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 199Coming soon
Cholangiocarcinoma: Biliary Tract Cancer
Cholangiocarcinoma (CCA) is a malignant tumour arising from biliary epithelium, classified by anatomical location: INTRAHEPATIC (iCCA, peripheral, mass-forming), PERIHILAR (pCCA, Klatskin tumour, 50-60%, biliary confluence), DISTAL (dCCA, 20-30%, between cystic duct and ampulla). For Zambian students, risk factors include PRIMARY SCLEROSING CHOLANGITIS (PSC), LIVER FLUKES (Opisthorchis, Clonorchis—rare in Zambia), HEPATOLITHIASIS, CHOLEDOCHAL CYSTS, and Thorotrast (historical). Clinical: iCCA: abdominal pain, weight loss, hepatomegaly, incidental mass. pCCA/dCCA: OBSTRUCTIVE JAUNDICE (painless, progressive), pruritus, pale stools, dark urine, weight loss. Cholangitis (if obstruction + infection). Diagnosis: iCCA: CECT/MRI: arterial phase rim enhancement, delayed central enhancement, capsular retraction. pCCA: MRCP: biliary stricture at hilum, pre-stenotic dilation. CA19-9 (elevated, not diagnostic). Tissue diagnosis: EUS-FNA (dCCA, lymph nodes), ERCP with brushings (pCCA, dCCA), percutaneous biopsy (iCCA, unresectable). Staging: CECT chest/abdomen/pelvis. Management: SURGICAL RESECTION is ONLY POTENTIAL CURE. iCCA: hepatectomy. pCCA: MAJOR RESECTION: biliary confluence resection + hepatectomy (often extended right) + portal lymphadenectomy + Roux-en-Y hepaticojejunostomy. dCCA: pancreaticoduodenectomy (Whipple). NEOADJUVANT THERAPY: emerging role (chemotherapy, chemoradiation). LOCALLY ADVANCED/UNRESECTABLE: LIVER TRANSPLANTATION (pCCA, highly selected, neoadjuvant chemoradiation protocol). PALLIATIVE: BILIARY STENTING (ERCP, PTBD), systemic chemotherapy (gemcitabine/cisplatin, FOLFOX), targeted therapy (FGFR2 fusions—iCCA, IDH1 mutations), immunotherapy (MSI-H). Prognosis: RESECTED: 5y survival 20-40%. UNRESECTABLE: median survival 6-12 months. Zambian context: CCA is RARE but underdiagnosed. Think CCA in patient with obstructive jaundice, biliary stricture on imaging, no stones. MRCP available tertiary. ERCP available (stenting). Surgical resection available (specialized centres). Liver transplant unavailable. Palliative stenting and chemotherapy (gemcitabine) accessible.
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Biliary Strictures: Benign vs Malignant
Biliary strictures are focal narrowings of the bile duct, posing a CRITICAL DIFFERENTIAL DIAGNOSIS: BENIGN vs MALIGNANT. For Zambian students, this distinction is essential—misdiagnosis leads to either unnecessary surgery for benign disease (high morbidity) or missed opportunity for curative resection of malignancy. ETIOLOGY: BENIGN: IATROGENIC (post-cholecystectomy—most common, clipping, thermal injury, ischaemia), ANASTOMOTIC (post-liver transplant, biliary-enteric anastomosis), INFLAMMATORY: CHRONIC PANCREATITIS, PRIMARY SCLEROSING CHOLANGITIS (PSC), IgG4-RELATED SCLEROSING CHOLANGITIS (IgG4-SC), RADIATION, INFECTIOUS (TB, HIV cholangiopathy, parasitic), MIRIZZI SYNDROME (stone in cystic duct/neck compressing common hepatic duct). MALIGNANT: CHOLANGIOCARCINOMA (pCCA, dCCA), PANCREATIC ADENOCARCINOMA, GALLBLADDER CANCER, AMPULLARY TUMOUR, METASTATIC (portal lymphadenopathy). CLINICAL: OBSTRUCTIVE JAUNDICE (painless, progressive—suggests malignancy), pain, pruritus, cholangitis (fever, RUQ pain, jaundice). HISTORY: prior biliary surgery (iatrogenic), pancreatitis, IBD (PSC), malignancy. DIAGNOSIS: LFTs: obstructive pattern (↑ALP, GGT, bilirubin). MRCP: level, morphology, multiplicity, associated masses. BENIGN: smooth, symmetric, tapering, short segment (<1cm), solitary (iatrogenic), multifocal/beaded (PSC). MALIGNANT: irregular, asymmetric, shouldered, long segment (>1cm), associated mass. EUS: wall thickening, masses, lymph nodes, tissue acquisition (FNA). ERCP: tissue acquisition (brushings, biopsy), therapeutic (stenting). SEROLOGY: CA19-9 (malignant, not specific), IgG4 (IgG4-SC). MANAGEMENT: BENIGN: IATROGENIC: endoscopic dilation + temporary stenting (sequential, 3-6 months). Surgical reconstruction (hepaticojejunostomy) if endoscopic failure. PSC: supportive (UDCA), endoscopic dilation for dominant stricture, transplant. IgG4-SC: CORTICOSTEROIDS (dramatic response). CHRONIC PANCREATITIS: endoscopic stenting, surgical bypass. MALIGNANT: RESECTABLE: surgical resection (pancreaticoduodenectomy, hilar resection, hepatectomy). UNRESECTABLE: biliary stenting (ERCP, PTBD), chemotherapy, palliative care. Zambian context: BILIARY STRICTURE IS A COMMON DIAGNOSTIC CHALLENGE. MRCP is key (available tertiary). ERCP with stenting available. IgG4 testing limited. Malignancy is common; resectability often late. Focus: distinguish benign vs malignant, relieve jaundice (stenting), refer for resection if possible.
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Topic 201Coming soon
Post-Cholecystectomy Bile Leak
Bile leak is a complication of cholecystectomy (0.5-2% laparoscopic), usually from CYSTIC DUCT STUMP (70%) or ACCESSORY DUCTS OF LUSCHKA (gallbladder fossa). For Zambian students, recognition and management are essential—most leaks are ENDOSCOPICALLY TREATABLE, avoiding re-operation. CLINICAL: PRESENTATION: 2-10 days post-op: persistent RUQ pain, fever, nausea, vomiting, biliary peritonitis (generalized pain, rigidity, distension), or DRAIN OUTPUT (bilious fluid). DIAGNOSIS: DRAIN FLUID: bilirubin >3x serum. ABDOMINAL ULTRASOUND: fluid collection (biloma). HIDA SCAN: nuclear medicine, tracer extravasation from bile duct, NON-VISUALIZATION OF CBD/DUODENUM (if complete leak). MRCP: fluid collection, identifies leak site, intact CBD (no retained stones). ERCP: GOLD STANDARD for DIAGNOSIS AND THERAPY. MANAGEMENT: STABLE PATIENT, DRAINED COLLECTION: ERCP + SPHINCTEROTOMY + BILIARY STENTING. Reduces transpapillary pressure gradient, diverts bile flow away from leak, allows healing. STENT REMOVAL: 4-6 weeks. PERCUTANEOUS DRAINAGE: image-guided drainage of biloma (if undrained). UNSTABLE PATIENT, PERITONITIS: URGENT SURGICAL REPAIR (laparoscopic or open). Antibiotics. Prognosis: EXCELLENT with prompt ERCP. Morbidity: retained stones, stricture, infection. Zambian context: Laparoscopic cholecystectomy is standard at tertiary centres. Bile leak occurs. ERCP is available (Lusaka, Ndola, Kitwe). HIDA scan NOT available. MRCP is available. Management pathway: SUSPECT leak (post-op pain, fever, drain output), CONFIRM (drain fluid bilirubin, ultrasound), REFER for ERCP + stenting. Do NOT re-operate immediately (unless peritonitis).
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Cystic Fibrosis Liver Disease
Cystic fibrosis (CF) is a multisystem disorder caused by CFTR mutations, leading to thick, viscous secretions. CF-associated liver disease (CFLD) is the THIRD LEADING CAUSE OF DEATH in CF (after pulmonary and transplant complications). For Zambian students, CF is RARE in indigenous African populations, but occurs. PATHOPHYSIOLOGY: CFTR dysfunction in biliary epithelium → impaired bicarbonate secretion, thick bile → bile duct plugging, obstruction → FOCAL BILIARY CIRRHOSIS → MULTILOBULAR CIRRHOSIS (10-15% of CF patients). CLINICAL: INFANTS: PROLONGED NEONATAL JAUNDICE (cholestasis). CHILDREN/ADULTS: ASYMPTOMATIC hepatomegaly, elevated ALP/GGT, steatosis (fatty liver, 20-60%, multifactorial), FOCAL BILIARY CIRRHOSIS, PORTAL HYPERTENSION (splenomegaly, varices, ascites), synthetic dysfunction (late). COMPLICATIONS: VARICEAL HAEMORRHAGE (leading cause of death in CFLD), synthetic failure. DIAGNOSIS: CF DIAGNOSIS (sweat chloride, genetic testing) + LIVER DISEASE (clinical, biochemical, imaging). Ultrasound: coarse echotexture, nodularity, splenomegaly. Transient elastography: elevated liver stiffness. Liver biopsy: focal biliary cirrhosis (pathognomonic), not routinely required. MANAGEMENT: URSODEOXYCHOLIC ACID (UDCA, 20-30 mg/kg/day): IMPROVES LFTs, histology, may slow progression. PORTAL HYPERTENSION: variceal screening (endoscopy), NSBB (propranolol), EVL. COMPLICATIONS: manage ascites, encephalopathy. LIVER TRANSPLANTATION: indicated for decompensated cirrhosis, refractory variceal haemorrhage, synthetic failure. Combined liver-lung transplant (advanced pulmonary disease). Prognosis: CFLD reduces survival. UDCA improves outcomes. Zambian context: CF is rare. Consider in child with recurrent respiratory infections, malabsorption, failure to thrive + hepatomegaly/elevated LFTs. Sweat chloride testing NOT available. Genetic testing NOT available. Diagnosis is clinical. UDCA is available. Liver transplant NOT available.
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Caroli Disease and Caroli Syndrome
Caroli disease is a rare congenital disorder characterized by NON-OBSTRUCTIVE, SACCULAR OR FUSIFORM DILATATION of the intrahepatic bile ducts. Caroli SYNDROME = Caroli disease + CONGENITAL HEPATIC FIBROSIS (ductal plate malformation). For Zambian students, it is a diagnostic consideration in young patients with recurrent cholangitis or portal hypertension. PATHOPHYSIOLOGY: Autosomal recessive (PKHD1 gene, fibrocystin). Ductal plate malformation → dilated, segmental, saccular intrahepatic bile ducts (central dot sign). Association with medullary sponge kidney, autosomal recessive polycystic kidney disease (ARPKD). CLINICAL: CAROLI DISEASE (dilatation only): RECURRENT CHOLANGITIS (fever, RUQ pain, jaundice), abdominal pain, hepatomegaly, intraductal stones (stasis). CAROLI SYNDROME (+ hepatic fibrosis): PORTAL HYPERTENSION (splenomegaly, varices, ascites) + cholangitis. Synthetic function PRESERVED until late. COMPLICATIONS: Cholangitis, intraductal stones, LIVER ABSCESS, CHOLANGIOCARCINOMA (10-15% lifetime risk). DIAGNOSIS: ULTRASOUND: dilated, saccular intrahepatic bile ducts, 'CENTRAL DOT SIGN' (portal vein branch protrudes into dilated duct—PATHOGNOMONIC). MRCP: segmental, saccular ectasia, communication with biliary tree. CT: similar. LIVER BIOPSY (Caroli syndrome): ductal plate malformation, portal fibrosis, preserved lobules. MANAGEMENT: CHOLANGITIS: antibiotics, ERCP (stone extraction, sphincterotomy—difficult, may not reach peripheral ducts). INTRAHEPATIC STONES: challenging, percutaneous transhepatic cholangioscopy and lithotripsy (if available). LOCALIZED DISEASE (unilobar): LIVER RESECTION (curative, eliminates cholangitis, cancer risk). DIFFUSE DISEASE: LIVER TRANSPLANTATION (indicated for recurrent cholangitis, portal hypertension, high cancer risk). CHOLANGIOCARCINOMA SURVEILLANCE: annual imaging, CA19-9. Prognosis: with transplant, excellent. Without transplant, recurrent cholangitis, cancer. Zambian context: EXTREMELY RARE. Consider in young adult with recurrent cholangitis, NO GALLSTONES, NO BILIARY OBSTRUCTION. Ultrasound: central dot sign. MRCP (tertiary) confirms. Liver resection available (tertiary). Liver transplant NOT available. Cholangiocarcinoma risk—surveillance challenging.
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Portal Vein Cavernous Transformation
Portal vein cavernous transformation (PVCT) is the formation of multiple, tortuous collateral veins in the porta hepatis, developing as a sequela of CHRONIC PORTAL VEIN THROMBOSIS (PVT). It represents a NATURAL PORTOSYSTEMIC SHUNT, but does NOT prevent complications of portal hypertension. For Zambian students, PVCT is an IMPORTANT DIAGNOSIS in patients with VARICEAL HAEMORRHAGE, SPLENOMEGALY, and a NORMAL LIVER (no cirrhosis). PATHOPHYSIOLOGY: Acute PVT → organization, recanalization failure → formation of portal cavernoma (6-20 days). Cavernous vessels are collaterals that bypass the obstructed portal vein, carrying splanchnic blood to the liver. They are NOT sufficient to fully decompress the portal system—PREHEPATIC PORTAL HYPERTENSION persists. ETIOLOGY: Underlying prothrombotic state in 60-80%: myeloproliferative neoplasm (JAK2+), protein C/S/antithrombin deficiency, antiphospholipid syndrome, PNH. LOCAL FACTORS: neonatal omphalitis, umbilical vein catheterization, pylephlebitis, pancreatitis, cirrhosis, abdominal surgery. In Africa: Idiopathic, pylephlebitis, TB. CLINICAL: PRESENTATION: VARICEAL HAEMORRHAGE (50-60%), SPLENOMEGALY (80-90%), HYPERSPLENISM (thrombocytopenia, leukopenia). LIVER SYNTHETIC FUNCTION IS NORMAL (no cirrhosis, no ascites, normal LFTs, no encephalopathy). BILIARY COMPLICATIONS: PORTAL BILIOPATHY—cavernoma compresses common bile duct → obstructive jaundice, cholangitis (10%). DIAGNOSIS: DOPPLER ULTRASOUND: portal vein replaced by multiple, serpiginous, venous channels, hepatopetal flow, splenomegaly. CT/MR VENOGRAPHY: confirms extent, cavernoma, biliary compression. THROMBOPHILIA SCREEN: JAK2V617F, protein C/S, antithrombin, lupus anticoagulant, anticardiolipin. LIVER BIOPSY: NORMAL (excludes cirrhosis). MANAGEMENT: PORTAL HYPERTENSION: NON-SELECTIVE BETA-BLOCKERS (propranolol, carvedilol) for primary/secondary prophylaxis of variceal haemorrhage. ENDOSCOPIC VARICEAL LIGATION (EVL). ANTICOAGULATION: INDICATED for ACUTE PVT (to prevent progression, promote recanalization). In chronic PVT with cavernoma, anticoagulation is CONTROVERSIAL. Consider if: persistent prothrombotic state, recurrent thrombosis, mesenteric vein involvement. SURGICAL SHUNT: MESO-REX SHUNT (restores physiologic portal flow, ideal for children with EHPVO, good SMV inflow). TIPS: technically challenging (cavernoma). BILIOPATHY: endoscopic stenting, surgical bypass. Prognosis: EXCELLENT with prophylaxis (NSBB, EVL). No liver disease. Morbidity from variceal bleeding, hypersplenism. Zambian context: CONSIDER PVCT in patient with variceal haemorrhage, splenomegaly, and NORMAL LFTs (no cirrhosis). Doppler ultrasound is diagnostic. Thrombophilia testing limited. NSBB (propranolol) is accessible, inexpensive. EVL available tertiary. Anticoagulation: LMWH/warfarin accessible. Meso-Rex shunt NOT available. TIPS NOT available. Portal biliopathy: ERCP available. This is a DIAGNOSABLE, TREATABLE cause of portal hypertension with NORMAL LIVER.
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Hypersplenism in Cirrhosis
Hypersplenism is a frequent complication of cirrhosis-related portal hypertension, characterized by SPLENOMEGALY and CYTOPENIAS (thrombocytopenia most common, leukopenia, anaemia). For Zambian students, hypersplenism is a DAILY CLINICAL PROBLEM. It is a MARKER OF PORTAL HYPERTENSION and ADVANCED LIVER DISEASE, but rarely requires specific intervention. PATHOPHYSIOLOGY: PORTAL HYPERTENSION → passive splenic congestion → SPLENOMEGALY → increased sequestration and destruction of blood cells (platelets, neutrophils, erythrocytes). Also: REDUCED THROMBOPOIETIN (TPO) synthesis by diseased liver contributes to thrombocytopenia. CLINICAL: THROMBOCYTOPENIA (platelets <150,000, often 50-100,000): MOST COMMON. LEUKOPENIA (neutropenia, ANC <1500). ANAEMIA (normocytic, normochromic, multifactorial). SPLENOMEGALY (palpable left upper quadrant mass). Bleeding risk: thrombocytopenia ALONE is rarely sufficient to cause spontaneous bleeding (need platelets <20,000 or additional coagulopathy). Infection risk: neutropenia is rarely severe enough to increase infection risk. DIAGNOSIS: CLINICAL (cirrhosis + splenomegaly + cytopenias). EXCLUDE other causes: vitamin B12/folate deficiency, iron deficiency, myelodysplasia, drug-induced, HIV, malaria. BONE MARROW: not required; if performed, shows NORMAL OR INCREASED MEGAKARYOCYTES (peripheral destruction, not central failure). MANAGEMENT: NO TREATMENT REQUIRED for mild-moderate cytopenias. INDICATIONS FOR INTERVENTION: severe thrombocytopenia (platelets <20,000) with bleeding, or platelet count below procedural threshold (invasive procedure: platelets <50,000 for liver biopsy, <30-50,000 for major surgery). SPLENECTOMY: HISTORICAL, AVOIDED. Increases risk of OVERWHELMING POST-SPLENECTOMY INFECTION (OPSI), worsens portal hypertension (splenic vein ligation). PARTIAL SPLENIC EMBOLIZATION (PSE): interventional radiology, reduces splenic volume, improves cytopenias, preserves splenic immune function. AVAILABILITY: interventional radiology required (limited in Zambia). TIPS: reduces portal pressure, reduces spleen size, improves cytopenias. Available in Zambia? NOT AVAILABLE. THROMBOPOIETIN RECEPTOR AGONISTS (TPO-RA): ELTROMBOPAG, AVATROMBOPAG. ORAL, increase platelet production. Indicated for thrombocytopenia in chronic liver disease (prior to invasive procedures, not for chronic management). COST: expensive, NOT AVAILABLE in Zambia. TRANSFUSION: platelet transfusion for active bleeding or peri-procedural. PROGNOSIS: Hypersplenism is a marker of PORTAL HYPERTENSION, not an independent predictor of mortality. Treat the underlying cirrhosis (aetiology, complications). Zambian context: Hypersplenism is COMMON. Platelet count is a readily available, inexpensive, surrogate marker for PORTAL HYPERTENSION and CIRRHOSIS. No specific treatment needed in most cases. Severe thrombocytopenia with bleeding is rare. Procedural thresholds: platelets <50,000 for high-risk procedures. Platelet transfusion is available. Splenectomy should be AVOIDED. TPO-RA NOT available. TIPS NOT available. FOCUS: diagnose cirrhosis, manage complications, avoid splenectomy.
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Topic 206Coming soon
Hereditary Hemorrhagic Telangiectasia
Hereditary hemorrhagic telangiectasia (HHT, Osler-Weber-Rendu syndrome) is an autosomal dominant disorder of FIBROVASCULAR DYSPLASIA, characterized by MUCUTANEOUS TELANGIECTASIAS and ARTERIOVENOUS MALFORMATIONS (AVMs) in visceral organs (lungs, liver, brain, GI tract). For Zambian students, HHT is a diagnostic consideration in patients with recurrent epistaxis, family history, and unexplained anaemia or hepatic bruit. PATHOPHYSIOLOGY: Mutations in ENG (endoglin, HHT1), ACVRL1 (ALK1, HHT2), or SMAD4 (JPHT). Impaired TGF-β/BMP9-10 signaling → abnormal angiogenesis, deficient mural cell coverage → direct arteriovenous connections (no intervening capillary bed) → telangiectasias, AVMs, high-output cardiac state. CLINICAL: CURAÇAO CRITERIA (≥3 = definite HHT): 1) EPISTAXIS (90-95%): spontaneous, recurrent, often childhood onset. 2) TELANGIECTASIAS: multiple, punctate, red, lips, tongue, fingers, nasal mucosa. 3) VISCERAL AVMs: PULMONARY (PAVM, 30-50%): right-to-left shunt, hypoxaemia, PARADOXICAL EMBOLISM (stroke, brain abscess), haemoptysis. HEPATIC (30-80%): three patterns—PORTAL HYPERTENSION (presinusoidal), BILIARY ISCHEMIA (sclerosing cholangitis-like), HIGH-OUTPUT HEART FAILURE (arteriovenous shunting, hepatomegaly, hepatic bruit—DIAGNOSTIC). CEREBRAL (10-20%): haemorrhage, seizure, headache. GI (20-30%): chronic occult bleeding, anaemia. 4) FAMILY HISTORY: first-degree relative with HHT. DIAGNOSIS: CLINICAL (Curacao criteria). GENETIC TESTING: confirmation, family screening. PAVM SCREENING: CONTRAST ECHOCARDIOGRAPHY (bubble study)—sensitive; positive requires CT angiography. HEPATIC AVMs: DOPPLER ULTRASOUND: dilated hepatic artery, tortuous intrahepatic vessels, arteriovenous shunting. CT/MR angiography. MANAGEMENT: EPISTAXIS: humidification, topical lubricants, laser photocoagulation, septodermoplasty. ANAEMIA: iron supplementation, transfusions. PAVM: EMBOLIZATION (coils, plugs) INDICATED for feeding artery ≥2-3mm. PREVENT paradoxical emboli. ANTIBIOTIC PROPHYLAXIS before dental/surgical procedures (PAVM). HEPATIC AVMs: asymptomatic → observe. HIGH-OUTPUT FAILURE: diuretics, afterload reduction, anti-angiogenic therapy (BEVACIZUMAB, IV, 5mg/kg q2 weeks x 4-6, then maintenance). LIVER TRANSPLANT: refractory high-output failure, biliary necrosis, portal hypertension. CEREBRAL AVMs: individualize (size, location, rupture risk). ANTIFIBRINOLYTICS: tranexamic acid (epistaxis, bleeding). Prognosis: Normal lifespan with surveillance and treatment of visceral AVMs. Leading causes death: CNS haemorrhage, PAVM complications, high-output failure. Zambian context: HHT is RARE, underdiagnosed. Suspect in recurrent epistaxis + telangiectasias + family history. Hepatic bruit = HHT until proven otherwise. PAVM screening (contrast echo) NOT AVAILABLE. Embolization (PAVM, hepatic) available limited. Bevacizumab NOT AVAILABLE. Focus: clinical diagnosis, iron for anaemia, epistaxis care, infection prophylaxis, genetic counselling.
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Topic 207Coming soon
Liver Abscess: Pyogenic vs Amoebic
Liver abscess is a common, life-threatening infection in tropical settings. For Zambian students, DISTINGUISHING PYOGENIC (PLA) from AMOEBIC (ALA) is essential—epidemiology, management, and prognosis differ. AMOEBIC LIVER ABSCESS (ALA): CAUSE: Entamoeba histolytica. PATHOGENESIS: faecal-oral, trophozoites invade colonic mucosa → portal circulation → liver. PROTEOLYTIC ENZYMES liquefy tissue. CLINICAL: YOUNG ADULT MALE (20-40y). SUBACUTE (2-4 weeks). FEVER (90%), RUQ PAIN (90%), HEPATOMEGALY (tender). Diarrhoea (20-30%). DYSPNOEA (rupture into pleural space). RISK: alcohol, malnutrition, institutionalization. DIAGNOSIS: ULTRASOUND/CT: ROUND or OVOID, HYPOECHOIC, WELL-DEFINED, ABUTTING DIAPHRAGM (right lobe 80%). Single (70%). SEROLOGY: E. histolytica antibodies (IgG) positive in 90-95% (past/current). STOOL: cysts/trophozoites (10-20%, insensitive). ASPIRATE: ANAEROBIC, ODORLESS, 'ANCHOVY SAUCE' (brown-red, sterile). PYOGENIC LIVER ABSCESS (PLA): CAUSE: POLYMICROBIAL (E. coli, Klebsiella, Streptococcus, anaerobes, Enterococcus). PATHOGENESIS: BILIARY (ascending cholangitis, 50-60%) → multiple, left lobe. PORTAL (pylephlebitis—appendicitis, diverticulitis). ARTERIAL (bacteraemia—endocarditis, dental). TRAUMA. CRYPTOGENIC (20%). CLINICAL: OLDER (>50y), diabetes, biliary disease. ACUTE (days). FEVER, CHILLS, RUQ PAIN, SEPSIS. JAUNDICE (biliary origin). DIAGNOSIS: ULTRASOUND/CT: IRREGULAR, COMPLEX, LOCULATED, MULTIPLE, BILATERAL. BLOOD CULTURES (50-80% positive). ASPIRATE CULTURE: aerobic, anaerobic. Gram stain: neutrophils, organisms. LABORATORY: ALA: mild leukocytosis, normal bilirubin/ALP, elevated CRP. PLA: marked leukocytosis, elevated ALP, bilirubin, transaminases. COMPLICATIONS: RUPTURE: pleural (empyema, hepatobronchial fistula), peritoneal (peritonitis), pericardial (left lobe). CHRONIC DRAINAGE. MANAGEMENT: AMOEBIC: METRONIDAZOLE 750mg TID IV/PO x 10 days (or tinidazole 2g/day x 5d). LUMINAL AGENT: paromomycin or diloxanide furoate (to eradicate colonic cysts). ASPIRATION: NOT ROUTINE. INDICATIONS: no response 72h, large abscess (>10cm), left lobe (pericardial risk), impending rupture, diagnostic uncertainty. PYOGENIC: IV ANTIBIOTICS (broad-spectrum, cover enterics/anaerobes: ceftriaxone + metronidazole, piperacillin-tazobactam, carbapenem) x 2-6 weeks. DRAINAGE: PERCUTANEOUS CATHETER DRAINAGE (PCD) is FIRST-LINE. Indications: all PLA >5cm. SURGICAL DRAINAGE: failed PCD, multiloculated, rupture, underlying intra-abdominal pathology. Prognosis: ALA: mortality <1% (treated). PLA: mortality 10-30% (sepsis, comorbidities). Zambian context: BOTH ARE COMMON. ALA more common (endemic). Ultrasound widely available—differentiates. ALA: serology (IHA, ELISA) available tertiary. PLA: biliary source common (CBD stones). Aspiration/drainage: PCD available (radiology, surgery). Antibiotics: metronidazole, ceftriaxone available. Amoebic = medical cure. Pyogenic = antibiotics + drainage.