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 253Coming soon
Anorectal Diseases: Fissure and Fistula
Anal fissure and anal fistula are common anorectal conditions with distinct pathophysiology and management. ANAL FISSURE: longitudinal tear in anoderm, distal to dentate line. ACUTE (<6 weeks) vs CHRONIC (>6 weeks). PATHOPHYSIOLOGY: trauma (hard stool), hypertonic internal anal sphincter → ischemia of posterior commissure (poor blood supply). LOCATION: POSTERIOR MIDLINE (90%). ATYPICAL location (lateral, multiple): consider CROHN'S DISEASE, TB, HIV, syphilis, malignancy. CLINICAL: SEVERE, SHARP PAIN with defecation, BRIGHT RED BLOOD (on toilet paper), sentinel tag (chronic). DIAGNOSIS: CLINICAL (gentle separation of buttocks). Anoscopy too painful (avoid). MANAGEMENT: ACUTE: CONSERVATIVE. HIGH-FIBRE DIET, FIBRE SUPPLEMENTS (psyllium), SITZ BATHS, TOPICAL ANALGESICS (lidocaine). HEALING >80% in 6-8 weeks. CHRONIC: MEDICAL: TOPICAL NITROGLYCERIN (0.2-0.4%, relaxes internal sphincter) or TOPICAL CALCIUM CHANNEL BLOCKERS (nifedipine 0.2%, diltiazem 2%). Healing 50-70%. SIDE EFFECTS: headache (GTN). BOTULINUM TOXIN INJECTION: internal sphincter, healing 60-80%, temporary. SURGICAL: LATERAL INTERNAL SPHINCTEROTOMY (LIS): GOLD STANDARD for CHRONIC FISSURE refractory to medical therapy. Divide internal sphincter, 95% healing, LOW INCONTINENCE RISK (<1% solid stool, 5-10% flatus). ANAL FISTULA: abnormal communication between anal canal (cryptoglandular) and perianal skin. PATHOPHYSIOLOGY: infection of anal gland → intersphincteric abscess → spontaneous drainage → epithelialized tract. CLASSIFICATION (Parks): INTERSPHINCTERIC (70%), TRANSSPHINCTERIC (25%), SUPRASPHINCTERIC (5%), EXTRASPHINCTERIC (1%). GOODSALL'S RULE: anterior external opening → straight radial fistula. posterior external opening → curvilinear tract to posterior midline. CLINICAL: perianal discharge (purulent, serous), recurrent abscess, pain, external opening. DIAGNOSIS: CLINICAL, PROBE TRACT. MRI PELVIS: GOLD STANDARD for complex fistula (recurrent, Crohn's, supralevator). EUS/EAUS. MANAGEMENT: FISTULOTOMY (lay open): SIMPLE, LOW FISTULA (<30% external sphincter). HIGH FISTULA (>30% external sphincter): SETON (draining or cutting), ADVANCEMENT FLAP, LIFT procedure, FIBRIN GLUE, ANAL FISTULA PLUG. CROHN'S FISTULA: SETON + BIOLOGICS (infliximab). Prognosis: SIMPLE FISTULA: 90-95% healing with fistulotomy. COMPLEX: variable, recurrence 20-30%, incontinence risk. Zambian context: FISSURE: COMMON. CONSERVATIVE: fibre, sitz baths. TOPICAL NITROGLYCERIN: available? Nifedipine/diltiazem: available? LIS: surgical procedure, available. FISTULA: COMMON. CLINICAL DIAGNOSIS, PROBE. MRI limited. FISTULOTOMY (low fistula) widely performed. SETON placement (draining, cutting) available. ADVANCEMENT FLAP, LIFT: limited expertise. CROHN'S FISTULA: uncommon; treat infection (seton), consider AZATHIOPRINE, BIOLOGICS (unavailable). TUBERCULOUS FISTULA: high index suspicion (HIV, chronic, atypical). DIAGNOSIS: biopsy, AFB, culture, PCR. TREAT: anti-TB therapy + surgery. FOCUS: FISSURE: fibre, topical nitrates/CCB, LIS if chronic. FISTULA: Goodsall's rule, determine fistula height, FISTULOTOMY (low), SETON (high), AVOID INCONTINENCE, exclude Crohn's, TB.
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Anorectal Abscess
Anorectal abscess is an acute infection of the cryptoglandular epithelium, originating in the intersphincteric space. For Zambian students, it is a COMMON SURGICAL EMERGENCY. CLASSIFICATION (by space): PERIANAL (60%, superficial), ISCHIORECTAL (20%, deeper, supralevator?), INTERSPHINCTERIC (5%), SUPRALEVATOR (rare, supralevator). CLINICAL: PERIANAL ABSCESS: THROBBING, CONSTANT PAIN, exacerbated by sitting, defecation. EXTERNAL SWELLING, ERYTHEMA, FLUCTUANCE. ISCHIORECTAL ABSCESS: DEEPER PAIN, fever, leukocytosis, NO external fluctuance (early), induration, gluteal asymmetry. SUPRALEVATOR ABSCESS: PELVIC PAIN, fever, NO perianal findings, difficult to diagnose. Risk factors: diabetes, Crohn's disease, immunosuppression (HIV). DIAGNOSIS: CLINICAL. Imaging (CT/MRI) for SUSPECTED DEEP, RECURRENT, ATYPICAL abscess (supralevator, Crohn's, malignancy). LABS: leukocytosis, CRP, glucose. MANAGEMENT: SURGICAL DRAINAGE IS DEFINITIVE. ANTIBIOTICS ARE ADJUNCTIVE, NOT CURATIVE. PERIANAL ABSCESS: INCISION AND DRAINAGE (I&D) under local anaesthesia. Cruciate incision, drain pus, break loculations, loosely pack. ISCHIORECTAL/ DEEP ABSCESS: I&D in operating room (spinal/general anaesthesia). SUPRALEVATOR ABSCESS: drainage via transrectal (preferred) or transperineal approach. ANTIBIOTICS: INDICATED for CELLULITIS, SYSTEMIC SEPSIS, IMMUNOCOMPROMISED, VALVULAR HEART DISEASE, EXTENSIVE DISEASE. Broad-spectrum (cover Gram-neg, anaerobes). COMPLICATIONS: FISTULA-IN-ANO (30-50% develop fistula), RECURRENCE, INCONTINENCE (sphincter damage). Prognosis: EXCELLENT with prompt drainage. Zambian context: ANORECTAL ABSCESS IS COMMON. PERIANAL: I&D in clinic/ED, local anaesthesia. DEEP: OR. HIGH INDEX SUSPICION in diabetics, HIV. CROHN'S DISEASE: consider in recurrent, complex, multiple abscesses. TUBERCULOUS ABSCESS: chronic, atypical, cold abscess. Diagnosis: biopsy, AFB, culture, PCR. TREAT: I&D + anti-TB therapy. FOCUS: PROMPT DRAINAGE (pain relief, source control). ANTIBIOTICS NOT ROUTINE. RECOGNIZE DEEP ABSCESS (ischiorectal, supralevator) requires OR. SUSPECT FISTULA (follow-up).
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Pilonidal Disease
Pilonidal disease is an acquired, chronic inflammatory condition of the SACROCOCCYGEAL (natal cleft) region, caused by penetration of loose hairs into the skin. For Zambian students, it is COMMON in hirsute young males. PATHOPHYSIOLOGY: Hair penetration → foreign body reaction → midline pits → infection → abscess → chronic draining sinuses (lateral extension). CLINICAL: ACUTE PILONIDAL ABSCESS: PAINFUL, ERYTHEMATOUS SWELLING at sacrococcygeal region, fluctuant. CHRONIC PILONIDAL DISEASE: intermittent, PAINLESS, SEROUS OR PURULENT DRAINAGE from MIDLINE PITS (± lateral sinuses). ASYMPTOMATIC: incidental pits. DIAGNOSIS: CLINICAL. MANAGEMENT: ACUTE ABSCESS: INCISION AND DRAINAGE (I&D) with LATERAL INCISION (preferred) or midline incision. CURETTAGE of hair, loosely packed. ANTIBIOTICS: NOT routine (unless cellulitis, immunocompromised). CHRONIC DISEASE: DEFINITIVE SURGERY. Simple excision and primary closure: high recurrence (20-40%). OFF-MIDLINE CLOSURE (Karydakis flap, Bascom cleft lift, rhomboid flap): LOWER RECURRENCE (<5%). PIT-PICKING (Bascom II): minimal excision of pits, lateral drainage. LAY OPEN (unroofing) ± marsupialization. LASER EPILATION: reduces recurrence (removes hair). CONSERVATIVE: good hygiene, shaving/ laser hair removal, can be effective for mild disease. Prognosis: EXCELLENT. Recurrence risk: 10-20% (overall). Modifiable: obesity, hirsutism, sedentary lifestyle, poor hygiene. Zambian context: PILONIDAL DISEASE IS COMMON. ACUTE ABSCESS: I&D (surgical registrars). CHRONIC: EXCISION + PRIMARY CLOSURE (common, high recurrence). FLAP PROCEDURES: limited expertise. LASER EPILATION: not available. FOCUS: ACUTE: I&D, pack, wound care. CHRONIC: ELECTIVE SURGERY (excision + off-midline closure preferred). PATIENT EDUCATION: weight loss, good hygiene, avoid prolonged sitting, hair removal (shaving, depilatory creams).
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Topic 256Coming soon
Short Bowel Syndrome
Short bowel syndrome (SBS) is a malabsorptive state resulting from extensive small bowel resection, leading to DIARRHOEA, DEHYDRATION, MALNUTRITION, and WEIGHT LOSS. For Zambian students, SBS is an UNDERDIAGNOSED, DEVASTATING CONDITION with HIGH MORTALITY, often caused by MESENTERIC ISCHEMIA, CROHN'S DISEASE, VOLVULUS, or TRAUMA. PATHOPHYSIOLOGY: Loss of absorptive surface area, loss of specific absorption sites (B12, bile acids, fat), loss of intestinal hormones, GASTRIC HYPERSECRETION, RAPID TRANSIT. ADAPTATION: structural and functional changes in remaining bowel (villous hyperplasia, increased crypt depth, dilation, prolonged transit). Occurs over 12-24 months. KEY FACTORS: Remaining small bowel LENGTH (<200cm symptomatic, <100cm severe, <50cm intestinal failure). Presence of COLON (preserves fluid, absorbs SCFA, salvage energy). Presence of ILEOCECAL VALVE (slows transit). CLINICAL: EARLY: PROFUSE WATERY DIARRHEA, DEHYDRATION, ELECTROLYTE DISTURBANCE (Na, K, Mg, Ca), HYPOVOLAEMIA, ACUTE RENAL FAILURE. LATE: MALNUTRITION, WEIGHT LOSS, FAT-SOLUBLE VITAMIN DEFICIENCY (A, D, E, K), B12 DEFICIENCY, IRON DEFICIENCY, OSTEOPOROSIS, NEPHROLITHIASIS (oxalate stones, colon intact), CHOLELITHIASIS (bile salt malabsorption), D-LACTIC ACIDOSIS (colon bacterial fermentation). INTESTINAL FAILURE ASSOCIATED LIVER DISEASE (IFALD): cholestasis, steatosis, fibrosis, cirrhosis (parenteral nutrition, sepsis). MANAGEMENT: INTENSIVE, MULTIDISCIPLINARY. PHASE 1: ACUTE (POST-RESECTION): FLUID AND ELECTROLYTE RESUSCITATION (IV). PARENTERAL NUTRITION (PN) via central line. GASTRIC ACID SUPPRESSION (PPI, H2RA). ANTI-DIARRHOEALS (loperamide, codeine, diphenoxylate). OCTREOTIDE (reduces secretions, slows transit). PHASE 2: ADAPTATION (2 weeks - 2 years): ENTERAL NUTRITION (continuous, elemental/semi-elemental). ORAL REHYDRATION SOLUTION (ORS, high sodium). GRADUAL ADVANCEMENT of enteral feeds. TAPER PN as enteral tolerance increases. PHASE 3: MAINTENANCE: HIGH-CARBOHYDRATE, HIGH-PROTEIN, LOW-FAT diet (if colon present). MEDIUM-CHAIN TRIGLYCERIDES (MCT) supplement (absorbed directly into portal vein). VITAMIN AND MINERAL SUPPLEMENTATION (B12 IM monthly, fat-soluble vitamins, iron, calcium, magnesium, zinc, selenium). URSODEOXYCHOLIC ACID (UDCA, gallstones). POTENTIALLY CURATIVE: INTESTINAL TRANSPLANTATION (life-threatening PN complications, irreversible liver disease, loss of central venous access). TEDUGLUTIDE (GLP-2 analogue): promotes intestinal adaptation, reduces PN requirements. Prognosis: SBS with <50cm small bowel and no colon: 5-year survival 50%. With multidisciplinary intestinal failure program, survival >80%. Zambian context: SBS IS RARE. ETIOLOGIES: VOLVULUS (extensive resection), MESENTERIC ISCHEMIA (post-op), TRAUMA, NEONATAL (necrotizing enterocolitis, atresia). PARENTERAL NUTRITION: LIMITED availability, high cost, infection risk. CENTRAL LINES: available. ENTERAL NUTRITION: elemental formula NOT AVAILABLE. MCT OIL: NOT AVAILABLE. ORS: available. TEDUGLUTIDE: NOT AVAILABLE. INTESTINAL TRANSPLANT: NOT AVAILABLE. FOCUS: AGGRESSIVE FLUID/ELECTROLYTE RESUSCITATION, NUTRITIONAL SUPPORT (PN if possible, enteral feeding with standard formula, high-calorie, high-protein), ANTI-DIARRHOEALS, PPI, VITAMIN/MINERAL REPLETION (B12, iron, calcium, vit D), PREVENT COMPLICATIONS (line sepsis, renal failure, gallstones, oxalate stones). PROGNOSIS: GUARDED. This is a CHALLENGING, HIGH-MORTALITY CONDITION.
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Topic 257Coming soon
Carcinoid Syndrome and Neuroendocrine Tumors
Neuroendocrine tumors (NETs) are rare neoplasms arising from neuroendocrine cells throughout the body. Carcinoid syndrome is the paraneoplastic syndrome associated with metastatic small intestinal NETs, caused by secretion of SEROTONIN and other vasoactive substances. For Zambian students, NETs are RARE, but must be recognized as a treatable cause of chronic diarrhoea and flushing. PATHOPHYSIOLOGY: Midgut NETs (ileum, appendix) produce serotonin, tachykinins, prostaglandins. SYNDROME OCCURS ONLY WITH LIVER METASTASES (or primary tumour with retroperitoneal invasion), because serotonin is metabolized by liver (first-pass). Bronchial and ovarian NETs can cause syndrome without metastases (venous drainage bypasses liver). CLINICAL: FLUSHING (90%): sudden, erythematous, face/neck/upper trunk, triggered by alcohol, exercise, stress. DIARRHOEA (70%): watery, secretory. RIGHT-SIDED HEART DISEASE (40-50%): tricuspid regurgitation, pulmonary stenosis; carcinoid heart disease. BRONCHOSPASM (15%). PELLAGRA (nicotinic acid deficiency): dermatitis, diarrhoea, dementia (tryptophan shunted to serotonin, not niacin). ABDOMINAL PAIN, INTESTINAL OBSTRUCTION (mesenteric fibrosis). DIAGNOSIS: 24-HOUR URINARY 5-HIAA (5-hydroxyindoleacetic acid), metabolite of serotonin. SENSITIVITY 70-90%. SERUM CHROMOGRANIN A (CgA): sensitive, non-specific. TUMOUR LOCALIZATION: CT/MRI (liver metastases, primary). OCTREOSCAN (somatostatin receptor scintigraphy) and Ga-68 DOTATATE PET/CT (GOLD STANDARD). COLONOSCOPY, CAPSULE ENDOSCOPY (small bowel primary). ECHOCARDIOGRAPHY (carcinoid heart disease). MANAGEMENT: SOMATOSTATIN ANALOGUES (SSA): OCTREOTIDE, LANREOTIDE. FIRST-LINE for symptom control, tumour stabilization. Reduces flushing, diarrhoea, 5-HIAA, may induce tumour regression. LONG-ACTING REPEATABLE (LAR) formulations monthly. TELOTRISTAT ETHYL (oral tryptophan hydroxylase inhibitor): reduces serotonin production, diarrhoea, flushing. TUMOUR DEBULKING: RESECTION of primary tumour, liver metastases (if resectable). LIVER-DIRECTED THERAPIES: embolization (TACE), radioembolization (Y-90), ablation (RFA). PEPTIDE RECEPTOR RADIONUCLIDE THERAPY (PRRT): 177Lu-DOTATATE (Lutathera), for metastatic, SSA-refractory NETs. EVEROLIMUS (mTOR inhibitor), SUNITINIB (tyrosine kinase inhibitor) for pancreatic NETs. CARCINOID HEART DISEASE: valve replacement surgery (high risk). Prognosis: INDOLENT. Metastatic midgut NET: median survival 5-10 years. Carcinoid heart disease: worse prognosis. Zambian context: NETS ARE EXTREMELY RARE. Consider in: chronic diarrhoea + flushing + right heart failure. URINARY 5-HIAA: NOT AVAILABLE. CHROMOGRANIN A: NOT AVAILABLE. OCTREOSCAN/DOTATATE: NOT AVAILABLE. DIAGNOSIS: CLINICAL, CT (liver metastases, mesenteric mass), ECHOCARDIOGRAPHY (carcinoid heart disease). SOMATOSTATIN ANALOGUES (octreotide): available (expensive). LIVER RESECTION: available. PRRT, everolimus, sunitinib, telotristat: NOT AVAILABLE. FOCUS: CLINICAL SUSPICION, CT ABDOMEN, ECHO, TRIAL OF OCTREOTIDE (if available), SYMPTOM CONTROL (loperamide, niacin supplementation).
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Topic 258Coming soon
Familial Adenomatous Polyposis
Familial adenomatous polyposis (FAP) is an autosomal dominant disorder caused by germline mutation in the APC gene, characterized by HUNDREDS TO THOUSANDS of colorectal adenomas, with NEARLY 100% LIFETIME RISK of COLORECTAL CANCER by age 40-50 years without prophylactic colectomy. For Zambian students, FAP is RARE but must be recognized for GENETIC COUNSELLING and LIFE-SAVING PROPHYLACTIC SURGERY. PATHOPHYSIOLOGY: APC gene (5q21) is a tumour suppressor, regulates beta-catenin. Loss of APC function → constitutive Wnt signalling → adenoma formation. CLASSIC FAP: >100 adenomas (often >1000), onset adolescence. ATTENUATED FAP (AFAP): 10-100 adenomas, later onset (40-50y). AUTOSOMAL RECESSIVE: MUTYH-associated polyposis (MAP). CLINICAL: COLORECTAL: ADENOMAS (tubular, villous, tubulovillous). Asymptomatic until cancer, or rectal bleeding, diarrhoea, abdominal pain. COLORECTAL CANCER: 100% risk by 40-50y (classic). EXTRACOLONIC MANIFESTATIONS: DUODENAL ADENOMAS (90%, periampullary, 5-10% cancer risk). GASTRIC FUNDIC GLAND POLYPS (benign, non-neoplastic). DESMOID TUMOURS (10-20%, aggressive fibromatosis, mesentery, abdominal wall, leading cause of death post-colectomy). OSTEOMAS (mandible, skull). EPIDERMOID CYSTS, FIBROMAS, LIPOMAS. CHRPE (congenital hypertrophy of retinal pigment epithelium, 80%, asymptomatic, useful marker). THYROID CANCER (papillary, 1-2%). HEPATOBLASTOMA (children <5y, 1-2%). PANCREATIC, BILIARY, CNS (medulloblastoma, Turcot syndrome) cancers. DIAGNOSIS: CLINICAL (colonoscopy, adenomas). GENETIC TESTING: APC mutation testing. If positive, test at-risk relatives. MAP: MUTYH testing. MANAGEMENT: COLECTOMY: PROPHYLACTIC, INDICATED in ALL classic FAP patients (typically age 15-25y). OPTIONS: TOTAL PROCTOCOLECTOMY WITH IPAA (ileal pouch-anal anastomosis): preserves continence, eliminates colorectal cancer risk. TOTAL COLECTOMY WITH ILEORECTAL ANASTOMOSIS (IRA): spares rectum, requires lifelong endoscopic surveillance of rectal stump (6-12 months). RISK RECTAL CANCER 10-30% at 20y. SURVEILLANCE: UPPER ENDOSCOPY (duodenal adenomas, Spigelman stage, surveillance intervals q6m-4y). DESMOID TUMOURS: NSAIDs (sulindac), anti-oestrogens (tamoxifen), chemotherapy, surgery (high recurrence). THYROID: annual ultrasound. HEPATOBLASTOMA: alpha-fetoprotein, liver ultrasound (age 0-5y). CHEMOPREVENTION: NSAIDs (sulindac, celecoxib) reduce adenoma burden, but NOT substitute for colectomy. Prognosis: EXCELLENT with prophylactic colectomy. DESMOID and DUODENAL CANCER are leading causes of death post-colectomy. Zambian context: FAP IS RARE. SUSPECT: young patient (<40y) with multiple colorectal adenomas, family history. COLONOSCOPY: available. GENETIC TESTING: NOT AVAILABLE. Diagnosis is CLINICAL (polyposis). COLECTOMY: TOTAL COLECTOMY WITH IRA, TOTAL PROCTOCOLECTOMY WITH IPAA available at specialized centres (Lusaka). UPPER ENDOSCOPY: available. DESMOID SURGERY: available. CHEMOPREVENTION: sulindac, celecoxib (available). FOCUS: CLINICAL DIAGNOSIS, PROMPT REFERRAL FOR COLECTOMY, FAMILY HISTORY (cascade screening), UPPER ENDOSCOPY SURVEILLANCE. This is a LIFE-SAVING intervention.
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Topic 259Coming soon
Lynch Syndrome
Lynch syndrome (LS), formerly hereditary nonpolyposis colorectal cancer (HNPCC), is the MOST COMMON HEREDITARY COLORECTAL CANCER SYNDROME (2-4% of all CRC), caused by germline mutations in DNA MISMATCH REPAIR (MMR) genes (MLH1, MSH2, MSH6, PMS2, EPCAM). For Zambian students, LS is RARE but IMPORTANT—identification enables CANCER PREVENTION in affected individuals and at-risk relatives. PATHOPHYSIOLOGY: Autosomal dominant, INCOMPLETE PENETRANCE. MMR deficiency → microsatellite instability (MSI-H), accelerated accumulation of mutations, carcinogenesis. ACCELERATED ADENOMA-CARCINOMA SEQUENCE (2-3 years vs 10 years sporadic). CLINICAL: EARLY-ONSET CRC (mean age 45y). PROXIMAL (RIGHT-SIDED) colon predominance (70%). SYNCHRONOUS/METACHRONOUS CRC (25-30% risk second CRC within 10y). EXTRACOLONIC CANCERS: ENDOMETRIAL (40-60% lifetime risk, female LS), OVARIAN, GASTRIC, SMALL BOWEL, HEPATOBILIARY, PANCREATIC, UROTHELIAL (ureter, renal pelvis), BRAIN (glioblastoma), SEBACEOUS NEOPLASMS (Muir-Torre variant). DIAGNOSIS: REVISED BETHESDA GUIDELINES: CRC diagnosed age <50y, synchronous/metachronous CRC or LS-associated tumour, CRC with MSI-H histology (Crohn's-like reaction, mucinous, signet ring, medullary), CRC in ≥1 first-degree relative with LS-associated tumour (one <50y), CRC in ≥2 first/second-degree relatives with LS-associated tumours (any age). AMSTERDAM II CRITERIA (research): ≥3 relatives with LS-associated cancers, ≥2 successive generations, ≥1 diagnosed <50y, exclude FAP. TUMOUR TESTING: IMMUNOHISTOCHEMISTRY (IHC) for MMR proteins (MLH1, MSH2, MSH6, PMS2). Loss of expression indicates which gene to test. MICROSATELLITE INSTABILITY (MSI) testing: PCR-based, MSI-High suggestive. GERMLINE GENETIC TESTING: definitive. MANAGEMENT: COLONOSCOPY SURVEILLANCE: q1-2y, starting age 20-25y (or 2-5y before earliest family CRC). PROPHYLACTIC COLECTOMY: NOT routine, consider for individuals with multiple adenomas, difficult surveillance, or patient preference (subtotal colectomy with IRA). GYNECOLOGIC: annual endometrial biopsy, transvaginal ultrasound (age 30-35y). PROPHYLACTIC HYSTERECTOMY + BILATERAL SALPINGO-OOPHORECTOMY: after childbearing completed, highly effective. GASTRIC: consider upper endoscopy with biopsies (H. pylori test and treat), especially in Asian populations. UROTHELIAL: urinalysis, consider ultrasound. ASPIRIN: chemoprevention (CAPP2 study, reduces CRC risk). Prognosis: MSI-H CRC has BETTER STAGE-FOR-STAGE PROGNOSIS than MSS CRC. LS patients have HIGH RISK of metachronous CRC and extracolonic cancers. Surveillance reduces mortality. Zambian context: LS IS RARE. SUSPECT in: early-onset CRC (<50y), family history of CRC/endometrial cancer, right-sided CRC, MSI-H histology. IHC for MMR proteins: NOT AVAILABLE. MSI testing: NOT AVAILABLE. GENETIC TESTING: NOT AVAILABLE. Diagnosis is CLINICAL (family history, Amsterdam/Bethesda criteria). SURVEILLANCE: COLONOSCOPY q1-2y (available). ENDOMETRIAL BIOPSY, TVUS: available. PROPHYLACTIC GYNECOLOGIC SURGERY: available. ASPIRIN: accessible. FOCUS: HIGH INDEX OF SUSPICION (early-onset, family history), AGGRESSIVE COLONOSCOPY SURVEILLANCE, GYNECOLOGIC SURVEILLANCE/PROPHYLAXIS, FAMILY HISTORY (cascade counselling). This is a PREVENTABLE CANCER SYNDROME.
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Topic 260Coming soon
Ischemic Colitis
Ischemic colitis (IC) is the MOST COMMON FORM of gastrointestinal ischemia, resulting from reduced blood flow to the colon, usually NON-OCCLUSIVE. For Zambian students, IC is an UNDERDIAGNOSED cause of LOWER GI BLEEDING, particularly in ELDERLY, HYPERTENSIVE, and DIALYSIS patients. PATHOPHYSIOLOGY: WATERSHED AREAS: SPLENIC FLEXURE (Griffith's point) and SIGMOID-RECTAL JUNCTION (Sudeck's point) are most vulnerable. Causes: HYPOPERFUSION (shock, sepsis, dehydration, cardiac failure, vasopressors), SMALL VESSEL DISEASE (diabetes, hypertension), VASCULITIS, DRUGS (cocaine, ergot, oral contraceptives, NSAIDs), COLONIC OBSTRUCTION. Usually NON-OCCLUSIVE. CLINICAL: TRIAD: SUDDEN, CRAMPY LEFT LOWER QUADRANT PAIN (mild to moderate), URGENCY, and BRIGHT RED OR MAROON BLOOD PER RECTUM (within 24h of pain). Haemodynamic instability is UNCOMMON (unless massive bleed, perforation). MILD, SELF-LIMITED (80%). SEVERE: peritonitis, gangrene, perforation. PHYSICAL EXAM: LLQ tenderness, distension. DIAGNOSIS: CLINICAL SUSPICION. CT ABDOMEN: segmental colonic wall thickening, fat stranding, thumbprinting, pneumatosis, portal venous gas (late). COLONOSCOPY: GOLD STANDARD (within 48h). Findings: segmental erythema, oedema, petechiae, ulceration, BLUISH NODULES (submucosal haemorrhage). HISTOLOGY: mucosal necrosis, haemosiderin-laden macrophages. AVOID HIGH INSUFFLATION (perforation risk). LABS: leukocytosis, metabolic acidosis, elevated lactate (late, severe). MANAGEMENT: MILD-MODERATE (no peritonitis, haemodynamically stable): CONSERVATIVE. IV FLUIDS, NPO, BOWEL REST, BROAD-SPECTRUM ANTIBIOTICS (controversial, but recommended in moderate-severe). SERIAL ABDOMINAL EXAMS. Most recover in 1-2 weeks. COLONOSCOPY in 4-6 weeks to document healing. SEVERE (peritonitis, pneumatosis, portal venous gas, gangrene): EMERGENCY SURGERY (segmental colectomy, Hartmann procedure). ANTICOAGULATION: NOT indicated (non-occlusive). Treat underlying cause (optimize cardiac output, discontinue vasopressors, vasodilators). Prognosis: EXCELLENT (mild). Recurrence <5%. Mortality: 5-10% (overall), >50% if gangrene/perforation. Zambian context: IC IS UNDERDIAGNOSED. SUSPECT in: elderly, hypertensive, cardiac failure, dialysis patient with sudden LLQ pain + hematochezia. CT available (tertiary). COLONOSCOPY available (early, gentle). CONSERVATIVE management (IVF, NPO, antibiotics) is mainstay. SURGERY: for peritonitis, gangrene (high mortality). FOCUS: CLINICAL DIAGNOSIS, CT/COLONOSCOPY, CONSERVATIVE CARE, SURGERY FOR COMPLICATIONS.
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Topic 261Coming soon
Radiation Proctitis
Radiation proctitis is injury to the rectum caused by ionizing radiation, a common complication of PELVIC RADIOTHERAPY (prostate, cervical, rectal, bladder, anal cancer). For Zambian students, with increasing access to radiotherapy (Lusaka), this is an EMERGING IATROGENIC CONDITION. ACUTE RADIATION PROCTITIS: occurs during or immediately after radiotherapy (<3 months). CHRONIC RADIATION PROCTITIS: develops 6-24 months after radiotherapy, can occur years later. PATHOPHYSIOLOGY: ACUTE: direct mucosal injury, inflammation, oedema. CHRONIC: progressive ENDARTERITIS OBLITERANS → ischemia, fibrosis, mucosal atrophy, neovascularization (telangiectasias). CLINICAL: ACUTE: URGENCY, FREQUENCY, TENESMUS, MUCOUS DISCHARGE, MILD RECTAL BLEEDING. SELF-LIMITED, resolves weeks after treatment. CHRONIC: PAINLESS RECTAL BLEEDING (hematochezia), chronic, intermittent, may be SEVERE, TRANSFUSION-DEPENDENT. URGENCY, DIARRHOEA, TENESMUS. COMPLICATIONS: STRICTURE, FISTULA (rare, rectovaginal, rectovesical), INCONTINENCE. DIAGNOSIS: HISTORY of pelvic radiotherapy. COLONOSCOPY: TELANGIECTASIAS (dilated, fragile blood vessels), mucosal pallor, friability, ulceration, stricture. HISTOLOGY: endothelial proliferation, hyalinization, fibrosis. EXCLUDE other causes (cancer recurrence, IBD, infection). MANAGEMENT: ACUTE: SUPPORTIVE. TOPICAL: sucralfate enemas, topical corticosteroids, lidocaine. ORAL: 5-ASA, steroids. Usually self-limited. CHRONIC: CONSERVATIVE: FIBRE SUPPLEMENTS (psyllium), LOPERAMIDE (diarrhoea). TOPICAL THERAPY (first-line for bleeding): SUCRALFATE ENEMAS (1g BID), 5-ASA/SALICYLATE ENEMAS, CORTICOSTEROID ENEMAS. ENDOSCOPIC THERAPY (refractory bleeding): ARGON PLASMA COAGULATION (APC) is GOLD STANDARD. Effective, safe, repeated sessions. FORMALIN (intrarectal instillation 4%). HYPERBARIC OXYGEN (systemic therapy, improves angiogenesis, tissue oxygenation). ORAL THERAPY: VITAMIN E, PENTOXIFYLLINE (limited). SURGERY: LAST RESORT (refractory bleeding, fistula, stricture). DIVERTING COLOSTOMY, PROCTECTOMY. Prognosis: ACUTE: excellent. CHRONIC: 80-90% respond to endoscopic therapy (APC). Recurrence common, repeat APC. Zambian context: RADIOTHERAPY is available (Lusaka, Cancer Hospital). ACUTE PROCTITIS: common, self-limited. CHRONIC PROCTITIS: emerging. TOPICAL THERAPY: sucralfate enemas (prepare from oral tablets), corticosteroid enemas, 5-ASA enemas (availability?). APC: available at tertiary endoscopy centres (Lusaka). FORMALIN: available. HYPERBARIC OXYGEN: NOT AVAILABLE. SURGERY: colostomy, proctectomy available. FOCUS: PREVENTION (modern radiotherapy techniques), RECOGNITION (history of pelvic RT, chronic bleeding), TOPICAL THERAPY (sucralfate), ENDOSCOPIC THERAPY (APC) for refractory bleeding.