h (>10%). GASTRIC EMPTYING BREATH TEST (13C-octanoate, spirulina). ENDOSCOPY: rule out mechanical obstruction (ulcer, tumour, pyloric stenosis). GASTRODUODENAL MANOMETRY: antral hypomotility, pylorospasm. MANAGEMENT: DIETARY: SMALL, FREQUENT, LOW-FAT, LOW-FIBRE MEALS. LIQUID NUTRIENTS (better tolerated). AVOID high-fat, high-fibre foods. HYDRATION. GLYCEMIC CONTROL (diabetic gastroparesis, insulin preferred). PHARMACOLOGIC: PROKINETICS: METOCLOPRAMIDE (5-10mg TID AC, IV for acute), dopamine antagonist, central antiemetic. BLACK BOX WARNING: tardive dyskinesia (long-term use). Limit to 12 weeks. DOMPERIDONE (peripheral dopamine antagonist, no CNS side effects, QT prolongation). ERYTHROMYCIN (motilin agonist, IV acute, oral tolerance). ANTIEMETICS: ondansetron, promethazine. NEUROMODULATORS: for pain (TCAs, gabapentin, pregabalin). REFRACTORY: GASTRIC PERORAL ENDOSCOPIC MYOTOMY (G-POEM): endoscopic pyloromyotomy, for pylorospasm. SURGICAL: JEJUNOSTOMY TUBE (feeding, venting), GASTRIC ELECTRICAL STIMULATION (controversial, humanitarian exemption). Prognosis: CHRONIC, RELAPSING. No cure. Diabetic gastroparesis: poor glycemic control accelerates progression. Idiopathic: stable course. Morbidity: malnutrition, bezoars, aspiration. Zambian context: GASTROPARESIS IS UNDERDIAGNOSED. DIABETES prevalence rising → diabetic gastroparesis increasing. ENDOSCOPY available (exclude obstruction). GASTRIC EMPTYING STUDY: NOT AVAILABLE. CLINICAL DIAGNOSIS (symptoms, delayed gastric emptying on barium meal/endoscopy, no obstruction). METOCLOPRAMIDE: available, inexpensive, use SHORT-TERM. DOMPERIDONE: available. ERYTHROMYCIN: available. ANTIEMETICS: available. G-POEM: NOT AVAILABLE. JEJUNOSTOMY: available (surgery). FOCUS: CLINICAL SUSPICION (diabetic with refractory nausea, vomiting, postprandial fullness), EXCLUDE OBSTRUCTION (endoscopy), DIETARY MODIFICATION, GLYCEMIC CONTROL, PROKINETICS (metoclopramide, domperidone), ANTIEMETICS, SURGICAL FEEDING TUBE (severe malnutrition).
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Functional Dyspepsia
Functional dyspepsia (FD) is a COMMON, CHRONIC disorder of GUT-BRAIN INTERACTION defined by ROME IV CRITERIA: one or more of bothersome postprandial fullness, early satiation, epigastric pain, or epigastric burning, with NO ORGANIC DISEASE to explain symptoms after appropriate investigation. For Zambian students, FD is a DAILY DIAGNOSIS OF EXCLUSION, often mislabeled as 'gastritis'. PATHOPHYSIOLOGY: HETEROGENEOUS. Delayed gastric emptying, impaired gastric accommodation, visceral hypersensitivity, duodenal eosinophilia, altered duodenal microbiota, impaired mucosal integrity, psychological distress (anxiety, depression). H. pylori-associated dyspepsia: subset. SUBTYPES (Rome IV): EPS (EPIGASTRIC PAIN SYNDROME): meal-unrelated pain/burning, localized to epigastrium, not generalized, not relieved by defecation/flatus. PDS (POSTPRANDIAL DISTRESS SYNDROME): bothersome postprandial fullness, early satiation. OVERLAP common. DIAGNOSIS: ROME IV CRITERIA + symptom duration ≥6 months, last 3 months active. INVESTIGATIONS to EXCLUDE ORGANIC DISEASE: Upper endoscopy (EGD) is GOLD STANDARD. Indicated for ALARM FEATURES: age >50, weight loss, dysphagia, odynophagia, haematemesis, melaena, iron deficiency anaemia, family history GI cancer, abdominal mass, lymphadenopathy, jaundice. NON-INVASIVE H. PYLORI TESTING (urea breath test, stool antigen). LIMITED, AGE-APPROPRIATE INVESTIGATION. In low-prevalence H. pylori, empiric PPI trial. MANAGEMENT: GENERAL: REASSURANCE, EXPLANATION (brain-gut axis, visceral hypersensitivity), DIETARY ADVICE (small, frequent meals, avoid fatty/spicy foods, trigger foods). H. PYLORI ERADICATION: Test-and-treat in endemic areas (cost-effective, 10-15% long-term symptom improvement). PHARMACOLOGIC: PDS: PROKINETICS (metoclopramide, domperidone) – limited efficacy, side effects. ACUPUNCTURE? EPS: PPI (standard dose, 4-8 weeks trial). H2RA (ranitidine, famotidine) alternative. REFRACTORY: NEUROMODULATORS: LOW-DOSE TCAs (amitriptyline 10-25mg nocte), mirtazapine (PDS, weight loss), SSRIs (less effective). PSYCHOLOGICAL THERAPIES: CBT, gut-directed hypnotherapy. Prognosis: CHRONIC, RELAPSING. Quality of life impaired. No increased mortality. Zambian context: FD IS COMMON. H. pylori prevalence is HIGH. TEST-AND-TREAT H. pylori is recommended (urea breath test, stool antigen limited; serology IgG not useful for active infection). EMPIRIC PPI TRIAL (omeprazole) is accessible. ENDOSCOPY: available tertiary, limited by cost/capacity. ALARM FEATURES = PRIORITY for endoscopy. PROKINETICS: metoclopramide, domperidone available. LOW-DOSE AMITRIPTYLINE: available, inexpensive, effective. DIETARY ADVICE: small, low-fat meals (culturally appropriate). FOCUS: EXCLUDE ORGANIC DISEASE (alarm features, endoscopy if indicated), H. pylori TEST-AND-TREAT (if accessible), EMPIRIC PPI (EPS), LOW-DOSE AMITRIPTYLINE (refractory, pain), REASSURANCE. DO NOT LABEL AS 'GASTRITIS' without endoscopy.
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Cyclic Vomiting Syndrome
Cyclic vomiting syndrome (CVS) is a chronic functional gastrointestinal disorder characterized by RECURRENT, STEREOTYPED EPISODES of INTENSE NAUSEA and VOMITING, separated by completely SYMPTOM-FREE INTERVALS. For Zambian students, CVS is UNDERDIAGNOSED, often mistaken for 'recurrent gastroenteritis' or 'billous vomiting'. PATHOPHYSIOLOGY: Unknown. Mitochondrial dysfunction, autonomic dysregulation, hypothalamic-pituitary-adrenal axis activation, cannabinoid hyperemesis syndrome (CHS, a mimicker). Associated with MIGRAINE (family history), anxiety, panic disorder. CLINICAL: FOUR PHASES: INTEREPISODIC (asymptomatic, normal). PRODROME (impending attack, nausea, pallor, diaphoresis). EMETIC (intense nausea, relentless vomiting, 1-6 episodes/hour, 4-12 vomitus/hour, duration 1-5 days). RECOVERY (symptoms resolve, hunger returns). TRIGGERS: emotional stress, infection, sleep deprivation, certain foods, menstruation, motion sickness. CANNABINOID HYPEREMESIS SYNDROME (CHS): cyclic vomiting + COMPULSIVE HOT BATHING/SHOWERING (relieves symptoms), heavy, long-term cannabis use. DIAGNOSIS: ROME IV CRITERIA. STEREOTYPED EPISODES with onset <1 week apart, ≥2 episodes in last 6 months, at least 1 episode in past 3 months. EXCLUDE OTHER CAUSES (anatomical, metabolic, neurologic). UPPER ENDOSCOPY, ABDOMINAL IMAGING (CT/MRI), LABS (pancreatic, liver, renal, metabolic panel), NEUROIMAGING (MRI brain) if neurologic signs. MANAGEMENT: LIFESTYLE: IDENTIFY AND AVOID TRIGGERS, regular sleep, stress reduction. CANNABIS CESSATION (CHS). PROPHYLAXIS (INTEREPISODIC): AMITRIPTYLINE (10-50mg nocte) – FIRST-LINE, 80% response. TOPIRAMATE, ZONISAMIDE, PROPRANOLOL, CYPROHEPTADINE. ABORTIVE (PRODROME): LORAZEPAM, ONDANSETRON, SUMATRIPTAN (nasal, SC). SUPPORTIVE (EMETIC PHASE): INTRAVENOUS FLUIDS, ELECTROLYTES, 5-HT3 ANTAGONISTS (ondansetron), benzodiazepines, APREPITANT (NK1 antagonist), TRIMEBUTINE. DARK, QUIET ROOM. Prognosis: CHRONIC, RELAPSING. No cure. 80% respond to amitriptyline. CHS: resolves with cannabis cessation. Zambian context: CVS IS UNDERDIAGNOSED. CANNABIS USE is common. SUSPECT CVS/CHS in young adult with recurrent, stereotyped vomiting episodes, asymptomatic intervals. CANNABIS HISTORY: ask about hot bathing/showering (CHS). DIAGNOSIS: clinical, EXCLUDE other causes (endoscopy, imaging). AMITRIPTYLINE: available, inexpensive, FIRST-LINE PROPHYLAXIS. ONDANSETRON: available. LORAZEPAM: available. IV FLUIDS: available. CANNABIS CESSATION COUNSELLING: essential. FOCUS: CLINICAL DIAGNOSIS, CANNABIS CESSATION (CHS), AMITRIPTYLINE PROPHYLAXIS, SUPPORTIVE CARE (IVF, ondansetron) during attacks.
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Rumination Syndrome
Rumination syndrome is a FUNCTIONAL GASTRODUODENAL DISORDER characterized by REGURGITATION of recently ingested food into the mouth, RE-CHEWING, and either RE-SWALLOWING or SPITTING OUT, occurring within minutes of eating, WITHOUT RETCHING or NAUSEA. For Zambian students, it is a DIAGNOSIS OF EXCLUSION, often MISDIAGNOSED as refractory GERD or bulimia. PATHOPHYSIOLOGY: BEHAVIORAL. Habitual, unconscious contraction of abdominal wall muscles (diaphragm, rectus abdominis) after eating, increasing intra-abdominal pressure, propelling gastric contents into esophagus and mouth. NO retrograde peristalsis. INCREASED ABDOMINAL PRESSURE as the mechanism. CLINICAL: ONSET: within 30 minutes of meal completion (often immediately). REGURGITATION (effortless, non-bilious, recognizable food, not sour/bitter). RE-CHEWING, RE-SWALLOWING, or SPITTING. NO NAUSEA, NO RETCHING, NO HEARTBURN. EPISODES cease when food becomes acidic (ruminants have alkaline saliva). Weight loss (common in adolescents, adults). Dental erosion, halitosis. PSYCHIATRIC COMORBIDITY: anxiety, depression, eating disorders. DIAGNOSIS: ROME IV CRITERIA. CLINICAL DIAGNOSIS (history, observation). HIGH- RESOLUTION ESOPHAGEAL MANOMETRY with IMPEDANCE: simultaneous R-waves (abdominal pressure spikes) with regurgitation, esophageal common cavity. ENDOSCOPY: exclude mechanical obstruction, GERD, eosinophilic esophagitis. GASTRIC EMPTYING STUDY: may be normal or delayed. EXCLUDE: bulimia nervosa (binge-purge, self-induced vomiting, body image disturbance), GERD, gastroparesis, achalasia. MANAGEMENT: PATIENT EDUCATION: explain mechanism (increased abdominal pressure, habit). REASSURANCE. DIAPHRAGMATIC BREATHING: CORNERSTONE THERAPY. Biofeedback: teach patient to relax abdominal wall during and after meals, breathe diaphragmatically. HABIT REVERSAL. SPEECH THERAPY, BEHAVIORAL THERAPY. PSYCHOLOGICAL: CBT for comorbid anxiety/depression. PHARMACOLOGY: baclofen (GABA-B agonist, reduces transient LES relaxations, case reports). SURGERY: Nissen fundoplication (rare, controversial). Prognosis: EXCELLENT with behavioural therapy (80% response). Chronic without treatment. Zambian context: RUMINATION SYNDROME IS RARE, UNDERDIAGNOSED. SUSPECT in patient with effortless regurgitation, immediately postprandial, no nausea. DIAGNOSIS: CLINICAL (history). MANOMETRY: NOT AVAILABLE. ENDOSCOPY: exclude other causes. DIAPHRAGMATIC BREATHING: simple, can be taught, effective. SPEECH THERAPY: limited. PSYCHOLOGY: limited. BACLOFEN: available. FOCUS: CLINICAL DIAGNOSIS, EXCLUDE OTHER CAUSES, PATIENT EDUCATION, DIAPHRAGMATIC BREATHING TRAINING. THIS IS NOT GERD.
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Bezoars
Bezoars are collections of indigestible foreign material accumulated in the gastrointestinal tract, most commonly the STOMACH. For Zambian students, bezoars are a RARE but important cause of GASTRIC OUTLET OBSTRUCTION, abdominal pain, and malnutrition. CLASSIFICATION: PHYTOBEZOAR (plant material, vegetables, fruit fibres, persimmon—diospyrobezoar) – MOST COMMON. TRICHOBEZOAR (hair, Rapunzel syndrome extends into small bowel). LACTIBEZOAR (milk curds, neonates, preterm infants). PHARMACOBEZOAR (medications: sucralfate, aluminum hydroxide, cholestyramine, extended-release nifedipine). PATHOPHYSIOLOGY: PREDISPOSING FACTORS: GASTRIC SURGERY (vagotomy, partial gastrectomy, pyloroplasty) → impaired motility, decreased acid, impaired grinding. GASTROPARESIS (diabetes, scleroderma). POOR MASTICATION, high-fibre diet, persimmon ingestion. PSYCHIATRIC DISORDERS (trichophagia, pica). CLINICAL: ASYMPTOMATIC (incidental). EPIGASTRIC PAIN (postprandial), NAUSEA, VOMITING, EARLY SATIETY, WEIGHT LOSS. GASTRIC OUTLET OBSTRUCTION. Trichobezoar: palpable abdominal mass (epigastric), halitosis, alopecia (hair pulling). Rapunzel syndrome: tail extends into small bowel, obstruction, perforation, intussusception. DIAGNOSIS: ENDOSCOPY: GOLD STANDARD. Visualize mass, assess size, composition, gastric mucosa (ulceration). UPPER GI SERIES (barium): filling defect, intraluminal mass. CT ABDOMEN: heterogeneous intraluminal mass, may have gas locules. MANAGEMENT: PHYTOBEZOAR: CONSERVATIVE (small, asymptomatic). DISSOLUTION: CELLULASE (1-2 ampules in 500mL water PO daily x 2-5 days). Coca-Cola lavage (endoscopic irrigation, 3L over 12-24h). NASOGASTRIC LAVAGE with Coca-Cola, cellulase. ENDOSCOPIC FRAGMENTATION: forceps, snare, lithotripter, laser, water jet. SURGERY: GASTROTOMY, bezoar removal. INDICATIONS: large, hard, refractory to endoscopic therapy, complications (obstruction, perforation, bleeding). TRICHOBEZOAR: ENDOSCOPIC REMOVAL (small). SURGICAL REMOVAL (gastrotomy) usually required (large, compacted, long tail). PSYCHIATRIC EVALUATION: trichotillomania, pica. LACTIBEZOAR: NPO, IV fluids, small frequent feeds, monitor electrolytes. SURGERY if obstruction. Prognosis: GOOD with removal. Recurrence common (10-20%). Psychiatric comorbidity requires treatment. Zambian context: BEZOARS ARE RARE. PHYTOBEZOAR: consider in patient with gastric surgery, poor dentition, high-fibre diet, persimmon ingestion (not common in Zambia?). TRICHOBEZOAR: rare, consider in young female with alopecia, abdominal mass, psychiatric illness. DIAGNOSIS: ENDOSCOPY (available). MANAGEMENT: ENDOSCOPIC FRAGMENTATION (snare, forceps). CELLULASE: NOT AVAILABLE. Coca-Cola: widely available, effective (endoscopic lavage, oral). SURGERY: available. PSYCHIATRIC REFERRAL: essential for trichobezoar. FOCUS: CLINICAL SUSPICION (gastric surgery, psychiatric history), ENDOSCOPY (diagnosis, attempted removal), CONSERVATIVE (Coca-Cola, endoscopic fragmentation), SURGERY (large, refractory, trichobezoar).
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Topic 276Coming soon
Eosinophilic Gastroenteritis: Diagnosis and Management
Eosinophilic gastroenteritis (EGE) is a rare, chronic inflammatory disorder characterized by EOSINOPHILIC INFILTRATION of the gastrointestinal wall (mucosa, muscularis, serosa), in the absence of secondary causes. For Zambian students, EGE is a DIAGNOSIS OF EXCLUSION, particularly in the tropics where parasitic infection is endemic. PATHOPHYSIOLOGY: Unknown, likely allergic/atopic (Th2-mediated). Food allergens? Peripheral eosinophilia (80%). MUCOSAL DISEASE (most common): eosinophilic infiltration of mucosa → abdominal pain, nausea, vomiting, diarrhoea, bleeding, malabsorption, protein-losing enteropathy. MUSCULARIS DISEASE: eosinophilic infiltration of muscularis propria → bowel wall thickening, obstruction (gastric outlet, small bowel). SEROSAL DISEASE (rare): eosinophilic ascites, high eosinophil count in ascitic fluid. CLINICAL: CHRONIC, RELAPSING. SYMPTOMS depend on layer and site: dysphagia (esophageal), epigastric pain, nausea, vomiting, early satiety (gastric), diarrhoea, weight loss (small bowel), obstruction (muscularis), ascites (serosal). Atopy (asthma, eczema, allergic rhinitis, food allergy) in 40-70%. DIAGNOSIS: HISTOLOGY (multiple biopsies, ≥6 from normal and abnormal areas). CRITERIA: EOSINOPHIL INFILTRATE in GI tract (≥20-30 eosinophils/HPF) in at least one site, with compatible symptoms, and EXCLUSION OF OTHER CAUSES. PERIPHERAL EOSINOPHILIA (50-80%). ELEVATED IgE (50%). ENDOSCOPY: normal, erythema, friability, nodularity, ulceration, polyps, thickened folds. MUCOSAL BIOPSIES: dense eosinophilic infiltration, eosinophilic cryptitis, microabscesses. SEROSAL DISEASE: EUS (thickened muscularis), paracentesis (eosinophilic ascites). CT: bowel wall thickening, ascites. EXCLUDE: PARASITES (Strongyloides, hookworm, Ascaris, Toxocara, Trichuris, Schistosoma). STOOL OVA AND PARASITES x 3, serology (Strongyloides). DRUGS (NSAIDs, antibiotics). HYPEREOSINOPHILIC SYNDROME (end-organ damage, heart). EGPA (eosinophilic granulomatosis with polyangiitis: asthma, vasculitis, neuropathy, renal, p-ANCA). IBD, celiac, lymphoma. MANAGEMENT: CORTICOSTEROIDS: FIRST-LINE. PREDNISONE 20-40mg/day, taper over weeks-months. Dramatic response. STEROID-SPARING: BUDESONIDE (ileal, right colon), ORAL BUDENOSIDE (systemic less). DIETARY THERAPY: ELEMENTAL DIET, SIX-FOOD ELIMINATION DIET (SFED: milk, wheat, egg, soy, peanut/tree nut, fish/shellfish). Limited efficacy (EGE vs EoE). ANTIHISTAMINES, MAST CELL STABILIZERS: limited. BIOLOGICS: MEPOLIZUMAB (anti-IL-5), RESLIZUMAB, OMALIZUMAB (anti-IgE). Refractory cases. SURGERY: obstruction, perforation (rare). Prognosis: CHRONIC, RELAPSING. Good response to steroids. Most require long-term, low-dose steroids. No malignant potential. Zambian context: EGE IS EXTREMELY RARE. STRONGYLOIDES and other parasites are COMMON. DO NOT DIAGNOSE EGE WITHOUT RIGOROUS EXCLUSION OF STRONGYLOIDES (stool microscopy, agar plate culture, serology). Strongyloides hyperinfection can be fatal if treated with corticosteroids. Other parasites: hookworm, Ascaris, Schistosoma. Eosinophilia + GI symptoms in Zambia = PARASITES until proven otherwise. ENDOSCOPY + BIOPSIES available. PATHOLOGY: eosinophil count. CORTICOSTEROIDS available. FOCUS: EXCLUDE PARASITES FIRST (multiple stool examinations, Strongyloides serology if available).
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Topic 277Coming soon
Collagenous Colitis
Collagenous colitis (CC) is a subtype of MICROSCOPIC COLITIS, characterized by chronic, watery, non-bloody diarrhoea, NORMAL COLONOSCOPY, and DIAGNOSTIC HISTOLOGY: THICKENED SUBCUTANEOUS COLLAGEN BAND (>10μm) beneath the surface epithelium. For Zambian students, CC is an EMERGING, UNDERDIAGNOSED cause of chronic diarrhoea, especially in older women. PATHOPHYSIOLOGY: Unknown. Immune-mediated? Aberrant response to luminal antigens (drugs, bacteria, bile acids) → inflammation, fibrosis. Associated with AUTOIMMUNE DISORDERS (celiac disease, thyroiditis, type 1 diabetes, RA, Sjögren's). DRUG-INDUCED: PROTON PUMP INHIBITORS (lansoprazole > omeprazole), NSAIDs, SSRIs, statins, beta-blockers, carbamazepine. SMOKING: strong risk factor. CLINICAL: CHRONIC, WATERY, NON-BLOODY DIARRHOEA (profuse, up to 5-15 episodes/day). NOCTURNAL DIARRHEA, URGENCY, FAECAL INCONTINENCE (common). ABDOMINAL PAIN (mild, crampy), WEIGHT LOSS (30-40%), FATIGUE. Sex: F > M (9:1). Age: peak 60-70 years. DIAGNOSIS: COLONOSCOPY: NORMAL or mild erythema, oedema, friability. KEY: MULTIPLE BIOPSIES (RIGHT AND LEFT COLON, segmental distribution). HISTOLOGY: THICKENED COLLAGEN BAND (>10μm, normally <5-7μm) beneath surface epithelium, increased intraepithelial lymphocytes, inflammation, capillary damage. BIOPSIES should be taken even if mucosa appears normal. LABS: normal inflammatory markers (ESR, CRP), negative faecal calprotectin (differentiates from IBD). CELIAC SEROLOGY (tTG-IgA): 10-20% have celiac; screen all. MANAGEMENT: STEPWISE. STEP 1: DISCONTINUE OFFENDING DRUGS (PPI, NSAIDs, others). SMOKING CESSATION. STEP 2: BUDESONIDE (ORAL, 9mg/day x 6-8 weeks) is FIRST-LINE, HIGHLY EFFECTIVE (80% response). INDUCES REMISSION. MAINTENANCE: BUDESONIDE (6mg/day) for RELAPSING DISEASE (60-70% relapse within 6 months). STEP 3: BISMUTH SUBSALICYLATE (9-12 tablets/day x 8 weeks) for mild disease, alternative. STEP 4: ANTIDIARRHOEALS: LOPERAMIDE, DIPHENOXYLATE. BILE ACID SEQUESTRANTS (CHOLESTYRAMINE): if bile acid malabsorption suspected. STEP 5: IMMUNOMODULATORS (AZATHIOPRINE, 6-MP, METHOTREXATE) for STEROID-DEPENDENT, REFRACTORY. BIOLOGICS (ANTI-TNF): case reports. SURGERY: DIVERTING ILEOSTOMY, COLECTOMY (EXTREMELY RARE, for refractory, severe). Prognosis: CHRONIC, RELAPSING. NOT PROGRESSIVE, NO INCREASED CANCER RISK. Quality of life impaired. Excellent response to budesonide. Zambian context: CC IS LIKELY UNDERDIAGNOSED. Consider in OLDER WOMAN with CHRONIC WATERY DIARRHOEA, NORMAL COLONOSCOPY, NEGATIVE STUDS (infectious, IBD, celiac). KEY: RANDOM COLONIC BIOPSIES are essential. PATHOLOGY (collagen band measurement) available at tertiary centres. BUDESONIDE: available (expensive). LOPERAMIDE, CHOLESTYRAMINE (if available), BISMUTH SUBSALICYLATE (availability?), AZATHIOPRINE (available). PPIs: widely used. Iatrogenic CC: consider drug-induced. FOCUS: SUSPECT CC, PERFORM COLONOSCOPY WITH BIOPSIES, DISCONTINUE PPIs, BUDESONIDE THERAPY. This is a TREATABLE, COMMON, OFTEN MISSED DIAGNOSIS.
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Topic 278Coming soon
Lymphocytic Colitis
Lymphocytic colitis (LC) is a subtype of MICROSCOPIC COLITIS, characterized by chronic, watery, non-bloody diarrhoea, NORMAL COLONOSCOPY, and DIAGNOSTIC HISTOLOGY: INCREASED INTRAEPITHELIAL LYMPHOCYTES (IELs) >20/100 enterocytes, with preserved crypt architecture and NO thickened collagen band. For Zambian students, LC is an EMERGING, UNDERDIAGNOSED cause of chronic diarrhoea. PATHOPHYSIOLOGY: Unknown. Immune-mediated? Aberrant immune response to intraluminal antigen (drugs, bacteria, food) in genetically susceptible host. Associated with AUTOIMMUNE DISORDERS (celiac disease, thyroiditis, type 1 diabetes, RA, Sjögren's). DRUG-INDUCED: PROTON PUMP INHIBITORS (lansoprazole > omeprazole), NSAIDs, SSRIs, statins, beta-blockers, carbamazepine. SMOKING: strong risk factor. CLINICAL: CHRONIC, WATERY, NON-BLOODY DIARRHOEA (profuse, up to 5-15 episodes/day). NOCTURNAL DIARRHEA, URGENCY, FAECAL INCONTINENCE (common). ABDOMINAL PAIN (mild, crampy), WEIGHT LOSS (30-40%), FATIGUE. Sex: F > M (3:1). Age: peak 60-70 years. DIAGNOSIS: COLONOSCOPY: NORMAL or mild erythema, oedema, friability. KEY: MULTIPLE BIOPSIES (RIGHT AND LEFT COLON, segmental distribution). HISTOLOGY: INCREASED INTRAEPITHELIAL LYMPHOCYTES (IELs) >20/100 enterocytes (normally <5-10), mixed inflammatory infiltrate in lamina propria, preserved crypt architecture, NO collagen band thickening. BIOPSIES should be taken even if mucosa appears normal. LABS: normal inflammatory markers (ESR, CRP), negative faecal calprotectin. CELIAC SEROLOGY (tTG-IgA): 10-20% of LC have celiac; screen all. MANAGEMENT: STEPWISE. STEP 1: DISCONTINUE OFFENDING DRUGS (PPI, NSAIDs, others). SMOKING CESSATION. STEP 2: BUDESONIDE (ORAL, 9mg/day x 6-8 weeks) is FIRST-LINE, HIGHLY EFFECTIVE (80% response). INDUCES REMISSION. MAINTENANCE: BUDESONIDE (6mg/day) for RELAPSING DISEASE (60-70% relapse within 6 months). STEP 3: BISMUTH SUBSALICYLATE (9-12 tablets/day x 8 weeks) for mild disease, alternative. STEP 4: ANTIDIARRHOEALS: LOPERAMIDE, DIPHENOXYLATE. BILE ACID SEQUESTRANTS (CHOLESTYRAMINE): if bile acid malabsorption suspected. STEP 5: IMMUNOMODULATORS (AZATHIOPRINE, 6-MP, METHOTREXATE) for STEROID-DEPENDENT, REFRACTORY. BIOLOGICS (ANTI-TNF): case reports. SURGERY: DIVERTING ILEOSTOMY, COLECTOMY (EXTREMELY RARE, for refractory, severe). Prognosis: CHRONIC, RELAPSING. NOT PROGRESSIVE, NO INCREASED CANCER RISK. Quality of life impaired. Excellent response to budesonide. Zambian context: LC IS LIKELY UNDERDIAGNOSED. Consider in OLDER PATIENT with CHRONIC WATERY DIARRHOEA, NORMAL COLONOSCOPY, NEGATIVE STUDS (infectious, IBD, celiac). KEY: RANDOM COLONIC BIOPSIES are essential. PATHOLOGY (IEL count) available at tertiary centres. BUDESONIDE: available (expensive). LOPERAMIDE, CHOLESTYRAMINE (if available), BISMUTH SUBSALICYLATE (availability?), AZATHIOPRINE (available). PPIs: widely used. Iatrogenic LC: consider drug-induced. FOCUS: SUSPECT LC, PERFORM COLONOSCOPY WITH BIOPSIES, DISCONTINUE PPIs, BUDESONIDE THERAPY. This is a TREATABLE, COMMON, OFTEN MISSED DIAGNOSIS.
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Topic 279Coming soon
Gastric Polyps
Gastric polyps are elevated mucosal lesions, most often ASYMPTOMATIC and INCIDENTAL findings on endoscopy. For Zambian students, gastric polyps are increasingly detected with greater access to endoscopy. CLASSIFICATION: EPITHELIAL (90%) and NON-EPITHELIAL (GIST, lipoma, carcinoid, etc). EPITHELIAL: FUNDIC GLAND POLYPS (FGP, 50-60%): most common. Small (<1cm), sessile, dome-shaped, same colour as mucosa. Sporadic (PPI use, female) or syndromic (FAP, attenuated FAP). Histology: cystic dilated glands, parietal and chief cells, NO dysplasia (sporadic), MAY HAVE dysplasia (FAP). NO MALIGNANT POTENTIAL (sporadic). HYPERPLASTIC POLYPS (30-40%): associated with chronic gastritis (H. pylori, autoimmune gastritis). Small, sessile or pedunculated, smooth, erythematous. Histology: elongated, dilated, branching pits, inflammation. LOW MALIGNANT POTENTIAL (1-2%, usually large >2cm, with dysplasia). ADENOMATOUS POLYPS (10%): PREMALIGNANT. Tubular, villous, tubulovillous. Associated with atrophic gastritis, familial syndromes (FAP). Risk of malignancy correlates with size, villous histology, high-grade dysplasia. CARCINOID (neuroendocrine tumour): Type 1 (chronic atrophic gastritis, hypergastrinemia, benign, small, multiple, endoscopic resection), Type 2 (MEN1/ZES, small, multiple), Type 3 (sporadic, large, solitary, metastatic potential, surgery). CLINICAL: ASYMPTOMATIC (most). Large polyps (>2cm): epigastric pain, bleeding (iron deficiency anaemia), obstruction (antral). DIAGNOSIS: ENDOSCOPY + BIOPSY (or polypectomy). HISTOLOGY: ESSENTIAL. MANAGEMENT: FUNDIC GLAND POLYPS: Sporadic: NO RESECTION, NO SURVEILLANCE. Discontinue PPI if possible. Syndromic (FAP): screening colonoscopy, colectomy. HYPERPLASTIC POLYPS: RESECT if LARGE (>1cm) or SYMPTOMATIC. Biopsy base. H. pylori eradication (if present). Surveillance: if large, multifocal, dysplasia. ADENOMA: COMPLETE ENDOSCOPIC RESECTION (EMR, polypectomy). SURGICAL RESECTION if invasive cancer, not amenable to endoscopic resection. SURVEILLANCE: 1 year then 3-5 years. CARCINOID: Type 1: endoscopic resection, surveillance. Type 2: treat gastrinoma. Type 3: surgical resection. Prognosis: EXCELLENT. Malignant potential low, except adenomas, large hyperplastic with dysplasia, Type 3 carcinoid. Zambian context: GASTRIC POLYPS ARE INCIDENTAL. ENDOSCOPY with biopsy/polypectomy available. HISTOPATHOLOGY available. H. pylori testing available. FAP: rare. Management: POLYPECTOMY (adenoma, large hyperplastic, symptomatic), H. pylori ERADICATION (hyperplastic polyps), NO RESECTION/SURVEILLANCE (sporadic FGP). FOCUS: HISTOLOGICAL DIAGNOSIS (biopsy/resect), ADENOMA = REMOVE, HYPERPLASTIC = remove if large, H. pylori test and treat, FUNDIC GLAND = leave alone, NO SURVEILLANCE (sporadic).