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 208Coming soon
Hepatic Cysts: Simple, Hydatid, and Polycystic
Hepatic cysts are common incidental findings, but may be complex (hydatid, neoplastic) or part of polycystic disease. For Zambian students, DISTINGUISHING BENIGN SIMPLE CYSTS from HYDATID CYSTS (Echinococcus) is critical—misdiagnosis leads to inappropriate aspiration (anaphylaxis, dissemination). SIMPLE HEPATIC CYSTS: PATHOLOGY: benign, congenital, lined by cuboidal epithelium. CLINICAL: INCIDENTAL (95%). Large cysts (>5cm): dull ache, early satiety, palpable mass. COMPLICATIONS: haemorrhage, rupture, infection (rare). DIAGNOSIS: ULTRASOUND: anechoic, smooth, thin-walled (<1mm), posterior acoustic enhancement, NO internal echoes, NO septations, NO calcification. WHOLE CYST. MANAGEMENT: ASYMPTOMATIC: NONE. SYMPTOMATIC: FENESTRATION (deroofing, laparoscopic/open), percutaneous aspiration + sclerotherapy (alcohol, doxycycline). HYDATID CYST (Echinococcus granulosus): ENDEMIC: pastoral communities (cattle, sheep, dogs). ZAMBIA: endemic in certain regions. PATHOLOGY: LARVA STAGE. THREE-LAYERED CYST: outer pericyst (host fibrous reaction), middle laminated membrane (acellular), inner germinal layer (produces brood capsules, protoscolices, hydatid sand). CLINICAL: SLOW GROWTH, often incidental. LARGE CYSTS: RUQ pain, mass, biliary obstruction, portal hypertension. COMPLICATIONS: CYST RUPTURE → ANAPHYLAXIS, peritoneal dissemination (secondary echinococcosis). BILIARY RUPTURE → cholangitis, obstructive jaundice. INFECTION. DIAGNOSIS: ULTRASOUND: WHO CLASSIFICATION (CL, CE1-CE5). CE1: unilocular, anechoic, HYATID SAND (snowflake sign). CE2: multiseptated, honeycomb, daughter cysts—PATHOGNOMONIC. CE3: detached membrane (water-lily sign). CE4/5: inactive, degenerated (calcified). SEROLOGY: ELISA, immunoblot (confirmation, 80-95% sensitive). AVOID ASPIRATION (diagnostic). MANAGEMENT: ALBENDAZOLE (15 mg/kg/day, continuous) x 3-6 months (pre-op, post-op, inoperable). PAIR: Puncture, Aspiration, Injection of scolicidal agent (95% ethanol, hypertonic saline), Re-aspiration. INDICATED for CE1, CE3 (selected). NOT for CE2 (multiseptated), biliary communication, superficial cysts (leak risk). SURGERY: PERICYSTECTOMY (total cyst removal), hepatic resection. INDICATED: large cysts (>10cm), CE2, biliary communication, failed PAIR, complicated cysts. POLYCYSTIC LIVER DISEASE (PCLD): autosomal dominant (ADPKD, PRKCSH, SEC63). MULTIPLE, BILATERAL cysts, normal liver function. Complications: MASS EFFECT (pain, early satiety, dyspnoea, portal hypertension). CYST INFECTION. MANAGEMENT: SYMPTOMATIC: aspiration + sclerotherapy, fenestration, hepatic resection, LIVER TRANSPLANT (rare). NO pharmacotherapy. Zambian context: Simple cysts: COMMON, incidental. Hydatid: ENDEMIC in livestock-rearing areas (Southern, Western provinces). SUSPECT in cystic lesion with septations, daughter cysts, calcification. SEROLOGY available (Veterinary? Human reference lab). ALBENDAZOLE available. PAIR: interventional radiology? Limited. SURGERY: pericystectomy available (tertiary). AVOID ASPIRATION of suspected hydatid.
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Topic 209Coming soon
Hepatic Adenoma
Hepatocellular adenoma (HCA) is a rare, benign, clonal proliferation of hepatocytes, strongly associated with ORAL CONTRACEPTIVE USE and other hormonal influences (androgens, pregnancy). For Zambian students, HCA is an important consideration in young women with a liver mass—distinction from FOCAL NODULAR HYPERPLASIA (FNH) is critical, as HCA carries RISK OF RUPTURE (haemorrhage, life-threatening) and MALIGNANT TRANSFORMATION (to HCC). PATHOPHYSIOLOGY: MOLECULAR CLASSIFICATION (4 subtypes, different risks): 1) HNF1A-INACTIVATED (30-40%): steatotic, lowest risk of transformation. 2) INFLAMMATORY (40-50%): JAK-STAT pathway, inflammatory infiltrate, highest risk of bleeding. 3) β-CATENIN-ACTIVATED (10-15%): highest risk of MALIGNANT TRANSFORMATION (HCC). 4) UNCLASSIFIED. ORAL CONTRACEPTIVES: duration, oestrogen dose. Androgens (anabolic steroids). Glycogen storage diseases (type I, III). CLINICAL: ASYMPTOMATIC, incidental (most). Large adenomas (>5cm): ABDOMINAL PAIN, PALPABLE MASS. ACUTE ABDOMEN: TUMOUR RUPTURE, HAEMORRHAGE (haemoperitoneum, shock)—MEDICAL EMERGENCY. Malignant transformation: slow growth, AFP normal. DIAGNOSIS: ULTRASOUND: variable. HNF1A: diffuse fat (homogeneous, rapid signal dropout). Inflammatory: marked hypervascularity. MRI: BEST NON-INVASIVE DIAGNOSIS. HNF1A: diffuse intralesional fat (chemical shift). Inflammatory: T2 hyperintense, MARKED ARTERIAL ENHANCEMENT, PERSISTENT DELAYED ENHANCEMENT (atypical for FNH). β-catenin: no specific features. BIOPSY: INDICATED if imaging non-diagnostic, β-catenin suspected (high transformation risk), or for molecular subtyping (guides management). DISTINGUISH FROM FNH: FNH = benign, NO rupture, NO malignant transformation. Imaging: CENTRAL SCAR (hypointense T2, delayed enhancement), arterial enhancement, isointense to liver on delayed phase. MANAGEMENT: RESECTION: INDICATED for: LARGE (>5cm), β-CATENIN ACTIVATED, SUSPECTED MALIGNANCY, or INCREASING SIZE on surveillance. LAPAROSCOPIC RESECTION preferred. RUPTURE/HAEMORRHAGE: HAEMODYNAMIC STABILISATION, transfusion, ANGIOGRAPHY WITH EMBOLIZATION (preferred), delayed resection. SURVEILLANCE: SMALL (<5cm), HNF1A or INFLAMMATORY (non-β-catenin): DISCONTINUE OCP, ANDROGENS. Repeat MRI at 6 months, 12 months, then annually. REGRESSION occurs in 50% after OCP cessation. PREGNANCY: INCREASED RISK OF GROWTH, RUPTURE. Multidisciplinary counselling. Prognosis: Excellent after resection. Rupture risk: 20-30% (tumours >5cm). Malignant transformation: 5-10% (β-catenin). Zambian context: HCA is UNDERDIAGNOSED. Think HCA in young woman on OCP with liver mass. MRI available tertiary. OCP widely used. RESECTION available (tertiary). Embolization (angio) available limited. β-catenin testing (IHC) NOT AVAILABLE. Management: OCP cessation, surveillance (ultrasound) if small, resection if large (>5cm). Rupture: emergency presentation, high mortality. Prevention: counsel young women on OCP regarding risk (low, but real).
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Topic 210Coming soon
Focal Nodular Hyperplasia
Focal nodular hyperplasia (FNH) is the SECOND MOST COMMON benign liver tumour (after haemangioma), a polyclonal, regenerative hepatocellular response to a local vascular anomaly (arterial malformation). For Zambian students, FNH is a CRITICAL DIFFERENTIAL DIAGNOSIS of HEPATIC ADENOMA—FNH is BENIGN, NO MALIGNANT POTENTIAL, NO RUPTURE RISK, and does NOT require resection or follow-up. PATHOPHYSIOLOGY: NOT a true neoplasm. Arteriovenous malformation (feeding artery) → hyperperfusion → hepatocellular hyperplasia, bile duct proliferation. Central fibrous scar (pathognomonic). NO association with OCP (but OCP may cause growth). NO malignant transformation. CLINICAL: INCIDENTAL (90%), young-middle aged women. Asymptomatic. Large lesions: rarely pain, mass effect. DIAGNOSIS: MRI (with hepatobiliary contrast agent—gadoxetate, gadobenate) is the NON-INVASIVE GOLD STANDARD. Imaging hallmarks: HOMOGENEOUS, ISOINTENSE to liver on T1/T2 (unless fat). CENTRAL SCAR: HYPOINTENSE T2, DELAYED HYPERENHANCEMENT. ARTERIAL PHASE: INTENSE, HOMOGENEOUS ENHANCEMENT. PORTAL VENOUS/DELAYED: ISOINTENSE to liver. HEPATOBILIARY PHASE (20 min): HYPERINTENSE or ISOINTENSE (uptake of contrast by hepatocytes, biliary excretion). This DISTINGUISHES FNH from ADENOMA (hypointense, no biliary uptake). CT: similar, central scar may not enhance early. ULTRASOUND: isoechoic, subtle, central scar (scarce). BIOPSY: RARELY REQUIRED. Indications: atypical imaging, inconclusive MRI, no hepatobiliary contrast agent available. Histology: nodular architecture, fibrous septa, ductular proliferation, MALFORMED VESSELS (no portal tracts). NO CYTOARCHITECTURAL ATYPIA. MANAGEMENT: NO TREATMENT. NO SURVEILLANCE (once diagnosis confirmed). DISCHARGE. If symptomatic (pain): surgical resection (rarely indicated). OCP: NO need to discontinue (no causal relationship, but may promote growth). Pregnancy: safe. Prognosis: EXCELLENT, benign. Zambian context: FNH is COMMON incidental finding on ultrasound. MRI is diagnostic (hepatobiliary contrast agents? May NOT be available). LIVER-SPECIFIC CONTRAST (gadoxetate, Primovist/Eovist) is EXPENSIVE, NOT AVAILABLE in Zambia. Therefore, IMAGING DIAGNOSIS MAY BE UNCERTAIN. In absence of hepatobiliary phase, FNH vs ADENOMA can be difficult. CLINICAL CONTEXT: young woman, OCP use, asymptomatic. MRI without hepatobiliary contrast: HOMOGENEOUS, CENTRAL SCAR, isointense on delayed phase, no intralesional fat. If TYPICAL, can diagnose FNH. If ATYPICAL or cannot exclude adenoma: BIOPSY. BIOPSY available (tertiary, ultrasound-guided). FNH = REASSURANCE, NO FOLLOW-UP. This is LIFE-ALTERING for patients (no surgery, no cancer worry).
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Topic 211Coming soon
Hepatic Hemangioma
Hepatic hemangioma is the MOST COMMON benign liver tumour, a congenital vascular malformation (cavernous venous channels) with NO malignant potential. For Zambian students, it is a FREQUENT INCIDENTAL FINDING on ultrasound. Recognition prevents unnecessary anxiety, biopsy (haemorrhage risk), and surgery. PATHOPHYSIOLOGY: Benign, non-neoplastic. Endothelial-lined vascular channels, slow-flow. Size: small (<5cm), giant (>10cm). CLINICAL: INCIDENTAL (90%), all ages, female predominance. Asymptomatic. GIANT HEMANGIOMA: abdominal pain, early satiety, palpable mass. RARE COMPLICATIONS: Kasabach-Merritt syndrome (consumptive coagulopathy—thrombocytopenia, hypofibrinogenaemia), spontaneous rupture (EXQUISITELY RARE, <1%). NO malignant transformation. DIAGNOSIS: ULTRASOUND: HYPERECHOIC, HOMOGENEOUS, WELL-DEFINED, posterior acoustic enhancement (bright). SMALL (<3cm) → DIAGNOSTIC. ATYPICAL: giant, heterogeneous, isoechoic, calcification. CONTRAST-ENHANCED ULTRASOUND (CEUS): peripheral nodular enhancement, CENTRIPETAL FILL-IN. CONTRAST-ENHANCED CT/MRI: DIAGNOSTIC. CT: hypodense, arterial phase: PERIPHERAL, NODULAR, DISCONTINUOUS ENHANCEMENT (same as aorta), PORTAL VENOUS/DELAYED: CENTRIPETAL FILL-IN, ISODENSE. MRI: T2: MARKED HYPERINTENSE ('light bulb' sign). Management: INCIDENTAL, TYPICAL: NO TREATMENT. REASSURE. NO SURVEILLANCE. GIANT, SYMPTOMATIC: RESECTION (enucleation) or INTERVENTION (rarely needed). Rupture: EMERGENCY, haemodynamic support, resection/embolization. Kasabach-Merritt: corticosteroids, interferon, resection. AVOID: BIOPSY (risk of major haemorrhage). OCP: NO contraindication. Pregnancy: safe (growth rare). Prognosis: EXCELLENT. Zambian context: HEMANGIOMA IS EXTREMELY COMMON. Ultrasound is widely available—TYPICAL APPEARANCE (hyperechoic, homogeneous, well-defined) is DIAGNOSTIC. Do NOT biopsy. Do NOT refer. Do NOT follow-up. REASSURE patient. This is one of the most important benign diagnoses to recognize and prevent iatrogenic harm. ATYPICAL FEATURES: heterogeneous, isoechoic, large size, calcification—requires CONFIRMATORY IMAGING (CEUS, CT, MRI) available at tertiary centres. MRI is diagnostic. Giant symptomatic haemangioma: surgical resection available (tertiary). This is RARE. MASTER HEPATIC HEMANGIOMA: RECOGNIZE, REASSURE, DO NOT BIOPSY, DO NOT FOLLOW.
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Topic 212Coming soon
Portal Hypertensive Gastropathy
Portal hypertensive gastropathy (PHG) is an endoscopic finding in patients with portal hypertension, characterized by a SNAKESKIN or MOSAIC-LIKE PATTERN of the gastric mucosa, with or without red spots. For Zambian students, PHG is a COMMON, OFTEN OVERLOOKED cause of CHRONIC GASTROINTESTINAL BLEEDING in cirrhotic patients. PATHOPHYSIOLOGY: PORTAL HYPERTENSION → passive congestion, gastric mucosal hyperaemia, arteriovenous shunting, impaired oxygenation → mucosal fragility, bleeding. CLINICAL: ASYMPTOMATIC (most). CHRONIC BLEEDING: iron deficiency anaemia, occult blood loss, positive faecal occult blood. ACUTE BLEEDING (15%): haematemesis, melaena, haemodynamic instability. CORRELATION: severity of PHG correlates with portal pressure, presence of varices. ENDOSCOPY: CLASSIFICATION: MILD: snakeskin, mosaic pattern. SEVERE: flat or bulging red spots (cherry-red spots), diffuse haemorrhagic gastritis. DISTINGUISH from GASTRIC VARICES (submucosal, compressible). MANAGEMENT: ACUTE BLEEDING: SOMATOSTATIN/OCTREOTIDE IV (reduces portal pressure) x 5 days. SUPPORTIVE: fluid resuscitation, blood transfusion (restrictive: Hb <7g/dL). PROTON PUMP INHIBITOR (PPI): if concomitant ulcer/erosions. PROPHYLAXIS (CHRONIC): NON-SELECTIVE BETA-BLOCKERS (NSBB: propranolol, carvedilol). Reduces portal pressure, improves PHG, reduces rebleeding. IRON SUPPLEMENTATION (oral, IV). REFRACTORY: TIPS (transjugular intrahepatic portosystemic shunt) effectively treats PHG (rebleeding <20%). Prognosis: PHG improves with NSBB. TIPS is definitive. Zambian context: PHG is COMMON. Endoscopy available tertiary. NSBB (propranolol) available, inexpensive. TIPS NOT available. Iron supplementation available. Recognize PHG as cause of chronic anaemia in cirrhosis.
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Topic 213Coming soon
Gastric Antral Vascular Ectasia
Gastric antral vascular ectasia (GAVE, 'watermelon stomach') is an uncommon but important cause of CHRONIC, SEVERE GASTROINTESTINAL BLEEDING and IRON DEFICIENCY ANAEMIA. For Zambian students, GAVE is distinct from PHG and requires different management. PATHOPHYSIOLOGY: Idiopathic. Associated with CIRRHOSIS (30%, especially primary biliary cholangitis, autoimmune hepatitis), connective tissue disease (scleroderma), chronic renal failure. NOT related to portal pressure. Histology: dilated, thrombosed mucosal capillaries, fibromuscular hyperplasia. CLINICAL: SEVERE, TRANSFUSION-DEPENDENT ANAEMIA. Occult bleeding (melena, haematochezia). Cirrhotic patients may have concomitant PHG. ENDOSCOPY: PATHOGNOMONIC: RED, VASCULAR, LINEAR STRIPES radiating from pylorus into antrum (watermelon stripes). May be diffuse (without stripes). DISTINGUISH from PHG: PHG = snakeskin, fundus/body. GAVE = antrum, linear stripes. MANAGEMENT: ENDOSCOPIC THERAPY is FIRST-LINE. ARGON PLASMA COAGULATION (APC): effective, safe, repeated sessions (2-4) often required to obliterate lesions. LASER (Nd:YAG), RADIOFREQUENCY ABLATION (RFA). INTRAVENOUS IRON: correct deficiency. TRANSFUSION: severe anaemia. MEDICAL THERAPY: limited efficacy. Corticosteroids, oestrogen-progesterone, tranexamic acid. REFRACTORY: SURGICAL ANTRECTOMY (rare, definitive). TIPS: NOT effective (GAVE is not portal pressure-dependent). Prognosis: Excellent response to APC. Recurrence common (20-30%), requires repeat sessions. Zambian context: GAVE is RARE, underdiagnosed. Consider in cirrhotic patient with severe, transfusion-dependent anaemia and NO variceal bleeding. Endoscopy is diagnostic. APC available at tertiary centres (Lusaka). Intravenous iron available. Surgery (antrectomy) available. High index suspicion.
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Topic 214Coming soon
Eosinophilic Esophagitis
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) 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%), FOOD IMPACTION (50-60%), HEARTBURN (GERD-like, refractory to PPI). 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 passage of scope), 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. 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) or ORAL BUDESONIDE (viscous suspension, 1-2mg/day). Swallow, NOT inhale. No systemic absorption. Dilation: ENDOSCOPIC DILATION for strictures (high perforation risk, gradual). 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. High index suspicion.
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Topic 215Coming soon
Gastroesophageal Reflux Disease
Gastroesophageal reflux disease (GERD) is a condition that develops when reflux of gastric contents causes TROUBLESOME SYMPTOMS (heartburn, regurgitation) and/or COMPLICATIONS (esophagitis, stricture, Barrett's esophagus, adenocarcinoma). For Zambian students, GERD is a DAILY, OFTEN SUBOPTIMALLY MANAGED condition, with increasing prevalence parallel to obesity and metabolic syndrome. PATHOPHYSIOLOGY: MULTIFACTORIAL: TRANSIENT LOWER ESOPHAGEAL SPHINCTER RELAXATIONS (tLESRs, most common), hypotensive LES, hiatal hernia, impaired esophageal clearance, delayed gastric emptying, obesity (increases intra-abdominal pressure). REFLUXATE: acid, pepsin, bile. CLINICAL: TYPICAL SYMPTOMS: HEARTBURN (retrosternal burning, postprandial, supine), REGURGITATION (effortless return of gastric contents). ATYPICAL SYMPTOMS: CHEST PAIN (non-cardiac), chronic cough, asthma, laryngitis (hoarseness, throat clearing), dental erosions. ALARM SYMPTOMS: dysphagia, odynophagia, weight loss, GI bleeding, anaemia, vomiting—require URGENT ENDOSCOPY. DIAGNOSIS: TYPICAL SYMPTOMS: EMPIRIC PPI TRIAL (4-8 weeks). Symptom relief = GERD. ENDOSCOPY: INDICATED for alarm symptoms, risk factors (age >50, male, white, obesity, long-term GERD, Barrett's screening), or PPI non-response. Findings: LA GRADE A-D esophagitis, stricture, Barrett's (salmon-coloured mucosa). BIOPSY: exclude eosinophilic esophagitis (if dysphagia), Barrett's (intestinal metaplasia). pH MONITORING: refractory symptoms, pre-surgical evaluation. MANAGEMENT: LIFESTYLE MODIFICATION: weight loss, head-of-bed elevation, avoid late meals, trigger foods (fatty, spicy, chocolate, coffee, alcohol). PHARMACOLOGIC: PROTON PUMP INHIBITORS (PPIs) are FIRST-LINE, MOST EFFECTIVE. Standard dose (omeprazole 20mg, pantoprazole 40mg, esomeprazole 40mg) 30-60min before breakfast. REFRACTORY GERD: double-dose PPI, check adherence, switch PPI, add H2RA at bedtime, endoscopy to exclude other causes. H2RA: alternative or adjunct (ranitidine, famotidine). ANTACIDS: rapid symptom relief, not healing. PROKINETICS: limited efficacy (metoclopramide, side effects). SURGERY: LAPAROSCOPIC NISSEN FUNDOPLICATION. INDICATIONS: PPI failure, PPI intolerance, large hiatal hernia, patient preference (avoid lifelong medication). ENDOSCOPIC THERAPIES (Stretta, TIF): emerging. COMPLICATIONS: PEPTIC STRICTURE: endoscopic dilation, PPI. BARRETT'S ESOPHAGUS: intestinal metaplasia, dysplasia risk, SURVEILLANCE endoscopy (q3-5y), ablation (dysplasia). ESOPHAGEAL ADENOCARCINOMA: prevention (GERD treatment, Barrett's surveillance). Zambian context: GERD IS COMMON AND INCREASING. PPI (omeprazole) widely available, inexpensive. Empiric PPI trial is appropriate. Endoscopy available tertiary. Barrett's is RARE in African populations, but occurs. Surgery (fundoplication) available. Focus: symptom control, PPI adherence, alarm features prompt endoscopy.
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Topic 216Coming soon
Barrett's Esophagus
Barrett's esophagus (BE) is a metaplastic change in which NORMAL SQUAMOUS EPITHELIUM of the distal esophagus is replaced by COLUMNAR EPITHELIUM WITH INTESTINAL METAPLASIA (goblet cells), a complication of chronic GERD. For Zambian students, BE is the ONLY KNOWN PRECURSOR to ESOPHAGEAL ADENOCARCINOMA, but the risk in African populations is low. PATHOPHYSIOLOGY: Chronic GERD → inflammation, oxidative stress → genetic/epigenetic alterations → metaplasia (goblet cells, CDX2 expression) → dysplasia (low-grade, high-grade) → adenocarcinoma. RISK FACTORS: chronic GERD (>5 years), age >50, male, white, obesity, hiatal hernia, family history. CLINICAL: NO SPECIFIC SYMPTOMS. Suspect in long-standing GERD. DIAGNOSIS: ENDOSCOPY: salmon-pink, velvety mucosa extending PROXIMAL to gastroesophageal junction (≥1cm). PRAGUE CLASSIFICATION: C (circumferential) and M (maximal) extent. BIOPSY: SEATTLE PROTOCOL: quadrantic biopsies q2cm, targeted of visible lesions. HISTOLOGY: INTESTINAL METAPLASIA (goblet cells, alcian blue stain positive). DYSPLASIA: low-grade (LGD), high-grade (HGD). MANAGEMENT: NON-DYSPLASTIC BE: SURVEILLANCE ENDOSCOPY q3-5 years. PPI (high-dose, indefinite). NO dysplasia = very low cancer risk (0.1-0.3%/year). LGD: CONFIRM by expert pathologist. SURVEILLANCE q12 months OR ENDOSCOPIC ABLATION (radiofrequency ablation, RFA). HGD: ENDOSCOPIC ERADICATION THERAPY (EET) is STANDARD. RFA, endoscopic mucosal resection (EMR) for visible lesions. SUBMUCOSAL INVASION (T1b): esophagectomy, endoscopic therapy (selected). Prognosis: Excellent with surveillance/ablation. Cancer risk: non-dysplastic 0.3%/year, LGD 0.5-1%/year, HGD 5-10%/year. Zambian context: BE IS RARE in indigenous Africans. Suspect in long-standing GERD, especially white, male, obese. Endoscopy available tertiary. Pathology: intestinal metaplasia diagnosis. PPI (omeprazole) available. RFA NOT AVAILABLE. EMR limited. Esophagectomy available (tertiary). High-grade dysplasia: consider esophagectomy (limited). Surveillance endoscopy: feasible, cost-prohibitive. Pragmatic: PPI, one surveillance endoscopy if BE confirmed, discharge if no dysplasia, low risk.