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 226Coming soon
Zollinger-Ellison Syndrome
Zollinger-Ellison syndrome (ZES) is a rare disorder caused by a GASTRIN-SECRETING NEUROENDOCRINE TUMOUR (GASTRINOMA), leading to HYPERGASTRINAEMIA, marked gastric acid hypersecretion, and SEVERE, REFRACTORY PEPTIC ULCER DISEASE. For Zambian students, ZES is a CONSIDERATION in patients with MULTIPLE ULCERS, ULCERS IN UNUSUAL LOCATIONS (post-bulbar), REFRACTORY TO STANDARD THERAPY, or ASSOCIATED WITH DIARRHOEA. PATHOPHYSIOLOGY: Gastrinoma (80-90% in 'gastrinoma triangle': cystic duct/common bile duct, second part duodenum, pancreatic head). 50-60% MALIGNANT (slow-growing). 25% associated with MULTIPLE ENDOCRINE NEOPLASIA TYPE 1 (MEN1: parathyroid hyperplasia, pituitary adenoma, pancreatic NET). Gastrin → parietal cell stimulation → gastric acid hypersecretion → mucosal injury. Acid also inactivates pancreatic lipase, damages small bowel mucosa → DIARRHOEA, STEATORRHOEA. CLINICAL: PEPTIC ULCER (90-95%): SEVERE, REFRACTORY, RECURRENT. MULTIPLE ulcers, UNUSUAL LOCATIONS (post-bulbar, distal duodenum, jejunum). COMPLICATIONS: bleeding, perforation, obstruction. DIARRHOEA (50-70%): watery, often prominent, may be sole manifestation. STEATORRHOEA (acid inactivation lipase). GERD (severe, erosive oesophagitis, stricture). MEN1: hyperparathyroidism (hypercalcaemia), pituitary tumour, family history. DIAGNOSIS: CLINICAL SUSPICION. FASTING SERUM GASTRIN: ELEVATED (>100 pg/mL, often >500-1000 pg/mL). PPI MUST BE WITHDRAWN (7-10d) for accurate measurement—may precipitate severe ulcer. SECRETIN STIMULATION TEST: GOLD STANDARD. IV secretin → gastrinoma: INCREASE in gastrin ≥120 pg/mL from baseline. Normal/atrophic gastritis: DECREASE. GASTRIC pH: <2.0 (hyperchlorhydria). TUMOUR LOCALIZATION: Endoscopic ultrasound (EUS), somatostatin receptor scintigraphy (Octreoscan), Ga-68 DOTATATE PET/CT (GOLD STANDARD), CT/MRI. MEN1 SCREENING: serum calcium, PTH, prolactin, pituitary MRI. MANAGEMENT: ACID SUPPRESSION: HIGH-DOSE PPIs (e.g., omeprazole 60mg BID, titrate to gastric pH >4, symptom control). LIFELONG therapy. Higher doses than typical PUD. TUMOUR RESECTION: SOLITARY, SPORADIC (non-MEN1): SURGICAL RESECTION (enucleation, pancreaticoduodenectomy). CURE rate 30-50%. METASTATIC DISEASE: debulking, somatostatin analogues (octreotide, lanreotide), peptide receptor radionuclide therapy (PRRT), chemotherapy, liver-directed therapy. MEN1: multiple tumours, rarely cured; manage acid hypersecretion, localize/ resect dominant tumours (>2cm). Prognosis: With PPI, excellent symptom control, normal life expectancy. Malignant gastrinoma: indolent; 10-year survival 90% (sporadic), 70% (MEN1). Liver metastases: worse. Zambian context: ZES IS RARE. Consider in REFRACTORY/ATYPICAL PUD. Fasting gastrin: NOT AVAILABLE. Secretin test: NOT AVAILABLE. Somatostatin receptor imaging: NOT AVAILABLE. Diagnosis is CLINICAL. High-dose PPI (omeprazole 40-80mg BID). If dramatic response, likely ZES. EUS available tertiary. CT available. Surgical resection available. MEN1 screening: calcium, PTH, prolactin available. Somatostatin analogues (octreotide) available. PRRT NOT AVAILABLE. This is a RARE, but important diagnostic consideration.
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Topic 227Coming soon
Non-Variceal Upper Gastrointestinal Bleeding
Non-variceal upper gastrointestinal bleeding (NVUGIB) is a COMMON MEDICAL EMERGENCY with significant morbidity and mortality (5-10%). For Zambian students, NVUGIB is a DAILY CLINICAL PROBLEM, predominantly caused by PEPTIC ULCER DISEASE (H. pylori, NSAIDs). MASTERY OF A SYSTEMATIC, PROTOCOL-DRIVEN APPROACH TO RESUSCITATION, RISK STRATIFICATION, ENDOSCOPIC THERAPY, AND POST-BLEEDING MANAGEMENT IS LIFE-SAVING. ETIOLOGY: PEPTIC ULCER (50-70%): DU > GU. EROSIVE DISEASE: gastritis, duodenitis, oesophagitis (NSAIDs, alcohol, stress). MALLORY-WEISS TEAR (5-15%). VASCULAR LESIONS: angiodysplasia, Dieulafoy lesion, gastric antral vascular ectasia (GAVE). ESOPHAGITIS. NEOPLASIA (gastric cancer, GIST). CLINICAL PRESENTATION: HAEMATEMESIS (fresh red blood, clots, or coffee-grounds). MELAENA (black, tarry, foul-smelling stool, >50mL blood, >8h transit). HAEMATOCHEZIA (maroon stool, bright red blood per rectum) = MASSIVE, RAPID UGI BLEED (>1000mL). HAEMODYNAMIC INSTABILITY: tachycardia, hypotension, shock. ASSESSMENT: AIRWAY, BREATHING, CIRCULATION. INITIAL MANAGEMENT: RESUSCITATION: IV ACCESS (2 large-bore 16-18G). IV FLUIDS (crystalloids, blood products). RESTRICTIVE TRANSFUSION STRATEGY: TRANSFUSE at Hb <7 g/dL (<8 g/dL if CAD, massive bleed). Target Hb 7-9 g/dL. AVOID EXCESSIVE TRANSFUSION (increases rebleeding, mortality). COAGULOPATHY: correct (vitamin K, FFP, platelets). ANTIPLATELET AGENTS: aspirin for secondary prevention? Hold; discuss cardiology. ANTICOAGULATION: reverse if possible. RISK STRATIFICATION: GLASGOW-BLATCHFORD SCORE (GBS): PRE-ENDOSCOPY. Variables: Hb, BUN, HR, SBP, melaena, syncope, hepatic disease, cardiac failure. GBS 0-1: LOW RISK, safe for OUTPATIENT management (discharge, early outpatient endoscopy). GBS ≥2: ADMIT, inpatient endoscopy. ROCKALL SCORE: POST-ENDOSCOPY. Predicts rebleeding, mortality. ENDOSCOPY: TIMING: URGENT (<12-24h) for high-risk patients (haemodynamic instability, ongoing bleeding, high GBS). Haemodynamically unstable: EMERGENT (<6h) after resuscitation. INTERVENTION: ENDOSCOPIC THERAPY for HIGH-RISK STIGMATA: ACTIVE BLEEDING (spurting, oozing), VISIBLE VESSEL (non-bleeding, pigmented protuberance), ADHERENT CLOT. DUAL THERAPY (injection + mechanical/thermal) is SUPERIOR. INJECTION: epinephrine 1:10,000-1:20,000 (dilutes, vasoconstricts, tamponade). MECHANICAL: HEMOCLIPS (endoclips)—preferred for visible vessel. THERMAL: HEATER PROBE, BIPOLAR COAGULATION, ARGON PLASMA COAGULATION (APC). ADHERENT CLOT: irrigate vigorously, consider cold snare polypectomy to expose underlying vessel, then treat. LOW-RISK STIGMATA: CLEAN BASE, FLAT SPOT (pigmented, non-protuberant). No endoscopic therapy required. POST-ENDOSCOPY MANAGEMENT: HIGH-DOSE IV PPI: IV bolus (80mg) then continuous infusion (8mg/h) x 72h for HIGH-RISK STIGMATA after successful endoscopic therapy. REDUCES REBLEEDING, MORTALITY. INTERMITTENT HIGH-DOSE IV PPI (e.g., pantoprazole 40mg IV q12h) may be equivalent. ORAL PPI: after 72h, BID for 4-8 weeks (ulcer healing). H. PYLORI TESTING: Biopsy at index endoscopy (rapid urease test, histology) or delayed (urea breath test). If POSITIVE: ERADICATION THERAPY (triple or quadruple). CONFIRM ERADICATION. NSAIDs: DISCONTINUE if possible. If must continue, PPI CO-THERAPY. SECOND-LOOK ENDOSCOPY: NOT ROUTINE. Indicated for high-risk rebleeding (large ulcer, visible vessel, haemodynamic instability at index). REBLEEDING (5-20%): REPEAT ENDOSCOPY WITH THERAPY is FIRST-LINE. ANGIOGRAPHY WITH EMBOLIZATION: if endoscopic therapy fails, or inaccessible lesion. SURGERY: LAST RESORT. INDICATIONS: failure of endoscopic + angiographic therapy, massive bleeding, perforation. Procedure: ulcer oversewing, vagotomy and antrectomy, partial gastrectomy. Prognosis: MORTALITY 5-10% (higher with age, comorbidities, in-hospital bleeding, rebleeding). REBLEEDING rate: with dual endoscopic therapy + IV PPI: 5-10%. Zambian context: NVUGIB IS COMMON. Endoscopy available tertiary (often limited availability, long waits). URGENT endoscopy (<24h) challenging. GBS score (Hb, BUN, HR, BP) is SIMPLE, NO ENDOSCOPY, can triage. RESTRICTIVE TRANSFUSION: feasible, save blood products. EPINEPHRINE INJECTION: widely available, inexpensive. HEMOCLIPS: available (cost). HEATER PROBE/APC: limited availability. IV PPI (omeprazole, pantoprazole) available. HIGH-DOSE IV PPI: IV bolus + infusion (cost). INTERMITTENT IV PPI (40mg q12h) acceptable alternative. ORAL PPI: widely available. H. pylori eradication: accessible. SURGERY available (tertiary). FOCUS: RESUSCITATE, TRANSFUSE RESTRICTIVELY, GBS TRIAGE, ENDOSCOPY (when available) + EPINEPHRINE + CLIPS, HIGH-DOSE IV PPI, H. PYLORI ERADICATION.
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Topic 228Coming soon
Gastric Cancer: Epidemiology and Pathogenesis
Gastric cancer (GC) is the FIFTH MOST COMMON CANCER and FOURTH LEADING CAUSE OF CANCER DEATH worldwide, with a disproportionately high burden in Eastern Asia, Central/South America, and Eastern Europe. For Zambian students, the incidence in indigenous Africans is RELATIVELY LOW, but increases with H. pylori prevalence, dietary factors, and possibly Epstein-Barr virus. However, with urbanization and dietary changes, incidence may rise. MASTERY OF GC EPIDEMIOLOGY, PATHOGENESIS, AND PREVENTION IS ESSENTIAL. HISTOLOGIC CLASSIFICATION: ADENOCARCINOMA (90-95%). LAURÉN CLASSIFICATION: INTESTINAL TYPE (well-differentiated, gland-forming, intestinal metaplasia precursor, H. pylori-associated, declining incidence). DIFFUSE TYPE (poorly differentiated, signet-ring cells, no gland formation, no intestinal metaplasia, hereditary, stable incidence). OTHER: lymphoma, GIST, carcinoid, squamous. ANATOMIC: CARDIA (proximal, GERD/obesity, increasing in West) vs NON-CARDIA (distal, H. pylori, declining). EPIDEMIOLOGY: MALE: FEMALE 2:1. Age >50. HIGH INCIDENCE REGIONS: Japan, Korea, China, Central/South America, Eastern Europe. LOW INCIDENCE: Africa (except high-risk pockets), South Asia, North America. RISK FACTORS: H. PYLORI: STRONGEST RISK FACTOR for NON-CARDIA GC. WHO GROUP I CARCINOGEN. Odds ratio 2-20. Chronic gastritis → atrophy → intestinal metaplasia → dysplasia → carcinoma (Correa cascade). H. pylori eradication REDUCES GC RISK. DIET: SALTED, SMOKED, PICKLED FOODS (high nitrate, nitrite). LOW FRUIT/VEGETABLE INTAKE. TOBACCO: increased risk. OBESITY, GERD: CARDIA GC. FAMILY HISTORY: diffuse type, hereditary diffuse gastric cancer (HDGC, CDH1/E-cadherin mutation), Lynch syndrome, FAP, Peutz-Jeghers. EPSTEIN-BARR VIRUS (EBV): 10% of GC, distinct molecular subtype (lymphoepithelioma-like, PD-L1 overexpression). GENETICS: CDH1 (hereditary diffuse), MLH1/MSH2 (Lynch), others. PATHOGENESIS: CORREA CASCADE (intestinal type): Normal → chronic gastritis (H. pylori) → atrophic gastritis → intestinal metaplasia (complete → incomplete) → dysplasia (low → high grade) → adenocarcinoma. Genetic alterations: TP53, KRAS, ERBB2, MSI, PIK3CA. Diffuse type: CDH1 loss, no precursor lesion. MOLECULAR CLASSIFICATION (TCGA): 1) EBV-positive, 2) MSI (microsatellite unstable), 3) genomically stable (including diffuse), 4) chromosomal instability (intestinal, TP53, receptor tyrosine kinase amplification). CLINICAL: EARLY GC: ASYMPTOMATIC. Screening in high-incidence countries (Japan, Korea) detects early, curable GC. ADVANCED GC: DYSPEPSIA, EPIGASTRIC PAIN, EARLY SATIETY, ANOREXIA, WEIGHT LOSS, NAUSEA, VOMITING (gastric outlet obstruction). DYSPHAGIA (cardia). ANAEMIA (chronic blood loss, iron deficiency). PALPABLE MASS. LEFT SUPRACLAVICULAR LYMPH NODE (Virchow's node). PERITONEAL DISSEMINATION: ascites, Krukenberg tumour (ovarian metastases), Blumer's shelf (rectal shelf). TROUSSEAU'S SIGN: migratory thrombophlebitis. DIAGNOSIS: ENDOSCOPY with BIOPSY (≥6-8 biopsies, suspicious lesions). Chromoendoscopy, virtual chromoendoscopy (NBI) enhance detection. STAGING: EUS (T stage, perigastric nodes). CT CHEST/ABDOMEN/PELVIS (M stage, nodal). PET-CT (equivocal). DIAGNOSTIC LAPAROSCOPY with PERITONEAL CYTOLOGY: occult peritoneal metastases (M1). STAGING: TNM (8th edition). PREVENTION: PRIMARY PREVENTION: H. pylori ERADICATION. Population-based screening and treatment in high-risk regions reduces GC incidence by 30-40%. HEALTHY DIET: reduced salt, increased fruit/vegetable intake. TOBACCO CESSATION. SECONDARY PREVENTION: ENDOSCOPIC SCREENING in high-incidence countries (Japan, Korea). Not cost-effective in low-incidence populations. Surveillance of PREMALIGNANT CONDITIONS: atrophic gastritis, intestinal metaplasia (limited, individualized). Zambian context: GC is LESS COMMON than HCC, esophageal SCC. H. pylori prevalence is VERY HIGH, but GC incidence is relatively low (African enigma? likely due to competing mortality, host genetics, bacterial strain differences). CORREA CASCADE occurs. ENDOSCOPY available tertiary. H. pylori eradication is accessible. SCREENING not feasible. Focus: EARLY DIAGNOSIS of symptomatic GC? most present late. REFERRAL for surgical resection (if early). PALLIATION for advanced disease (chemotherapy, symptom control).
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Topic 229Coming soon
Gastric Cancer: Staging and Multidisciplinary Management
Gastric cancer (GC) management has evolved significantly, with a paradigm shift toward MULTIDISCIPLINARY, PERIOPERATIVE, AND INDIVIDUALIZED THERAPY. For Zambian students, while many advanced therapies may not be available, understanding the principles of STAGING and the HIERARCHY OF TREATMENT OPTIONS is essential for appropriate referral and counselling. STAGING: TNM (8th edition). T (TUMOUR DEPTH): T1: lamina propria/muscularis mucosae/submucosa. T1a: mucosa. T1b: submucosa. T2: muscularis propria. T3: subserosa. T4a: perforates serosa. T4b: invades adjacent structures. N (LYMPH NODES): N1: 1-2, N2: 3-6, N3a: 7-15, N3b: >16. M (METASTASIS): M1: distant metastases (including positive peritoneal cytology). STAGE GROUPINGS: Stage 0 (Tis), Stage I (T1N0, T2N0), Stage II, Stage III, Stage IV (M1). MANAGEMENT: MULTIDISCIPLINARY TEAM (surgery, oncology, gastroenterology, radiology, pathology). STAGE 0 (Tis, HIGH-GRADE DYSPLASIA): ENDOSCOPIC RESECTION (EMR, ESD). CURATIVE. STAGE IA (T1aN0): ENDOSCOPIC RESECTION (ESD) if well-differentiated, <2cm, no ulceration, no lymphovascular invasion. SURGICAL RESECTION if high-risk features. STAGE IB-IIIC (RESECTABLE, NON-METASTATIC): GASTRECTOMY with D2 LYMPHADENECTOMY is the SURGICAL GOLD STANDARD. SUBTOTAL GASTRECTOMY: distal tumours (antrum). TOTAL GASTRECTOMY: proximal/mid-body, limits plastica. D1 LYMPHADENECTOMY: perigastric nodes (stations 1-6). D2 LYMPHADENECTOMY: D1 + stations 7-12 (left gastric, common hepatic, coeliac, splenic, hepatoduodenal). STANDARD IN ASIA, improves survival, requires surgical expertise. SPLENECTOMY: NOT routine (increases morbidity). PERIOPERATIVE CHEMOTHERAPY: STANDARD OF CARE in Europe/North America. MAGIC TRIAL: preoperative (epirubicin/cisplatin/5-FU, ECF) x 3 cycles + surgery + postoperative x 3 cycles. IMPROVES 5-YEAR SURVIVAL (36% vs 23%). FLOT REGIMEN (docetaxel/oxaliplatin/5-FU/leucovorin) SUPERIOR to ECF. ADJUVANT CHEMORADIATION: SWOG/INT-0116: postoperative chemoradiation (5-FU/leucovorin + 45Gy) improved survival. Used in US if D2 not performed, positive margins. ADJUVANT CHEMOTHERAPY alone: D2 resection + S-1 (Japan) or capecitabine/oxaliplatin (CLASSIC trial, Asia). NEOADJUVANT CHEMORADIATION: emerging. STAGE IV (METASTATIC): PALLIATIVE INTENT. CHEMOTHERAPY: FIRST-LINE: Platinum/fluoropyrimidine doublet (oxaliplatin/cisplatin + 5-FU/capecitabine) ± trastuzumab (HER2+). HER2 TESTING: 15-20% of GC, trastuzumab adds survival benefit. SECOND-LINE: ramucirumab (VEGFR2) + paclitaxel, irinotecan, trifluridine/tipiracil. THIRD-LINE: pembrolizumab (MSI-H, PD-L1+), nivolumab (CheckMate 649). SURGERY: No survival benefit for routine gastrectomy in metastatic disease. PALLIATION: GASTRIC OUTLET OBSTRUCTION: endoscopic stenting (SEMS), surgical gastrojejunostomy. BLEEDING: endoscopic therapy, radiotherapy, embolization. PAIN: analgesics, coeliac plexus block. NUTRITION: dietary counselling, feeding jejunostomy. PROGNOSIS: STAGE I: 5-year survival 80-90%. STAGE II: 60%. STAGE III: 30-40%. STAGE IV: 5-10%, median survival 8-12 months. PROGNOSTIC FACTORS: stage, grade, lymphovascular invasion, HER2, MSI-H (better prognosis). Zambian context: GASTRIC CANCER IS LESS COMMON. LATE PRESENTATION (Stage IV) is the norm. ENDOSCOPY available tertiary. STAGING CT available. EUS limited. DIAGNOSTIC LAPAROSCOPY available. SURGICAL RESECTION (gastrectomy, D1 lymphadenectomy) available at tertiary centres (Lusaka, Ndola). D2 lymphadenectomy expertise limited. PERIOPERATIVE CHEMOTHERAPY: EPIRUBICIN, CISPLATIN, 5-FU, CAPECITABINE, OXALIPLATIN? Available at Cancer Hospital (Lusaka). FLOT? Docetaxel available. TRASTUZUMAB (HER2): may be available. HER2 testing: NOT routinely available. RADIOTHERAPY: available (Lusaka). PALLIATIVE CHEMOTHERAPY: fluorouracil/cisplatin, capecitabine/oxaliplatin accessible? Cost. ENDOSCOPIC STENTING: available. SURGICAL BYPASS: available. FOCUS: DIAGNOSIS (endoscopy + biopsy), STAGING (CT), REFERRAL (surgery, oncology), PALLIATION (symptom control).
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Topic 230Coming soon
Gastrointestinal Stromal Tumors
Gastrointestinal stromal tumors (GISTs) are the MOST COMMON MESENCHYMAL NEOPLASMS of the gastrointestinal tract, arising from the INTERSTITIAL CELLS OF CAJAL (pacemaker cells). For Zambian students, GIST is an important differential diagnosis for subepithelial masses and GI bleeding. The availability of TYROSINE KINASE INHIBITORS (IMATINIB) has transformed a highly chemotherapy-resistant sarcoma into a CHRONIC, MANAGEABLE DISEASE. PATHOPHYSIOLOGY: 80-90% harbor activating mutations in KIT (CD117) or PDGFRA genes. Imatinib targets these mutated tyrosine kinases. Location: STOMACH (50-60%), SMALL INTESTINE (30-40%), colon/rectum, esophagus, omentum/mesentery (rare). CLINICAL: WIDE SPECTRUM. Small GISTs (<2cm): INCIDENTAL (endoscopy, imaging). Large GISTs: GASTROINTESTINAL BLEEDING (mucosal ulceration, 40-50%), ABDOMINAL PAIN (20-30%), PALPABLE MASS, OBSTRUCTION, PERFORATION (rare). DIAGNOSIS: ENDOSCOPY: SUBEPITHELIAL MASS (smooth, intact mucosa). CENTRAL UMBILICATION (ulceration). EUS: hypoechoic, homogeneous, well-defined mass arising from muscularis propria (4th layer). FNA/CORE BIOPSY: essential for tissue diagnosis. IMMUNOHISTOCHEMISTRY: CD117 (KIT, 95%), DOG1 (95%), CD34 (70%). Mutational analysis (KIT, PDGFRA): predicts imatinib response. CT/MRI: well-defined, enhancing mass, often exophytic. Calcification, necrosis, metastasis (liver, peritoneum). STAGING: Tumour size, mitotic rate (per 50 HPF), tumour rupture. RISK STRATIFICATION (Miettinen, AFIP criteria) predicts recurrence risk after resection (very low, low, moderate, high). MANAGEMENT: LOCALIZED RESECTABLE: SURGICAL RESECTION (COMPLETE, R0) is GOLD STANDARD. Laparoscopic resection for small, favourable locations. LYMPHADENECTOMY NOT required (rarely metastasize to nodes). NEOADJUVANT IMATINIB: for locally advanced, borderline resectable, or to reduce surgical morbidity (e.g., esophageal, rectal). IMATINIB 400mg daily x 6-12 months. ADJUVANT IMATINIB: HIGH-RISK GIST (size >10cm, mitotic rate >10/50 HPF, tumour rupture, non-gastric location). 3 years imatinib (significant survival benefit). INTERMEDIATE-RISK: 1 year? SELECTED. UNRESECTABLE/METASTATIC: IMATINIB 400mg daily is FIRST-LINE. RESPONSE RATE: 80-90%. Disease control: median 2-3 years. PROGRESSION: IMATINIB DOSE ESCALATION (400mg → 800mg daily). SECOND-LINE: SUNITINIB. THIRD-LINE: REGORAFENIB. SURGERY: metastasectomy in selected patients (responding disease, limited progression). VERY LOW RISK (<2cm, low mitotic rate): SURVEILLANCE (EUS) vs RESECTION. Gastric GIST <2cm, low-risk features: observation with EUS q1-2y. Prognosis: RESECTED, LOW RISK: 5y survival >90%. RESECTED, HIGH RISK: 5y survival 50-70% (adjuvant imatinib improves). METASTATIC: median survival 5 years (imatinib era). Zambian context: GIST is RARE but underdiagnosed. Consider in SUBEPITHELIAL MASS, GI BLEEDING of unknown origin. EUS available tertiary. IHC (CD117, DOG1) available at reference pathology labs. MUTATIONAL ANALYSIS NOT AVAILABLE. SURGICAL RESECTION available. IMATINIB is available (WHO Essential Medicines, Zambia Cancer Hospital?). Expensive. ADJUVANT IMATINIB for high-risk: may be accessible. UNRESECTABLE/METASTATIC: IMATINIB first-line. SUNITINIB, REGORAFENIB NOT AVAILABLE. FOCUS: DIAGNOSIS (EUS + biopsy, IHC), SURGICAL RESECTION (low/intermediate risk, localized), IMATINIB (high-risk, metastatic).
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Topic 231Coming soon
Celiac Disease
Celiac disease (CD) is a chronic, immune-mediated enteropathy triggered by ingestion of GLUTEN (storage proteins in wheat, barley, rye) in genetically susceptible individuals (HLA-DQ2/DQ8). For Zambian students, CD was historically considered RARE in Africa, but is increasingly recognized with urbanization, Western diet adoption, and improved diagnostic capacity. It is a GREAT MIMICKER of other GI disorders and nutritional deficiencies. MASTERY OF CD IS ESSENTIAL. PATHOPHYSIOLOGY: Gluten peptides (gliadin) resist digestion, cross intestinal epithelium, are deamidated by tissue transglutaminase (tTG) in lamina propria. Deamidated gliadin binds HLA-DQ2/DQ8 on antigen-presenting cells, activating CD4+ T-cells → Th1 response (IFN-γ) → mucosal inflammation, crypt hyperplasia, villous atrophy. Autoantibodies: anti-tTG, anti-endomysial (EMA), anti-deamidated gliadin peptides (DGP). CLINICAL: CLASSIC PHENOTYPE (infants/young children): chronic diarrhoea, failure to thrive, abdominal distension, muscle wasting, irritability. MODERN PHENOTYPE (older children/adults): NON-SPECIFIC, EXTRAINTESTINAL. Iron deficiency anaemia (most common presentation in adults). Chronic fatigue, aphthous stomatitis, dental enamel defects. Dermatitis herpetiformis (intensely pruritic, papulovesicular rash on elbows, knees, buttocks—PATHOGNOMONIC). Osteoporosis/osteopenia, short stature, delayed puberty. Elevated transaminases. Neurologic: ataxia, peripheral neuropathy, epilepsy. Reproductive: infertility, recurrent miscarriage. ASSOCIATED CONDITIONS: Type 1 diabetes, autoimmune thyroiditis, autoimmune hepatitis, IgA deficiency, Down syndrome, Turner syndrome. DIAGNOSIS: SEROLOGY: FIRST-LINE: IgA ANTI-TISSUE TRANSGLUTAMINASE (tTG-IgA). Sensitivity/sensitivity >95% (untreated). TOTAL IgA: RULE-OUT IgA DEFICIENCY (1:400). If IgA deficient: IgG DGP or IgG tTG. ANTI-ENDOMYSIAL ANTIBODY (EMA-IgA): highly specific (>99%), operator-dependent. DECREASING USE. ENDOSCOPY WITH DUODENAL BIOPSY: GOLD STANDARD. Required for CONFIRMATION in adults. Findings: scalloping, fissuring, loss of folds, mosaic pattern. HISTOLOGY: MARSH CLASSIFICATION: Marsh 0: normal. Marsh 1: increased intraepithelial lymphocytes (IELs) >25/100 enterocytes. Marsh 2: + crypt hyperplasia. Marsh 3: + villous atrophy (3a: partial, 3b: subtotal, 3c: total). Marsh 3 is diagnostic (in appropriate clinical/serologic context). HLA-DQ2/DQ8 TYPING: HIGH NEGATIVE PREDICTIVE VALUE (excludes CD). Not diagnostic. MANAGEMENT: LIFELONG, STRICT GLUTEN-FREE DIET (GFD). Elimination of wheat, barley, rye. Oats: pure, uncontaminated oats are tolerated by most. DIETICIAN REFERRAL essential. NUTRITIONAL DEFICIENCIES: iron, folate, B12, calcium, vitamin D, zinc—replete. VACCINATIONS: pneumococcal (hyposplenism risk). MONITORING: Symptom response, serology (tTG-IgA) decline (6-12 months), repeat biopsy if non-response. REFRACTORY CELIAC DISEASE (RCD): persistent symptoms/villous atrophy despite ≥12 months strict GFD. RCD I: normal IEL phenotype. RCD II: aberrant IEL phenotype (clonal, worse prognosis). MANAGEMENT: corticosteroids (budesonide, prednisone), immunosuppression (azathioprine), biologics (anti-IL-15). COMPLICATIONS: Enteropathy-associated T-cell lymphoma (EATL): RARE, severe, poor prognosis. Small bowel adenocarcinoma (increased risk). Prognosis: EXCELLENT with strict GFD. Quality of life normal. Increased mortality if untreated or non-adherent. Zambian context: CD IS RARE but underdiagnosed. Consider in: iron deficiency anaemia (unexplained), chronic diarrhoea, malabsorption, autoimmune disease, family history. SEROLOGY (tTG-IgA) available at reference lab (Lusaka). ENDOSCOPY + BIOPSY available (tertiary). HLA typing not available. GFD: culturally challenging (nshima—maize, cassava is gluten-free, wheat bread common in urban areas). DIETICIAN SUPPORT limited. Support groups: nascent. Focus: HIGH INDEX OF SUSPICION, SEROLOGIC TESTING, ENDOSCOPY/BIOPSY CONFIRMATION, DIETARY COUNSELLING.
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Topic 232Coming soon
Tropical Sprue
Tropical sprue (TS) is an acquired, chronic malabsorption syndrome of unclear etiology, affecting residents of or visitors to TROPICAL REGIONS (Caribbean, Central/South America, India, Southeast Asia). For Zambian students, TS is a DIAGNOSIS OF EXCLUSION in patients with malabsorption, but its existence in Africa is controversial; some experts consider it rare or non-existent in sub-Saharan Africa. However, it remains in the differential of chronic diarrhoea and nutritional deficiencies. PATHOPHYSIOLOGY: Unknown, likely INFECTIOUS (bacterial overgrowth, Klebsiella, coliforms). Environmental factors, malnutrition, altered gut microbiota. Diffuse, continuous small bowel mucosal injury (duodenum > jejunum > ileum). Villous atrophy (partial, not total), crypt hyperplasia, chronic inflammation. Impaired B12 and folate absorption (ileum). CLINICAL: ACUTE PHASE: acute diarrhoeal illness (watery diarrhoea, fever, malaise) → persists. CHRONIC PHASE: MALABSORPTION (diarrhoea, steatorrhoea, weight loss), MULTIPLE NUTRIENT DEFICIENCIES: MEGALOBLASTIC ANAEMIA (B12, folate), iron deficiency, hypoalbuminaemia, hypocalcaemia, vitamin D deficiency, vitamin K deficiency (prolonged INR). DISTENSION, flatulence, anorexia. Geographic link: stay in endemic area. DIAGNOSIS: DIAGNOSIS OF EXCLUSION. HISTORY: residence/travel in endemic region, protracted diarrhoea. LABS: megaloblastic anaemia, low B12, low folate, low iron, low albumin. STOOL: negative for parasites (Strongyloides, Giardia, Cryptosporidium, Cyclospora, Isospora), negative bacterial culture. ENDOSCOPY: non-specific; may be normal or show scalloping, fissuring. HISTOLOGY: partial villous atrophy, crypt hyperplasia, chronic inflammation, intraepithelial lymphocytes (variable). NOT diagnostic. DISTINGUISH FROM: CELIAC DISEASE: HLA-DQ2/DQ8, tTG/EMA serology positive, responds to GFD. ENVIRONMENTAL ENTEROPATHY: asymptomatic or mild, growth faltering, no megaloblastic anaemia. PARASITIC INFECTION: Strongyloides, Giardia, Cyclospora, Isospora, Cryptosporidium (HIV, immunocompetent). WHIPPLE'S DISEASE: PAS-positive macrophages, Tropheryma whipplei. HIV ENTEROPATHY. IMMUNOPROLIFERATIVE SMALL INTESTINAL DISEASE (IPSID): alpha-heavy chain disease, lymphoma. MANAGEMENT: ANTIBIOTICS: TETRACYCLINE (250mg QID) OR DOXYCYCLINE (100mg BID) x 3-6 months. FOLIC ACID: 5mg daily (rapid haematologic response). VITAMIN B12: intramuscular (if deficient). IRON, calcium, vitamin D, multivitamins. NUTRITIONAL SUPPORT. Prognosis: EXCELLENT with appropriate antibiotics and vitamin repletion. Relapse may occur. Zambian context: TS is LIKELY RARE OR NON-EXISTENT in Zambia. MOST 'tropical sprue' diagnoses in Africa are likely UNDIAGNOSED PARASITIC INFECTIONS (Strongyloides, Giardia, Cyclospora, Isospora), TROPICAL ENTEROPATHY, HIV enteropathy, or CELIAC DISEASE. DO NOT DIAGNOSE TS without exhaustive exclusion of parasites, HIV, celiac disease, and other causes. Strongyloides hyperinfection in immunocompromised can mimic. If strong clinical suspicion and no other cause, consider DOXYCYCLINE 100mg BID + FOLIC ACID + B12. Focus: EXCLUDE OTHER CAUSES FIRST.
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Topic 233Coming soon
Environmental Enteric Dysfunction
Environmental enteric dysfunction (EED), formerly tropical enteropathy, is a subclinical, diffuse small bowel disorder affecting infants and children in LOW-INCOME, UNSANITARY ENVIRONMENTS. For Zambian students, EED is a MAJOR, UNDERAPPRECIATED PUBLIC HEALTH PROBLEM, contributing to STUNTING, VACCINE FAILURE, and IMPAIRED CHILD DEVELOPMENT. PATHOPHYSIOLOGY: Chronic, repeated faecal-oral microbial exposure → small intestinal inflammation, villous blunting (partial), crypt hyperplasia, increased permeability, reduced absorptive capacity, microbial translocation. Histology: NOT PATHOGNOMONIC. Similar to celiac (but milder, no gluten trigger, no autoantibodies). Biomarkers: fecal calprotectin (elevated), fecal neopterin, fecal alpha-1-antitrypsin, plasma LPS, sCD14, I-FABP (intestinal fatty acid binding protein). DUAL SUGAR ABSORPTION TEST (lactulose:mannitol ratio): increased permeability (not widely available). CLINICAL: ASYMPTOMATIC (infants, children). MANIFESTATIONS: LINEAR GROWTH FALTERING (stunting, height-for-age Z-score <-2). ORAL VACCINE FAILURE (polio, rotavirus, cholera). Micronutrient deficiencies (iron, zinc, vitamin A). No overt diarrhoea. DIAGNOSIS: NO SINGLE DIAGNOSTIC TEST. Clinical diagnosis: child living in poverty, poor sanitation, stunting, no other cause of malabsorption. EED is a diagnosis of exclusion. ENDOSCOPY/BIOPSY (rarely performed, research). MANAGEMENT: NO PROVEN THERAPY. INTERVENTIONS: IMPROVED SANITATION, WATER, HYGIENE (WASH). Maternal education, breastfeeding, complementary feeding, micronutrient supplementation. PROBIOTICS, PREBIOTICS? Inconsistent. ANTI-INFLAMMATORY (5-ASA)? Not recommended. ANTIBIOTICS? Not recommended (routine). AZITHROMYCIN mass drug administration? Research. Prognosis: EED is reversible with improved sanitation and nutrition. Early childhood stunting has lifelong consequences (reduced adult height, lower educational attainment, decreased economic productivity). Zambian context: EED IS HIGHLY PREVALENT. Stunting prevalence in Zambia: 35-40% (under-5 children). EED is a MAJOR DRIVER. No diagnostic tests available. FOCUS: PREVENTION (WASH, nutrition, breastfeeding, vaccination), EARLY DETECTION OF STUNTING (growth monitoring), NUTRITIONAL INTERVENTIONS. EED is a CRITICAL, YET NEGLECTED, DETERMINANT OF CHILD HEALTH. You will see it every day. Address the root causes: poverty, sanitation, nutrition.
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Coming soon
Topic 234Coming soon
Whipple's Disease
Whipple's disease (WD) is a RARE, CHRONIC, MULTISYSTEM INFECTION caused by Tropheryma whipplei, a Gram-positive actinobacterium. For Zambian students, WD is an EXOTIC, UNLIKELY DIAGNOSIS, but it is CLASSIC and must be recognized because it is CURABLE with antibiotics. Failure to diagnose can be fatal. PATHOPHYSIOLOGY: T. whipplei infects macrophages in small intestinal lamina propria, mesenteric lymph nodes, and disseminates systemically. Macrophages accumulate intracellular organisms (PAS-positive granules). Intestinal villi are blunted, contain foamy, PAS-positive macrophages and dilated lymphatics (lymphangiectasia). Genetic susceptibility (HLA-DRB1*13, DQB1*06). CLINICAL: CLASSIC TRIAD (only 10-15%): ARTHRALGIA/ARTHRITIS (migratory, large joints, precedes other symptoms by YEARS), CHRONIC DIARRHOEA (steatorrhoea, malabsorption, weight loss), ABDOMINAL PAIN. OTHER: SYSTEMIC: FEVER, NIGHT SWEATS, LYMPHADENOPATHY, HYPERPIGMENTATION (sun-exposed skin). CARDIAC: endocarditis (culture-negative, blood culture-negative, valve destruction), pericarditis. NEUROLOGIC (5-10%): COGNITIVE IMPAIRMENT, DEMENTIA, OPHTHALMOPLEGIA, Oculomasticatory myorhythmia (OCM) and Oculo-facial-skeletal myorhythmia (OFSM) are PATHOGNOMONIC (but rare). PULMONARY: cough, pleural effusion. DIAGNOSIS: ENDOSCOPY: pale, yellow, shaggy, friable mucosa with dilated lymphatics (DUODENUM). HISTOLOGY (duodenal biopsy): FOAMY, PAS-POSITIVE MACROPHAGES in lamina propria (diastase-resistant). Confirmatory: IMMUNOHISTOCHEMISTRY (anti-T. whipplei antibody), PCR (stool, saliva, blood, tissue, CSF). ELECTRON MICROSCOPY: trilamellar cell wall (bacillary bodies). CSF analysis: pleocytosis, elevated protein, PCR+ (neurologic involvement). Differential: MACROPHAGE INFILTRATION (MAI—Mycobacterium avium intracellulare, in HIV; PAS-positive, but acid-fast positive; WD is acid-fast negative). MANAGEMENT: ANTIBIOTIC THERAPY. INDUCTION: CEFTRIAXONE 2g IV daily OR PENICILLIN G IV x 2-4 weeks. MAINTENANCE: TMP-SMX DS (160/800mg) BID OR DOXYCYCLINE 100mg BID + HYDROXYCHLOROQUINE 200mg TID x 12 months. Alternatives: ceftriaxone induction followed by TMP-SMX. NEUROLOGIC WD: longer therapy, CSF monitoring. IMMUNE RECONSTITUTION INFLAMMATORY SYNDROME (IRIS): upon treatment initiation, corticosteroids. Prognosis: EXCELLENT with early treatment. Relapse possible (especially neurologic). Late diagnosis: irreversible CNS damage. Zambian context: WHIPPLE'S DISEASE IS EXTREMELY RARE IN AFRICA. Almost certainly never seen. Do NOT consider unless ALL other causes of malabsorption (TB, MAI, parasites, HIV, celiac) are excluded. However, it is a 'must-know' for examinations and global awareness. If suspected, refer to tertiary centre (endoscopy, histology with PAS, PCR). Treatment: ceftriaxone, TMP-SMX are available. Diagnosis: requires PAS staining (available). IHC, PCR: NOT available.