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 …
Read more
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.
-
Coming soon
Topic 235Coming soon
Small Intestinal Bacterial Overgrowth
Small intestinal bacterial overgrowth (SIBO) is defined as excessive bacteria in the small bowel (>10^3-10^5 CFU/mL) causing malabsorption and gastrointestinal symptoms. For Zambian students, SIBO is a COMMON, UNDERDIAGNOSED cause of chronic diarrhoea, bloating, and malabsorption, particularly in patients with PREDISPOSING CONDITIONS (gastric surgery, hypochlorhydria, dysmotility, chronic pancreatitis, cirrhosis, immunosuppression). PATHOPHYSIOLOGY: MECHANISMS: DISRUPTED MIGRATING MOTOR COMPLEX (diabetes, scleroderma, opioids), ANATOMIC ABNORMALITIES (small bowel diverticula, blind loop, strictures, fistulae), HYPOCLORHYDRIA (PPI use, atrophic gastritis), IMMUNE DEFICIENCY (IgA deficiency, HIV, common variable immunodeficiency). Bacteria deconjugate bile acids (steatorrhoea), ferment carbohydrates (gas, bloating, diarrhoea), consume vitamin B12 (megaloblastic anaemia), produce folate (elevated serum folate). CLINICAL: BLOATING, ABDOMINAL DISTENSION (postprandial), FLATULENCE, DIARRHOEA (watery, steatorrhoea), ABDOMINAL PAIN, NAUSEA. NUTRITIONAL DEFICIENCIES: B12 deficiency (neuropathy, anaemia), fat-soluble vitamin deficiency (A, D, E, K), weight loss. DIAGNOSIS: GOLD STANDARD: JEJUNAL ASPIRATE CULTURE >10^3 CFU/mL (coliforms) or >10^5 CFU/mL (total). Invasive, not widely available. NON-INVASIVE: GLUCOSE BREATH TEST (GBST) OR LACTULOSE BREATH TEST (LBST). Measure exhaled H2 (and methane) after ingestion of substrate. RISE IN H2 >20 ppm above baseline indicates SIBO. METHANE PREDOMINANCE: associated with constipation (Methanobrevibacter smithii). Sensitivity/specificity: 60-90%. PPI: discontinue 1 week before test. EMPIRIC THERAPY: In high-risk patient with typical symptoms, no access to breath testing, trial of antibiotics. MANAGEMENT: TREAT PREDISPOSING CONDITION (if possible). ANTIBIOTICS: RIFAXIMIN 550mg TID x 14 days: FIRST-LINE, non-absorbable, E. coli coverage, effective. METRONIDAZOLE 250mg TID: anaerobes. CIPROFLOXACIN 500mg BID: Gram-negative. DOXYCYCLINE 100mg BID. AMOXICILLIN-CLAVULANATE. Rotate antibiotics (relapse common). PROKINETICS: if dysmotility (low-dose erythromycin, prucalopride). NUTRITIONAL REPLETION: B12, iron, calcium, vitamin D, fat-soluble vitamins. ELEMENTAL DIET: severe, refractory. Prognosis: SIBO is chronic, relapsing. Long-term antibiotics often required. Rifaximin is effective, but expensive. Zambian context: SIBO IS LIKELY COMMON (cirrhosis, hypochlorhydria, HIV, TB, post-gastric surgery, chronic pancreatitis, diabetes). DIAGNOSIS: breath testing NOT AVAILABLE. Jejunal aspirate NOT AVAILABLE. Diagnosis is CLINICAL: chronic bloating, diarrhoea, B12 deficiency, predisposing condition. EMPIRIC THERAPY: doxycycline, metronidazole, amoxicillin-clavulanate (available, inexpensive). RIFAXIMIN: expensive, not on essential medicines list, limited availability. B12 injections available. Focus: HIGH INDEX OF SUSPICION, EMPIRIC ANTIBIOTICS, B12 REPLETION.
-
Coming soon
Topic 236Coming soon
Protein-Losing Enteropathy
Protein-losing enteropathy (PLE) is a syndrome of excessive serum protein loss into the gastrointestinal tract, leading to HYPOPROTEINAEMIA and OEDEMA, in the absence of other causes (renal, hepatic, nutritional). For Zambian students, PLE is a CLINICAL DIAGNOSIS, with a BROAD DIFFERENTIAL (infectious, inflammatory, neoplastic, lymphatic). PATHOPHYSIOLOGY: Three mechanisms: 1) EROSIVE/MUCOSAL INJURY (ulceration, inflammation) → exudative loss. 2) NON-EROSIVE/MUCOSAL DISEASE (celiac, Ménétrier's) → increased mucosal permeability. 3) LYMPHATIC OBSTRUCTION/increased pressure (congestive heart failure, constrictive pericarditis, primary intestinal lymphangiectasia, lymphoma, TB) → leakage of lymph (protein, lymphocytes, triglycerides). ETIOLOGY: INFECTIOUS: TB (ileal), HIV enteropathy, parasites (Strongyloides, Giardia), Whipple's. INFLAMMATORY: Crohn's disease, ulcerative colitis, celiac disease. NEOPLASTIC: lymphoma, gastric cancer, colon cancer. HYPERTROPHIC GASTROPATHY: Ménétrier's disease (giant gastric folds, hypochlorhydria, CMV, H. pylori). LYMPHATIC: Primary intestinal lymphangiectasia (congenital, Waldmann's disease), secondary (right heart failure, constrictive pericarditis, TB, lymphoma, retroperitoneal fibrosis). OTHER: Sarcoidosis, systemic lupus erythematosus. CLINICAL: HYPOPROTEINAEMIA (low albumin, low total protein), OEDEMA (peripheral, periorbital, ascites, pleural effusion), DIARRHOEA (may be absent in lymphatic disorders), LYMPHOPENIA (loss of lymphocytes into gut, primary/secondary lymphangiectasia), hypogammaglobulinaemia (increased infection risk), fat-soluble vitamin deficiency, steatorrhoea (lymphangiectasia). DIAGNOSIS: CONFIRM PROTEIN LOSS: SPOT FECAL ALPHA-1-ANTITRYPSIN CLEARANCE (or 24h stool collection). Alpha-1-antitrypsin is resistant to intestinal degradation, reflects protein loss. Not widely available. 24h URINE PROTEIN: exclude nephrotic syndrome. LFTs, PT/INR: exclude synthetic dysfunction (cirrhosis). DIAGNOSIS OF UNDERLYING ETIOLOGY: ENDOSCOPY + BIOPSY (celiac, Ménétrier's, Crohn's, eosinophilic gastroenteritis, amyloid, GIST, cancer). COLONOSCOPY (IBD, cancer). SMALL BOWEL IMAGING: CT enterography, MR enterography (Crohn's, lymphoma). ECHOCARDIOGRAPHY (constitutive pericarditis, heart failure). LYMPHOSCINTIGRAPHY (primary lymphangiectasia). INFECTIOUS WORKUP: TB (chest X-ray, sputum, abdominal CT, ascitic fluid), HIV, stool parasites (Strongyloides, Giardia). MANAGEMENT: TREAT UNDERLYING CAUSE. DIETARY: LOW-FAT DIET + MEDIUM-CHAIN TRIGLYCERIDES (MCTs) for LYMPHANGIECTASIA. MCTs are absorbed directly into portal vein, bypassing lymphatics. DIURETICS: symptomatic oedema. ALBUMIN INFUSION: temporary, not chronic. IMMUNOSUPPRESSION: corticosteroids, azathioprine, infliximab (Crohn's, lupus). PROGNOSIS: Depends on etiology. Primary intestinal lymphangiectasia: good with MCT diet. Ménétrier's: spontaneous remission possible (children), adults: cetuximab (EGF receptor inhibitor). Zambian context: PLE IS COMMON, but underdiagnosed. ETIOLOGIES: TB (ileal, peritoneal), HIV enteropathy, intestinal lymphoma (EBV-associated, endemic Burkitt), Strongyloides, Giardia, right heart failure (cor pulmonale, RHD), constrictive pericarditis (TB). Ménétrier's: CMV, H. pylori. Primary lymphangiectasia: rare. DIAGNOSIS: Clinical (hypoalbuminaemia, oedema, no proteinuria, normal LFTs, no malnutrition). CONFIRM: fecal alpha-1-antitrypsin (NOT AVAILABLE). Endoscopy, biopsy, TB workup, echocardiography are available. MCT oil: limited availability. Albumin: expensive. Focus: SEARCH FOR UNDERLYING CAUSE (TB, HIV, lymphoma, parasites, heart failure). TREAT THE CAUSE.
-
Coming soon
Topic 237Coming soon
Intestinal Lymphangiectasia
Intestinal lymphangiectasia (IL) is a disorder characterized by dilation and dysfunction of intestinal lymphatic vessels, leading to leakage of lymph into the gut lumen → PROTEIN-LOSING ENTEROPATHY, LYMPHOPENIA, and STEATORRHOEA. For Zambian students, PRIMARY IL (Waldmann's disease) is RARE, but SECONDARY IL is MORE COMMON (TB, lymphoma, retroperitoneal fibrosis, heart failure, constrictive pericarditis). PATHOPHYSIOLOGY: PRIMARY IL: congenital malformation of enteric lymphatics. PRESENTATION: infancy/early childhood. SECONDARY IL: obstruction of lymphatic drainage (mesenteric, retroperitoneal) by infection (TB, filariasis), malignancy (lymphoma, retroperitoneal sarcoma), inflammation (retroperitoneal fibrosis, pancreatitis), or increased central venous pressure (constitutive pericarditis, right heart failure). Dilated lacteals rupture, lymph leaks into bowel lumen. Loss of protein, lymphocytes (T-cells), immunoglobulins, and chylomicrons. CLINICAL: HYPOPROTEINAEMIA (severe, hypoalbuminaemia), OEDEMA (peripheral, periorbital, ascites, pleural effusion), LYMPHOPENIA (CD4+ T-cell depletion), HYPOGAMMAGLOBULINAEMIA, STEATORRHOEA (fat malabsorption, diarrhoea). CHYLOUS ASCITES, chylothorax, chylous effusions. DIAGNOSIS: ENDOSCOPY: SNOWFLAKE APPEARANCE, scattered white spots (dilated lacteals), oedematous mucosa, chyle leak. HISTOLOGY: MARKEDLY DILATED LACTEALS in villi and submucosa, blunted villi, normal inflammatory infiltrate. CAPSULE ENDOSCOPY: diffuse, white villi. SMALL BOWEL FOLLOW-THROUGH: thickened folds, nodularity. LYMPHOSCINTIGRAPHY, MR LYMPHANGIOGRAPHY: assess lymphatic anatomy, leak. SECONDARY IL: ECHO (constitutive pericarditis, RHF), CT ABDOMEN (retroperitoneal mass, lymphoma, TB), lymph node biopsy. MANAGEMENT: PRIMARY IL: DIETARY: LOW-FAT DIET + MEDIUM-CHAIN TRIGLYCERIDES (MCTs). MCTs are absorbed directly into portal vein, bypass lymphatics. REDUCES chyle production, decreases protein loss. FAT-SOLUBLE VITAMIN SUPPLEMENTATION (A, D, E, K). ALBUMIN INFUSION: severe oedema, short-term. OCTREOTIDE: reduces lymphatic flow (case reports). SURGERY: segmental resection (localized disease). SECONDARY IL: TREAT UNDERLYING CAUSE. Tuberculosis: anti-TB therapy. Lymphoma: chemotherapy. Constitutive pericarditis: pericardiectomy. Heart failure: diuresis, afterload reduction. Prognosis: PRIMARY IL: good with dietary management. Chronic, relapsing course. SECONDARY IL: depends on etiology. Zambian context: PRIMARY IL: RARE. SECONDARY IL: MORE COMMON. TB (abdominal, retroperitoneal) is #1 cause. Lymphoma (Burkitt, DLBCL, HIV-associated) is another. Constitutive pericarditis (TB) is common. DIAGNOSIS: Endoscopy available tertiary. Histology (dilated lacteals) diagnostic. ECHO (constitutive pericarditis), CT abdomen (TB, lymphoma) available. DIETARY: low-fat diet feasible. MCT oil: limited availability, expensive. Albumin: expensive, limited. ANTI-TB THERAPY available. Chemotherapy (lymphoma) available (Lusaka). FOCUS: SUSPECT IL in patient with severe hypoalbuminaemia, oedema, lymphopenia. ENDOSCOPY + BIOPSY. TREAT SECONDARY CAUSE.
-
Coming soon
Topic 238Coming soon
Eosinophilic Gastroenteritis
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 (parasites, drugs, hypereosinophilic syndrome, EGPA). 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).
-
Coming soon
Topic 239Coming soon
Ménétrier's Disease
Ménétrier's disease (MD) is a rare, acquired, hypertrophic gastropathy characterized by GIANT RUGAL FOLDS (cerebriform) in the gastric body/fundus, with FOVEOLAR HYPERPLASIA (mucous cell hyperplasia), glandular atrophy, and HYPOPROTEINAEMIA (protein-losing gastropathy). For Zambian students, MD is a RARE but CLASSIC cause of PLE. CMV (children) and H. pylori (adults) are associated. PATHOPHYSIOLOGY: Overexpression of TRANSFORMING GROWTH FACTOR-ALPHA (TGF-α) in gastric mucosa → activation of epidermal growth factor receptor (EGFR) → excessive mucous cell proliferation, gland destruction, decreased acid secretion. Protein loss occurs through leaky tight junctions. CLINICAL: ADULTS: EPIGASTRIC PAIN, NAUSEA, VOMITING, WEIGHT LOSS, OEDEMA (hypoalbuminaemia), DIARRHOEA. HYPOCLORHYDRIA (achlorhydria). CHILDREN: often associated with CMV infection, acute presentation (nausea, vomiting, abdominal pain, oedema), SELF-LIMITED. PHYSICAL EXAM: epigastric tenderness, peripheral oedema. DIAGNOSIS: ENDOSCOPY: GIANT, TORTUOUS, CEREBRIFORM GASTRIC FOLDS (body, fundus, sparing antrum), thickened mucosa, erosions, superficial ulceration. HISTOLOGY: FOVEOLAR HYPERPLASIA (elongated, tortuous gastric pits), GLANDULAR ATROPHY (loss of parietal, chief cells), edema, smooth muscle hyperplasia, MILD inflammation. NO malignancy. EUS: thickened mucosal layer (2nd layer). LABS: HYPOPROTEINAEMIA (low albumin, low total protein), NORMAL LFTs, NO proteinuria. LOW GASTRIN, LOW PEPSINOGEN I. H. pylori testing. CMV testing (children, immunocompromised adults). COMPLICATIONS: VENOUS THROMBOEMBOLISM (protein-losing state). GASTRIC ADENOCARCINOMA: INCREASED RISK (2-15%). Surveillance endoscopy. MANAGEMENT: SUPPORTIVE: HIGH-PROTEIN DIET, NUTRITIONAL SUPPORT. DIURETICS for oedema. ACID SUPPRESSION: PPI (for erosions). ANTICOAGULATION: VTE prophylaxis. H. PYLORI ERADICATION: if positive, may induce remission. CMV: antiviral therapy (ganciclovir) in children/immunocompromised. CORTICOSTEROIDS: limited efficacy. OCTREOTIDE: case reports. CETUXIMAB: monoclonal antibody against EGFR. Case series demonstrate dramatic improvement in protein loss, histology. Expensive. GASTRECTOMY: REFRACTORY, SEVERE DISEASE (intractable protein loss, bleeding, high cancer risk). CURATIVE. Prognosis: ADULTS: chronic, progressive. High morbidity (protein loss, thrombosis). Cancer risk: surveillance endoscopy. CHILDREN: self-limited, good prognosis. Zambian context: MD IS EXTREMELY RARE. Consider in patient with: giant gastric folds + hypoalbuminaemia + oedema + no other cause of PLE. ENDOSCOPY + BIOPSY available (tertiary). H. pylori testing available. CMV: serology, PCR limited. Cetuximab: NOT AVAILABLE. Gastrectomy available (tertiary surgical centres). Surveillance endoscopy available. Focus: DIAGNOSIS (endoscopy, biopsy, exclude malignancy), H. pylori eradication (if positive), nutritional support, GASTRECTOMY (if severe).
-
Coming soon
Topic 240Coming soon
Acute Diarrhea in Adults
Acute diarrhea (≥3 loose stools/day, <14 days) is one of the MOST COMMON PRESENTATIONS worldwide. For Zambian students, it is a DAILY CLINICAL PROBLEM, with infectious etiologies dominating. MASTERY OF SYNDROMIC DIAGNOSIS, REHYDRATION, SELECTIVE TESTING, AND APPROPRIATE ANTIBIOTIC USE IS ESSENTIAL. ETIOLOGY: VIRAL (50-70%): Norovirus (winter, outbreaks), Rotavirus (children, vaccine), Adenovirus, Astrovirus. BACTERIAL (15-20%): E. coli (ETEC, EAEC—traveler's), Campylobacter, Salmonella, Shigella, Vibrio cholerae (epidemic), C. difficile (antibiotics, healthcare). PARASITIC (<5%): Giardia, Cryptosporidium, Cyclospora, Entamoeba histolytica (bloody), Strongyloides. CLINICAL SYNDROMES: ACUTE WATERY DIARRHEA: viral, ETEC, V. cholerae, Giardia, Cryptosporidium. DYSENTERY (BLOODY DIARRHEA): Shigella, Campylobacter, Salmonella, EHEC, E. histolytica. TYPHOID FEVER: Salmonella typhi, paratyphi. STEP-UP APPROACH: SEVERITY ASSESSMENT: DEHYDRATION (thirst, dry mucous membranes, decreased skin turgor, tachycardia, hypotension, oliguria, lethargy/comma). SHOCK. Volume status determines site of care. DIAGNOSIS: MOST CASES ARE SELF-LIMITED, NO TESTING REQUIRED. INDICATIONS FOR STOOL TESTING: SEVERE DEHYDRATION, BLOODY DIARRHEA, FEVER ≥38.5°C, DURATION >7 days, IMMUNOCOMPROMISED (HIV, chemotherapy), HEALTHCARE-ASSOCIATED, OUTBREAK, TRAVEL HISTORY. TESTS: STOOL MICROSCOPY (ova, parasites), CULTURE (Salmonella, Shigella, Campylobacter, E. coli), E. COLI O157:H7 CULTURE (bloody), C. DIFFICILE TOXIN/PCR (antibiotics, healthcare), CHOLERA STOOL CULTURE (epidemic), FAECAL LEUKOCYTES/LACTOFERRIN (inflammation, bacterial). BLOOD CULTURES: if febrile, suspected enteric fever. MANAGEMENT: REHYDRATION IS CORNERSTONE. ORAL REHYDRATION SOLUTION (ORS): low-osmolarity (75 mEq Na, 75 mmol glucose). ZINC: 20mg/day x 10-14 days (children, reduces duration, severity). IV FLUIDS: severe dehydration (Ringer's lactate, normal saline). ANTIMOTILITY AGENTS: LOPERAMIDE (2mg after each loose stool, max 16mg/day). NOT in DYSENTERY, suspected EHEC (risk HUS), C. difficile. BISMUTH SUBSALICYLATE: symptomatic relief. ANTIBIOTICS: NOT ROUTINE. INDICATIONS: SEVERE, BACTERIAL SUSPECTED (dysentery, >8 stools/day, febrile, immunocompromised), SHIGELLOSIS (ciprofloxacin, azithromycin, ceftriaxone), CAMPYLOBACTER (azithromycin), CHOLERA (doxycycline, azithromycin), C. DIFFICILE (oral vancomycin, fidaxomicin, metronidazole), TRAVELER'S DIARRHEA (azithromycin, rifaximin, fluoroquinolone). ENTERIC FEVER: ceftriaxone, azithromycin. AVOID FLUOROQUINOLONES (resistance). PROBIOTICS: Saccharomyces boulardii, Lactobacillus (modest benefit). PREVENTION: HANDWASHING, SAFE FOOD/WATER, VACCINES (cholera, rotavirus). Prognosis: EXCELLENT. Mortality <1% (dehydration, sepsis, HUS). Zambian context: ACUTE DIARRHEA IS UBIQUITOUS. ETIOLOGIES: Viral (Norovirus, Rotavirus), bacterial (ETEC, Campylobacter, Shigella, Salmonella, Cholera—epidemic), parasitic (Cryptosporidium—HIV, Giardia, E. histolytica). HIV ENTEROPATHY: chronic. CHOLERA: seasonal, epidemic. ORS is widely available, LIFE-SAVING. ZINC: available. STOOL CULTURE: limited. STOOL MICROSCOPY: available. C. DIFFICILE testing: limited. ANTIBIOTICS: ciprofloxacin, azithromycin, ceftriaxone, doxycycline, metronidazole available. LOPERAMIDE: available. FOCUS: REHYDRATION (ORS, IVF), ZINC, SELECTIVE ANTIBIOTICS (dysentery, cholera, severe), PUBLIC HEALTH (cholera surveillance, WASH).
-
Coming soon
Topic 241Coming soon
Chronic Diarrhea: Diagnostic Approach
Chronic diarrhea (≥4 weeks) is a common, challenging presentation with a BROAD DIFFERENTIAL. For Zambian students, a SYSTEMATIC, STEPWISE APPROACH is essential to avoid unnecessary testing and delayed diagnosis. ETIOLOGIES (CATEGORIES): WATERY (OSMOTIC vs SECRETORY), INFLAMMATORY, FATTY (MALABSORPTION/STEATORRHOEA). STEP 1: HISTORY, PHYSICAL, STOOL CHARACTERISTICS. OSMOTIC DIARRHEA: stops with fasting, high osmotic gap (>100 mOsm/kg). Causes: lactose intolerance, sorbitol, magnesium, laxatives. SECRETORY DIARRHEA: persists with fasting, normal osmotic gap (<50). Causes: microscopic colitis, bile acid malabsorption, neuroendocrine tumours (VIPoma, gastrinoma, carcinoid), IBS-D. INFLAMMATORY DIARRHEA: blood, pus, fever, abdominal pain. Causes: IBD (Crohn's, UC), infectious (TB, Yersinia, amebic), ischemia, radiation. FATTY DIARRHEA (STEATORRHOEA): greasy, foul, floating, difficult to flush. Causes: malabsorption (celiac, tropical sprue, Whipple's), maldigestion (chronic pancreatitis, pancreatic insufficiency). STEP 2: BASIC LABS: CBC, CRP/ESR, electrolytes, BUN/creatinine, albumin, calcium, vitamin B12, folate, iron studies, TSH, IgA tTG (celiac). STOOL: OVA AND PARASITES x 3, fecal calprotectin/lactoferrin (inflammation), fecal elastase-1 (pancreatic insufficiency), Sudan stain (fat), stool electrolytes (osmolality, osmotic gap), C. difficile toxin (if antibiotic exposure). STEP 3: ENDOSCOPY: COLONOSCOPY with ILEAL INTUBATION + BIOPSIES (random, segmental) for suspected IBD, microscopic colitis, TB, cancer. EGD + DUODENAL BIOPSIES (celiac, Whipple's, tropical sprue, eosinophilic gastroenteritis, Crohn's, amyloid, abetalipoproteinemia). STEP 4: IMAGING: CT ENTEROGRAPHY/MR ENTEROGRAPHY (Crohn's, lymphoma, TB, small bowel tumours). SMALL BOWEL FOLLOW-THROUGH (SBT). ABDOMINAL CT (chronic pancreatitis, neuroendocrine tumours). STEP 5: SPECIALIZED TESTS: 24h fecal fat quantification, fecal bile acids, serum chromogranin A, gastrin, VIP, 5-HIAA, secretin test, hydrogen breath tests (lactose, fructose, SIBO). COMMON ETIOLOGIES IN ZAMBIA: INFECTIOUS: TB (ileocecal), HIV enteropathy, parasites (Strongyloides, Giardia, Cryptosporidium, Cyclospora, Isospora, Schistosoma mansoni), tropical sprue (rare). INFLAMMATORY: Crohn's disease (uncommon), ulcerative colitis (rare). MALABSORPTION: celiac disease (rare, emerging), chronic pancreatitis (alcohol, tropical calcific), pancreatic insufficiency, post-infectious (post-dysentery IBS-D). ENDOCRINE: hyperthyroidism, diabetes. DRUGS: ARVs, antibiotics, PPIs, metformin, NSAIDs. MANAGEMENT: TREAT UNDERLYING CAUSE. Symptomatic: LOPERAMIDE, DIPHENOXYLATE, BILE ACID SEQUESTRANTS (cholestyramine), OCTREOTIDE (neuroendocrine tumours). Prognosis: Depends on etiology. Zambian context: CHRONIC DIARRHEA IS COMMON. ETIOLOGIES: HIV enteropathy (#1), TB (#2), parasites (Strongyloides, Giardia, Cryptosporidium, Schistosoma), chronic pancreatitis (alcohol), post-infectious IBS-D, celiac (rare, but suspect in refractory cases). DIAGNOSTIC APPROACH: Stepwise, using available resources: STOOL MICROSCOPY (ova, parasites, AFB—Cryptosporidium, Cyclospora, Isospora), HIV TESTING, CHEST X-RAY (TB), ABDOMINAL CT (TB, pancreatitis, lymphoma), ENDOSCOPY + BIOPSY (TB, IBD, celiac, lymphoma). FOCUS: EXCLUDE INFECTIOUS CAUSES FIRST (HIV, TB, parasites), THEN INVESTIGATE OTHER CAUSES.
-
Coming soon
Topic 242Coming soon
Irritable Bowel Syndrome
Irritable bowel syndrome (IBS) is a common, chronic disorder of GUT-BRAIN INTERACTION, characterized by recurrent abdominal pain associated with defecation or a change in bowel habits. For Zambian students, IBS is a DIAGNOSIS OF EXCLUSION, but it is REAL, COMMON, and causes significant morbidity. It is NOT 'all in the head'. PATHOPHYSIOLOGY: MULTIFACTORIAL. VISCERAL HYPERSENSITIVITY (increased perception of physiological stimuli). ALTERED GUT MOTILITY. GUT-BRAIN AXIS DYSREGULATION. LOW-GRADE MUCOSAL INFLAMMATION, IMMUNE ACTIVATION. ALTERED GUT MICROBIOTA (dysbiosis). INTESTINAL PERMEABILITY. PSYCHOSOCIAL FACTORS (anxiety, depression, stress, abuse history). POST-INFECTIOUS IBS (10-30%): develops after acute gastroenteritis (bacterial, viral, parasitic). CLINICAL: ROME IV CRITERIA: Recurrent abdominal pain, ON AVERAGE ≥1 DAY/WEEK in last 3 months, associated with ≥2 of: related to defecation, change in stool frequency, change in stool form (appearance). Symptom onset ≥6 months ago. SUBTYPES: IBS-C (constipation predominant, >25% hard/lumpy stools, <25% loose/watery). IBS-D (diarrhea predominant, >25% loose/watery, <25% hard/lumpy). IBS-M (mixed). IBS-U (unclassified). RED FLAGS (ALARM FEATURES): Age >50 with new symptoms, rectal bleeding (not from fissure/hemorrhoids), nocturnal diarrhea, weight loss, fever, family history of IBD/colon cancer, abdominal mass, abnormal exam. These REQUIRE INVESTIGATION. DIAGNOSIS: CLINICAL (Rome IV criteria). LIMITED INVESTIGATIONS to exclude organic disease: CBC, CRP, fecal calprotectin (exclude IBD), CELIAC SEROLOGY (tTG-IgA). COLONOSCOPY: INDICATED if alarm features, age ≥45 (or ≥50) for colorectal cancer screening, or suspected IBD. In low-risk, young patients with typical IBS symptoms and negative screening tests, colonoscopy is NOT required. MANAGEMENT: THERAPEUTIC RELATIONSHIP is paramount. Validate symptoms, explain pathophysiology (gut-brain axis, visceral hypersensitivity). DIET: FODMAP DIET (low fermentable oligosaccharides, disaccharides, monosaccharides, polyols). Trial 4-6 weeks, then reintroduction. AVOID triggers (caffeine, alcohol, fatty foods, gas-producing foods). FIBER: Soluble fiber (psyllium, ispaghula) for IBS-C (may worsen bloating). Insoluble fiber (bran) NOT recommended. LIFESTYLE: Exercise, stress reduction, sleep hygiene. PHARMACOTHERAPY: IBS-C: LUBIPROSTONE, LINACLOTIDE (guanylate cyclase-C agonist), PLEGOTIDE. Not available in Zambia. POLYETHYLENE GLYCOL (PEG, macrogol) for constipation. IBS-D: LOPERAMIDE (symptomatic). ELUXADOLINE (mixed opioid, not available). RIFAXIMIN (550mg TID x14d, re-treat) for IBS-D. IBS PAIN: ANTISPASMODICS (hyoscine, mebeverine, peppermint oil). LOW-DOSE TRICYCLIC ANTIDEPRESSANTS (TCA: amitriptyline 10-25mg nocte)—FIRST-LINE for pain, global symptoms. SSRIs (fluoxetine, citalopram) for IBS-C (with anxiety). PSYCHOLOGICAL THERAPIES: CBT, gut-directed hypnotherapy. Probiotics: limited evidence (Bifidobacterium, Lactobacillus). Prognosis: CHRONIC, RELAPSING. Quality of life impaired. NOT life-threatening. Zambian context: IBS IS COMMON. DIAGNOSIS OF EXCLUSION. HIGH PREVALENCE OF INFECTIOUS CAUSES (parasites, TB, HIV) MIMICKING IBS. DO NOT DIAGNOSE IBS WITHOUT EXCLUDING THESE FIRST. Rome criteria, alarm features. Fecal calprotectin: NOT AVAILABLE. Celiac serology: available (limited). Colonoscopy: available (tertiary). DIETARY ADVICE: low-FODMAP challenging, impractical. Simple advice: reduce gas-producing foods (beans, onions, cabbage), caffeine, alcohol. PSYLLIUM (ispaghula) available. LOPERAMIDE available. ANTISPASMODICS (hyoscine, mebeverine) available. AMITRIPTYLINE: available, inexpensive, effective. SSRIs: available. RIFAXIMIN: expensive, not available. Probiotics: available (expensive). FOCUS: EXCLUSION OF ORGANIC DISEASE (HIV, TB, parasites, celiac, IBD), REASSURANCE, DIETARY ADVICE, SYMPTOMATIC TREATMENT (loperamide, antispasmodics, amitriptyline).
-
Coming soon
Topic 243Coming soon
Diverticulitis: Acute Management
Acute diverticulitis is inflammation of colonic diverticula, a common surgical presentation. For Zambian students, incidence is RISING with urbanization and low-fibre diet. UNCOMPLICATED (phlegmon, 75%): LLQ pain, fever, leukocytosis, NO abscess/perforation. CT is gold standard (wall thickening, fat stranding). MANAGEMENT: OUTPATIENT (stable, tolerating oral): oral antibiotics (7-10d, cover Gram-neg/anaerobes: amoxicillin-clavulanate, ciprofloxacin+metronidazole), liquid diet, analgesia. INPATIENT (severe, comorbid, failed outpatient): IV antibiotics (ceftriaxone+metronidazole, piperacillin-tazobactam), bowel rest. COMPLICATED (25%): abscess, fistula, obstruction, free perforation. CT essential. ABSCESS: <4cm: antibiotics alone. >4cm or refractory: PERCUTANEOUS DRAINAGE (CT/US-guided) + IV antibiotics. SURGERY if drainage fails. FREE PERFORATION (peritonitis): EMERGENCY SURGERY (Hartmann procedure: sigmoidectomy + end colostomy). Resection + primary anastomosis + diverting ileostomy (selected stable patients). ELECTIVE COLECTOMY: INDICATIONS: recurrent attacks (≥2), complicated diverticulitis treated non-operatively, immunocompromised, persistent symptoms. Laparoscopic sigmoidectomy preferred. ELECTIVE COLONOSCOPY: mandatory 6-8 weeks post-resolution to exclude cancer. Prognosis: uncomplicated: 70-80% no recurrence. Complicated: higher recurrence. Zambian context: CT limited, ultrasound alternative. Surgery available. Antibiotics available. Focus: STAGE with CT/US, CONSERVATIVE care first, PERCUTANEOUS drainage for abscess, SURGERY for perforation/recurrent.