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MBBS FINAL PROF - COMPREHENSIVE NOTES

Medicine & Surgery - High-Yield Complete Reference

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PART I: MEDICINE

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SECTION 1: CARDIOVASCULAR SYSTEM

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TOPIC 1: HEART FAILURE (HF)

Definition

Classification

• Both types are approximately equally common
• HFpEF is common in elderly, hypertensive, diabetic, and obese patients

Etiology / Precipitating Causes

• Coronary artery disease (CAD) / Myocardial Infarction - most common in Western world
• Hypertension (pressure overload)
• Valvular heart disease (aortic stenosis, mitral regurgitation)
• Diabetes mellitus
• Cardiomyopathies (dilated, hypertrophic, restrictive)
• Congenital heart defects
• Anemia (high-output failure)
• Alcoholism (alcoholic cardiomyopathy)
• Viral myocarditis

Pathophysiology - LV Remodeling (KEY CONCEPT)

1. Precipitating injury → LV remodeling: stretching, dilation, reduced LV function
2. Neurohormonal activation:
   • RAAS (renin-angiotensin-aldosterone system): Angiotensin II causes myocyte apoptosis, hypertrophy, ventricular fibrosis + aldosterone secretion
   • SNS (sympathetic nervous system): Catecholamines cause beta-adrenoceptor-mediated calcium overload, myocyte toxicity, receptor downregulation
   • Endothelin-1: Vasoconstriction
   • Inflammatory cytokines: Endothelial dysfunction
3. Cellular: MMPs increase → cardiac fibrosis + collagen deposition; calcium flux alterations; shift to glycolysis from FFA oxidation
4. Remodeling is reversible with appropriate therapy

Clinical Features (Symptoms)

• Dyspnea on exertion (earliest)
• Orthopnea (breathlessness lying flat)
• Paroxysmal nocturnal dyspnea (PND)
• Cardiac asthma
• Fatigue, reduced exercise tolerance

• Peripheral pitting edema (ankles, legs)
• Raised jugular venous pressure (JVP)
• Hepatomegaly, ascites
• Weight gain

• Tachycardia, S3 gallop (pathognomonic of HFrEF)
• Displaced apex beat
• Basal crepitations (pulmonary edema)
• Pleural effusion

NYHA Classification of HF

Investigations

• ECG: LVH, AF, LBBB (suggests dyssynchrony)
• CXR: Cardiomegaly (CTR > 0.5), Kerley B lines, upper lobe diversion, bat-wing pulmonary edema
• Echo (most important): Assess EF, wall motion, valves, diastolic function
• BNP / NT-proBNP: Elevated - best biomarker for HF diagnosis and prognosis
• FBC, U&E, LFTs, TFTs, glucose: Identify precipitants
• Cardiac catheterization: If ischemic etiology suspected

Management of HFrEF (Pharmacological)

1. ACE inhibitor (or ARB if ACE intolerant) - blocks RAAS, reduces remodeling; e.g., ramipril, enalapril
2. Beta-blocker - blocks SNS; e.g., carvedilol, bisoprolol, metoprolol succinate
3. Aldosterone antagonist (MRA) - e.g., spironolactone, eplerenone; added because aldosterone "escapes" ACE inhibition
4. SGLT2 inhibitor - e.g., dapagliflozin, empagliflozin (newer addition, proven mortality benefit)

• Loop diuretics (furosemide) - for symptomatic relief of congestion (do NOT reduce mortality)
• Digoxin - reduces hospitalizations, no mortality benefit; useful in AF + HF
• Ivabradine - reduces heart rate if sinus rhythm + HR > 70 despite beta-blocker
• ARNi (sacubitril/valsartan) - replaces ACE inhibitor/ARB, superior to enalapril (PARADIGM-HF trial)
• Hydralazine + nitrate - alternative if ACE/ARB intolerant, especially in Black patients

• ICD - if EF < 35% after 3 months optimal medical therapy
• CRT (biventricular pacing) - if EF < 35% + LBBB (QRS > 150 ms)
• CRT-D - combined CRT + ICD

• No proven mortality-reducing therapy
• Treat underlying cause (BP control, rate control in AF)
• Diuretics for congestion
• SGLT2 inhibitors show emerging benefit

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TOPIC 2: ACUTE MYOCARDIAL INFARCTION (AMI)

Definition

Classification

Pathophysiology

• Atherosclerotic plaque rupture → platelet aggregation → thrombus → coronary occlusion
• Ischemia: 20-40 min → irreversible necrosis (infarction)
• Reperfusion injury if vessel opens (free radicals, calcium overload)

Clinical Features

• Chest pain: Severe, crushing/squeezing, central, radiating to left arm/jaw/neck; lasting > 20 min; not relieved by nitrates
• Sweating, nausea, vomiting
• Anxiety ("sense of impending doom")
• Dyspnea, palpitations
• Silent MI: Common in diabetics, elderly, women

ECG Changes in STEMI (time sequence)

1. Hyperacute T-waves (within minutes)
2. ST elevation (within hours) - key diagnostic finding
3. T-wave inversion (hours to days)
4. Pathological Q-waves (persist - indicate old infarction)

Localization of MI on ECG

Biomarkers

• Troponin I/T: Most sensitive and specific; rises 4-6h, peaks 12-24h, stays raised 7-14 days
• CK-MB: Rises 4-6h, peaks 12-24h, normalizes by 72h (useful for reinfarction)
• LDH: Rises 24-48h, peaks 3-6 days, elevated 8-14 days

Management of STEMI ("TIME IS MUSCLE")

• Aspirin 300 mg (loading dose) - give immediately
• P2Y12 inhibitor: Ticagrelor 180 mg or clopidogrel 300-600 mg
• Anticoagulation: UFH or LMWH
• Nitrates (sublingual/IV) - if ongoing pain, NOT if BP low/RV infarct
• Morphine - for pain (use cautiously)
• O2 - only if SpO2 < 94%
• IV access, monitoring

• Primary PCI (preferred): Door-to-balloon time < 90 minutes; stent placement
• Thrombolysis (fibrinolysis): If PCI not available within 120 min; use streptokinase or alteplase; door-to-needle < 30 min
• Contraindications to thrombolysis: Recent surgery/trauma, active bleeding, hemorrhagic stroke, severe HTN

• Dual antiplatelet (aspirin + P2Y12 for 12 months minimum)
• Statin (high-intensity: atorvastatin 80 mg)
• ACE inhibitor / ARB
• Beta-blocker
• Cardiac rehabilitation

Complications of MI

• Early (0-48h): Arrhythmias (VF most common cause of death in first hour), cardiogenic shock, acute LVF
• Days 2-7: Pericarditis, free wall rupture (3-5 days post-MI → hemopericardium → death), VSD, papillary muscle rupture (severe MR)
• Late (weeks): Dressler's syndrome (autoimmune pericarditis, 1-10 weeks post-MI), LV aneurysm, heart failure

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TOPIC 3: HYPERTENSION

Definition

• Stage 1: SBP 130-139 or DBP 80-89 mmHg
• Stage 2: SBP ≥ 140 or DBP ≥ 90 mmHg (JNC-8/ACC/AHA criteria)
• Hypertensive urgency: BP ≥ 180/120 with NO end-organ damage
• Hypertensive emergency: BP ≥ 180/120 WITH end-organ damage

Classification

• Primary (Essential) - 90-95%; no identifiable cause
• Secondary - 5-10%; identifiable cause:
  • Renal: CKD, renal artery stenosis (most common secondary cause)
  • Endocrine: Primary hyperaldosteronism (Conn's), pheochromocytoma, Cushing's, hyperthyroidism
  • Drug-induced: OCPs, NSAIDs, steroids, cocaine
  • Coarctation of aorta (young patients with arm-leg BP differential)

End-Organ Damage (ABCD)

• A: Arteries - atherosclerosis, peripheral vascular disease
• Brain: Stroke, hypertensive encephalopathy
• Cardiac: LVH, IHD, HF
• Diabetes-related + Kidneys: Nephrosclerosis, CKD
• Also: Hypertensive retinopathy (grade I-IV)

Management

• DASH diet (low sodium < 2g/day)
• Weight reduction
• Exercise
• Alcohol reduction, smoking cessation

• A: ACE inhibitors/ARBs (especially DM, CKD, HF, post-MI)
• B: Beta-blockers (especially with IHD, HF, tachyarrhythmia, pregnancy)
• C: Calcium channel blockers (elderly, isolated systolic HTN, Afro-Caribbean)
• D: Diuretics (thiazides: low-dose; aldosterone antagonists: Conn's)

• Target: Reduce MAP by 25% in first hour, then to 160/100 over next 2-6h
• Agents: IV labetalol, IV nitroprusside, IV nicardipine, IV hydralazine (in pregnancy)
• Exception: Acute ischemic stroke - do NOT lower BP aggressively unless > 220/120 or thrombolysis planned

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TOPIC 4: DIABETES MELLITUS

Classification

Diagnostic Criteria (WHO/ADA)

• Fasting glucose: ≥ 7.0 mmol/L (126 mg/dL)
• 2h OGTT: ≥ 11.1 mmol/L (200 mg/dL)
• Random glucose + symptoms: ≥ 11.1 mmol/L
• HbA1c: ≥ 6.5% (48 mmol/mol)
• Pre-diabetes: FPG 6.1-6.9, HbA1c 6.0-6.4%, OGTT 7.8-11.0

Pathophysiology

• Type 1: T-cell mediated autoimmune destruction of islet beta-cells → absolute insulin deficiency
• Type 2: Peripheral insulin resistance (muscle, liver, adipose) + progressive beta-cell dysfunction + increased glucagon → relative insulin deficiency; linked to obesity, inactivity, genetics

Complications

• Nephropathy: Earliest marker = microalbuminuria (30-300 mg/day); leads to proteinuria → CKD → ESRD
• Retinopathy: Background (dot hemorrhages, hard exudates, microaneurysms) → Pre-proliferative → Proliferative (new vessels → vitreous hemorrhage, tractional retinal detachment); maculopathy is leading cause of visual loss
• Neuropathy: Symmetrical distal sensorimotor polyneuropathy (stocking-glove); autonomic neuropathy (postural hypotension, gastroparesis, diarrhea, impotence, bladder dysfunction)

• Ischemic heart disease (MI), cerebrovascular accident, peripheral arterial disease
• Haffner showed: DM patients without prior MI have same MI risk as non-diabetic post-MI patients

• Diabetic foot: Neuropathy + PVD + infection
• Infections: Mucormycosis, UTIs, skin infections, TB
• Lipoatrophy / lipohypertrophy (insulin injection)

Management of Type 2 DM

1. Lifestyle (diet, exercise, weight loss)
2. Metformin (1st line): Reduces hepatic gluconeogenesis; reduces CV events (UKPDS); contraindicated in eGFR < 30; SE: GI upset, lactic acidosis (rare)
3. Add 2nd agent if HbA1c not at target:
   • SGLT2 inhibitor (empagliflozin/dapagliflozin): Glycosuria, weight loss, BP reduction; cardioprotective, renoprotective; SE: UTI, genital thrush, DKA
   • GLP-1 agonist (semaglutide/liraglutide): Weight loss, CV benefit; SE: nausea, vomiting
   • DPP-4 inhibitor (sitagliptin): Weight neutral; SE: nasopharyngitis
   • Sulfonylurea (glipizide/gliclazide): Risk of hypoglycemia, weight gain
   • Pioglitazone: Insulin sensitizer; SE: fluid retention, fractures, bladder cancer
4. Insulin if HbA1c persistently elevated (start with basal insulin)

• Statin for all T2DM + CVD or high risk (CARDS trial: atorvastatin)
• ACE inhibitor if microalbuminuria/proteinuria
• Aspirin if established CVD
• BP target < 130/80

Diabetic Ketoacidosis (DKA) - Emergency

• Typically Type 1 (can occur in Type 2)
• Triad: Hyperglycemia (usually > 14 mmol/L) + Ketosis (ketonuria/ketonemia) + Metabolic acidosis (pH < 7.3, HCO3 < 15)
• Precipitants: Infection, missed insulin, new-onset T1DM, MI, surgery
• Symptoms: Polyuria, polydipsia, N/V, abdominal pain, Kussmaul breathing (deep, rapid), acetone breath, reduced consciousness
• Management (FLUID, INSULIN, K+):
  • IV normal saline: 1L in first hour, then based on response
  • Insulin infusion: 0.1 units/kg/hour (NOT until K+ > 3.5 mEq/L)
  • Potassium replacement (DKA causes total body K+ depletion): Replace throughout
  • Monitor glucose hourly; add dextrose when glucose < 14 mmol/L
  • Treat precipitant

Hyperosmolar Hyperglycemic State (HHS) - Type 2 Emergency

• Glucose often > 35 mmol/L, marked dehydration, serum osmolarity > 320 mOsm/kg
• NO significant ketoacidosis
• Slower onset, older patients
• Higher mortality than DKA
• Treatment: Gentle rehydration (0.9% saline), low-dose insulin, anticoagulation (high DVT risk)

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TOPIC 5: PNEUMONIA

Definition

Classification

• CAP (Community-Acquired Pneumonia)
• HAP (Hospital-Acquired/Nosocomial Pneumonia): > 48h after admission
• VAP (Ventilator-Associated Pneumonia): > 48-72h after intubation
• Aspiration Pneumonia: Inhalation of oropharyngeal secretions

Common Organisms by Presentation

Pathophysiology

• Consolidation of alveoli with exudate → impaired gas exchange
• V/Q mismatch: Increased perfusion to shunt (consolidated) and low V/Q regions
• Mild-moderate hypoxemia: Shunt fraction 7.5%, low V/Q 4.2%
• Severe pneumonia (on ventilator): Shunt 21.9%, low V/Q 10.9% - proportional to severity
• Response to O2 depends on degree of shunt

Clinical Features

• Fever, rigors, productive cough (rusty sputum in pneumococcal)
• Pleuritic chest pain
• Dyspnea, tachypnea
• On exam: Dullness to percussion, bronchial breathing, increased tactile vocal fremitus, crackles

Investigations

• CXR: Consolidation (homogeneous opacity) - lobar/segmental or patchy bilateral (atypical)
• FBC: Leukocytosis (neutrophilia in bacterial; lymphocytosis in viral)
• Sputum C&S, blood cultures
• Urine antigen: For Legionella and pneumococcal
• ABG: Assess severity/hypoxemia
• CURB-65 score (severity assessment for CAP):
  • C - Confusion
  • U - Urea > 7 mmol/L
  • R - Respiratory rate > 30/min
  • B - Blood pressure < 90/60
  • 65 - Age > 65
  • Score 0-1: Outpatient; 2: Hospital; 3-5: ICU

Management

• Amoxicillin 500mg TDS × 5 days
• If atypical suspected: Add clarithromycin (macrolide)

• IV amoxicillin + IV clarithromycin (dual coverage for typical + atypical)

• Co-amoxiclav (or 3rd-generation cephalosporin) + clarithromycin/azithromycin
• Cover MRSA if risk factors: Add vancomycin/linezolid

• Piperacillin-tazobactam OR 3rd-gen cephalosporin + antipseudomonal cover
• Add vancomycin if MRSA risk

• Oxygen (target SpO2 94-98%)
• Adequate hydration
• Physiotherapy
• DVT prophylaxis
• Treat complications (empyema, sepsis)

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TOPIC 6: PULMONARY EMBOLISM (PE)

Risk Factors (Virchow's Triad)

• Venous stasis: Prolonged immobility, long flights, obesity
• Hypercoagulability: OCP, pregnancy, malignancy, thrombophilia (Factor V Leiden, antiphospholipid syndrome, protein C/S deficiency)
• Endothelial injury: Surgery, trauma, central venous catheters

Clinical Features

• Massive PE: Sudden collapse, severe dyspnea, syncope, cardiogenic shock, hypoxia
• Submassive PE: Dyspnea, pleuritic chest pain, hemoptysis, tachycardia, hypoxia
• Small PE: May be asymptomatic or minimal symptoms
• Classically: Pleuritic chest pain + dyspnea + hemoptysis (pulmonary infarction)
• Important: PE may occur WITHOUT hypoxemia; up to 12% of proven PE had PaO2 > 80 mmHg (Urokinase PE Trial)

Investigations

• D-dimer: Sensitive (> 99%) but NOT specific; use to RULE OUT PE if pre-test probability is low
• CTPA (CT pulmonary angiography): Gold standard diagnostic test; shows filling defect
• ECG: Sinus tachycardia (most common); S1Q3T3 (classical but uncommon); RBBB; RV strain
• ABG: Hypoxia, low pCO2 (hyperventilation), raised A-a gradient; but can be normal
• CXR: Often normal; Hampton's hump (wedge-shaped opacity = infarct); Westermark sign (oligemia)
• Echo: RV dilation, D-septum, McConnell's sign (RV free wall hypokinesia with apical sparing)
• V/Q scan: Alternative to CTPA; for renal impairment or contrast allergy
• Leg Doppler US: DVT confirms diagnosis

Management

• Anticoagulation (cornerstone): Start immediately if clinical suspicion
  • DOAC (apixaban, rivaroxaban) - first line
  • LMWH (enoxaparin) - first line in cancer, pregnancy
  • IV UFH - if high bleeding risk or massive PE (for rapid reversal)
  • Warfarin (with LMWH overlap for 5 days until INR 2-3)
• Duration: Provoked PE = 3 months; unprovoked = 3-6 months (consider lifelong); cancer = lifelong DOAC/LMWH
• Massive PE with hemodynamic instability: Systemic thrombolysis (alteplase) - if no contraindications; surgical embolectomy if thrombolysis fails/contraindicated
• Catheter-directed thrombolysis: For submassive with high bleeding risk

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TOPIC 7: STROKE & CEREBROVASCULAR DISEASE

Classification

• Lacunar (small vessel): Deep white matter, basal ganglia; hypertension
• Atherothrombotic (large vessel): Extracranial or intracranial atherosclerosis
• Cardioembolic: AF (most common cardiac cause), endocarditis, LV thrombus
• Cryptogenic: No identified cause

TIA (Transient Ischemic Attack)

• Focal neurological deficit lasting < 24 hours (usually < 1 hour) with no infarction on imaging
• High-risk emergency: ABCD2 score guides urgency
• 5-10% stroke risk within 2 days → urgent investigation and secondary prevention

Clinical Syndromes

Investigations (URGENT)

• Immediate CT brain (non-contrast): Rule out hemorrhage before giving thrombolysis
• MRI brain + DWI (diffusion-weighted): More sensitive for early ischemia
• CT angiography / MRA: Vessel imaging for large vessel occlusion (LVO)
• ECG: Rule out AF
• Echo, carotid Doppler US
• FBC, coagulation, lipids, glucose

Management of Ischemic Stroke

• IV thrombolysis (tPA - alteplase): If < 4.5 hours of onset, no hemorrhage on CT, no contraindications
  • Contraindications: Hemorrhagic stroke, recent surgery/trauma, severe hypertension (> 185/110 before treatment), coagulopathy, platelet < 100k
• Mechanical thrombectomy (MT): For LVO (M1/M2, basilar); up to 6-24 hours (DAWN/DEFUSE-3 trials); door-to-groin < 90 min
• Do NOT lower BP aggressively in acute ischemic stroke unless > 220/120 (or > 185/110 if giving tPA)
• Aspirin 300 mg (after excluding hemorrhage, and 24h after tPA)

• DVT prophylaxis (compression stockings)
• Swallowing assessment before oral intake
• Urinary catheterization if retention
• Glucose and temperature control
• Physiotherapy, speech therapy, occupational therapy

• Antiplatelet (aspirin + dipyridamole OR clopidogrel alone)
• Anticoagulation if AF (warfarin or DOAC)
• Carotid endarterectomy if stenosis 70-99% (symptomatic)
• Statins, BP control, DM management, smoking cessation

Hemorrhagic Stroke

• Causes: HTN (most common, basal ganglia/thalamus/pons), AVM, anticoagulants, amyloid angiopathy (elderly, lobar)
• Management: Reverse anticoagulation, BP control (target < 140), neurosurgical evacuation in selected cases (lobar hematoma with deterioration), ICP monitoring

• Worst headache of life ("thunderclap headache")
• Cause: Ruptured Berry aneurysm (most common site: anterior communicating artery)
• Complications: Re-bleed (highest risk 24h), hydrocephalus, vasospasm (3-14 days, treat with nimodipine)
• Investigations: CT (blood in subarachnoid space); if CT negative → LP for xanthochromia
• Management: Neurosurgical (coil/clip aneurysm), nimodipine (prevents vasospasm), supportive

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TOPIC 8: CHRONIC KIDNEY DISEASE (CKD)

Definition

Classification (KDIGO - by GFR)

Common Causes

1. Diabetic nephropathy (most common in developed world)
2. Hypertension / renovascular disease
3. Glomerulonephritis (IgA nephropathy most common)
4. Polycystic kidney disease (PKD)
5. Recurrent pyelonephritis / reflux nephropathy

Complications

• Anemia: Normochromic normocytic; EPO deficiency (treat with EPO + iron)
• Metabolic acidosis: Accumulation of acids
• Hyperkalemia: Dangerous; restrict dietary K+; K-binders
• Renal osteodystrophy: Low Ca++, high PO4, high PTH, low vit D → osteitis fibrosa cystica, osteoporosis
• Cardiovascular disease: Accelerated; main cause of death in CKD
• Fluid overload: Hypertension, pulmonary edema
• Uremia: Pericarditis, encephalopathy, coagulopathy (platelet dysfunction), itch

Management

• Treat underlying cause
• BP control: Target < 130/80; ACE inhibitor/ARB (especially in DM/proteinuria; REIN study)
• Dietary: Low protein, low K+, low Na+, low PO4
• Erythropoiesis-stimulating agent (ESA) for anemia (target Hb 10-12 g/dL)
• Phosphate binders: Calcium carbonate, sevelamer (non-calcium)
• Calcitriol / active Vitamin D for renal osteodystrophy
• Statins for CV risk reduction
• Avoid nephrotoxins (NSAIDs, aminoglycosides, contrast)
• Renal replacement therapy: Hemodialysis, peritoneal dialysis, renal transplantation (best long-term outcome)

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TOPIC 9: ANEMIA

Classification by MCV

Iron Deficiency Anemia (IDA) - Most Common Anemia

• Causes: Blood loss (GI - most common in adults; menorrhagia), malabsorption (celiac), poor dietary intake
• CBC: Low Hb, low MCV, low MCH, low MCHC, high RDW
• Blood film: Microcytosis, hypochromia, anisocytosis, pencil cells
• Serum ferritin (most sensitive early marker): Low
• Iron studies: Low serum iron, low ferritin, HIGH TIBC
• Treatment: Oral ferrous sulfate/fumarate; IV iron if severe/malabsorption; treat underlying cause

B12/Folate Deficiency (Megaloblastic Anemia)

• B12 causes: Pernicious anemia (autoimmune; anti-intrinsic factor antibodies - most common cause of B12 def in UK), vegan diet, terminal ileum disease/resection
• Folate causes: Poor dietary intake (most common), alcohol, pregnancy, methotrexate, phenytoin
• Features: Anemia + lemon-yellow skin + glossitis + angular stomatitis
• B12 also causes: Subacute combined degeneration of the spinal cord (dorsal + lateral column demyelination → loss of vibration/proprioception + UMN signs)
• Blood film: Oval macrocytes, hypersegmented neutrophils (> 5 lobes)
• Bone marrow: Megaloblasts
• Treatment: IM hydroxocobalamin (B12) for pernicious anemia; oral folic acid

Sickle Cell Disease

• Autosomal recessive; HbS (Glu → Val substitution in beta-globin chain)
• HbSS = sickle cell disease; HbAS = sickle cell trait (usually asymptomatic; protection against malaria)
• Deoxygenated HbS polymerizes → sickle-shaped RBCs → hemolysis + vaso-occlusion

• Painful vaso-occlusive crisis (bone marrow infarction, dactylitis in infants)
• Acute chest syndrome (pneumonia/infarction of lung - leading cause of death)
• Stroke (5-10% of children with SCD)
• Splenic sequestration (children) → functional asplenia (adults) → susceptibility to encapsulated organisms (pneumococcus, meningococcus, H. influenzae)
• Aplastic crisis (parvovirus B19 → temporary marrow arrest)
• Avascular necrosis (femoral head)
• Retinopathy, leg ulcers, priapism, cholelithiasis (pigment stones)

• Hydroxyurea (increases HbF, reduces crises)
• Penicillin prophylaxis (after functional asplenia)
• Vaccines (pneumococcal, meningococcal, Hib)
• Folate supplementation
• Pain: Analgesics, hydration, opioids for severe crises
• Exchange transfusion: Acute chest syndrome, stroke, priapism

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TOPIC 10: TUBERCULOSIS (TB)

Microbiology

• Mycobacterium tuberculosis - aerobic, acid-fast bacillus (AFB)
• Ziehl-Neelsen stain: AFBs appear red on blue background
• Slow-growing; culture takes 4-8 weeks (Lowenstein-Jensen media)
• Spread: Airborne droplet nuclei (< 5 microns)

Types

• Primary TB: Initial infection; Ghon focus (usually mid-zone) + hilar lymphadenopathy = Ghon complex; usually asymptomatic
• Post-primary (Reactivation) TB: Reactivation in immunocompromised or in adulthood; upper lobe; cavitation
• Latent TB: Infection without active disease; LTBI treated to prevent reactivation
• Military TB: Hematogenous dissemination; millet-seed appearance on CXR; can cause meningitis, pericarditis, peritonitis, Addison's disease

Clinical Features (Pulmonary TB)

• Chronic cough > 3 weeks + hemoptysis
• Constitutional: Night sweats, weight loss, evening fever, anorexia, malaise
• On exam: Signs of consolidation/cavitation (upper zones)

Diagnosis

• Sputum AFB smear + culture (gold standard): 3 sputum specimens
• GeneXpert MTB/RIF (Xpert): Rapid molecular test; detects TB + rifampicin resistance
• Tuberculin skin test (Mantoux): PPD injection; measure induration at 48-72h; positive if ≥ 10mm (≥ 5mm in immunocompromised/HIV)
• IGRA (Interferon Gamma Release Assay): QuantiFERON-TB Gold; blood test; not affected by BCG vaccination; better specificity
• CXR: Cavitation, upper lobe infiltrates, hilar lymphadenopathy

Treatment (Directly Observed Therapy - DOT)

• 2 months RIPE (Intensive phase): Rifampicin + Isoniazid + Pyrazinamide + Ethambutol
• 4 months RI (Continuation phase): Rifampicin + Isoniazid

• MDR-TB: Resistant to rifampicin + INH
• XDR-TB: MDR + resistance to fluoroquinolone + at least one 2nd-line injectable
• Treatment: Bedaquiline, linezolid, clofazimine-based regimens (18-24 months)

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SECTION 2: SURGERY

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TOPIC 1: ACUTE ABDOMEN & APPENDICITIS

Definition

Key Causes by Location

Appendicitis

• Classic: Periumbilical pain migrating to right iliac fossa (McBurney's point)
• Nausea, vomiting, low-grade fever
• Anorexia (important - almost always present)
• Signs: Tenderness + guarding at McBurney's point (1/3 between ASIS and umbilicus)
• Rovsing's sign: Palpation of LIF causes pain in RIF
• Psoas sign: Extension of hip worsens pain (retrocaecal appendix)
• Obturator sign: Internal rotation of hip worsens pain (pelvic appendix)

• Alvarado score (clinical scoring):
  • Migration of pain to RIF (1)
  • Anorexia (1)
  • Nausea/Vomiting (1)
  • RIF tenderness (2)
  • Rebound tenderness (1)
  • Elevated temp (1)
  • Leucocytosis (2) → Max 10
  • Score < 5: Low risk; 5-6: Possible (investigate); ≥ 7: Likely appendicitis
• FBC (leukocytosis), CRP
• Urine dipstick (rule out UTI)
• USS abdomen (especially young women, children, pregnancy)
• CT abdomen/pelvis (most sensitive/specific; reserve for diagnostic uncertainty)
• Pregnancy test (women)

• Appendicectomy (laparoscopic preferred): DEFINITIVE treatment
• Pre-op: IV antibiotics (co-amoxiclav), IV fluids, NBM
• Perforated appendicitis: Emergency laparotomy, washout, drain placement
• Conservative (antibiotics only): Some centers for uncomplicated appendicitis - higher recurrence risk

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TOPIC 2: INTESTINAL OBSTRUCTION

Classification

• Mechanical: Physical blockage
  • Small bowel: Adhesions (most common in adults after previous surgery), hernia, Crohn's
  • Large bowel: Colorectal carcinoma (most common), volvulus, diverticular stricture
• Functional (Ileus/Pseudo-obstruction): No mechanical cause; decreased peristalsis
  • Post-op ileus, electrolyte imbalance, drugs (opioids)

Clinical Features

• Colicky periumbilical pain (frequent episodes)
• Vomiting (early, bilious)
• Abdominal distension (modest)
• Tinkling bowel sounds (early) → absent (late)
• Constipation (absolute if complete)

• Colicky, lower abdominal pain
• Distension (marked)
• Vomiting (late, feculent)
• Absolute constipation (no flatus)

Investigations

• AXR (Abdominal X-ray):
  • SBO: Central dilated loops (> 3 cm), valvulae conniventes (cross whole bowel width)
  • LBO: Peripheral dilated loops (> 6 cm), haustral folds (incomplete)
  • Free gas under diaphragm = perforation
• CT abdomen: Best investigation; identifies cause and level
• FBC, U&E, amylase, blood gas

Management

• Drip and Suck: IV fluids (correct dehydration + electrolytes) + NGT (nasogastric tube) decompression
• Urinary catheterization to monitor output
• Strangulation (compromised blood supply) = surgical emergency → signs: Fever, leukocytosis, peritonism, constant pain
• Surgical: If conservative fails, or strangulation/complete obstruction
  • SBO: Division of adhesions, resection if ischemic bowel
  • LBO: Hartmann's procedure; or decompressing colostomy + elective resection
• Volvulus: Sigmoid - rigid sigmoidoscopy + rectal tube; caecal - resection

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TOPIC 3: PEPTIC ULCER DISEASE (PUD) & COMPLICATIONS

Etiology

• H. pylori (most important) - gram-negative spiral bacterium; disrupts mucosal defense
• NSAIDs (second most important) - inhibit COX-1 (prostaglandin synthesis) → reduced mucus + bicarbonate secretion + reduced mucosal blood flow
• Cigarette smoking (doubles risk)
• Zollinger-Ellison syndrome (ZES): Gastrinoma → massive acid secretion → refractory multiple ulcers
• Stress ulcers (Curling's - burns; Cushing's - head injury)
• Steroids alone (less significant than NSAIDs)

Types

• Duodenal ulcer (DU): 1st part of duodenum; more common; pain relieved by food, worse 2-3h later; H. pylori in > 90%
• Gastric ulcer (GU): Lesser curve; pain worsened by food; H. pylori in 70%; MUST biopsy to exclude malignancy
• Ulcers occur at junctions of different epithelial types (least acid-resistant)

Diagnosis

• Endoscopy (OGD): Gold standard; allows biopsy
• H. pylori testing: Urea breath test, stool antigen, CLO test (biopsy at endoscopy), serology (remains positive after eradication - not useful for cure)
• Barium meal (less common now)

H. pylori Eradication (Triple Therapy - 7 days)

• PPI + Clarithromycin + Amoxicillin (or metronidazole if penicillin allergic)
• Confirm eradication: Urea breath test 4 weeks after completing antibiotics (stop PPI 2 weeks before)
• Quadruple therapy if first line fails

Complications

• Hematemesis (fresh blood/coffee ground) + melena
• Rockford Classification (Forrest) for endoscopic risk:
  • Ia: Spurting (active) - highest risk
  • Ib: Oozing
  • IIa: Visible vessel
  • IIb: Adherent clot
  • IIc: Flat pigmented spot
  • III: Clean base (lowest risk)
• Management: Resuscitate → Endoscopy → Hemostasis (adrenaline injection, clips, coagulation)
• High-dose PPI infusion post-endoscopy (omeprazole 80mg bolus then 8mg/h infusion for 72h)
• Failed endoscopy → Interventional radiology or Surgery

• Sudden severe epigastric pain → generalized peritonitis
• Rigid board-like abdomen, absent bowel sounds
• CXR: Free gas under diaphragm (pneumoperitoneum) - pathognomonic
• Management: Resuscitate → IV antibiotics → Emergency laparotomy/laparoscopy → Graham Omental Patch repair

• Repeated vomiting (no bile - pyloric level), projectile
• Succussion splash (fluid in distended stomach)
• Metabolic alkalosis + hypokalemia + hypochloremia (loss of HCl in vomitus)
• Management: NG decompression, correct electrolytes → Endoscopic balloon dilation or surgery

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TOPIC 4: GASTROINTESTINAL BLEEDING

Upper GI Bleeding (UGIB) - Proximal to Ligament of Treitz

• Peptic ulcer disease (most common, 35-50%)
• Gastritis/erosions (NSAIDs, alcohol)
• Oesophageal varices (in portal hypertension)
• Mallory-Weiss tear (forceful vomiting → mucosal tear at GEJ)
• Oesophagitis, Dieulafoy lesion

• Age, shock (HR/BP), comorbidity, diagnosis, endoscopic stigmata

• Resuscitate: IV access (2 large bore), bloods (FBC, coag, X-match), IV fluids, blood transfusion (Hb < 8 or hemodynamically unstable)
• OGD within 24h (emergency < 6h if hemodynamically unstable)
• PPI: High dose IV pre- and post-endoscopy
• Varices: Terlipressin (splanchnic vasoconstrictor), prophylactic antibiotics (ciprofloxacin/norfloxacin), urgent endoscopic band ligation or sclerotherapy; TIPS if uncontrolled
• Tranexamic acid: Not routinely recommended (HALT-IT trial negative)
• Target: Hb > 8 g/dL (restrictive transfusion better than liberal in most UGIB)

Lower GI Bleeding (LGIB) - Distal to Ligament of Treitz

• Diverticular disease (most common cause of massive LGIB)
• Colorectal cancer
• Colitis (ischemic, IBD, infective)
• Angiodysplasia (especially elderly)
• Hemorrhoids (most common overall cause of bright red rectal bleeding)
• Polyps

• Stable: Colonoscopy (diagnosis + treatment)
• Unstable: CT mesenteric angiography → embolization
• Persistent: Surgery (segmental colectomy)

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TOPIC 5: COLORECTAL CANCER (CRC)

Epidemiology & Risk Factors

• 3rd most common cancer worldwide; 2nd leading cause of cancer death
• Risk factors: Age > 50, family history, FAP (APC gene), HNPCC/Lynch syndrome (MLH1, MSH2 genes), IBD (especially UC), high red/processed meat diet, obesity, alcohol, smoking, low fiber diet

Adenoma-Carcinoma Sequence (Vogelstein model)

Pathology

• 90% adenocarcinoma
• Right colon (cecum/ascending): Iron deficiency anemia (occult bleeding), mass, weight loss; rarely obstruct
• Left colon (descending/sigmoid): Change in bowel habit, rectal bleeding, obstruction
• Rectum: Tenesmus, rectal bleeding, mucus

TNM Staging (Dukes' correlation)

Investigations

• Colonoscopy + biopsy (gold standard diagnosis)
• CT chest/abdomen/pelvis (staging)
• MRI pelvis (rectal cancer - local staging, circumferential resection margin)
• CEA (carcinoembryonic antigen) - not diagnostic; used for monitoring recurrence

Management

• Surgery (curative intent):
  • Right hemicolectomy (cecum/ascending)
  • Left hemicolectomy (descending)
  • Anterior resection (sigmoid/upper rectum)
  • Abdominoperineal resection (APR) - for low rectal cancer; permanent colostomy
• Neo-adjuvant chemoradiotherapy: For locally advanced rectal cancer (before surgery)
• Adjuvant chemotherapy: Stage III (lymph node positive); FOLFOX (5-FU + oxaliplatin)
• Metastatic CRC: FOLFOX/FOLFIRI ± targeted therapy (bevacizumab, cetuximab)
• Screening: Colonoscopy at 50 (or earlier if family history); stool FOB testing in population screening programs

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TOPIC 6: ACUTE PANCREATITIS

Causes ("I GET SMASHED")

• Idiopathic
• Gallstones (most common, ~45%)
• Ethanol/Alcohol (2nd most common, ~35%)
• Trauma
• Steroids
• Mumps/viral
• Autoimmune (IgG4-related pancreatitis)
• Scorpion venom, Snake bite
• Hyperlipidemia (hypertriglyceridemia > 1000 mg/dL), Hypercalcemia
• ERCP (post-procedural)
• Drugs (azathioprine, thiazides, valproate, tetracycline)

Pathophysiology

• Inappropriate activation of trypsin within acinar cells → autodigestion of pancreas → inflammation + necrosis

Clinical Features

• Severe epigastric pain radiating to back (band-like), relieved by leaning forward
• Nausea, vomiting, fever
• Tachycardia, hypotension (severe)
• Signs of severe disease:
  • Grey-Turner's sign: Flank bruising (hemorrhagic pancreatitis - 5-7 days)
  • Cullen's sign: Periumbilical bruising

Investigations

• Serum amylase > 3× upper limit (or lipase - more sensitive and specific, remains elevated longer)
• FBC, U&E, LFTs (raised LFTs suggest gallstone cause), glucose, Ca++, LDH
• CXR: Left pleural effusion (common)
• USS abdomen: Look for gallstones (cause)
• CECT abdomen (CT with contrast): After 48-72h if severe; gold standard for necrosis
  • Balthazar score/CT severity index

Severity Assessment - Glasgow/Ranson Criteria

• PaO2 < 8 kPa
• Age > 55
• Neutrophils/WBC > 15 × 10⁹/L
• Calcium < 2 mmol/L
• Renal: Urea > 16 mmol/L
• Enzymes: LDH > 600 U/L
• Albumin < 32 g/L
• Sugar: Glucose > 10 mmol/L

Management

• "Drip and Rest": Aggressive IV fluids (Hartmann's preferred), analgesia (opioids + NSAIDs), NBM initially, then early enteral nutrition
• Nasojejunal feeding (not TPN) preferred if unable to eat
• Do NOT use antibiotics routinely (no benefit for infected necrosis prevention in sterile pancreatitis)
• ERCP: If gallstone pancreatitis with cholangitis or biliary obstruction (within 72h)
• Infected pancreatic necrosis: Antibiotics (carbapenems), drainage (percutaneous or endoscopic); surgery (necrosectomy) as last resort
• Complications: Pancreatic necrosis, abscess, pseudocyst, ARDS, renal failure, DIC

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TOPIC 7: THYROID DISEASE & THYROID SURGERY

Thyroid Nodule Assessment

• USS + FNA (Fine Needle Aspiration Cytology): Bethesda classification
  • I: Non-diagnostic
  • II: Benign
  • III: AUS/FLUS (Atypia of undetermined significance)
  • IV: Follicular neoplasm
  • V: Suspicious for malignancy
  • VI: Malignant

Thyroid Cancer Types

• MEN2A: MTC + pheochromocytoma + hyperparathyroidism
• MEN2B: MTC + pheochromocytoma + marfanoid habitus + mucosal neuromas
• Caused by RET proto-oncogene mutations
• Prophylactic thyroidectomy based on mutation:
  • ATA-HST (M918T): Total thyroidectomy within first year of life
  • ATA-H (C634/A883F): By age 5 years
  • ATA-MOD (all others): Annual screening from age 5, thyroidectomy guided by calcitonin

Hyperthyroidism

• Graves' disease (most common): Autoimmune; TSH receptor-stimulating antibodies (TSI/TRAb); diffuse goiter + exophthalmos + pretibial myxedema
• Toxic multinodular goiter
• Toxic adenoma (Plummer's disease)
• Subacute thyroiditis (de Quervain's) - painful
• Factitious (excessive T4 ingestion)

• Antithyroid drugs: Carbimazole (propylthiouracil in pregnancy) - first line; monitor for agranulocytosis
• Beta-blocker (propranolol): Symptomatic relief
• Radioiodine (I-131): Definitive; contraindicated in pregnancy, active Graves' ophthalmopathy
• Surgery (total thyroidectomy): Large goiter, compression, malignancy, failed medical therapy
• Thyroid storm: IV propranolol, high-dose carbimazole, potassium iodide (Lugol's iodine), dexamethasone, supportive

Hypothyroidism

• Hashimoto's thyroiditis (most common in iodine-sufficient areas): Autoimmune; anti-TPO, anti-thyroglobulin antibodies
• Iodine deficiency (most common worldwide)
• Post-radioiodine/thyroidectomy
• Drug-induced: Amiodarone, lithium

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TOPIC 8: HERNIAS

Definition

Types of Abdominal Hernias

Terminology

• Reducible: Contents can be returned to cavity
• Irreducible (Incarcerated): Cannot be reduced; not necessarily ischemic
• Obstructed: Bowel herniated; obstruction but no ischemia
• Strangulated: Blood supply compromised → ischemia/necrosis → emergency

Inguinal Hernia

• Most common hernia type (75% of all hernias)
• Male > Female (indirect > direct)
• Indirect: More common, congenital, follows spermatic cord, can descend to scrotum
• Direct: Acquired, due to weakness; pushes through Hesselbach's triangle medially; does NOT descend to scrotum

• Groin swelling, aching discomfort
• Cough impulse present
• Indirect: Controlled by pressure at deep ring (mid-point of inguinal ligament)
• Direct: Returns on release of pressure; does not transilluminate

• Elective repair for symptomatic hernias
• Lichtenstein repair (open mesh): Gold standard open technique
• Laparoscopic repair (TEP/TAPP): Better for bilateral and recurrent hernias; less post-op pain; quicker return to work
• Strangulated hernia: Emergency surgery; bowel viability assessed; resect if non-viable

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TOPIC 9: SURGICAL PRINCIPLES - TRAUMA (ATLS)

Primary Survey - ABCDE

• Airway (with cervical spine control): Clear airway; jaw thrust (not head tilt if C-spine injury); intubation if needed; C-collar
• Breathing: Expose chest; look for life-threatening chest injuries (tension pneumothorax, open pneumothorax, massive hemothorax, flail chest, cardiac tamponade)
• Circulation (with hemorrhage control): 2 large-bore IV access; 2L IV crystalloid bolus; cross-match; control external bleeding (direct pressure); blood products early (1:1:1 = pRBC:FFP:platelets)
• Disability: GCS, pupils, glucose
• Exposure: Remove clothing + log-roll; prevent hypothermia

Immediately Life-Threatening Chest Injuries ("ATOM FC")

• Airway obstruction
• Tension pneumothorax → needle decompression (2nd ICS MCL) → chest drain
• Open pneumothorax → 3-sided dressing → chest drain
• Massive hemothorax → chest drain + IV fluids + surgical control
• Flail chest → analgesia + mechanical ventilation if failing
• Cardiac tamponade → pericardiocentesis → thoracotomy (Beck's triad: Low BP + raised JVP + muffled heart sounds)

Hemorrhage Shock Classification

Damage Control Surgery (DCS)

• For critically unstable patients
• Phase 1: Abbreviated surgery to control hemorrhage + contamination (packs, clamps, staples)
• Phase 2: ICU resuscitation (correct "lethal triad": Hypothermia, acidosis, coagulopathy)
• Phase 3: Definitive surgery when stable

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TOPIC 10: BREAST DISEASE

Breast Lumps - Triple Assessment

1. Clinical examination
2. Imaging: USS (< 35 yrs) or Mammography (> 35 yrs) or Both
3. Histology/Cytology: Core biopsy (preferred) or FNAC

Common Benign Conditions

• Fibroadenoma ("breast mouse"): Young women, highly mobile, smooth, firm; no treatment usually needed if confirmed
• Breast cyst: Perimenopausal women; USS + aspiration (if symptomatic)
• Fibrocystic change: Cyclical pain, nodularity
• Duct ectasia: Older women; nipple discharge (dark/green); periareolar
• Fat necrosis: Post-trauma; can mimic cancer on imaging

Breast Cancer

• Female sex, age > 50 (most cases)
• Family history (BRCA1 chromosome 17q, BRCA2 chromosome 13q mutations)
• BRCA1: Breast + ovarian + triple-negative
• BRCA2: Breast (male and female) + ovarian
• Early menarche, late menopause, nulliparity, late first pregnancy
• HRT (combined estrogen + progesterone)
• Previous breast cancer/DCIS/LCIS

• Ductal carcinoma in situ (DCIS): Pre-invasive; comedocarcinoma (central necrosis)
• Invasive ductal carcinoma (IDC/NST): 75-80%; most common invasive type
• Invasive lobular carcinoma (ILC): 10%; "Indian file" pattern on histology
• Inflammatory breast cancer: Peau d'orange skin, red/warm, no discrete lump; worse prognosis
• Paget's disease of nipple: Eczema-like nipple change; underlying ductal carcinoma

• T1 (< 2cm) → T2 (2-5cm) → T3 (> 5cm) → T4 (skin/chest wall invasion)
• N0-3 (lymph node status)
• M0/M1 (metastasis - most common sites: bone, lung, liver, brain)

• Wide local excision (WLE) + axillary surgery + radiotherapy = equivalent to mastectomy for early disease (NSABP B-06 trial)
• Mastectomy (simple or modified radical): For large tumors, multicentric disease, BRCA carriers; can add immediate reconstruction
• Axillary surgery: Sentinel lymph node biopsy (SLNB) first; axillary clearance if nodes positive

• ER+/PR+ (Hormone receptor positive): Tamoxifen (pre-menopausal: blocks estrogen receptor) OR aromatase inhibitor (post-menopausal: letrozole, anastrozole, exemestane, reduces estrogen synthesis)
• HER2+ (ERBB2 amplified): Trastuzumab (Herceptin) + pertuzumab + chemotherapy
• Triple negative (ER-/PR-/HER2-): Chemotherapy (no targeted therapy); BRCA-associated → PARP inhibitors

• FEC (5-fluorouracil + epirubicin + cyclophosphamide)
• Taxanes (docetaxel, paclitaxel)
• AC-T, FEC-T regimens

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TOPIC 11: VASCULAR SURGERY

Peripheral Arterial Disease (PAD)

• ABPI (Ankle-Brachial Pressure Index): Normal 0.9-1.3; Claudication 0.5-0.9; CLI < 0.5; Incompressible (calcified) > 1.4 (diabetics)
• Duplex Doppler USS: First-line
• CT angiography: Pre-operative planning
• MR angiography

• Risk factor modification: Stop smoking (most important single intervention), BP control, diabetes control, statins, aspirin
• Supervised exercise program (first line for claudication; 30-60 min, 3x/week)
• Clopidogrel (antiplatelet)
• Cilostazol (phosphodiesterase inhibitor): Improves claudication distance
• Revascularization (for CLI or disabling claudication):
  • Angioplasty ± stent (endovascular): First line for suitable lesions
  • Bypass surgery (surgical): For complex/occlusive disease; vein grafts preferred over prosthetic
• Amputation: For non-viable limb or failed revascularization

Abdominal Aortic Aneurysm (AAA)

• Symptomatic AAA (any size) - urgent
• Elective: Diameter ≥ 5.5 cm (men), ≥ 5.0 cm (women), or rapid expansion > 1 cm/year

• EVAR (Endovascular aneurysm repair): Less invasive, faster recovery; requires suitable anatomy (neck, iliac arteries); risk of endoleak, requires surveillance
• Open surgical repair: More durable; higher peri-operative mortality (3-5%)

• Classic triad: Severe back/abdominal pain + pulsatile mass + hypotension (shock)
• 80% mortality (hospital mortality 40-50%)
• Permissive hypotension (target SBP 50-70 mmHg until aorta clamped)
• Emergency EVAR or open repair

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SECTION 3: RAPID-REVIEW TABLE

Key Mnemonics & High-Yield Memory Aids

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Key Numbers to Remember (MEDICINE)

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Key Numbers to Remember (SURGERY)

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HOW TO USE THESE NOTES

• Braunwald's Heart Disease (CVS topics)
• Goldman-Cecil Medicine (internal medicine)
• Murray & Nadel's Respiratory Medicine (pulmonology)
• Bailey & Love's Short Practice of Surgery (surgery topics)
• Sabiston Textbook of Surgery (thyroid, vascular)
• Textbook of Family Medicine (DM, HF, common conditions)
• Grainger & Allison's Diagnostic Radiology (stroke imaging)
• Harrison's Principles of Internal Medicine 22E

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TOPICS COVERED

MEDICINE (10 Topics)

1. Heart Failure - HFrEF vs HFpEF, LV remodeling, NYHA, ABCD drugs, devices
2. Myocardial Infarction - STEMI/NSTEMI classification, ECG localization, biomarkers, management
3. Hypertension - Classification, secondary causes, ABCD drugs, hypertensive emergency
4. Diabetes Mellitus - Type 1 vs 2, DKA, HHS, microvascular/macrovascular complications, drug ladder
5. Pneumonia - CAP/HAP organisms, V/Q mismatch mechanism, CURB-65, antibiotic protocols
6. Pulmonary Embolism - Virchow's triad, D-dimer, CTPA, anticoagulation, thrombolysis
7. Stroke - Ischemic vs hemorrhagic, TIA, clinical syndromes, tPA window, thrombectomy
8. CKD - KDIGO staging, complications, CKD-mineral bone disease, RRT
9. Anemia - IDA, B12/folate, sickle cell disease (all complications + management)
10. Tuberculosis - AFB, RIPE regimen, side effects table, MDR-TB, latent TB

SURGERY (11 Topics)

1. Acute Abdomen & Appendicitis - Key causes, Alvarado score, laparoscopic appendicectomy
2. Intestinal Obstruction - SBO vs LBO, AXR findings, drip and suck, strangulation
3. Peptic Ulcer Disease - H. pylori, NSAIDs, Forrest classification, perforation (CXR), triple therapy
4. GI Bleeding - UGIB/LGIB causes, Rockall score, variceal management, terlipressin
5. Colorectal Cancer - Adenoma-carcinoma sequence, Dukes'/TNM staging, surgery types, adjuvant chemo
6. Acute Pancreatitis - I GET SMASHED, Glasgow criteria (PANCREAS), CECT, management
7. Thyroid Disease & Surgery - MEN2/RET mutations, prophylactic thyroidectomy timing, hypo/hyperthyroidism
8. Hernias - Direct vs indirect inguinal, Hesselbach's triangle, Lichtenstein repair, strangulation
9. ATLS Trauma - Primary survey ABCDE, ATOM FC chest injuries, shock classification table, DCS
10. Breast Disease - Triple assessment, BRCA1/2, receptor status, surgical options, adjuvant therapy
11. Vascular Surgery - PAD (Fontaine), ABPI values, AAA repair thresholds, ruptured AAA triad

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• Learn the key numbers tables by heart (both medicine and surgery sections at the end)
• For each topic, practice writing out the management steps from memory
• Focus on drugs + doses + side effects for medicine
• For surgery, know the investigations → management sequence clearly
• The mnemonics are tested frequently as MCQs and SAQ prompts

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MBBS FINAL PROF - COMPLETE ORTHOPAEDICS NOTES

All Topics | Detailed | Exam-Ready

Sources: Campbell's Operative Orthopaedics 15th Ed 2026, Bailey & Love's Short Practice of Surgery 28th Ed, Grainger & Allison's Diagnostic Radiology, Rosen's Emergency Medicine, Goldman-Cecil Medicine, Robbins Basic Pathology

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PART 1: FUNDAMENTALS OF ORTHOPAEDICS

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CHAPTER 1: BONE STRUCTURE & PHYSIOLOGY

Bone Composition

• Organic (35%): Type I collagen (90%), proteoglycans, non-collagen proteins (osteocalcin, osteonectin)
• Inorganic (65%): Hydroxyapatite [Ca10(PO4)6(OH)2] - gives rigidity and compressive strength

Bone Cells

Bone Types

• Cortical (compact) bone: Dense, outer shell; 80% of skeleton; slow turnover; provides strength
• Cancellous (trabecular/spongy) bone: Inner honeycomb; 20% of skeleton; faster turnover; metabolically active; found at epiphyses and vertebral bodies

Bone Remodeling (Wolff's Law)

• Bone remodels in response to mechanical stress - laid down along lines of force
• Remodeling unit (BMU): Osteoclasts resorb → osteoblasts form → net balance maintained
• Key regulators: PTH, Vitamin D, estrogen, cortisol, growth hormone, thyroid hormone
• RANK/RANK-L/OPG axis: Central to osteoclast activation
  • RANK-L (on osteoblasts/stromal cells) binds RANK (on osteoclast precursors) → osteoclast activation
  • OPG (osteoprotegerin) is a decoy receptor that blocks RANK-L → inhibits resorption

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CHAPTER 2: FRACTURES - GENERAL PRINCIPLES

Definition

Classification

By Skin Integrity

• Closed (simple): Skin intact
• Open (compound): Skin breached, bone communicates with external environment → infection risk

Gustilo-Anderson Classification of Open Fractures

• IV antibiotics (co-amoxiclav + gentamicin) within 1 hour of injury
• Photograph wound, cover with saline-soaked gauze
• Splint + NV assessment
• Debridement in theatre within 6 hours (highly contaminated) or within 24h (clean)

By Pattern

By Displacement

• Undisplaced: Bone ends in anatomical position
• Displaced: Described as:
  • Translation: Shift sideways (in AP or lateral plane)
  • Angulation: Direction of the apex/distal fragment
  • Rotation: Twist around long axis (clinical sign: rotational malalignment)
  • Shortening: Overlap of fragments
  • Distraction: Fragments pulled apart

Epiphyseal (Growth Plate) Fractures - Salter-Harris Classification

• Type II most common (75%)
• Type V worst prognosis (growth plate crushed)

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Fracture Healing (Bailey & Love / Grainger's Radiology)

Two Mechanisms

• Requires absolute stability + cortical apposition (no movement, no gap)
• NO callus formation
• Osteoclastic cutting cones cross fracture line → osteoblasts lay lamellar bone
• Achieved by: Compression plating (ORIF), interfragmentary screws

• Requires relative stability (some controlled movement at fracture site)
• Involves callus formation
• Perren's Strain Theory: Amount of interfragmentary strain determines tissue type:
  • Strain > 100% → Fibrous tissue (no healing)
  • Strain 10-100% → Fibrocartilage
  • Strain < 10% → Soft callus
  • Strain < 2% → Hard callus → Bone (mineralization)
  • "A little movement is good, too much is bad"

Stages of Indirect Fracture Healing

1. Inflammatory stage (Days 1-7):
   • Hematoma forms at fracture site
   • Inflammatory cells (PMNs → macrophages) infiltrate
   • Cytokines released: IL-1, IL-6, TNF-α, TGF-β, BMPs (bone morphogenetic proteins)
   • Clot acts as scaffold
2. Soft callus stage (Weeks 1-3):
   • Mesenchymal stem cell proliferation + differentiation
   • Woven bone and cartilage formed (enchondral ossification)
   • Fracture stabilizes clinically (no longer painful to move)
   • Callus visible on X-ray by 2-3 weeks
3. Hard callus stage (Weeks 3-12):
   • Cartilage mineralized and replaced by woven bone
   • Fracture radiologically healed (callus bridges the fracture)
4. Remodeling stage (Months to years):
   • Woven bone replaced by lamellar bone (Haversian systems)
   • Medullary canal re-established
   • Bone returns to near-normal shape (Wolff's Law)
   • Children remodel significantly; adults much less

Terminology

• Union: Healed clinically + radiologically; can bear physiological loads
• Delayed union: Not healed within expected time frame (no fixed definition)
• Non-union: Fracture has NOT healed AND has no potential to heal without intervention
  • Hypertrophic non-union: "Elephant foot" - adequate biology, inadequate stability; treat with stable fixation
  • Atrophic non-union: No callus, no biology; inadequate blood supply; treat with bone grafting + fixation
  • Infected non-union: Requires eradication of infection + fixation + bone graft
• Malunion: Fracture healed in abnormal position (angulation, rotation, shortening)

Factors Affecting Fracture Healing

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Fracture Management Principles ("3 Rs")

• Closed reduction: Manipulation under anesthesia (MUA)
• Open reduction (ORIF): Surgical exposure of fracture

• Early mobilization prevents complications (DVT, muscle wasting, pressure sores, joint stiffness)

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Complications of Fractures

Immediate (at time of injury)

• Vascular injury
• Nerve injury
• Visceral injury (e.g., bladder in pelvic fracture, urethra)
• Skin damage / open fracture

Early (hours to days)

• Compartment syndrome (see below)
• Infection (open fractures)
• Fat embolism
• DVT / PE
• Shock (especially long bone, pelvic fractures - large blood loss)

Late (weeks to months/years)

• Delayed union / Non-union / Malunion
• Avascular necrosis (AVN)
• Post-traumatic OA
• Complex regional pain syndrome (CRPS / Sudeck's atrophy)
• Myositis ossificans
• Growth disturbance (children)
• Stiffness / contractures
• Osteomyelitis

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CHAPTER 3: COMPARTMENT SYNDROME

Definition

Critical Pressure Thresholds

• Normal compartment pressure: 0-8 mmHg
• Critical pressure (Fasciotomy indicated):
  • Absolute: > 30 mmHg
  • OR within 30 mmHg of diastolic BP (Delta P = diastolic BP - compartment pressure < 30 mmHg) - more physiological criterion

Causes

• Most common: Long bone fracture (tibia most common site), crush injury
• Reperfusion injury (after arterial repair / revascularization of ischemic limb) - free radicals + lipid peroxidation + intracellular Ca++ influx → edema → raised compartment pressure
• Combined arterial + venous injury
• Tight plaster/bandage
• Burns
• Prolonged limb compression (unconscious patient)

Pathophysiology

• Edema (from fracture, bleeding, reperfusion) → raised compartment pressure → venous outflow obstructed → further edema → capillary perfusion pressure falls below tissue oxygen demand → ischemia → necrosis

"6 Ps" - Clinical Features (in order of appearance)

1. Pain out of proportion to injury (earliest + most sensitive sign)
2. Pain on passive stretch (most specific sign - stretch muscles in compartment)
3. Pressure (tense compartment on palpation)
4. Paresthesia (tingling/numbness - earliest neurological sign)
5. Paralysis (weakness - late sign; indicates significant nerve/muscle damage)
6. Pallor + Pulselessness (very late; irreversible damage likely already done)

Key point: Pulses may remain present even in compartment syndrome - do NOT wait for absent pulse before acting!

Compartments (by site)

• Leg (most common site): 4 compartments - anterior, lateral, posterior superficial, posterior deep
• Forearm: 3 compartments - volar, dorsal, mobile wad
• Foot: Multiple compartments
• Thigh: 3 compartments - anterior, posterior, medial
• Hand, gluteal: Can also occur

Investigations

• Clinical diagnosis - do not delay for investigations
• Compartment pressure measurement (Stryker device): Confirm if diagnosis uncertain
• Monitor all patients with significant fractures at risk

Treatment

• EMERGENCY FASCIOTOMY - all fascial compartments must be opened
• Release tight casts/dressings IMMEDIATELY as temporary measure
• Do NOT elevate limb above heart level (reduces perfusion pressure)
• Wounds left open; re-inspected at 48h
• Delayed primary closure or skin grafting
• Time is critical: Irreversible muscle necrosis occurs within 4-8 hours
• Missed compartment syndrome → Volkmann's ischemic contracture (forearm), equinus deformity (leg)

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PART 2: SPECIFIC FRACTURES & DISLOCATIONS

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CHAPTER 4: UPPER LIMB FRACTURES

4.1 Fractures of the Clavicle

• Most common: Middle 1/3 (80%)
• Mechanism: FOOSH (fall on outstretched hand) or direct blow to shoulder
• Clinical: Deformity, tenderness, arm held adducted
• Management:
  • Most: Broad arm sling for 4-6 weeks (conservative)
  • ORIF (plate fixation): Significant displacement, open fracture, vascular/nerve injury, threatened skin, bilateral, polytrauma
• Complications: Non-union (figure-of-8 bandage increases risk), malunion, subclavian vessel/brachial plexus injury

4.2 Shoulder Dislocation

• Anterior dislocation (95%): Most common joint dislocation in body
  • Mechanism: Forced abduction + external rotation (FOOSH, tackle in sport)
  • Subcoracoid position (most common subtype)
  • Clinical: Arm held abducted, loss of shoulder contour, prominent acromion, "sulcus sign"
  • Associated injuries:
    • Bankart lesion: Avulsion of anterior glenoid labrum (causes recurrence)
    • Hill-Sachs lesion: Posterior humeral head impaction fracture
    • HAGL lesion: Avulsion of inferior glenohumeral ligament
    • Axillary nerve injury: Test sensation over "regimental badge area" (lateral deltoid)
  • Reduction techniques: Kocher's, Hippocratic, Milch, scapular manipulation
  • Post-reduction: Sling 3-6 weeks; physiotherapy
  • Recurrence risk: Very high in young (< 25 years), athletic patients (> 80%)
  • Surgery (Bankart repair): For recurrent dislocations
• Posterior dislocation (rare, < 5%):
  • Mechanism: Epileptic seizure, electrocution, direct posterior blow ("Lightening stroke")
  • Clinical: Arm in internal rotation, cannot externally rotate, flattening of anterior shoulder
  • Often missed on AP X-ray! - Look for "Light bulb sign" (humeral head symmetrical)
  • Management: Reduce under GA; may need surgical stabilization

4.3 Proximal Humerus Fractures

• Common in elderly (osteoporotic)
• Neer classification (4 parts: greater tuberosity, lesser tuberosity, humeral head, humeral shaft)
• Management:
  • 1-2 part, undisplaced: Conservative (collar and cuff sling, mobilize early)
  • Displaced 2-4 part fractures: ORIF (locking plate) or Hemiarthroplasty/RSA (reverse shoulder arthroplasty) in elderly
• Complication: AVN of humeral head (especially 4-part fractures - all blood supply disrupted)

4.4 Shaft of Humerus Fractures

• Radial nerve injury in up to 18% (runs in spiral groove)
  • Signs: Wrist drop, loss of extension of fingers + thumb, loss of sensation first dorsal web space
  • Mostly neuropraxia; most recover within 3 months
• Management:
  • Conservative: Hanging arm cast or functional brace (most shaft fractures heal well)
  • ORIF: Open fractures, vascular injury, polytrauma, pathological, bilateral, radial nerve injury at exploration

4.5 Supracondylar Fracture of Humerus

• Most common elbow fracture in children (peak age 5-8 years)
• Mechanism: FOOSH with hyperextension (extension type - 95%)
• Extension type most common: Distal fragment displaced posteriorly
• Critical neurovascular structures at risk:
  • Anterior interosseous nerve (AIN) branch of median nerve: Most commonly injured; tests: "OK sign" - flex thumb IP joint + flex index DIP joint; cannot make "OK" sign
  • Radial nerve: Less common
  • Brachial artery: Antecubital fossa; risk of vascular injury
• Baumann's angle on AP X-ray (angle between long axis of humerus and capitellar physeal line): Normal ~70-75°; use to assess angulation
• Fat pad signs: Anterior fat pad elevation (normal can be seen) + posterior fat pad (sail sign) = pathological = hemarthrosis = fracture until proven otherwise

• Cubitus varus ("gunstock deformity"): Malunion with medial angulation; cosmetic problem; corrective osteotomy if severe
• Volkmann's ischemic contracture (from compartment syndrome/vascular injury)
• Myositis ossificans

4.6 Colles' Fracture

• Most common fracture in adults (> 40 years, post-menopausal women)
• Mechanism: FOOSH with wrist extended + supinated
• Site: Distal radius fracture < 3 cm from articular surface

• Dorsal displacement + dorsal angulation of distal fragment
• Radial shortening + radial deviation
• Supination deformity

• Dorsal tilt (normal 11° volar tilt → reversed to dorsal)
• Radial height loss
• Radial inclination reduced (normally 23°)

• Undisplaced: POP backslab × 6 weeks
• Displaced: Closed reduction (MUA) under haematoma block + below elbow plaster × 6 weeks
  • Mnemonics for reduction: Disimpact → Hyperflex → Ulnar deviate → Pronate
• Unstable/intra-articular: ORIF with volar locking plate (preferred for active patients)

• Malunion (most common complication)
• Median nerve injury (carpal tunnel syndrome)
• Rupture of extensor pollicis longus (EPL) tendon
• CRPS/Sudeck's atrophy
• Stiffness

• Volar displacement of distal fragment ("garden spade deformity")
• Mechanism: Fall on flexed wrist
• Usually needs ORIF (volar locking plate) - unstable

4.7 Scaphoid Fracture

• Most common carpal bone fracture (70% of carpal fractures)
• Most common in young males (20-30 years)
• Mechanism: FOOSH with wrist extended and radially deviated

• Blood supply enters distally → waist and proximal pole fractures risk AVN
• Proximal pole fracture: Highest AVN risk (100% of blood supply at risk)
• Waist fracture: 70-80% of scaphoid fractures; intermediate AVN risk
• Distal pole: Lowest AVN risk

• Anatomical snuffbox tenderness (between EPL + ECRL/ERCB tendons at base of thumb)
• Tenderness over scaphoid tubercle
• Pain on axial compression of thumb

• Suspect scaphoid fracture clinically even with normal X-ray
• Repeat X-ray in 10-14 days (OR CT scan for early definitive diagnosis)
• MRI: Most sensitive (can diagnose day 1)

• Undisplaced waist: Below elbow POP (scaphoid cast, thumb included) × 8-12 weeks
• Displaced (> 1mm), proximal pole, unstable: Percutaneous headless compression screw (Herbert screw) (ORIF) → faster return to sport/work
• Established non-union: Bone grafting (Russe graft) ± fixation

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CHAPTER 5: LOWER LIMB FRACTURES

5.1 Hip (Proximal Femur) Fractures

• Extremely common in elderly (osteoporotic); major source of morbidity and mortality
• 1-year mortality: ~30% (hip fracture surgery reduces but doesn't eliminate mortality)
• Mechanism: Low-energy fall (in elderly); high-energy trauma (in young)

Classification (by anatomical region)

• Surgery within 36-48 hours (unless medically unfit; delay increases mortality/complications)
• Hemiarthroplasty: Replaces femoral head only; cemented preferred in elderly
• Total Hip Replacement (THR/THA): For displaced intracapsular in active, cognitively intact elderly with pre-existing OA
• DHS (Dynamic Hip Screw): Lag screw in femoral head + side plate; allows sliding/controlled collapse → compression at fracture site; for intertrochanteric fractures
• Cephalomedullary nail: IM nail + proximal screw into femoral head; for subtrochanteric and unstable intertrochanteric fractures

• AVN of femoral head (intracapsular fractures)
• Non-union
• Implant failure
• Venous thromboembolism (DVT/PE) - high risk → chemical + mechanical prophylaxis
• Pressure sores
• Pneumonia, UTI, delirium (in elderly)
• Periprosthetic fracture (after arthroplasty)

5.2 Femoral Shaft Fractures

• Significant energy required in young; low energy in elderly/osteoporotic
• Large blood loss: 1-1.5 liters into thigh (can cause shock)
• Classification: Winquist (degree of comminution)
• Management: Locked intramedullary nail (gold standard)
  • Load-sharing device; allows early mobilization
  • Static locking prevents rotation and shortening
• Complications: Fat embolism, neurovascular injury, malrotation, non-union

5.3 Tibial Shaft Fractures

• Most common long bone fracture
• Mechanism: Direct blow, road traffic accident, twisting
• Compartment syndrome - highest risk in tibial shaft fractures
• Management:
  • Isolated, stable: Long leg cast or functional brace
  • Displaced/unstable: Intramedullary tibial nail (gold standard)
  • Open fractures: External fixator initially; convert to nail when wounds clean

5.4 Ankle Fractures

• Bony tenderness at posterior edge of distal 6 cm of fibula OR malleolar zone AND unable to walk 4 steps at scene + in ED → X-ray indicated
• Apply also to foot (navicular, 5th metatarsal base) → Ottawa Foot Rules

5.5 Calcaneum Fractures

• Usually high-energy (fall from height); axial loading
• Associated with: Vertebral compression fractures (10%), contralateral calcaneal fracture, spinal + pelvic injuries
• Bohler's angle: Normal 20-40°; reduced in calcaneal fracture
• Management:
  • Undisplaced: Plaster + non-weight bearing × 6-8 weeks
  • Displaced (Sanders classification): ORIF (delayed 10-14 days for swelling to settle)
• Complications: Subtalar OA, peroneal tendon impingement, malunion, chronic pain

5.6 Pelvic Fractures

• High-energy injuries (RTA, fall from height)
• Life-threatening hemorrhage risk (retroperitoneal): Can lose > 2 liters
• Associated injuries: Bladder (10%), urethra (5% - males > females), bowel, sacral nerve roots

• Type A: Stable; posterior arch intact (pubic ramus fractures, acetabular)
• Type B: Rotationally unstable; vertically stable (open book/compression injuries)
• Type C: Rotationally AND vertically unstable (shear injuries)

• Immediate: ATLS → IV access → blood transfusion, pelvic binder (emergent hemorrhage control)
• Pelvic binder: Applied at trochanters (NOT iliac crests)
• Interventional radiology: Angioembolization for persistent hemorrhage
• External fixator: Emergency damage control
• Definitive: ORIF for unstable fractures (delayed 5-7 days)

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CHAPTER 6: SPINAL INJURIES

Anatomy Review

• Vertebral column: 7 cervical, 12 thoracic, 5 lumbar, 5 sacral (fused), 4 coccygeal
• Spinal cord ends at L1-L2 (conus medullaris)
• Below L2: Cauda equina (collection of nerve roots)

Denis Three-Column Model (for stability)

• Stable fracture: Only ONE column disrupted
• Unstable fracture: TWO or more columns disrupted

Cervical Spine Injuries

• Flexion, extension, axial compression, rotation, distraction

1. Jefferson Fracture (C1 burst fracture): Axial loading → blowout of C1 ring (4-point fracture); usually stable if transverse ligament intact; "rule of Spence" on open-mouth X-ray
2. Odontoid (Dens) Fracture (C2):
   • Type I: Tip of dens (rare, stable)
   • Type II: Base of dens - most common and highest non-union risk; often needs fixation
   • Type III: Through body of C2 - usually heals in halo
3. Hangman's Fracture (C2 traumatic spondylolisthesis): Bilateral C2 pedicle fractures; hyperextension + distraction; paradoxically often neurologically intact
4. Teardrop Fracture: Hyperflexion; anterior inferior corner avulsion + severe posterior element disruption; HIGH cord injury risk (most dangerous cervical fracture mechanism)
5. Clay-Shoveler's Fracture: Avulsion of spinous process (C6/C7); stable; benign
6. Facet Dislocation: Unilateral (rotational injury, 25% subluxation on lateral X-ray, nerve root injury) or bilateral (pure flexion, 50% subluxation, often cord injury)

• No midline tenderness
• No focal neurological deficit
• Normal alertness
• No intoxication
• No distracting painful injury

Spinal Cord Injury (SCI)

• Complete injury: No preservation of motor OR sensory at S4-S5 (perianal sensation, voluntary anal contraction)
• Incomplete injury: Some preservation below level - better prognosis

• Immediate flaccid paralysis + loss of all reflexes below injury level
• Lasts hours to days after injury
• Bulbocavernosus reflex return = end of spinal shock (S3-S4 arc; squeeze glans penis → anal sphincter contracts)

• Loss of sympathetic outflow → peripheral vasodilation + loss of cardiac acceleration
• Hypotension + bradycardia (distinguishes from hypovolemic shock)
• Treatment: IV fluids ± vasopressors (noradrenaline); avoid aggressive fluid overload

Management of SCI

• Primary survey (ATLS) - suspect SCI in any trauma with neck pain, unconsciousness, or mechanism
• Immobilize C-spine (rigid collar + blocks + tape - "triple immobilization")
• Avoid secondary injury: Maintain MAP > 85-90 mmHg for first 7 days (spinal perfusion pressure)
• Methylprednisolone: No longer routinely recommended (controversy; NASCIS trials)
• Surgical decompression: Urgent (< 24h) for incomplete injuries with worsening neurology
• Rehabilitation: Multidisciplinary; physiotherapy, occupational therapy, psychology, social work

Disc Disease & Degenerative Spine

• Most common levels: L4-L5 (L5 nerve root) and L5-S1 (S1 nerve root) → 95% of lumbar disc herniations
• Cervical: C5-C6 and C6-C7 most common

• Back pain radiating to leg (radiculopathy / sciatica)
• Dermatomal sensory loss
• Myotomal weakness
• Diminished/absent reflexes
• Positive straight leg raise (SLR/Lasegue's test): Pain reproduced < 60° (L4/L5/S1 root)
• Crossed SLR: More specific for large central/sequestered disc

• Large central L4-L5 disc compresses multiple cauda equina roots
• Features: Bilateral sciatica + saddle anesthesia (S3-S5) + bladder/bowel dysfunction (retention or incontinence) + sexual dysfunction
• Urgent MRI + emergency surgical decompression (within 24-48h)
• Delay → permanent incontinence

• Age < 20 or > 55 (new onset)
• History of cancer
• Night pain / pain at rest
• Weight loss, fever (infection/tumor)
• Saddle anesthesia, bladder/bowel dysfunction
• Bilateral neurological symptoms
• Thoracic back pain (uncommon; think tumor, infection)

1. Conservative (90% improve within 6 weeks): NSAIDs, physiotherapy, activity modification, epidural steroid injection
2. Surgical (microdiscectomy / discectomy): If:
   • Cauda equina syndrome (emergency)
   • Progressive neurological deficit
   • Failed 6-12 weeks conservative treatment with persistent radiculopathy

• Narrowing of spinal canal (central) or neural foramina (lateral) due to degenerative changes
• Neurogenic claudication (bilateral leg pain/weakness on walking; relieved by sitting/forward flexion - "shopping trolley sign")
• Distinguishes from vascular claudication: Neurogenic - relieved by stopping + sitting; vascular - relieved by stopping alone
• Management: Conservative first; decompressive laminectomy if conservative fails

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PART 3: JOINT DISEASES

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CHAPTER 7: OSTEOARTHRITIS (OA)

Definition

Classification

• Primary OA: No identifiable cause; genetic + age-related; more common in women
  • Typical distribution: Hands (DIP joints → Heberden's nodes, PIP joints → Bouchard's nodes, CMC joint of thumb), hips, knees, 1st MTP joint, apophyseal joints of spine
• Secondary OA: Identifiable underlying cause:
  • Trauma (most common secondary cause - post-traumatic OA)
  • Metabolic: Hemochromatosis, Wilson's disease, ochronosis (alkaptonuria)
  • Endocrine: Acromegaly, hypothyroidism, hyperparathyroidism, diabetes
  • Crystal deposition: CPPD, gout
  • Inflammatory arthritis: RA, AS
  • Paget's disease, bone/joint dysplasias

Pathology

• Loss of articular cartilage (chondrocyte dysfunction + matrix degradation by MMPs)
• Subchondral bone exposed → eburnation (ivory-like hardening)
• Subchondral bone cysts (synovial fluid forced into bone)
• Osteophyte formation (periosteal bone overgrowth at margins)
• Synovial thickening (reactive)
• Loss of joint space

Radiological Features (X-ray) - "LOSS" or "4 Signs of OA"

1. Loss of joint space (narrowing - uniform in OA; asymmetric)
2. Osteophytes (bony spurs at joint margins)
3. Subchondral sclerosis (increased density in bone adjacent to cartilage loss)
4. Subchondral cysts (translucent areas in subchondral bone)

Clinical Features

• Deep, aching joint pain - worse with activity, better with rest (early); later continuous pain
• Morning stiffness < 30 minutes (> 45 min suggests inflammatory arthritis)
• Joint swelling (effusion, osteophytes)
• Crepitus on movement
• Decreased range of motion
• Bony enlargement (Heberden's/Bouchard's nodes)
• Varus/valgus deformity (knee OA)
• Antalgic gait

Management

Non-Pharmacological

• Weight loss (each kg of weight loss = 4 kg less force on knee)
• Exercise (low impact: swimming, cycling, hydrotherapy)
• Physiotherapy + strengthening
• Walking aids, orthoses, bracing

Pharmacological

1. Topical NSAIDs + topical capsaicin (first line for knee/hand OA)
2. Paracetamol (limited evidence; used cautiously)
3. Oral NSAIDs (ibuprofen, diclofenac, naproxen) - with PPI gastroprotection
4. Intra-articular corticosteroid injection (short-term relief, 4-8 weeks)
5. Intra-articular hyaluronic acid (viscosupplementation): Variable evidence
6. Duloxetine: For OA pain with central sensitization

Surgical

• Total Joint Replacement (TJR): Gold standard for end-stage OA
  • Total Knee Replacement (TKR): Prosthetic tibiofemoral + patellar components
  • Total Hip Replacement (THR): Prosthetic acetabular cup + femoral stem/head
  • Indications: Severe pain unresponsive to conservative treatment, significant functional limitation, X-ray evidence of joint space loss
  • NICE criteria: Radiographic OA + severe pain + impaired QoL + failed conservative treatment ≥ 3 months
• High Tibial Osteotomy (HTO): Unilateral medial compartment knee OA in young active patients; realigns load to lateral compartment
• Arthroscopic debridement/lavage: NOT recommended for OA (no benefit over sham surgery - Moseley RCT)
• Joint fusion (arthrodesis): Small joints (wrist, ankle, MTP); eliminates pain but sacrifices motion
• Core decompression: Early AVN of femoral head

Knee OA - Special Points

• Medial compartment most commonly involved → varus deformity
• "Medial joint line pain + bony crepitus + varus deformity = knee OA"
• X-ray: Weight-bearing views mandatory (non-WB misses joint space narrowing)

Hip OA - Special Points

• Groin/buttock/thigh pain (referred to knee in 20%)
• Loss of internal rotation first (capsular pattern)
• Trendelenburg gait (abductor weakness)
• Limb shortening (in end-stage)

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CHAPTER 8: RHEUMATOID ARTHRITIS (RA) - Orthopaedic Aspects

Pathology

• Autoimmune; synovial inflammation → pannus formation → articular cartilage destruction → joint destruction

Orthopaedic Features

• Ulnar drift at MCPJs
• Swan neck deformity: PIP hyperextension + DIP flexion (intrinsic muscle tightness)
• Boutonniere deformity: PIP flexion + DIP hyperextension (central slip rupture)
• Rheumatoid nodules (extensor surface, olecranon)
• Z-thumb deformity
• Carpal tunnel syndrome (median nerve compression)

• Forefoot valgus, hallux valgus
• Clawing of toes (MTPJ subluxation)

• Atlanto-axial instability (AAI): Odontoid process subluxation anteriorly due to transverse ligament destruction → risk of cord compression
  • Screen with flexion/extension C-spine X-rays
  • Pre-operative assessment MANDATORY before general anesthesia (neck movement during intubation can cause cord injury)
  • Treatment: Posterior C1-C2 fusion (Magerl/Goel-Harms technique)

Drug-Related Surgical Considerations

• Methotrexate: Continue perioperatively (stopping increases disease flare)
• DMARDs/Biologics: Generally stop 1-2 half-lives before surgery (infection risk)
• Steroids: Continue; stress dose if on long-term steroids (adrenal suppression)

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CHAPTER 9: SEPTIC ARTHRITIS

Definition

Organisms

• Staphylococcus aureus: Most common at all ages; most virulent
• Kingella kingae: Children under 5; previously underdiagnosed; presents with near-normal inflammatory markers
• Neisseria gonorrhoeae: Sexually active young adults (most common cause of septic arthritis in this age group)
• Streptococcus: Any age
• Gram-negative organisms (Pseudomonas, Enterococcus): Elderly, IV drug users, immunocompromised
• Salmonella: Sickle cell disease patients

Pathogenesis

• Haematogenous seeding (most common): Bacteria seed joint from bloodstream
• Direct inoculation: Trauma, joint aspiration, surgery
• Contiguous spread: From adjacent osteomyelitis
• Destruction mechanism: Bacterial toxins + host neutrophil proteases + cytokines → cartilage destruction within 24-48 hours → irreversible damage

Clinical Features

• Hot, swollen, painful joint with restricted range of motion (all movements painful)
• Fever, malaise, elevated inflammatory markers (ESR, CRP, WBC)
• Patient holds joint in position of least capsular tension:
  • Hip: Flexed, abducted, externally rotated
  • Knee: Slightly flexed
• Key: Pain on ANY passive motion (distinguishes from cellulitis where pain on weight-bearing only)

Kocher Criteria (Septic Arthritis vs Transient Synovitis in Children)

• 4 criteria: 99.6% probability of septic arthritis
• 0 criteria: < 0.2% probability

Investigations

• Joint aspiration (arthrocentesis) - most important investigation
  • Send: MC&S (Gram stain + culture), cell count, glucose, protein, crystals
  • WBC > 50,000/mm³ suggests septic arthritis (but overlap with crystal arthropathy)
  • WBC > 100,000 strongly suggests infection
  • Glucose low (compared to plasma)
• Blood cultures (positive in 50%)
• FBC, ESR, CRP
• X-ray (baseline; early changes: widened joint space; late: joint destruction, osteomyelitis)
• MRI: For adjacent osteomyelitis, complex joints (hip in children), poor clinical progress
• USS hip: Child with suspected septic hip - confirm effusion and guide aspiration

Management - SURGICAL EMERGENCY (act within hours)

1. Joint washout (arthrotomy or arthroscopic) + drainage + debridement
   • Hip: Open arthrotomy (urgent)
   • Knee, shoulder, wrist: Arthroscopic washout preferred
2. IV antibiotics (start after joint aspiration, not before):
   • Empirical: IV flucloxacillin (+ gentamicin if at risk for gram-negatives)
   • MRSA risk: IV vancomycin
   • IV for 2 weeks then oral for 4+ weeks (total 4-6 weeks)
3. Splinting in functional position
4. Regular re-aspiration/lavage if not improving

Complications (if delayed treatment)

• Avascular necrosis (especially in hip, from raised intra-articular pressure)
• Cartilage destruction → Post-infective OA
• Growth disturbance in children
• Osteomyelitis (contiguous spread)
• Chronic infection / sinuses

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CHAPTER 10: OSTEOMYELITIS

Routes of Infection

1. Haematogenous (most common in children): Blood-borne seeding
2. Direct inoculation: Open fracture, surgery, penetrating injury
3. Contiguous spread: From adjacent soft tissue infection or septic arthritis

Why Metaphysis in Children?

• Rich, sluggish blood supply in metaphyseal sinusoids → bacteria seed and proliferate
• Absence of phagocytic lining cells in metaphyseal sinusoids
• In neonates/infants: Metaphyseal vessels penetrate growth plate → joint involvement (higher risk of septic arthritis + growth disturbance)

Organisms by Patient Group (Grainger's Radiology)

Pathology

• Bony edema → vascular congestion → thrombosis of small vessels → devascularized bone
• Pus accumulates: Elevates periosteum → subperiosteal abscess → soft tissue involvement

• Sequestrum: Dead devascularized bone (nidus of infection)
• Involucrum: New periosteal bone formation surrounding sequestrum
• Cloaca: Holes in involucrum through which pus discharges
• Sinus tract: Chronic discharging track to skin surface
• Brodie's abscess: Subacute/chronic osteomyelitis; well-defined lytic lesion with sclerotic rim on X-ray; commonly in proximal tibia; most common in adolescents

Clinical Features

• Fever, malaise, severe limb pain
• Localized tenderness, warmth, swelling (over metaphysis usually)
• Restricted movement of adjacent joint
• May appear septic/toxic (especially in young children)

• Persistent/recurrent discharge through sinuses
• Low-grade pain, swelling, thickening of bone
• Intermittent acute exacerbations

Investigations

• Blood cultures: Positive in 50% of acute cases
• FBC, CRP, ESR: Leukocytosis, elevated inflammatory markers
• X-ray: Normal for first 7-14 days; then soft tissue swelling → cortical irregularity/bony destruction → periosteal reaction
• MRI (gold standard): Highest sensitivity + specificity; shows bone marrow edema, subperiosteal abscess, soft tissue involvement; penumbra sign in subacute osteomyelitis
• Bone scan (Tc-99m MDP): Sensitive early; good for multifocal disease
• USS: Quick, bedside; detects subperiosteal abscess in children; guides aspiration
• CT: Defines cortical destruction, sequestra; pre-operative planning

Management

1. IV antibiotics (after blood cultures, aspirate if possible):
   • Empirical: IV flucloxacillin (+ gentamicin if < 3 months or gram-negative risk)
   • IV 2 weeks → oral 4 weeks (minimum 4-6 weeks total)
   • MRSA: IV vancomycin
2. Surgical drainage: If:
   • No improvement within 24-48h of antibiotics
   • Subperiosteal abscess on imaging
   • Adjacent septic arthritis
   • Neurological compression (spinal)

• Sequestrectomy (remove sequestrum), saucerization (remove involucrum/dead bone + open to allow drainage)
• Wound management (VAC dressing)
• Prolonged antibiotics (often 3-6 months; guided by bone biopsy culture)
• Bone grafting for defects
• Soft tissue coverage (flaps)
• Ilizarov technique (bone transport) for massive bone defects

Cierny-Mader Classification (Chronic Osteomyelitis)

Pott's Disease (Tuberculous Spondylitis)

• TB of the spine; most common form of skeletal TB
• Most common: Lower thoracic + upper lumbar
• Vertebral body destruction → disc space loss → vertebral collapse → gibbus deformity (angular kyphosis)
• Paravertebral abscess → psoas abscess (tracks to groin)
• Spinal cord compression (Pott's paraplegia)
• Investigations: MRI (gold standard), ESR, biopsy
• Treatment: Anti-TB chemotherapy (RIPE × 12-18 months) + surgical drainage/decompression/fusion if:
  • Spinal instability
  • Progressive neurological deficit
  • Large abscess
  • Diagnostic uncertainty

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PART 4: METABOLIC BONE DISEASE

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CHAPTER 11: OSTEOPOROSIS

Definition

Diagnosis (WHO - DXA Scan T-score)

Risk Factors (FRAX tool)

• Age (most important)
• Female sex (estrogen deficiency post-menopause - accelerated bone loss)
• Low BMI
• Family history of hip fracture
• Previous fragility fracture
• Secondary causes: Long-term steroids (most common secondary cause), hypogonadism, alcohol, malabsorption (celiac), inflammatory disease (RA), CKD, hyperthyroidism/hyperparathyroidism
• Smoking
• Glucocorticoids (current or recent use > 3 months)

Common Osteoporotic Fractures (WRIST, SPINE, HIP, SHOULDER)

• Distal radius (Colles') - age 50-60
• Vertebral compression fractures - age 60-70 (most common osteoporotic fracture overall)
• Hip (proximal femur) - age > 70 (highest morbidity/mortality)
• Proximal humerus

Management

• Weight-bearing exercise
• Fall prevention (home hazard assessment, occupational therapy, physiotherapy)
• Calcium 1000-1200 mg/day (dietary preferred) + Vitamin D 800-1000 IU/day

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CHAPTER 12: RICKETS & OSTEOMALACIA

Definition

• Rickets: Defective mineralization of the growing skeleton (children - affects growth plates)
• Osteomalacia: Defective mineralization of adult bone matrix (osteoid accumulates)

Causes

• Vitamin D deficiency (most common worldwide): Inadequate sunlight, poor diet, malabsorption (celiac, short bowel), chronic liver/renal disease, drugs (anticonvulsants)
• Calcium deficiency: Rare
• Phosphate deficiency: X-linked hypophosphatemic rickets (PHEX gene mutation) - most common genetic rickets
• Renal osteodystrophy: CKD → reduced 1α-hydroxylase activity → low calcitriol
• Vitamin D-resistant rickets: Mutations in VDR, CYP27B1

Biochemistry

Clinical Features of Rickets (Children)

• Bone deformities: Bow legs (genu varum) or knock knees (genu valgum), saber tibia
• Rachitic rosary: Widened, beaded costochondral junctions
• Harrison's sulcus: Groove along lower ribs (diaphragm pull on soft ribs)
• Frontal bossing: Enlarged frontal bones
• Craniotabes: Softened skull (ping-pong ball sensation)
• Widened wrist epiphyses (cupping + fraying of metaphyses on X-ray)
• Delayed fontanelle closure
• Hypotonia, delayed walking
• Dental hypoplasia, dental caries

Clinical Features of Osteomalacia (Adults)

• Bone pain and tenderness (diffuse, back, hips, ribs)
• Proximal muscle weakness (difficulty climbing stairs)
• Looser's zones (pseudofractures): Symmetrical lucent bands perpendicular to cortex (pathognomonic of osteomalacia); common in scapula, femoral neck, pubic rami, ribs
• Waddling gait
• Fragility fractures

X-ray in Rickets

• Cupping, fraying, widening of metaphyses (especially distal radius, knee)
• Looser's zones (adolescents/adults)
• Reduced bone density

Management

• Nutritional D deficiency: Cholecalciferol (Vitamin D3) high-dose loading then maintenance; calcium supplementation
• X-linked hypophosphatemia: Phosphate + calcitriol (NOT vitamin D alone - requires PHEX correction); now burosumab (anti-FGF23 antibody) for children and adults
• Renal osteodystrophy: 1α-calcitriol (active vitamin D; bypasses defective hydroxylation in kidney)

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CHAPTER 13: PAGET'S DISEASE OF BONE

Definition

Epidemiology

• Common in Europeans > 55 years; M = F; incidence increasing with age
• UK prevalence ~2-3% in > 55 years

Pathology

• Abnormal osteoclasts (larger, more nuclei, increased activity)
• Rapid but disorganized bone formation → woven bone (not lamellar)
• Bone is larger, more vascular, structurally weaker

Clinical Features

• Often asymptomatic (incidental finding on X-ray or elevated ALP)
• Bone pain (deep, aching)
• Bone deformity: Bowing of tibia ("sabre tibia"), enlarged skull
• Warmth over bone (hypervascular bone)
• Deafness (compression of CN VIII in skull base)
• Pathological fractures (especially femur - "banana fractures" - transverse through deformed bone)
• Sarcomatous change (osteosarcoma): Rare (< 1%), but major complication; suspect if sudden increase in pain + ALP

Investigations

• Elevated alkaline phosphatase (ALP) (bone fraction) - key marker; reflects osteoblast activity
• Normal calcium + phosphate (usually)
• X-ray: Osteoporosis circumscripta (lytic phase in skull), "cotton wool" skull (blastic), "blade of grass" lytic advancing edge in long bone, bowing, cortical thickening
• Bone scan: Localize extent (whole body) - areas of intense uptake

Management

• Bisphosphonates (zoledronate first choice - single IV infusion, durable response; or oral risedronate):
  • Inhibit osteoclasts → normalize bone turnover
  • Target: Normalize ALP
• Analgesia (NSAIDs for pain)
• Surgery for: Fractures, joint replacement for OA secondary to Paget's, decompression of nerves, corrective osteotomy for severe deformity, resection for sarcomatous change

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PART 5: BONE TUMORS

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CHAPTER 14: CLASSIFICATION OF BONE TUMORS

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CHAPTER 15: SPECIFIC BONE TUMORS

15.1 Osteosarcoma

• Most common primary malignant bone tumor (excluding myeloma)
• Age: Bimodal - peak in adolescence (10-20 years; related to rapid bone growth) and > 60 years (Paget's/irradiation-related)
• Location: Metaphysis of long bones; distal femur (most common) > proximal tibia > proximal humerus
  • "Sunburst" pattern around knee
• Codman's triangle: Periosteal reaction - periosteum lifted by tumor → triangular reactive bone
• Sunburst/Sunray appearance: Spiculated periosteal reaction (new bone along vessels)
• Histology: Malignant osteoblasts producing osteoid
• Staging: Enneking system (Grade + Compartment + Metastasis)

• Pain + swelling around knee (most common site)
• Local warmth, tenderness
• Pathological fracture (late)
• Metastases: Lung (most common - "cannon ball" metastases on CXR)

• X-ray (bone destruction + periosteal reaction)
• MRI (local staging, extent in bone, soft tissue involvement)
• CT chest (lung metastases)
• Bone scan (skip lesions, multifocal)
• Biopsy (trucut/core biopsy - through planned excision window)
• LDH and ALP elevated (markers of disease activity)

• Neoadjuvant chemotherapy → limb-salvage surgery (wide excision + reconstruction) → adjuvant chemotherapy
• Chemotherapy: MAP regimen (Methotrexate + Adriamycin/doxorubicin + Cisplatin)
• Assess chemotherapy response: % tumor necrosis on resected specimen (> 90% necrosis = good response = good prognosis)
• Limb salvage (> 90% of cases now): Endoprosthesis (modular implant), allograft, rotationplasty
• Amputation: If adequate margins cannot be achieved with limb salvage
• 5-year survival: ~70% if localized; ~20% if metastatic at presentation

15.2 Ewing's Sarcoma

• Second most common primary malignant bone tumor in children/young adults
• Age: 5-25 years; slightly more common in males
• Location: Diaphysis of long bones (femur most common); flat bones (pelvis, ribs, scapula)
• "Onion skin" periosteal reaction (layers of periosteal new bone) - classic appearance
• Histology: Small round blue cells; t(11;22) translocation → EWS-FLI1 fusion gene (pathognomonic); positive for CD99 (MIC2)
• Highly aggressive; metastasizes early (lung + bone)

• Pain + swelling
• Fever, elevated ESR (can mimic osteomyelitis)
• Hot, tender swelling
• Systemic symptoms (weight loss, malaise)

• Chemotherapy + local treatment (surgery or radiotherapy) + adjuvant chemotherapy
• VIDE protocol (vincristine, ifosfamide, doxorubicin, etoposide)
• Surgery if resectable (limb salvage)
• Radiotherapy (highly radiosensitive): If surgery not possible
• 5-year survival: ~65-70% localized; ~30% metastatic

15.3 Chondrosarcoma

• Most common in adults (40-70 years); M > F
• Location: Central (medullary) in axial skeleton (pelvis most common site), femur, humerus
• Arises de novo (primary) OR from malignant transformation of enchondroma/osteochondroma (secondary)
• Radiosensitive and chemoresistant: Surgery only curative treatment
• Management: Wide surgical excision; no chemotherapy benefit
• Prognosis depends on grade:
  • Grade 1 (low): Rarely metastasizes; 90% 5-yr survival
  • Grade 3 (high): Aggressive; 30% 5-yr survival

15.4 Giant Cell Tumor (GCT) of Bone

• Locally aggressive, rarely malignant
• Age: 20-40 years (skeletally mature, NOT in immature bone)
• Location: Epiphysis of long bones (distal femur most common, proximal tibia, distal radius)
  • Extended to subchondral bone (abuts articular surface)
• X-ray: Eccentric, lytic lesion; "soap bubble" appearance; no matrix mineralization; extends to articular surface; no sclerotic rim

• Intralesional curettage + adjuvants (phenol, liquid nitrogen, cement/bone graft)
• Wide excision: For expendable bones (distal radius, fibula, clavicle), recurrence
• Denosumab (RANK-L inhibitor): For locally advanced/unresectable/metastatic GCT
• Recurrence rate: ~25% after curettage

15.5 Osteochondroma (Exostosis)

• Most common benign bone tumor
• Bony outgrowth with cartilage cap; sessile or pedunculated
• Direction away from growth plate (pointing away from joint)
• Grows during childhood; stops when skeletal maturity reached
• Multiple hereditary exostoses (MHE): Autosomal dominant; EXT1/EXT2 mutations; higher risk of malignant transformation
• Risk of malignant transformation to chondrosarcoma: Solitary < 1%; MHE ~5-10%
• Suspect malignant change if: Growth after skeletal maturity, cap > 2 cm, soft tissue mass
• Management: Observe if asymptomatic; excision if symptomatic/cosmetic/nerve irritation

15.6 Osteoid Osteoma

• Age: 10-35 years; M > F (3:1)
• Location: Femoral neck (most common), tibia, humerus
• X-ray/CT: Radiolucent nidus (< 2 cm) surrounded by dense reactive sclerosis
• Classic symptom: Night pain, dramatically relieved by NSAIDs/aspirin
• MRI: Extensive surrounding bone marrow edema (disproportionate)
• Management: NSAIDs (long-term; some resolve spontaneously); CT-guided radiofrequency ablation (RFA) - minimally invasive, treatment of choice; surgical excision (nidus must be removed)

15.7 Multiple Myeloma - Bone Lesions

• Most common primary malignant bone tumor in adults overall
• Plasma cell malignancy → osteoclast activation via RANK-L + DKK-1 (Wnt inhibitor)
• "Punched-out" lytic lesions on X-ray/skeletal survey; NO sclerotic rim
• Bone scan usually COLD (no osteoblast activity; hence bone scan unreliable in myeloma; use PET-CT or whole-body MRI)
• Complications: Pathological fractures, hypercalcemia, spinal cord compression
• Orthopedic management: Prophylactic fixation of impending fractures (> 50% cortex destruction; mirel's score), vertebroplasty/kyphoplasty for vertebral fractures
• Bisphosphonates reduce skeletal events

15.8 Metastatic Bone Disease

• Most common malignant bone tumor overall (much more common than primary)
• Primary sites (Mnemonic "BLTKP" - "Bloody Lungs Try Killing People"):
  • Breast (most common in women; mixed lytic + blastic)
  • Lung (lytic; poor prognosis)
  • Thyroid (lytic; highly vascular)
  • Kidney (lytic; highly vascular)
  • Prostate (most commonly blastic/sclerotic; most common in men)
• Sites: Spine (most common) > pelvis > ribs > skull > proximal femur > proximal humerus
• Mirel's score (impending fracture risk assessment):

  Variable	1	2	3
  Site	Upper limb	Lower limb	Peritrochanteric
  Pain	Mild	Moderate	Functional
  Lesion type	Blastic	Mixed	Lytic
  Size (% cortex)	< 1/3	1/3-2/3	> 2/3

  • Score ≥ 9: Prophylactic fixation recommended
• Management: Analgesia, radiotherapy (bisphosphonates, surgical fixation, spinal decompression)

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PART 6: PEDIATRIC ORTHOPAEDICS

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CHAPTER 16: DEVELOPMENTAL DYSPLASIA OF THE HIP (DDH)

Definition

Incidence & Risk Factors

• Female > Male (6:1)
• Left hip more common (75%; position of fetus)
• Risk factors (FLAGGED):
  • Female
  • Family history (first-degree relative)
  • Breech presentation
  • Oligohydramnios
  • Other orthopaedic conditions (club foot, torticollis)
  • First born

Clinical Examination - Neonatal Screening

• Hips in 90° flexion; abduct and gently pull anteriorly
• Positive: Feel/hear a "clunk" as dislocated femoral head is reduced back into acetabulum

• Hips in 90° flexion; adduct and gently push posteriorly
• Positive: Feel femoral head slip posteriorly out of acetabulum

Note: After 3 months these tests become negative (muscles contract around dislocated hip)

• Asymmetrical skin creases (multiple vs. few)
• Limited hip abduction (< 60°)
• Apparent shortening of affected limb
• Positive Galeazzi sign (Allis sign): Knees at different heights with hips + knees at 90°
• Trendelenburg gait + waddling gait (bilateral DDH)
• Delayed walking

Investigations

• USS (ultrasound): Gold standard in infants < 6 months (growth plate not yet ossified)
  • Graf classification: Based on alpha angle (> 60° = normal) and beta angle
  • Alpha angle < 60°: Hip dysplasia
  • Performed at 6 weeks (earlier USS not reliable)
• X-ray (AP pelvis): Once ossification centers appear (> 4-6 months)
  • Shenton's line: Should be smooth arc; broken = subluxation/dislocation
  • Hilgenreiner's line (horizontal through triradiate cartilage)
  • Perkin's line (vertical from lateral acetabular margin)
  • Ossific nucleus should be in lower inner quadrant
  • Wiberg's centre-edge angle: < 20° = dysplastic

Management (Age-Dependent) - Campbell's Operative Orthopaedics 2026

• Flexion-abduction orthosis; allows some movement but prevents extension/adduction
• Success rate ~85-95% in infants < 3 months
• Worn 23 hours/day for 6-12 weeks
• Monitor for avascular necrosis (Pavlik disease)
• Failure: Consider ultrasound-guided abduction bracing

• Arthrogram to confirm reduction
• "Safe zone" of reduction (Ramsey zone)
• If closed reduction fails: Open reduction

• Redirects acetabulum over femoral head
• Femoral derotation/shortening osteotomy to reduce tension

• Palliative (salvage) procedures; attempts at anatomic reduction carry high AVN risk
• Total hip replacement when adult if symptomatic OA

Complications

• Avascular necrosis (AVN) of femoral head - most serious complication of treatment
• Residual dysplasia (secondary OA in adulthood)
• Re-dislocation
• Growth disturbance

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CHAPTER 17: PERTHES' DISEASE (Legg-Calvé-Perthes Disease)

Definition

Epidemiology

• Age: 4-8 years (range 2-12 years)
• Male : Female = 4-5:1
• Bilateral in 10-15%
• White children predominantly
• Associated with delayed skeletal maturity (bone age < chronological age)

Pathophysiology

• Unknown cause of vascular insult → ischemia → necrosis of femoral head epiphysis → revascularization (takes 2-4 years) → remodeling
• During avascular phase: Epiphysis vulnerable to deformation (collapse)
• Outcome depends on extent of necrosis and sphericity of femoral head at healing

Clinical Features

• Limp (onset often insidious) + pain (groin, thigh, or knee)
• Restricted hip movements (especially internal rotation + abduction) - remember "Perthes Internal Rotation + Abduction = loss")
• Muscle wasting (thigh)
• Hip held in flexion + external rotation + adduction

X-ray Stages (Waldenstrom/Catterall)

1. Necrosis/Initial: Sclerosis (white/dense) femoral epiphysis; small capital epiphysis
2. Fragmentation: Lucency in femoral head; subchondral fracture (crescent sign)
3. Re-ossification: New bone formation; gradual restoration
4. Healing/Residual: Remodeling; may be spherical or misshapen (coxa magna, coxa plana)

Management

• Conservative (most cases):
  • Physiotherapy, anti-inflammatory analgesia
  • Activity restriction during fragmentation phase
  • Bracing (controversial; limited evidence for abduction casts/Scottish Rite orthosis)
• Surgical (Herring B/C, older age, > 50% head involvement):
  • Femoral varus derotation osteotomy (VDRO): Redirects femoral head into acetabulum
  • Salter innominate osteotomy (pelvic): Redirects acetabulum over femoral head
  • Triple pelvic osteotomy for older children

• Better prognosis: Young age (< 6 yrs), female (surprisingly), Herring A
• Worse prognosis: Older age (> 8 yrs), Herring C, > 50% head involvement
• Long-term: Risk of early OA in adulthood (coxa magna)

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CHAPTER 18: SLIPPED UPPER FEMORAL EPIPHYSIS (SUFE / SCFE)

Definition

Epidemiology

• Age: Adolescence (M: 10-16 yrs; F: 10-14 yrs - slightly earlier due to earlier puberty)
• Male > Female (2:1)
• Obese children (most common risk factor)
• Left > right; bilateral in 20-40%
• Associated: Hypothyroidism, growth hormone therapy, hypogonadism, renal osteodystrophy (if atypical age)

Pathophysiology

• Weakened physis (physeal widening from hormonal changes + growth) + excess body weight → posterior/medial displacement of epiphysis
• Metaphysis (femoral neck) moves anterolaterally; epiphysis (femoral head) stays in socket

Clinical Features

• Limp + groin/thigh/knee pain (knee pain alone in 20% → missed diagnosis!)
• Hip held in external rotation (obligate ER - flexing hip causes external rotation)
• Loss of internal rotation (hallmark sign)
• Restricted abduction + flexion
• Shortening of limb

Classification

• Stable SUFE: Child can weight-bear (with/without crutches); AVN risk low (~0%)
• Unstable SUFE: Cannot weight-bear; AVN risk 25-50% → orthopedic emergency

• Mild: < 1/3 of femoral head width slipped
• Moderate: 1/3 - 1/2
• Severe: > 1/2

Investigations

• X-ray (AP + frog-lateral views):
  • Klein's line (AP view): Line along superior femoral neck should intersect the lateral 1/4 of femoral head; in SUFE it does not intersect the head (Trethowan's sign)
  • "Ice cream falling off cone" appearance
  • Widened physis (early sign)
  • "Posterior tilting" visible on frog lateral

Management - SURGICAL EMERGENCY (prevent further slip + AVN)

1. In-situ fixation with single cannulated screw: Standard treatment for stable SUFE
   • Screw placed centrally into epiphysis across the physis; epiphysis NOT reduced
   • Do NOT attempt to reduce a stable SUFE (increases AVN risk)
2. Unstable SUFE: Gentle reduction (if severe displacement) + in-situ fixation
   • Attempt reduction within 24h (? benefit controversial)
3. Prophylactic contralateral fixation: Controversial; indicated in endocrinopathy/renal disease (high bilateral risk)
4. Subtrochanteric osteotomy: For severe chronic slip causing deformity

Complications

• AVN (most feared): From disrupted blood supply (retinacular vessels)
  • More common in unstable SUFE
  • Leads to collapse, leg shortening, early OA
• Chondrolysis: Cartilage dissolution; pin penetration into joint
• Early OA
• Femoroacetabular impingement (FAI): From healed deformity → cam impingement

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CHAPTER 19: CLUB FOOT (TALIPES EQUINOVARUS - TEV)

Definition

• Cavus (high arch)
• Adductus (forefoot adducted)
• Varus (heel in varus/inversion)
• Equinus (plantarflexed; heel up)

Classification

• Idiopathic (most common): Unknown cause; may have genetic component; bilateral in 50%
• Secondary: Neuromuscular (spina bifida, cerebral palsy), arthrogryposis, skeletal dysplasia

Incidence

• 1-2 per 1000 live births; Male > Female (2:1)

Management: Ponseti Method (Gold Standard)

1. Serial plaster casting (started at birth, ideally < 2 weeks):
   • Weekly cast changes
   • Sequence: C-A-V first (corrects cavus, then adductus, then varus), then Equinus last
   • ~5-7 casts over 6-8 weeks
2. Percutaneous Achilles tenotomy: After casts; performed percutaneously in clinic under LA; corrects equinus; 3 weeks in cast post-tenotomy
3. Foot abduction bracing (Denis-Browne boots + bar): After casting
   • ESSENTIAL to prevent relapse
   • Worn 23h/day for 3 months, then 12-16h/day (nights + naps) until age 4-5 years
4. Tibialis anterior transfer: If persistent forefoot supination/relapse after bracing phase

Complications of Untreated Club Foot

• Walking on dorsum of foot
• Severe disability
• Early OA of ankle and foot joints

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CHAPTER 20: COMMON PEDIATRIC CONDITIONS

Transient Synovitis (Irritable Hip)

• Most common cause of acute hip pain in children (2-12 years)
• Benign, self-limiting synovial inflammation
• Often follows viral upper respiratory tract infection
• Clinical: Hip pain + limited ROM; may be low-grade fever
• Normal inflammatory markers (or only mildly elevated)
• Diagnosis of exclusion (must rule out septic arthritis!)
• Use Kocher criteria (see septic arthritis chapter)
• Management: Rest, NSAIDs; resolves in 2-4 weeks
• Recurrence in ~15%; small risk of Perthes' disease in future

Osgood-Schlatter Disease

• Traction apophysitis of tibial tuberosity at patellar tendon insertion
• Age: 10-15 years (adolescent growth spurt); athletic children
• Clinical: Pain + tenderness + swelling at tibial tuberosity; worse with activity
• X-ray: Fragmentation of tibial tuberosity (confirms but not always present)
• Management: Activity modification, NSAIDs, physiotherapy, quadriceps stretching
• Usually self-limiting; resolves when growth plate fuses

Sinding-Larsen-Johansson (SLJ) Disease

• Traction apophysitis at inferior pole of patella
• Similar age group and mechanism to Osgood-Schlatter
• Pain at inferior patella, worse with activity
• Management: Same as Osgood-Schlatter

Scoliosis

• Idiopathic (most common, 80%):
  • Infantile (< 3 yrs), Juvenile (3-10 yrs), Adolescent (AIS > 10 yrs) - most common
  • AIS: Female > Male; right thoracic most common curve pattern
• Neuromuscular: Cerebral palsy, muscular dystrophy, spina bifida
• Congenital: Vertebral malformation (hemivertebra, vertebral bar)
• Secondary: Leg length discrepancy, pain (disappears in prone position)

• Lines drawn parallel to end vertebrae (most tilted at top and bottom of curve)
• Angle between these lines = Cobb angle

• Uneven shoulders, prominent shoulder blade, uneven waist
• Adam's forward bending test: Rib hump (rotation) on bending forward - hallmark of structural scoliosis (vs. functional which disappears)
• Scoliometer: Measures angle of trunk rotation (ATR)

• Curves > 50° progress in adulthood → respiratory compromise, cosmetic deformity, pain

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PART 7: SHOULDER, KNEE & SPORTS INJURIES

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CHAPTER 21: ROTATOR CUFF DISEASE

Rotator Cuff Anatomy ("SITS")

• Supraspinatus: Initiates abduction (0-15°); most commonly injured
• Infraspinatus: External rotation
• Teres minor: External rotation
• Subscapularis: Internal rotation; protects anterior shoulder

Impingement Syndrome (Subacromial Impingement)

• Supraspinatus tendon compressed between humeral head and coracoacromial arch
• Causes: Acromial morphology (type III = hooked), AC joint OA, poor posture, muscle imbalance
• Neer's sign: Forward flexion with internal rotation - pain reproduced
• Hawkins-Kennedy test: Forward flexed elbow + internal rotation - pain
• Painful arc: Pain between 60-120° of abduction (supraspinatus impingement zone)
• Management: Physiotherapy, subacromial corticosteroid injection, NSAIDs; surgical decompression (subacromial decompression/acromioplasty) if conservative fails

Rotator Cuff Tears

• Partial thickness or full thickness tears
• Mostly supraspinatus (due to poor vascularity at "critical zone" - 1 cm from insertion)
• Causes: Degenerative (most common; > 50 years), acute trauma (younger patients)
• Clinical:
  • Drop arm test: Cannot hold arm at 90° abduction (supraspinatus tear)
  • Empty can test (Jobe's): Arm at 90° forward flexion, 30° horizontal abduction, thumb down → resistance against gravity; weakness/pain = supraspinatus
  • External rotation lag sign: Cannot maintain external rotation (infraspinatus)
• Investigations: MRI (gold standard for tear size and extent), USS
• Management:
  • Partial/small tears: Conservative (physio, injection)
  • Full-thickness, symptomatic, young patient: Arthroscopic rotator cuff repair
  • Massive irreparable tears: Superior capsule reconstruction, tendon transfer, reverse shoulder arthroplasty

Adhesive Capsulitis (Frozen Shoulder)

• Fibrotic contracture of glenohumeral joint capsule + synovium → global loss of movement
• Age: 40-60 years; female > male; associated with diabetes, thyroid disease
• Phases:
  • Freezing (painful, 2-9 months): Severe pain + stiffening
  • Frozen (stiff, 4-12 months): Pain decreases; marked stiffness
  • Thawing (12-24 months): Gradual return of movement
• Clinical: Global restriction of active AND passive ROM (all planes equally restricted - "capsular pattern")
• Management: NSAIDs, physiotherapy, intra-articular steroid injection, hydrodilatation; surgery (arthroscopic capsular release) if fails

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CHAPTER 22: KNEE INJURIES

Anatomy of Key Structures

• ACL (Anterior Cruciate Ligament): Prevents anterior translation of tibia; resists internal rotation; most commonly injured knee ligament in sport
• PCL (Posterior Cruciate Ligament): Prevents posterior translation; stronger than ACL; rarely injured
• MCL (Medial Collateral Ligament): Resists valgus stress
• LCL (Lateral Collateral Ligament): Resists varus stress
• Medial meniscus: C-shaped; less mobile (attached to MCL); more commonly torn than lateral
• Lateral meniscus: O-shaped; more mobile; less commonly torn

ACL Injury

• Mechanism: Non-contact twisting/pivoting; sudden deceleration; landing from jump; valgus collapse
• Most common in young athletes (football, basketball, skiing)
• Clinical features:
  • Acute: "Pop" heard/felt; immediate swelling (hemarthrosis from middle genicular artery); unable to continue activity
  • Chronic: "Giving way" episodes; instability on pivoting
• Tests:
  • Lachman test (most sensitive): Knee at 20-30° flexion; anterior drawer on tibia; soft/absent endpoint
  • Anterior drawer test: Knee at 90°; anterior pull; less sensitive than Lachman
  • Pivot shift test (most specific for ACL): Most specific functional test; reduced by muscle spasm acutely
• Investigations: MRI (confirms tear + associated injuries - meniscus, MCL)
• Management:
  • Conservative: Quadriceps + hamstring rehab; bracing; for lower demand patients/older patients
  • Surgical (ACL reconstruction): For young, active patients with instability; autograft (hamstring tendon or bone-patellar tendon-bone); allograft; synthetic
  • Return to sport: ~9-12 months post-reconstruction

Meniscal Tears

• Mechanism: Twisting on semi-flexed, weight-bearing knee; degenerative tears in older patients (no trauma)
• Types: Vertical (bucket-handle, longitudinal), horizontal, radial, complex
• Bucket-handle tear: Longitudinal tear; displaced central fragment (handle) → locked knee (cannot fully extend)

• Joint line tenderness (medial > lateral)
• Joint effusion (delayed onset > hemarthrosis of ACL)
• McMurray's test: Rotate foot with knee in flexion + extension; clunk/pain at joint line
• Thessaly test: Knee at 20° flexion; rotate medially/laterally; pain/catching = meniscal tear
• Apley's test: Prone; compress + rotate (compresses meniscus) vs distract + rotate (stresses ligaments)
• Locked knee (bucket-handle tear = extension block)

• Conservative: Degenerative tears, partial tears, elderly; physiotherapy
• Arthroscopic surgery: For traumatic tears, failed conservative, locked knee
  • Meniscal repair: Young, peripheral "red-red zone" tear (vascular); suture repair
  • Partial meniscectomy: Central tears (avascular "white-white zone"); trim degenerative/unstable parts
  • Total meniscectomy: Avoid if possible (→ accelerated OA)

Patellofemoral Problems

• Lateral dislocation most common (trochlear dysplasia, increased Q-angle, lateral ligamentous laxity)
• Medial patellofemoral ligament (MPFL) tears
• Reduction: Extend knee + push patella medially
• Post-reduction: Immobilize briefly, then physiotherapy
• Recurrence: Common; surgical MPFL reconstruction for recurrent dislocations

• Softening and fibrillation of patellar articular cartilage
• Young women, athletes
• Anterior knee pain worse going down stairs, prolonged sitting ("movie sign"), squatting
• Management: Physiotherapy (VMO strengthening), NSAIDs; arthroscopy (debridement) in resistant cases

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PART 8: NERVE & TENDON INJURIES

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CHAPTER 23: PERIPHERAL NERVE INJURIES

Seddon Classification

Sunderland Classification (I-V)

• I = Neuropraxia
• II = Axonotmesis (endoneurium intact)
• III = Axon + endoneurium disrupted (perineurium intact)
• IV = Axon + endoneurium + perineurium disrupted (epineurium intact)
• V = Complete transection (Neurotmesis)

Key Nerve Injuries by Location

• Wrist drop (loss of wrist + finger extension)
• Loss of sensation: 1st dorsal web space
• Injured in: Humeral shaft fracture (spiral groove), posterior interosseous nerve in radial tunnel (resistant lateral epicondylitis)
• Saturday night palsy / crutch palsy: Compression neuropraxia

• Proximal lesion (elbow): Loss of forearm pronation, wrist flexion (radial side), all FDP to index/middle, FPL → "Hand of Pope" (only ring + little finger can flex)
• Distal lesion (wrist/carpal tunnel): Loss of LOAF muscles (Lumbricals I&II, Opponens pollicis, Abductor pollicis brevis, Flexor pollicis brevis) → wasting of thenar eminence, loss of thumb opposition
• Sensation: Radial 3.5 fingers (thumb, index, middle, radial ½ ring)
• Carpal tunnel syndrome: Phalen's test (wrist flexion × 60s → numbness), Tinel's over carpal tunnel; Mx: Splint/steroid injection/carpal tunnel decompression

• "Claw hand" (ring + little fingers in MCP hyperextension + IP flexion)
• Wasting of hypothenar eminence + interossei + medial 2 lumbricals
• Loss of sensation: Ulnar 1.5 fingers (little finger + ulnar ½ ring)
• Froment's sign: Cannot pinch without thumb IP joint flexion (compensates for lost adductor pollicis)
• Injured in: Medial epicondyle fracture (elbow), cubital tunnel, Guyon's canal (wrist)
• Note: Ulnar paradox - low ulnar nerve injury causes worse clawing than high ulnar nerve injury (FDP to ring/little retained)

• Injured in shoulder dislocation, surgical neck of humerus fracture
• Deltoid weakness (shoulder abduction 15-90°)
• Loss of sensation: Regimental badge area (lateral upper arm)

• Injured by shoulder surgery, trauma, radical mastectomy
• Serratus anterior weakness → Winging of scapula (medial border of scapula protrudes posteriorly when pushing against wall)

• Injured at fibular neck (fracture, prolonged squatting, plaster pressure)
• Foot drop (loss of dorsiflexion + eversion)
• High-stepping gait (to clear foot)
• Loss of sensation: Dorsum of foot + 1st web space
• Recover with foot drop orthosis (AFO); often neuropraxia → good recovery

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PART 9: COMMON ORTHOPAEDIC CONDITIONS

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CHAPTER 24: CARPAL TUNNEL SYNDROME

• Most common peripheral nerve compression syndrome
• Compression of median nerve in carpal tunnel
• Risk factors: Female, obesity, pregnancy, hypothyroidism, diabetes, RA, amyloidosis, repetitive wrist movement, acromegaly
• Clinical: Numbness + tingling in radial 3.5 fingers, nocturnal symptoms (wakes from sleep), worse with wrist flexion, thenar wasting (late)
• Tests: Phalen's (wrist flexion test): Symptoms within 60s; Tinel's sign: Percussion over carpal tunnel → tingling; Durkan's compression test: Direct carpal tunnel pressure
• Investigations: Nerve conduction studies (NCS) + EMG (gold standard)
• Management:
  • Mild/moderate: Wrist splint (neutral, especially at night), steroid injection into carpal tunnel
  • Severe/refractory: Open or endoscopic carpal tunnel decompression (release flexor retinaculum)

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CHAPTER 25: PLANTAR FASCIITIS

• Most common cause of heel pain
• Degenerative/inflammatory condition of plantar fascia at calcaneal insertion
• Classic symptom: First-step pain in morning (eases with walking then worsens)
• Risk factors: Obesity, prolonged standing, high arches, tight Achilles
• X-ray: May show heel spur (plantar calcaneal osteophyte) - often incidental, not causative
• Management: Heel padding/insoles, stretching (plantar fascia + Achilles stretching protocol), NSAIDs, ice; Extracorporeal Shock Wave Therapy (ESWT) for resistant cases; steroid injection (short-term); surgical plantar fascia release (last resort)

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CHAPTER 26: HALLUX VALGUS

• Lateral deviation of great toe at 1st MTP joint with medial deviation of 1st metatarsal
• Female >> Male; family history, narrow shoes, flat feet
• Bunion: Bursa over medial eminence of 1st MTP
• Clinical: Pain, footwear difficulty, callosity, lesser toe deformities (hammer toes)
• X-ray: HVA (hallux valgus angle) > 15°; IMA (intermetatarsal angle) > 9°
• Management:
  • Conservative: Wide footwear, bunion pads, orthotics
  • Surgical: Multiple osteotomy options based on severity:
    • Mild: Chevron (Austin) osteotomy (distal metatarsal)
    • Moderate: Scarf osteotomy (oblique metatarsal shaft)
    • Severe (high IMA): Proximal metatarsal osteotomy (e.g., Ludloff)
    • Severe + OA: 1st MTP joint fusion (arthrodesis) - best long-term results

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PART 10: EXAMINATION SKILLS & ASSESSMENT FRAMEWORKS

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CHAPTER 27: ORTHOPAEDIC EXAMINATION - "LOOK, FEEL, MOVE"

Standard Framework for Any Joint

• Skin: Scars, sinuses, bruising, erythema
• Shape: Deformity, swelling, wasting
• Position: Abnormal posture/alignment
• Compare bilaterally

• Temperature
• Tenderness (localize: medial/lateral joint line, ligaments, tendons, bony prominences)
• Swelling: Effusion (patellar tap, bulge sign for knee), synovitis vs bony
• Crepitus

• Active first (patient moves), then passive (examiner moves)
• Document angles
• Note pain, restriction, instability, crepitus
• Special tests (specific to joint)

• Peripheral pulses, capillary refill
• Sensation (dermatomes), motor (myotomes)
• Reflexes

• Gait, walking aids
• ADL ability (dressing, stairs)

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CHAPTER 28: KEY GAIT PATTERNS

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KEY NUMBERS & HIGH-YIELD FACTS FOR EXAMS

Fractures & Orthopedic Numbers

Pediatric Orthopaedics Numbers

Bone Tumor High-Yield Points

Osteoporosis

Orthopaedic Mnemonics Summary