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KATHMANDU UNIVERSITY - July 2025

Paper II: Musculoskeletal System (Upper and Lower Limb)

Complete Answers

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SECTION "B" - A. Short Answer Questions

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ANATOMY [12 marks]

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Q1. Draw a well-labeled diagram of the femoral triangle

                 INGUINAL LIGAMENT (Base)
                /                        \
        Sartorius                    Adductor Longus
        (lateral border)             (medial border)
               \                        /
                \  ___________________/
                 \|                   |
                  |  Floor:           |
                  |  - Iliopsoas (lat)|
                  |  - Pectineus (med)|
                  |                   |
                  |  Contents (L→M):  |
                  |  N - Femoral Nerve|
                  |  A - Femoral Art. |
                  |  V - Femoral Vein |
                  |  L - Lymphatics   |
                  \                   /
                   \                 /
                    APEX (→ Adductor Canal)

• Base (superior): Inguinal ligament
• Lateral border: Medial margin of sartorius
• Medial border: Medial margin of adductor longus
• Floor: Iliopsoas (laterally) + Pectineus and Adductor longus (medially)
• Roof: Fascia lata with cribriform fascia (pierced by great saphenous vein)
• Apex: Opens into the adductor canal inferiorly

• N - Femoral Nerve (outside femoral sheath)
• A - Femoral Artery
• V - Femoral Vein
• Y - Lymph nodes and lymphatics (femoral canal)

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Q2. Enlist the ligaments of the shoulder joint

1. Superior glenohumeral ligament - resists inferior translation of humeral head
2. Middle glenohumeral ligament - resists anterior translation at 45° abduction
3. Inferior glenohumeral ligament (anterior and posterior bands) - most important; primary stabilizer at 90° abduction; resists anterior dislocation

• Runs from base of coracoid process to greater and lesser tubercles of humerus
• Strengthens superior capsule; stabilizes the long head of biceps tendon

• Bridges the intertubercular groove (bicipital groove)
• Retains the tendon of the long head of biceps brachii

• Runs from coracoid process to acromion
• Forms the "coracoacromial arch" - prevents superior dislocation of humeral head

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Q3. Write short notes on the sciatic nerve with its applied aspects

• Largest nerve in the body
• Arises from the sacral plexus: anterior rami of L4, L5, S1, S2, S3
• Two components: tibial part (anterior divisions L4-S3) + common fibular part (posterior divisions L4-S2)

1. Exits pelvis through the greater sciatic foramen, inferior to piriformis
2. Passes between ischial tuberosity and greater trochanter (midpoint = safe injection zone superolateral quadrant)
3. Descends deep to gluteus maximus
4. Enters posterior compartment of thigh
5. Usually divides into common fibular nerve and tibial nerve at the apex of the popliteal fossa (may divide higher)

• In thigh: motor branches to all posterior compartment muscles (biceps femoris, semitendinosus, semimembranosus) and ischial part of adductor magnus
• Common fibular nerve: supplies anterior and lateral leg + dorsum of foot
• Tibial nerve: supplies posterior leg and plantar foot

1. Sciatica - Compression at L4/L5/S1 disc level causes radiating pain down the leg along its distribution (buttock → posterior thigh → leg → foot)
2. Piriformis syndrome - Nerve compressed by a hypertrophied or inflamed piriformis muscle
3. Intramuscular injection injury - Wrong site injections in the gluteal region can injure the nerve; safe zone is the superolateral quadrant of the buttock
4. Hip surgery - At risk during total hip replacement, posterior approach
5. Posterior thigh injuries - Complete division causes loss of knee flexion + all movement below knee + sensory loss over lateral leg and foot

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Q4. Write short notes on great saphenous vein

1. Passes anterior to the medial malleolus
2. Ascends along the medial side of the leg (with saphenous nerve)
3. Passes posterior to the medial condyle of the femur at the knee
4. Ascends along the medial thigh
5. Passes through the saphenous opening (cribriform fascia) in the deep fascia in the upper thigh
6. Drains into the femoral vein in the femoral triangle (about 3-4 cm below the inguinal ligament)

• Medial superficial femoral vein
• Anterolateral superficial femoral vein
• Superficial iliac circumflex vein
• Superficial inferior epigastric vein
• Superficial external pudendal vein

1. Varicose veins - Incompetent valves cause dilatation; treated by high ligation and stripping
2. Cutdown site for intravenous access in emergencies (anterior to medial malleolus)
3. Coronary artery bypass grafting (CABG) - Used as graft vessel
4. Peripheral vascular bypass surgery - Used as conduit
5. Long saphenous nerve block for foot/ankle anesthesia

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Q5. Enlist the branches of axillary artery

1. Superior (Supreme) thoracic artery - supplies upper 2 intercostal spaces

• Circumflex scapular artery
• Thoracodorsal artery

1. Anterior circumflex humeral artery
2. Posterior circumflex humeral artery (passes through quadrilateral space with axillary nerve)

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Q6. Formation and branches of posterior cord of brachial plexus

• Formed by the union of the posterior divisions of all three trunks (upper, middle, and lower trunks)
• Equivalent to contributions from roots C5, C6, C7, C8, T1 (all roots)
• Located posterior to the axillary artery (hence "posterior cord")

1. Upper subscapular nerve (C5, C6) - supplies subscapularis (upper part)
2. Thoracodorsal nerve (C6, C7, C8) - supplies latissimus dorsi (middle subscapular nerve)
3. Lower subscapular nerve (C5, C6) - supplies subscapularis (lower part) + teres major
4. Axillary nerve (C5, C6) - terminal branch; exits via quadrilateral space; supplies:
   • Deltoid muscle
   • Teres minor
   • Skin over lower deltoid (upper lateral cutaneous nerve of arm)
5. Radial nerve (C5-T1) - terminal branch (largest branch of brachial plexus); supplies:
   • All extensor muscles of arm, forearm
   • Skin of posterior arm, forearm, and lateral dorsum of hand

• "Saturday night palsy" (radial nerve injury at spiral groove)
• Wrist drop (inability to extend wrist/fingers)
• Loss of deltoid function

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BIOCHEMISTRY [4 marks]

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Q7. Enlist the different markers of skeletal muscle damage

• CK-MM = skeletal muscle specific (vs. CK-MB = cardiac, CK-BB = brain)
• Troponin I/T - cardiac specific; rarely elevated in pure skeletal muscle injury

• Rhabdomyolysis - massive CK elevation (>10,000 U/L), myoglobinuria, risk of acute renal failure
• Muscular dystrophies (Duchenne's - CK 50-100x normal)
• Inflammatory myopathies (polymyositis, dermatomyositis)
• Crush injuries, burns, strenuous exercise
• Drug-induced myopathy (statins)

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Q8. Differentiate between Type I and Type II muscle fibers

• Type IIa - intermediate (both aerobic and anaerobic)
• Type IIb/IIx - purely glycolytic, fastest but most fatigable

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MICROBIOLOGY [2 marks]

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Q9. List the causative agents of osteomyelitis

• Staphylococcus aureus - #1 cause at all ages (including MRSA strains)

• Sickle cell disease: Salmonella species (alongside S. aureus)
• Intravenous drug users: Pseudomonas aeruginosa, Candida
• Immunocompromised: Fungal organisms, atypical mycobacteria
• Vertebral osteomyelitis (Pott's spine): Mycobacterium tuberculosis
• Post-surgical/Implant: Staphylococcus epidermidis (coagulase-negative)
• Puncture wound (foot): Pseudomonas aeruginosa
• Diabetic foot: Polymicrobial (S. aureus + anaerobes + gram-negatives)
• Brucellosis: Brucella melitensis/abortus (cattle-endemic regions)

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PATHOLOGY [6 marks]

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Q10. Discuss Pott's spine

• Primary focus usually in lungs (or GIT)
• Hematogenous spread to vertebral body (rich blood supply)
• Begins in the anterior part of the vertebral body near the disc
• Caseous necrosis destroys the disc space (disc has no blood supply, avascular - vulnerable once adjacent bone is infected)
• Spreads to adjacent vertebrae (typically two vertebrae involved)
• "Cold abscess" (paravertebral/psoas abscess) forms - tracks along fascial planes

• Caseous granulomatous inflammation
• Bone destruction without reactive sclerosis (unlike pyogenic)
• Disc space narrowing/destruction
• Vertebral collapse → Kyphotic deformity (Gibbus deformity)

• Insidious onset back pain
• Local tenderness
• Gibbus deformity (angular kyphosis - characteristic)
• Constitutional symptoms (fever, night sweats, weight loss)
• Paraplegia (Pott's paraplegia) - from cord compression by abscess, granulation tissue, or collapsed vertebra

• X-ray: Disc space loss, vertebral body erosion, paravertebral shadow (abscess)
• MRI: Gold standard (shows cord compression, abscess extent)
• ESR elevated; Mantoux positive
• Culture and biopsy for confirmation

• Anti-tubercular therapy (ATT): HRZE for 2 months, then HR for 10 months (12 months total)
• Surgery: For paraplegia, instability, large abscess, no response to ATT

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Q11. Write in short about etiopathogenesis of Gout

• Idiopathic; multifactorial genetic predisposition
• Defects in purine metabolism:
  • Decreased renal excretion of uric acid (most common, 90%)
  • Overproduction of uric acid (10%)
• Rare enzyme defects: HPRT deficiency (Lesch-Nyhan syndrome), PRPP synthetase overactivity

• Increased production: Myeloproliferative disorders (leukemia), polycythemia, hemolytic anemia, psoriasis, cytotoxic drugs (tumour lysis)
• Decreased excretion: Chronic renal disease, diuretics (thiazides, furosemide), low-dose aspirin, cyclosporine, alcohol
• Diet: High purine diet (red meat, organ meat, shellfish), fructose-sweetened drinks

1. Hyperuricemia (serum uric acid >7 mg/dL in men, >6 mg/dL in women)
2. MSU crystal deposition in joints (predilection for cooler peripheral joints - 1st MTP joint "podagra")
3. Acute gouty arthritis: MSU crystals phagocytosed by neutrophils → IL-1β, IL-6, TNF-α released → intense inflammatory response → painful acute arthritis
4. Chronic tophaceous gout: Repeated attacks → deposition of urate tophi in soft tissues (auricle of ear, tendons, bursae) and joints
5. Renal involvement: Urate nephropathy, uric acid stones

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Q12. Define fracture. Enumerate the types of fracture.

• Closed (Simple): No communication with external environment
• Open (Compound): Wound communicates with fracture site (infection risk)

• Undisplaced vs. Displaced (angulation, translation, rotation, shortening)

• Complete vs. Incomplete (greenstick, torus, crack)

• Epiphyseal fractures (Salter-Harris I-V): In children involving growth plate
• Colles fracture: Distal radius, dorsal angulation (FOOSH injury)
• Smith fracture: Distal radius, volar angulation
• Boxer fracture: 5th metacarpal neck

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PHARMACOLOGY [4 marks]

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Q13. Write down the therapeutic uses of skeletal muscle relaxants

• Intubation facilitation: Succinylcholine (depolarizing), Rocuronium (non-depolarizing)
• Surgical muscle relaxation during general anesthesia: Pancuronium, Vecuronium, Atracurium
• Mechanical ventilation in ICU: Cisatracurium
• Electroconvulsive therapy (ECT): Succinylcholine (to prevent injury from convulsions)

1. Spasticity - MS, cerebral palsy, stroke: Baclofen, tizanidine, dantrolene
2. Acute muscle spasm (back pain, neck pain): Cyclobenzaprine, methocarbamol
3. Tetanus: Diazepam + neuromuscular blockers
4. Malignant hyperthermia: Dantrolene (life-saving)
5. Physiotherapy: To relax muscles before passive stretching exercises

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Q14. Enumerate the advantages of selective COX inhibitors (NSAIDs) with suitable examples

• COX-1 is constitutive: protects gastric mucosa, platelet aggregation, renal function
• COX-2 is inducible: mediates inflammation, pain, fever

• Celecoxib (Celebrex) - most widely used
• Etoricoxib (Arcoxia)
• Parecoxib (IV formulation for post-operative pain)
• Meloxicam (preferential COX-2 selectivity)
• Nimesulide (preferential)

• Increased cardiovascular risk (TXA2 inhibition reduced but prostacyclin also reduced → prothrombotic state; risk of MI, stroke) - Rofecoxib (Vioxx) withdrawn for this reason
• More expensive than traditional NSAIDs
• Renal effects similar to non-selective NSAIDs
• Contraindicated in patients with established cardiovascular disease

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PHYSIOLOGY [2 marks]

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Q15. Write the differences between isometric and isotonic muscle contraction

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SECTION "B" - B. Clinical Based Questions [4Q×5=20 marks]

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ANATOMY [10 marks]

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Q16. 20-year-old female - Fractured lower end of humerus + displaced head of radius

• Capitulum (lateral): Rounded, articulates with head of radius
• Trochlea (medial): Pulley-shaped, articulates with trochlear notch of ulna

• Coronoid fossa (anterior): Accommodates coronoid process of ulna during flexion
• Radial fossa (anterior, lateral): Accommodates head of radius during full flexion
• Olecranon fossa (posterior): Accommodates olecranon of ulna during extension

• Medial epicondyle - Non-articular; gives origin to forearm flexors; ulnar nerve passes in groove behind it
• Lateral epicondyle - Non-articular; gives origin to forearm extensors; weaker prominence

• Flexion (0-145°): Biceps brachii, brachialis, brachioradialis
• Extension (145°-0°): Triceps brachii, anconeus
• Pronation (90°): Pronator teres, pronator quadratus
• Supination (90°): Supinator, biceps brachii (most powerful)

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Q17. 15-year-old boy - Right ankle sprain, X-ray normal

1. Tibia - medial malleolus + distal articular surface (tibial plafond)
2. Fibula - lateral malleolus
3. Talus - superior surface (trochlea of talus)

• Tibionavicular
• Tibiocalcaneal
• Anterior tibiotalar
• Posterior tibiotalar

• Anterior talofibular ligament (ATFL) - most commonly torn (weakest)
• Calcaneofibular ligament (CFL) - second most injured
• Posterior talofibular ligament (PTFL) - strongest; rarely torn

• Anterior inferior tibiofibular ligament
• Posterior inferior tibiofibular ligament
• Interosseous ligament

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PHYSIOLOGY [10 marks]

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Q18. 55-year-old woman - Muscle cramps, tingling, serum calcium 6.5 mg/dL (Hypocalcemia)

1. Action potential travels down the motor nerve → releases acetylcholine (ACh) at NMJ
2. ACh generates an action potential in the sarcolemma
3. Action potential travels down T-tubules (transverse tubules)
4. T-tubule depolarization activates DHPR (dihydropyridine receptors) - voltage-gated L-type Ca²+ channels
5. DHPR mechanically activates RyR1 (ryanodine receptor) on the sarcoplasmic reticulum (SR)
6. SR releases calcium (Ca²+) into the cytosol (sarcoplasmic Ca²+ rises from 10⁻⁷ to 10⁻⁵ M)
7. Ca²+ binds to troponin C (of the troponin complex on thin filament)
8. Conformational change moves tropomyosin away from the myosin-binding sites on actin
9. Myosin heads can now attach to actin → cross-bridge cycling → force + shortening
10. Relaxation: Ca²+ pumped back into SR by SERCA pump

Z disc — I band — A band (with H zone + M line) — I band — Z disc

• A band (dark): Contains thick myosin filaments + overlapping actin; remains CONSTANT
• I band (light): Contains only thin actin filaments; extends from Z disc to edge of A band
• H zone: Central part of A band with only myosin (no actin overlap)
• M line: Centre of H zone; proteins holding myosin together
• Z disc: Marks boundary of sarcomere; thin filaments anchored here

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Q19. Goma, 46-year-old woman - Myasthenia Gravis (MG)

1. Autoantibodies (IgG) produced against nicotinic acetylcholine receptors (anti-AChR antibodies) on the postsynaptic membrane (~85% of cases)
2. These antibodies:
   • Block ACh binding to receptors
   • Accelerate receptor degradation (receptor endocytosis)
   • Activate complement → damage/destroy the postsynaptic membrane (simplification of junctional folds)
3. Result: Fewer functional AChR available → reduced end plate potential amplitude
4. With repeated stimulation (repetitive nerve stimulation), the readily releasable pool of ACh vesicles is depleted → progressive reduction in end plate potential → decremental response on EMG
5. This manifests clinically as fatiguable weakness - weakness worsens with activity (proximal muscles, ocular, bulbar muscles most affected)

1. Action potential arrives at the presynaptic terminal of the motor neuron
2. Depolarization of the presynaptic membrane opens voltage-gated Ca²+ channels (P/Q-type, Cav2.1)
3. Ca²+ influx into the presynaptic terminal
4. Ca²+ binds to synaptotagmin (calcium sensor protein on synaptic vesicles)
5. Synaptotagmin interacts with SNARE proteins: synaptobrevin (VAMP), syntaxin, SNAP-25
6. SNARE complex formation causes vesicle fusion with the presynaptic membrane
7. Exocytosis of ACh into the synaptic cleft (quantal release - ~1 quantum = ~5,000-10,000 ACh molecules)
8. ACh diffuses across cleft → binds postsynaptic nAChR → depolarization → muscle contraction

• Lambert-Eaton Myasthenic Syndrome (LEMS) - autoantibodies against presynaptic P/Q-type voltage-gated Ca²+ channels → reduced ACh release → weakness (proximal, unlike MG)
• Aminoglycosides block Ca²+ channels at NMJ → potentiate neuromuscular blockade

1. Acetylcholinesterase (AChE) - primary mechanism:
   • Located in the synaptic cleft (basal lamina) and postsynaptic membrane
   • Hydrolyzes ACh → acetic acid + choline
   • Reaction is extremely fast (one AChE molecule can hydrolyze ~25,000 ACh/sec)
   • This ensures brief, precise muscle activation
2. Diffusion away from the synapse (minor role at NMJ)
3. Reuptake of choline into the presynaptic terminal via high-affinity choline transporter (CHT1) for ACh resynthesis (choline acetyltransferase reconverts choline + acetyl-CoA → ACh)

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