Locomotor – 2024

• Aspirin (acetylsalicylic acid) irreversibly acetylates a serine residue at the active site of COX.

• This permanent inactivation lasts for the lifetime of the enzyme.

• Platelets, which lack nuclei, cannot synthesize new COX → aspirin’s antiplatelet effect lasts 7–10 days (life span of platelets).

• This unique mechanism explains why aspirin is used in low doses for cardioprotection (anti-thrombotic effect via inhibition of thromboxane A2).

❌Why Other Options Are Incorrect

• Acetaminophen – not a classic NSAID, weak COX inhibitor in peripheral tissues (acts mainly in CNS, antipyretic/analgesic but not anti-inflammatory). Also reversible.

• Diclofenac – reversible NSAID.

• Mefenamic acid – reversible NSAID.

• Naproxen – reversible NSAID.

• NAC is the specific antidote for acetaminophen poisoning.

• It acts by:

  1. Replenishing glutathione stores → allowing detoxification of NAPQI.

  2. Acting as a direct sulfhydryl donor to neutralize NAPQI.

  3. Improving microcirculatory blood flow in the liver, aiding recovery.

• The earlier NAC is given (within 8–10 hours), the more effective it is.

❌Why the Other Options are Incorrect

• Activated charcoal – useful if given within 1 hour of ingestion to prevent absorption, but not an antidote.

• Protamine sulfate – antidote for heparin toxicity, not acetaminophen.

• Sodium bicarbonate – used for tricyclic antidepressant overdose (to counter arrhythmias), and in metabolic acidosis, not here.

• Sulphapyridine – not an antidote, rather an antimicrobial sometimes used in inflammatory bowel disease.

Aspirin is contraindicated in children with viral illnesses (e.g., chickenpox, influenza) because it is associated with Reye’s syndrome, a rare but potentially fatal condition.

• Reye’s syndrome = acute encephalopathy + liver failure (microvesicular fatty change in hepatocytes).

• The exact mechanism is unclear, but aspirin is thought to impair mitochondrial function in the liver during viral infections.

• Clinical features: vomiting, confusion, seizures, coma, elevated liver enzymes, hyperammonemia.

❌ Why the other options are incorrect:

• Fanconi syndrome → Proximal tubule dysfunction, not aspirin-related.

• Gastric bleeding → Possible with aspirin but not specific to children with viral illness.

• Nephrotoxicity → Seen with NSAIDs in general, not the major contraindication here.

• Thrombocytopenia → Aspirin impairs platelet aggregation, but not the reason for contraindication in viral illness.

The first step in fracture repair is hematoma formation.

• Blood vessels at the fracture site tear → bleeding occurs.

• A hematoma (blood clot) forms within hours.

• This provides the initial framework for inflammatory cells and fibroblasts to migrate in.

• Only after this step do fibrocartilaginous callus, bony callus, and finally bone remodeling occur.

❌ Why the other options are incorrect:

• Bone remodeling → Final stage, restores bone to original shape.

• Bony callus formation → Later stage, replaces fibrocartilage with spongy bone.

• Vascularization of site → Happens after hematoma, when granulation tissue forms.

• Fibrocartilaginous callus formation → Intermediate stage, stabilizes fracture.

The major risk factor for osteoporosis is postmenopausal status in women. After menopause, estrogen levels fall sharply, and estrogen normally inhibits osteoclast activity (bone resorption). With reduced estrogen:

• Osteoclast activity increases

• Bone resorption > Bone formation

• Bone mineral density (BMD) progressively decreases

This leads to fragile bones and increased fracture risk, especially vertebral compression fractures, Colles’ fractures, and hip fractures.

❌ Why the other options are incorrect:

• High body weight: Actually protective, as increased mechanical load stimulates bone formation.

• Regular weight-bearing exercise: Protective, improves bone density.

• Adequate calcium and vitamin D intake: Protective, reduces risk of osteoporosis.

• Male gender: Less risk compared to females, especially postmenopausal women.

A greenstick fracture is an incomplete fracture in which the bone breaks on one side and bends on the other—much like how a young, green twig snaps partially but remains partially intact. This pattern is characteristic of pediatric bones, which are more pliable and have a thicker periosteum than adult bones. Falling on an outstretched arm is a classic mechanism producing such injuries in children.

❌ Why the other options are incorrect:

• Comminuted fracture: Involves the bone being shattered into three or more fragments—occurs after high-energy trauma, not a partial bend.

• Transverse fracture: A complete horizontal break across the bone shaft—doesn’t describe one-sided bending with an intact opposite cortex.

• Spiral fracture: Result of a twisting force producing a helical fracture line—does not match the described bending pattern.

• Oblique fracture: A complete diagonal break across the bone—again, not an incomplete, one-sided bend typical of greenstick injuries.

Age and Gender: The patient is a 65-year-old woman. This demographic is at high risk for osteoporosis, particularly post-menopause.

Clinical Presentation:

• • Multiple fractures with minor trauma: This is a classic sign of osteoporosis, as the bones are fragile and easily break.
  • Stooped posture (kyphosis): This is often caused by vertebral compression fractures, another common feature of osteoporosis.
  • Low Bone Mineral Density (BMD): This is the diagnostic criterion for osteoporosis.

Laboratory Findings:

• • Normal calcium and phosphate: This helps rule out primary hyperparathyroidism or vitamin D deficiency/excess as the primary cause, which would typically show abnormal calcium and/or phosphate levels.
  • Decreased estrogen: This is the key piece of information. Postmenopausal women experience a significant drop in estrogen levels.
• The Role of Estrogen:
  • Estrogen plays a crucial role in regulating bone remodeling. It inhibits osteoclast activity. Osteoclasts are the cells responsible for bone resorption (breaking down bone).
  • With the decrease in estrogen after menopause, the inhibitory effect on osteoclasts is lost.
  • This leads to increased osteoclast activity and a higher rate of bone resorption compared to bone formation (osteoblastic activity).
  • While the patient’s parathyroid hormone levels are not given, it is important to understand that the drop in estrogen leads to an increase in the sensitivity of the skeleton to the resorptive effects of PTH, and also to a compensatory increase in PTH secretion in an attempt to maintain calcium homeostasis.
  • The net result is a shift in the balance towards bone breakdown, leading to a progressive loss of bone mass and the development of osteoporosis.

❌Why the other options are incorrect:

• Increased osteoblastic activity leading to excessive bone formation: This would result in denser bones, not osteoporosis.
• Decreased osteoclast activity resulting in dense but fragile bones: Decreased osteoclast activity would lead to increased bone density, not osteoporosis. This describes conditions like osteopetrosis (“marble bone disease”).
• Decreased oestrogen levels leading to increased osteoblast activity and bone resorption: The first part of this statement is incorrect. Decreased estrogen does not lead to increased osteoblast activity; it leads to increased osteoclast activity.
• Excessive vitamin D leading to hyper mineralisation of bones: Excessive vitamin D leads to hypercalcemia and potentially renal stones, not necessarily hypermineralization. A deficiency, not excess, is more commonly associated with bone issues (osteomalacia/rickets).

• A comminuted fracture is when the bone is shattered into three or more fragments.

• Commonly results from severe trauma (e.g., car accidents, falls from height).

• Healing is often complicated because of the multiple bone fragments, requiring surgical fixation.

❌ Why the others are incorrect:

• Greenstick fracture: Incomplete fracture, common in children → bone bends and cracks.

• Transverse fracture: Break is straight across the bone, perpendicular to its axis.

• Spiral fracture: Results from twisting force, fracture line is helical.

• Oblique fracture: Break runs diagonally across the bone.

• Parathyroid hormone (PTH) is secreted by the parathyroid glands in response to low serum calcium.

• Its actions increase serum calcium and decrease serum phosphate by:

  1. Bone: Stimulates osteoclast activity indirectly (via osteoblasts) → ↑ bone resorption → release of calcium and phosphate into blood.

  2. Kidney: Increases calcium reabsorption in distal tubules, decreases phosphate reabsorption in proximal tubules.

  3. Vitamin D activation: Stimulates 1-α hydroxylase in the kidney → ↑ calcitriol (active vitamin D) → increases intestinal absorption of calcium.

❌ Why the others are incorrect:

• Calcitonin: Secreted by thyroid C-cells, does the opposite → inhibits osteoclasts, lowering calcium.

• Insulin: Anabolic hormone, no direct role in calcium homeostasis.

• Thyroxine (T4): Excess can cause bone loss, but not the main regulator.

• Testosterone: Supports bone density, not calcium regulation.

• Alkaline phosphatase (ALP) is present in many tissues, but especially high in the liver (bile canaliculi) and bone (osteoblasts).

• Elevated ALP levels are clinically significant in:

  • Liver disease → especially obstructive jaundice and cholestasis, where bile duct obstruction increases ALP release.

  • Bone disease → conditions with high osteoblastic activity, e.g., rickets, osteomalacia, Paget’s disease, bone metastases.

• To differentiate liver vs bone source of ALP, clinicians also check Gamma-glutamyl transferase (GGT) →

  • If both ALP and GGT are raised → source is liver.

  • If ALP is raised but GGT is normal → source is bone.

❌ Why the others are incorrect:

• AST (Aspartate aminotransferase): Primarily a marker of liver injury (also heart, muscle), but not bone disease. 

• ALT (Alanine aminotransferase): More specific to liver damage, not bone.

• GGT (Gamma glutamyl transferase): A marker of liver/biliary disease and alcoholism, but not bone.

• Osteocalcin: Specific marker of bone formation, but not used as a liver function test.

• The kidneys are the primary organs responsible for phosphate excretion.

• In renal failure, the glomerular filtration rate (GFR) decreases, meaning less phosphate is filtered out and excreted.

• This leads to hyperphosphatemia (elevated phosphate levels in the blood).

❌ Why the others are incorrect:

• Hyperparathyroidism → Causes hypophosphatemia, since PTH increases phosphate excretion in urine.

• Osteoporosis → Bone mineral density decreases, but phosphate levels in blood are usually not significantly elevated.

• Rickets → Caused by vitamin D deficiency; may have low or normal phosphate depending on type.

• Thymoma → Associated with myasthenia gravis, not phosphate imbalance.

• In the skin, 7-dehydrocholesterol (derived from cholesterol) absorbs UVB radiation and is converted into cholecalciferol (vitamin D₃).

• This cholecalciferol then enters the circulation and undergoes hydroxylation in the liver (25-hydroxylase → calcidiol) and later in the kidney (1-α hydroxylase → calcitriol, the active form).

❌ Why others are incorrect:

• Cholecalciferol → The product formed in skin after UV light acts, not the precursor.

• Cholesterol → The parent compound, but not the immediate skin precursor.

• Ergocalciferol → Plant-derived vitamin D₂, obtained from diet, not skin.

•  Ergosterol → Precursor for vitamin D₂ in plants, not in humans.

• Vitamin D₃ (cholecalciferol) is first converted in the liver to 25-hydroxycholecalciferol (calcidiol) by the enzyme 25-hydroxylase.

• In the kidney (proximal tubule), 1-α hydroxylase converts 25-hydroxy D₃ into 1,25-dihydroxycholecalciferol (calcitriol), which is the active form of vitamin D.

• This enzyme is regulated by:

  • Parathyroid hormone (PTH) → stimulates it.

  • Phosphate levels → low phosphate stimulates activity.

  • Calcitriol itself → provides negative feedback.

❌ Why others are incorrect:

•  24 hydroxylase → Inactivates vitamin D by converting it to 24,25-dihydroxycholecalciferol.

• 25 hydroxylase → Acts in the liver, not the kidney.

•  7-dehydrocholesterol reductase → Enzyme in skin for cholesterol metabolism, unrelated to activation.

•  17-β hydroxysteroid dehydrogenase → Steroid hormone metabolism, not vitamin D.

Dystrophin is a key structural protein that links the cytoskeleton of muscle fibers (actin filaments) to the extracellular matrix via the dystrophin–glycoprotein complex. This provides mechanical stability during contraction and relaxation.

• When dystrophin is absent or defective (as in Duchenne and Becker muscular dystrophies), the sarcolemma (muscle cell membrane) becomes fragile.

• Contraction-induced stress leads to microtears in the sarcolemma → leakage of intracellular enzymes like creatine kinase into the blood.

• This explains the high serum CK and progressive muscle weakness in the patient.

❌ Why other options are incorrect:

• Defective cross bridge formation → Caused by actin–myosin interaction problems, but dystrophin is not part of the cross-bridge cycle.

• Defective SERCA pump → Leads to impaired Ca²⁺ reuptake into the SR (seen in some metabolic myopathies), but not in dystrophin mutations.

•  Impaired acetylcholine release → This would be a neuromuscular junction issue (e.g., botulism), unrelated to dystrophin.

•  Reduced binding of calcium to troponin C → Would prevent contraction initiation, but dystrophin has no role in calcium–troponin binding.

• Dystrophin is a large cytoskeletal protein that connects actin filaments of the muscle cytoskeleton to the extracellular matrix via the dystrophin–glycoprotein complex.

• Its role is crucial in stabilizing the sarcolemma during muscle contraction and relaxation.

• Mutations or absence of dystrophin lead to muscular dystrophies such as Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD).

• Without dystrophin, the sarcolemma becomes fragile, leading to repeated injury, degeneration, and progressive weakness.

❌ Why Other Options Are Incorrect:

•  Actin → Actin is a cytoskeletal protein involved in contraction (thin filaments), but it does not anchor the cytoskeleton to the extracellular matrix.

• Myosin → Thick filament motor protein that interacts with actin for contraction, not for attachment to ECM.

• Titin → A giant protein that provides elasticity and stabilizes myosin, but does not link cytoskeleton to ECM.

• Troponin→ Regulatory protein in contraction, binds calcium to initiate actin-myosin interaction, not involved in cytoskeletal attachment.

• Inside the sarcoplasmic reticulum (SR) of skeletal muscle, calcium must be stored efficiently until it is released during contraction.

• The storage protein responsible for this is calsequestrin, which binds large amounts of calcium ions while keeping the free concentration low.

• This helps maintain a steep calcium gradient between the SR and cytosol, ensuring rapid calcium release during excitation–contraction coupling.

❌ Why Other Options Are Incorrect:

• Calbindin → Calcium-binding protein found mainly in intestine and kidney for Ca²⁺ transport.

• Calcineurin → Calcium/calmodulin-dependent phosphatase, involved in T-cell activation and muscle remodeling, not SR storage.

• Calexcitin → A neuronal calcium-binding protein involved in learning and memory, not skeletal muscle SR.

• Calmodulin → Cytosolic calcium-binding protein that activates enzymes (e.g., MLCK), not for SR calcium storage.

Correct Answer: Laterally….. pierced by saphenous nerve ❌ (Odd one out)

The femoral sheath is a funnel-shaped fascial sleeve derived from transversalis fascia (anteriorly) and iliac fascia (posteriorly). It surrounds the femoral vessels below the inguinal ligament and is divided by two vertical septa into three compartments:

1. Lateral compartment – contains the femoral artery.

2. Intermediate compartment – contains the femoral vein.

3. Medial compartment – known as the femoral canal, containing lymph nodes (notably Cloquet’s node), lymphatics, and loose connective tissue.

The saphenous nerve does NOT pass through the femoral sheath. It lies outside the sheath, traveling in the adductor canal with the femoral artery but pierces the fascia lata more distally. Hence, the statement “laterally… pierced by saphenous nerve” is incorrect and is the odd one out.

Why the others are correct:

• Medial compartment → femoral canal ✅
  Correct — this is the narrow medial compartment that contains lymphatics and serves as a potential space for femoral hernias.

• Lateral compartment → femoral artery ✅
  Correct — the femoral artery lies in the lateral part of the sheath.

• Intermediate compartment → femoral vein ✅
  Correct — the femoral vein is between the artery and the canal.

• Medially → inguinal lymph nodes ✅
  Correct — Cloquet’s (deep inguinal) lymph node lies in the femoral canal, which is medial.

Correct Answer: Obturator artery ❌ (does not participate)

The trochanteric anastomosis is a rich vascular network around the greater trochanter of the femur. Its purpose is to provide blood supply to the head and neck of the femur — particularly important in case of fractures where direct blood flow might be disrupted.

The main contributors are:

• Superior gluteal artery (descending branch)

• Inferior gluteal artery (ascending branch)

• Lateral circumflex femoral artery (ascending branch)

• Medial circumflex femoral artery (ascending branch)

Notice that the obturator artery is not part of this anastomosis. Instead, the obturator artery gives off the acetabular branch, which contributes to blood supply of the femoral head via the ligament of the head of femur (ligamentum teres). That’s important, but it’s separate from the trochanteric anastomosis.

Why the others are part of the trochanteric anastomosis:

• Superior gluteal artery ✅

  • Descending branch contributes directly to the anastomosis.

• Inferior gluteal artery ✅

  • Ascending branch participates in the network.

• Lateral circumflex femoral artery ✅

  • The ascending branch is a key contributor.

• Medial circumflex femoral artery ✅

  • The ascending branch is especially important in supplying the head and neck of femur.

Correct Answer: Ilioinguinal nerve ✅

The ilioinguinal nerve arises from the L1 spinal nerve (sometimes with a contribution from T12). It provides cutaneous innervation to the skin of the upper medial thigh, root of the penis and anterior scrotum (in males), or mons pubis and labium majus (in females). Because of its derivation from T12–L1, this is the nerve in the list that matches the question.

Medial femoral cutaneous nerve ❌
This nerve is a branch of the femoral nerve (L2–L4). It supplies skin over the medial thigh, but not from T12–L1.

Obturator nerve ❌
The obturator nerve originates from L2–L4. It innervates the medial thigh muscles (adductors) and gives off a cutaneous branch to the medial thigh, but again, it is not from T12–L1.

Lateral femoral cutaneous nerve ❌
This nerve comes from L2–L3. It supplies sensation to the lateral thigh, but not T12–L1.

Genitofemoral nerve ❌
The genitofemoral nerve arises from L1–L2, not T12. It divides into genital and femoral branches, supplying the skin of the anterior scrotum/labium majus and upper anterior thigh.

Correct Answer: Popliteus ✅

The popliteus is called the “key to the knee.” During the last phase of extension, the knee joint becomes locked because the femur rotates slightly medially on the tibia. This provides stability for standing. To begin flexion again, the joint must first be unlocked. The popliteus achieves this by laterally rotating the femur on the tibia in a weight-bearing limb or medially rotating the tibia on the femur in a non–weight-bearing limb. This unlocking allows full knee movement to be restored.

Soleus ❌
Acts only at the ankle joint as a plantarflexor. It does not cross the knee and plays no role in unlocking.

Plantaris ❌
A small, vestigial muscle. Though it crosses the knee, its weak action is limited to minor assistance in plantarflexion and knee flexion. It cannot unlock the knee.

Gastrocnemius ❌
Crosses the knee and contributes to knee flexion, but its role is in power generation, not the delicate unlocking mechanism.

Peroneus tertius ❌
Located in the anterior compartment of the leg. Its functions are dorsiflexion and eversion of the foot, unrelated to the knee.

Correct Answer

✅ It lies in superficial fascia

The oval opening described is the saphenous opening (fossa ovalis) in the fascia lata of the thigh. It is an important landmark where the great saphenous vein pierces to drain into the femoral vein.

• It is saphenous opening ✅ (true) → Correct identification of the structure.

• Closed by cribriform fascia ✅ (true) → The saphenous opening is covered by the cribriform fascia, which is pierced by veins and lymphatics.

• Lateral border is sharpest ✅ (true) → The lateral margin forms the falx inguinalis (falciform margin), a sharp curved edge.

• Great saphenous vein passes into it ✅ (true) → This vein pierces the opening to join the femoral vein.

• It lies in superficial fascia ❌ (false) → The saphenous opening lies in the deep fascia (fascia lata), not in the superficial fascia.

👉 That makes this the odd one out.

Correct Answer

✅ Anterior talofibular ligament (ATFL)

The most common ankle sprain injury occurs with inversion and plantarflexion, which stretches and tears the anterior talofibular ligament. This ligament runs between the lateral malleolus (fibula) and the talus. It is the weakest part of the lateral ligament complex (anterior talofibular, calcaneofibular, posterior talofibular).

👉 Clinical pearl: “Always Tears First Ligament” is a mnemonic for ATFL.

• Anterior tibiofibular ligament ❌ → part of the syndesmosis between tibia and fibula. Injured in high ankle sprains, not simple inversion injuries.

• Calcaneofibular ligament ❌ → may be torn in more severe inversion injuries, but it is usually the second to be affected after ATFL.

• Deltoid ligament ❌ → a strong medial ligament resisting eversion. Rarely injured without an associated fracture of the medial malleolus.

• Posterior talofibular ligament ❌ → the strongest part of the lateral complex. Only injured in severe ankle dislocations.

The muscle that inserts into the iliotibial tract is the gluteus maximus.

Key facts about gluteus maximus:

Gluteus maximus is actually a:

• Lateral rotator of the thigh

• Not a medial rotator

Medial rotation is performed by muscles like:

• Gluteus medius (anterior fibers)

• Gluteus minimus

• Tensor fascia lata

Correct Answer

✅ Mid-palmar space infection

Explanation

Why Mid-palmar Space is Correct

• The mid-palmar space lies deep to the flexor tendons of the medial four fingers (ring, middle, little, and index partly) and superficial to the interossei.

• Infection here → pain, swelling, and difficulty in flexion of the medial four fingers, since the flexor tendons pass through this space.

• Clinically: presents with palmar swelling, painful finger movements, and sometimes extension of infection into the forearm via the carpal tunnel.

Why the Other Options are Incorrect

• Dorsal subaponeurotic ❌
  This space lies on the dorsum of the hand, deep to extensor tendons. Infection causes dorsal hand swelling, not difficulty flexing fingers.

• Hypothenar ❌
  Contains hypothenar muscles (abductor, flexor, opponens digiti minimi). Infection here affects the little finger region, not all medial four fingers.

• Superficial pulp of the fingers ❌
  Infection here causes felon (localized abscess at fingertip pulp). Leads to throbbing pain in one finger, not all medial four.

• Thenar ❌
  Thenar space infection affects thumb movements (thenar muscles and index finger), not the medial four fingers.

Correct Answer

✅ Deep peroneal nerve

Explanation

Key Concept

• The deep peroneal (fibular) nerve supplies the skin between the first and second toes — i.e., the first dorsal web space.

• This area is a classic sensory landmark for testing deep peroneal nerve integrity.

• Motor: supplies anterior compartment muscles (dorsiflexors of foot and toes).

• Clinical correlation: injury → foot drop (loss of dorsiflexion) + sensory loss in first web space.

Why the Other Options are Incorrect

• Superficial peroneal ❌
  Provides cutaneous innervation to most of the dorsum of the foot, except the first web space.

• Saphenous nerve ❌
  A branch of the femoral nerve, it supplies the medial side of the leg and foot, not the dorsum between the first and second toes.

• Sural nerve ❌
  Provides sensation to the posterolateral aspect of the leg and lateral side of the foot. No role in the first web space.

• Medial plantar nerve ❌
  Branch of tibial nerve, supplies medial plantar surface of the foot and medial 3½ toes on the sole, not the dorsal web space.

Correct Answer

✅ 7

Explanation

Tarsal Bones of the Foot

There are 7 tarsal bones in each foot, arranged in two rows:

1. Proximal row:

   • Talus (ankle bone)

   • Calcaneus (heel bone)

2. Distal row:

   • Navicular

   • Cuboid

   • 3 Cuneiforms (medial, intermediate, lateral)

👉 Total = 7.

Clinical Note

• These bones form the tarsus, which contributes to the arches of the foot.

• The calcaneus bears weight during standing and provides attachment for the Achilles tendon.

• Fractures of calcaneus often occur from falls (“lover’s fracture”), important in orthopedic practice.

Why the Other Options are Incorrect

• 3 ❌ → Too few, does not account for the complex structure of the hindfoot/midfoot.

• 5 ❌ → Less than the actual number (may confuse with number of metatarsal bones in hand vs foot context).

• 9 ❌ → Too many; might confuse with total number of tarsal + metatarsals combined.

• 11 ❌ → Incorrect; total number of bones in one foot (tarsals, metatarsals, phalanges) is much higher.

Correct Answer

✅ Flexes and adducts

Explanation

Anatomy of Pectineus

• Origin: Superior ramus of pubis (pecten pubis).

• Insertion: Pectineal line of femur, just below the lesser trochanter, blending with linea aspera.

• Innervation: Primarily by the femoral nerve (L2–L4); sometimes also receives a branch from the obturator nerve (making it a transitional muscle between anterior and medial compartments).

Actions

• Flexion of thigh at hip (because it runs anterior to the hip joint).

• Adduction of thigh (because it lies close to the medial compartment muscles and pulls the thigh inward).

• It also assists in medial rotation to a minor extent.

Why the Other Options are Incorrect

• Flexes and abducts ❌
  Pectineus does flex, but instead of abducting, it adducts. Abduction is done by gluteus medius/minimus.

• Extends and adducts ❌
  Extension at hip is done by gluteus maximus and hamstrings, not pectineus.

• Extends and abducts ❌
  Same issue: pectineus is a flexor, not an extensor. Abduction again is incorrect.

• Extends and rotates ❌
  Pectineus is not a primary rotator or extensor. Rotation is a minor action, but flexion + adduction are the key.

Correct Answer

✅ 150°

Explanation

Normal Angles of Femoral Neck–Shaft

• The angle formed between the neck of the femur and the shaft is called the angle of inclination.

• This angle decreases with age:

  • At birth / in children: ~150°

  • In adults: ~125°

  • In the elderly: ~120° or even less (due to bone remodeling, osteoporosis, and changes in posture).

Why it matters

• A larger angle in children helps accommodate growth and rapid changes in gait.

• As people age, the angle decreases because of weight-bearing forces and remodeling of the proximal femur.

• Abnormalities:

  • Coxa vara → angle reduced (<120°) → short limb, limp.

  • Coxa valga → angle increased (>135°) → instability at hip.

Why the Other Options are Incorrect

• 130° ❌ → closer to the adult range, not typical for children.

• 140° ❌ → higher than adults, but still less than the normal child value.

• 155° ❌ & 160° ❌ → excessively high, not seen physiologically; would predispose to hip instability.

Correct Answer

✅ Infraspinatus

Explanation

Why Infraspinatus is Correct

• The infraspinatus muscle is one of the four rotator cuff muscles (SITS: Supraspinatus, Infraspinatus, Teres minor, Subscapularis).

• Its primary action: lateral (external) rotation of the arm at the shoulder joint.

• Nerve supply: Suprascapular nerve (C5–C6).

• Clinical relevance: Weakness or injury → impaired lateral rotation (e.g., difficulty combing hair, reaching back pocket).

• Pain and weakness in shoulder movements, especially lifting and rotating, are typical features of a rotator cuff injury.

Why the Other Options are Incorrect

• Pectoralis minor ❌
  Attaches from ribs 3–5 to coracoid process. Action: stabilizes scapula by pulling it forward and downward. No role in arm rotation.

• Subscapularis ❌
  Another rotator cuff muscle, but it is a medial rotator of the arm. If this were affected, the patient would have difficulty with internal rotation, not lateral rotation.

• Biceps brachii ❌
  A flexor of the elbow and supinator of the forearm. Does not act directly on shoulder rotation.

• Triceps brachii ❌
  Extends the elbow (long head also extends/adducts the arm). No role in lateral rotation of the shoulder.

Correct Answer

✅ Superior gluteal nerve

Explanation

Understanding Trendelenburg’s Test

• Trendelenburg’s test checks the function of the hip abductor muscles: gluteus medius and gluteus minimus.

• These muscles are innervated by the superior gluteal nerve (L4, L5, S1).

• Their job: stabilize the pelvis during the stance phase of walking.

👉 Positive Trendelenburg sign: when the patient stands on the affected leg, the pelvis drops on the opposite side because the abductors cannot hold the pelvis level.

Why Superior Gluteal Nerve is Correct

• Damage to the superior gluteal nerve paralyzes gluteus medius and minimus, leading to pelvic instability and positive Trendelenburg sign.

• Clinical gait: “waddling” or “lurching” gait to compensate.

Why the Other Options are Incorrect

• Femoral nerve ❌
  Supplies anterior thigh muscles (quadriceps) for knee extension. Damage causes weak knee extension, not pelvic drop.

• Sciatic nerve ❌
  Supplies posterior thigh and all muscles below the knee. Damage causes foot drop and hamstring weakness, but not Trendelenburg sign specifically.

• Inferior gluteal nerve ❌
  Innervates gluteus maximus, which is an extensor of the hip (important in rising from sitting or climbing stairs). Injury impairs powerful hip extension, but pelvis does not drop.

• Pudendal nerve ❌
  Supplies perineum (external anal sphincter, urethral sphincter, sensory to genitalia). Damage affects continence, not walking or hip stabilization.

Correct Answer

✅ Biceps brachii

Explanation

Why Biceps brachii is Correct

• The biceps brachii inserts onto the radial tuberosity of the radius.

• It also sends the bicipital aponeurosis medially into the deep fascia of the forearm.

• Function: powerful supinator of the forearm and flexor of the elbow.

• Clinical relevance: during supination (like turning a screwdriver), the tendon pulls on the radial tuberosity, rotating the radius.

Why the Other Options are Incorrect

• Triceps ❌
  Inserts onto the olecranon process of the ulna. It is the primary extensor of the elbow, not attached to the radius.

• Brachioradialis ❌
  Inserts onto the lateral surface of the distal radius (styloid process region). It flexes the elbow, especially in mid-pronation, but not on the radial tuberosity.

• Brachialis ❌
  Inserts onto the ulnar tuberosity and coronoid process of ulna. It is a strong flexor of the elbow, but acts only on the ulna (does not rotate radius).

• Teres major ❌
  Inserts onto the medial lip of the intertubercular sulcus of the humerus. Its role is adduction and medial rotation of the arm, not related to the radius.

Correct Answer

✅ Deep posterior compartment muscles

Explanation

Step 1: Analyze the findings

• Inability to flex the toes → Flexion of the toes is carried out by:

  • Flexor hallucis longus (big toe)

  • Flexor digitorum longus (lateral four toes)
    Both are in the deep posterior compartment of the leg.

• Foot drop → Classically due to paralysis of the anterior compartment muscles (dorsiflexors: tibialis anterior, extensor hallucis longus, extensor digitorum longus).
  However, here the key clue is flexion of toes is also lost. This means not just dorsiflexors, but the toe flexors (deep posterior group) are involved.

👉 The only way to explain both toe flexion loss + foot drop is damage to the tibial nerve, which supplies the deep posterior compartment (toe flexors) and contributes via branches to balance dorsiflexion/plantarflexion actions.

Step 2: Why other options are wrong

• Anterior compartment ❌
  Lesion here causes foot drop (loss of dorsiflexion) but toe flexion is preserved.

• Lateral compartment ❌
  These muscles (fibularis longus and brevis) are everters of the foot, not toe flexors. Injury here would cause loss of eversion, not toe flexion.

• Anterior compartment (duplicate) ❌
  Same reasoning as above.

• Posterior compartment (general) ❌
  Includes both superficial (gastrocnemius, soleus) and deep muscles. Superficial group does plantarflexion (not toe flexion). The specific dysfunction here points to the deep group only.

Correct Answer

✅ Popliteal artery

Explanation

The popliteal fossa contains important neurovascular structures arranged from superficial → deep in a very specific order.

Arrangement of structures (posterior to anterior):

1. Tibial nerve (most superficial of the deep structures)

2. Popliteal vein

3. Popliteal artery (most deep, directly against the popliteal surface of the femur, joint capsule, and popliteus muscle)

Additionally:

• Common fibular (peroneal) nerve runs along the superolateral boundary, not deeply placed.

• Small saphenous vein and posterior cutaneous nerve of thigh are even more superficial, draining and supplying skin.

So the popliteal artery is the deepest and most protected structure. Clinically, this is important because:

• It is difficult to palpate unless the knee is flexed.

• It is at risk in posterior knee dislocations.

Why the Other Options are Incorrect

• Small saphenous vein ❌
  Very superficial; drains into the popliteal vein. Not deep.

• Tibial nerve ❌
  It is the most superficial of the neurovascular bundle inside the fossa.

• Common fibular nerve ❌
  Runs laterally along the biceps femoris tendon; not the deepest structure.

• Posterior cutaneous nerve of thigh ❌
  A purely cutaneous nerve, very superficial; not part of the deep contents.

Correct Answer

✅ Subtalar and transverse tarsal joint

Explanation

Why This is Correct

• Inversion (sole turns inward) and eversion (sole turns outward) are side-to-side movements of the foot.

• These are not produced at the ankle (talocrural) joint, which is only a hinge for dorsiflexion and plantarflexion.

• Instead, they occur at:

  1. Subtalar (talocalcaneal) joint – between talus and calcaneus.

  2. Transverse tarsal joint – a functional combination of the talonavicular and calcaneocuboid joints.

Together, these joints let the foot adapt to uneven ground and maintain balance.

Why the Other Options are Wrong

• Subtalar and calcaneocuboid joint ❌
  Calcaneocuboid joint is indeed part of the transverse tarsal complex, but without including the talonavicular joint, this answer is incomplete.

• Subtalar and ankle joint ❌
  The ankle (talocrural) joint only allows dorsiflexion and plantarflexion. It does not participate in inversion/eversion.

• Talocalcaneonavicular joint ❌
  This is part of the transverse tarsal joint (talonavicular portion), but on its own, it cannot account for the complete inversion/eversion range.

• Intertarsal joints (general) ❌
  While technically true that these are intertarsal movements, the answer is too vague. Not all intertarsal joints participate meaningfully; only subtalar and transverse tarsal joints play the primary role.

Correct Answer

✅ Axillary nerve

Explanation

Why the Axillary Nerve is Correct

The surgical neck of the humerus is closely related to the axillary nerve and the posterior circumflex humeral artery.

• The axillary nerve arises from the posterior cord of the brachial plexus (C5–C6).

• It innervates the deltoid muscle (responsible for abduction of the arm beyond the first 15°) and the teres minor.

• Damage leads to:

  • Inability to abduct the arm at the shoulder

  • Loss of the rounded contour of the shoulder

  • Sensory loss over the regimental badge area (skin over deltoid).

Thus, in this case — fracture at the surgical neck + inability to abduct = axillary nerve injury.

Why the Other Options are Incorrect

• Median nerve ❌
  Runs in the arm but does not supply muscles of the shoulder. Mainly responsible for forearm flexors and thenar muscles. Injury → hand deformities (“ape hand”), not inability to abduct the shoulder.

• Musculocutaneous nerve ❌
  Innervates anterior arm flexors (biceps, brachialis, coracobrachialis). Injury causes weak flexion and supination, but does not affect abduction at the shoulder joint.

• Radial nerve ❌
  Runs along the radial groove of the humerus (midshaft). Injury → wrist drop due to paralysis of wrist extensors. This nerve is endangered in midshaft fractures, not surgical neck fractures.

• Ulnar nerve ❌
  Passes behind the medial epicondyle of the humerus (the “funny bone”). Damage here affects intrinsic hand muscles and causes “claw hand,” not shoulder abduction weakness.

Correct Answer

✅ Type I

Explanation

Why Type I is Correct

Type I collagen is the most abundant collagen in the human body and the primary collagen of bone, tendons, ligaments, dentin, and skin.
In bone, it forms the organic matrix (osteoid), which provides tensile strength. Minerals like calcium hydroxyapatite are then deposited on this framework, making bone strong yet slightly flexible.
Defective Type I collagen is seen in osteogenesis imperfecta, where bones become brittle and fracture easily — a clinical correlation that underscores its importance.

Why the Other Options are Incorrect

• Type II ❌
  Found mainly in cartilage, vitreous body, and nucleus pulposus. It resists compression, not the main collagen in bone.
  👉 Memory aid: “Type II = carTWOlage.”

• Type III ❌
  Forms reticular fibers that support skin, blood vessels, and internal organs. Important in tissues requiring flexibility. Defects are linked to Ehlers-Danlos syndrome (vascular type).

• Type IV ❌
  Special because it forms a mesh (not fibrils). It’s the principal collagen in the basement membrane (basal lamina), anchoring epithelium to underlying tissue. Not found in bone matrix.

• Type V ❌
  Present in placenta, hair, and interstitial tissues. Often found alongside Type I collagen and regulates fibril assembly, but is not the dominant collagen of bone.

Answer: ✅ Iliopsoas

Explanation:
The iliopsoas is the most powerful flexor of the hip joint and plays a vital role in activities like walking, running, and standing from a seated position. It is formed by the fusion of the psoas major and iliacus muscles. Sudden contraction during vigorous activity can lead to strain or pain, particularly in athletes or active individuals.

Let’s break down the incorrect options:

• ❌ Articular genu – This is a small muscle that pulls the synovial membrane of the knee joint during extension, not involved in hip flexion.

• ❌ Pectineus – Though it assists in hip flexion and adduction, it is not the primary or most powerful hip flexor.

• ❌ Vastus medialis – A part of the quadriceps, it extends the knee—not involved in hip flexion.

• ❌ Vastus lateralis – Also part of the quadriceps group responsible for knee extension, not hip flexion.

✅ Correct Answer: Gastrocnemius & Soleus

The tendocalcaneus, also known as the Achilles tendon, is formed by the convergence of two powerful calf muscles: the gastrocnemius and the soleus. These muscles collectively insert into the posterior surface of the calcaneus. When this tendon is tapped, it stretches these muscles, triggering a deep tendon reflex that causes plantar flexion at the ankle — an important part of neurological testing to assess the integrity of the S1 spinal segment.

Why the other options are incorrect:

• Flexor Digitorum Longus & Flexor Hallucis Longus: These are deep posterior compartment muscles of the leg. They do not contribute to the Achilles tendon but instead pass separately behind the medial malleolus to flex toes.

• Flexor Digitorum Longus & Gastrocnemius: Only gastrocnemius is part of the Achilles tendon. FDL is not; it has a distinct insertion on the distal phalanges of lateral toes.

• Flexor Hallucis Longus & Soleus: Soleus is a correct component of the Achilles tendon, but FHL is not. FHL independently inserts on the distal phalanx of the great toe.

• Flexor Digitorum Longus & Soleus: Again, soleus is correct, but FDL does not contribute to the Achilles tendon.

Answer: ✅ Femoral vein

The great saphenous vein is the longest vein in the body. It ascends along the medial side of the leg and thigh and ultimately drains into the femoral vein through the saphenous opening in the fascia lata, located just below the inguinal ligament. This makes the femoral vein its direct point of termination.

Why the other options are incorrect:

• Dorsal venous arch: This is where the great saphenous vein originates, not where it ends. It collects blood from the superficial veins of the foot.

• External iliac vein: This vein lies proximal to the femoral vein. The great saphenous vein does not drain directly into it.

• Popliteal vein: The small saphenous vein drains into the popliteal vein at the level of the knee, not the great saphenous vein.

• Plantar venous arch: Located on the sole of the foot, this arch is far distal to the termination point of the great saphenous vein.

✅ Correct Answer: Medial Border on Costal Surface (Medial Margin of Costal Surface)

The subscapularis muscle is one of the four rotator cuff muscles, and it is responsible for medial rotation of the humerus and stabilizing the glenohumeral joint.

• Origin:
  It arises from the subscapular fossa, which is the concave anterior (costal) surface of the scapula.
  Specifically, its broad origin includes the medial margin (border) of the costal surface.

• Insertion:
  The lesser tubercle of the humerus.

• Function:

  • Medial rotation of the arm.

  • Adduction of the arm (assists).

  • Stabilizes the head of the humerus in the glenoid cavity.

❌ Why the Other Options Are Incorrect:

• Acromion Process:
  This is part of the scapula’s lateral superior projection, but no muscle originates here; the deltoid inserts here.

• Coracoid Process:
  Serves as the origin of short head of biceps brachii, coracobrachialis, and pectoralis minor, but not subscapularis.

• Dorsal Surface:
  The posterior surface of the scapula. Muscles like infraspinatus and supraspinatus originate here, but subscapularis arises from the anterior/costal surface.

• Inferior Angle:
  Muscles like teres major may originate here, but not subscapularis.

• • Actin (thin) filaments are anchored to the Z line via proteins like α-actinin.

  • The lateral spacing (distance) between adjacent actin filaments within the same sarcomere is organized and fixed at the Z line.

  • This spacing determines the hexagonal lattice arrangement of thin filaments.

  So when asked:

  “Distance between one actin filament and the next actin filament on the same sarcomere”

  It refers to the structural anchoring and spacing point, which is the Z line.

  ---

  Why the other options are incorrect ❌

  • M line ❌
    → Anchors myosin (thick) filaments, not actin.

  • I band ❌
    → Region containing actin only, but does not define spacing.

  • A band ❌
    → Region of overlap of actin and myosin; spacing is not set here.

  • H zone ❌
    → Contains only myosin; no actin filaments.

• Length of muscle at rest: This matters because of the length–tension relationship. There is an optimal sarcomere length (~2.0–2.2 μm) that gives maximal overlap of actin and myosin. However, this is not the primary determinant of whole muscle contraction strength.
• Number of muscle fibres recruited: The more motor units (each motor neuron + the fibres it innervates) that are activated, the greater the overall force. This is the primary determinant of contraction strength in vivo. ✅
• Number of ACh receptors: Important for neuromuscular transmission efficiency (e.g., reduced in myasthenia gravis), but not the main determinant under normal physiology.
• Thickness of Sarcolemma: This does not play a major role in determining contraction strength.
• The type of muscle fibre: This influences endurance vs strength (slow oxidative vs fast glycolytic), but recruitment of fibres is still the dominant factor for acute contraction strength.

✅ Correct Answer: Number of muscle fibres recruited

✅ Correct Answer:

Fenn Effect

• Described by Wallace O. Fenn (1923).
• States that the amount of energy liberated (ATP hydrolyzed) during muscle contraction is proportional to the work performed.
• If the muscle shortens and does work → more ATP is consumed.
• If it contracts isometrically (no shortening) → less ATP is consumed.

❌ Why not the others?

• Actin PowerStroke theory → Describes the physical movement of actin by myosin heads, not the proportionality of ATP use to work.
•  Crossbridge theory → Explains how myosin heads bind, pivot, and detach, fueled by ATP. It’s the mechanism, not the energy–work correlation.
•  Power stroke → The actual movement of myosin head pulling actin.
•  Ratchet theory of contraction → Old explanation for repeated crossbridge cycling, not about ATP-work proportionality.

✅ Correct Answer: High myoglobin content and oxidative metabolism

• Slow muscle fibers (Type I fibers) are designed for endurance and sustained contractions.
• They have:
  • High myoglobin (which gives them a red color, hence also called “red fibers”)
  • Numerous mitochondria → supports oxidative phosphorylation
  • Rich capillary supply → ensures continuous oxygen delivery
• These features allow them to resist fatigue and sustain long-duration activities (like marathon running, posture maintenance).

❌ Extensive sarcoplasmic reticulum

• This is more characteristic of fast muscle fibers (Type II), which require rapid calcium release and reuptake for quick, powerful contractions.

❌ Largest size and glycolytic enzymes

• Again, this is a property of fast glycolytic fibers (Type IIb), which are thick, pale, and rely heavily on glycolysis for short bursts of power.

❌ Rapid contraction and fewer mitochondria

• This describes fast fibers (low mitochondria → less oxidative capacity), not slow fibers.

❌ Small nerve fibers and rapid excitation

• Slow fibers are indeed innervated by small motor neurons, but their excitation is slower (not rapid). The rapid part here makes it incorrect.

✅ Correct Answer:

Tetanization

🔎 Explanation

• A muscle twitch = single contraction–relaxation cycle from one action potential.
• If another stimulus arrives before full relaxation, the effects add together → summation.
• With rapid repeated stimuli:
  • The muscle doesn’t relax completely.
  • The force of contraction keeps adding up.
  • Eventually, it reaches a sustained, smooth contraction = tetanus (tetanization).

This is the additive effect of twitches → increased strength.

❌ Why not the other options?

•  Treppe (“staircase phenomenon”) → Strength increases gradually with repeated twitches due to improved Ca²⁺ handling, but it’s stepwise, not continuous summation.
•  Muscle tone → Baseline partial contraction for posture, unrelated to twitch addition.
•  Muscle fatigue → Decline in force after prolonged activity, not increase.
•  Isotonic contraction → Muscle changes length (shortens/lengthens) under constant load; not about twitch summation.

✅ Correct Answer:

. Complete overlap of actin filaments

🔎 Explanation

• Active tension in muscle is described by the length–tension relationship.
• Optimal sarcomere length for maximum force: ~2.0–2.2 μm (enough actin–myosin overlap without interference).
• If sarcomere length shortens below ~1.6 μm:
  • Actin filaments from opposite Z-discs overlap each other.
  • This blocks myosin binding sites and interferes with cross-bridge formation.
  • Result → active tension falls to zero even though ATP and calcium may still be present.

❌ Why not the other options?

• . Crumpling of myosin filaments → Myosin doesn’t crumple; the issue is actin–actin interference.
• . Lack of ATP availability → That causes rigor mortis, not this physiological length–tension effect.
• . Low calcium release → Would reduce contraction in general, but not specifically when sarcomere <1.6 μm.
•  Maximum overlap of myosin cross bridges → This is what gives maximum tension (at optimal length), not zero.

✅ Correct Answer:

Lack of ATP prevents myosin detachment from actin

Why it’s correct:

• Normally, after the power stroke, ATP must bind to the myosin head to release it from actin and allow a new contraction cycle.
• After death, ATP production stops. Without ATP, myosin heads remain bound to actin filaments → cross-bridges stay locked → muscles stiffen = rigor mortis.

❌ Excessive calcium causes continuous contraction

Calcium does leak from the sarcoplasmic reticulum after death, exposing actin binding sites. But this alone doesn’t cause rigor mortis. Without ATP, myosin heads cannot detach — that’s the direct mechanism.

❌ Increased ATP leads to sustained contraction

This is the opposite of what happens. ATP levels fall, they don’t rise. Without ATP, cross-bridge cycling stops.

❌ Lactic acid accumulation locks muscle fibers

Lactic acid buildup lowers pH but does not cause the actin–myosin cross-bridge locking seen in rigor mortis.

❌ Troponin-tropomyosin breakdown freezes muscles

These proteins regulate actin–myosin binding, but rigor mortis is not due to their breakdown. It’s due to lack of ATP.

✅ Correct Answer:

Eccentric contraction

Why it’s correct:

In an eccentric contraction, the muscle generates force while lengthening.

Here, the quadriceps are active but lengthening to slow the body against gravity during downhill running. This controlled lengthening protects joints and regulates movement, though it can cause delayed-onset muscle soreness (DOMS).

❌ Concentric contraction

Force is produced while shortening the muscle (e.g., quadriceps contracting to stand up from a squat). Not happening here since the muscle is lengthening, not shortening.

❌ Isometric contraction

Force is generated without a change in length (e.g., holding a squat position). Not the case here, as the muscle length is changing.

❌ Isotonic contraction

A general term for muscle contraction that changes muscle length under constant tension. It includes both concentric and eccentric contractions. The question asks for the specific type.

❌ Isokinetic contraction

Muscle contracts at a constant speed (usually measured with special equipment in labs/rehab). Not relevant in natural running conditions.

✅ Correct Answer:

Fatty acids

Why it’s correct:

After 2–3+ hours of steady endurance work, muscle and liver glycogen are largely depleted, and skeletal muscle relies mainly on aerobic oxidation of fatty acids for ATP. Fat metabolism is slower but sustainable, making it the dominant fuel late in a marathon.

❌ Amino acids

Minor contribution (~5–10%) during prolonged exercise; primarily a backup when glycogen is low, not the main fuel.

❌ Blood glucose

Still used (from hepatic output), but limited supply; cannot meet most of the energy demand compared with fatty acid oxidation this late.

❌ Creatine phosphate

Supports only the first 5–10 seconds of maximal effort; irrelevant during steady-state hours into a race.

❌ Muscle glycogen

Key early fuel; by 20 miles much is depleted (“hitting the wall”), so it’s no longer predominant.

✅ Correct Answer:

Creatine phosphate system

Why it’s correct:

For efforts lasting ~0–10 seconds at maximal intensity, ATP is regenerated primarily by the phosphagen (ATP-PCr) system. Creatine phosphate (phosphocreatine, PCr) rapidly donates its phosphate to ADP via creatine kinase, restoring ATP almost instantaneously to fuel explosive contractions at the start and throughout a 100 m sprint.

❌ Fatty acid

Too slow (requires aerobic β-oxidation and mitochondrial processing). Dominates during prolonged, lower-intensity exercise—not a 10-second sprint.

❌ Oxidative phosphorylation

High ATP yield but slow activation kinetics (needs sufficient oxygen delivery and mitochondrial steps). Insufficient to meet the immediate, maximal power demand of a 100 m dash.

❌ Glycogen pathway

Refers to anaerobic glycolysis from muscle glycogen—important for ~10–60 seconds bouts (e.g., 200–400 m), but it lags the phosphagen system and is not the primary source in the first ~10 seconds.

❌ Blood glucose

Contribution is minimal in the first seconds; uptake/processing is too slow relative to the instantaneous ATP demand.

✅ Correct Answer:

Creatine phosphate system

Why it’s correct:

For efforts lasting ~0–10 seconds at maximal intensity, ATP is regenerated primarily by the phosphagen (ATP-PCr) system. Creatine phosphate (phosphocreatine, PCr) rapidly donates its phosphate to ADP via creatine kinase, restoring ATP almost instantaneously to fuel explosive contractions at the start and throughout a 100 m sprint.

❌ Fatty acid

Too slow (requires aerobic β-oxidation and mitochondrial processing). Dominates during prolonged, lower-intensity exercise—not a 10-second sprint.

❌ Oxidative phosphorylation

High ATP yield but slow activation kinetics (needs sufficient oxygen delivery and mitochondrial steps). Insufficient to meet the immediate, maximal power demand of a 100 m dash.

❌ Glycogen pathway

Refers to anaerobic glycolysis from muscle glycogen—important for ~10–60 seconds bouts (e.g., 200–400 m), but it lags the phosphagen system and is not the primary source in the first ~10 seconds.

❌ Blood glucose

Contribution is minimal in the first seconds; uptake/processing is too slow relative to the instantaneous ATP demand.

✅ Correct Answer:

Creatine phosphate system

Why it’s correct:

For efforts lasting ~0–10 seconds at maximal intensity, ATP is regenerated primarily by the phosphagen (ATP-PCr) system. Creatine phosphate (phosphocreatine, PCr) rapidly donates its phosphate to ADP via creatine kinase, restoring ATP almost instantaneously to fuel explosive contractions at the start and throughout a 100 m sprint.

❌ Fatty acid

Too slow (requires aerobic β-oxidation and mitochondrial processing). Dominates during prolonged, lower-intensity exercise—not a 10-second sprint.

❌ Oxidative phosphorylation

High ATP yield but slow activation kinetics (needs sufficient oxygen delivery and mitochondrial steps). Insufficient to meet the immediate, maximal power demand of a 100 m dash.

❌ Glycogen pathway

Refers to anaerobic glycolysis from muscle glycogen—important for ~10–60 seconds bouts (e.g., 200–400 m), but it lags the phosphagen system and is not the primary source in the first ~10 seconds.

❌ Blood glucose

Contribution is minimal in the first seconds; uptake/processing is too slow relative to the instantaneous ATP demand.

✅ Correct Answer:

A-alpha fibres

Explanation:

• Aα fibres are the largest diameter, heavily myelinated fibres in the peripheral nervous system.
• They include:
  • Ia fibres → from muscle spindles (sense muscle length → proprioception).
  • Ib fibres → from Golgi tendon organs (sense muscle tension → proprioception).
  • Alpha motor neurons → innervate extrafusal skeletal muscle fibers (motor control).
• Their fast conduction velocity (~80–120 m/s) makes them ideal for quick reflexes and coordinated movement.

❌ A-beta fibres

• Function: touch, vibration, pressure.
• They do not carry motor commands.

❌ A-delta fibres

• Function: fast pain and temperature.
• Thinly myelinated, slower than Aα and Aβ.

❌ B fibres

• Small, myelinated autonomic preganglionic fibers.
• Not related to skeletal muscle or proprioception.

❌ C fibres

• Function: slow pain, crude touch, temperature.
• Unmyelinated, slowest conduction.

✅ Correct Answer:

A-alpha fibres

Explanation:

• Aα fibres are the largest diameter, heavily myelinated fibres in the peripheral nervous system.
• They include:
  • Ia fibres → from muscle spindles (sense muscle length → proprioception).
  • Ib fibres → from Golgi tendon organs (sense muscle tension → proprioception).
  • Alpha motor neurons → innervate extrafusal skeletal muscle fibers (motor control).
• Their fast conduction velocity (~80–120 m/s) makes them ideal for quick reflexes and coordinated movement.

❌ A-beta fibres

• Function: touch, vibration, pressure.
• They do not carry motor commands.

❌ A-delta fibres

• Function: fast pain and temperature.
• Thinly myelinated, slower than Aα and Aβ.

❌ B fibres

• Small, myelinated autonomic preganglionic fibers.
• Not related to skeletal muscle or proprioception.

❌ C fibres

• Function: slow pain, crude touch, temperature.
• Unmyelinated, slowest conduction.

Explanation:

• Titin is a giant elastic protein that extends from the Z-line to the M-line within the sarcomere.
• It plays two critical roles:
  • Structural support → keeps thick (myosin) filaments properly aligned within the sarcomere.
  • Elasticity → acts like a spring, allowing the sarcomere to return to resting length after being stretched.
• Without titin, sarcomeres would lose stability, and muscle fibers would not recoil efficiently after stretch.

❌ Anchoring of actin filaments to the Z-line

• This is the job of α-actinin, not titin.

❌ Anchoring of myosin filaments to the Z-line

• Myosin is centered at the M-line.
• Titin spans between Z-line and M-line, but its role is elasticity and support, not just “anchoring.”

❌ Initiating the power stroke of myosin heads

• The power stroke comes from ATP hydrolysis by the myosin head, not titin.

❌ Regulating the contraction speed of myosin

• Contraction speed is determined by the myosin ATPase isoform (fast vs slow fibers), not titin.

Explanation:

• The resting membrane potential (RMP) of neurons is typically about –70 mV.
• The primary reason is the selective permeability of the membrane to potassium (K⁺).
• At rest:
  • The neuronal membrane is much more permeable to K⁺ (due to leak channels) than to Na⁺ or Cl⁻.
  • K⁺ tends to diffuse out of the cell (down its concentration gradient), leaving behind negatively charged proteins → creating a negative inside.
  • The exact RMP is determined largely by the K⁺ equilibrium potential (E_K), modified slightly by Na⁺ leak and the Na⁺/K⁺ pump.
• Thus, while the sodium-potassium pump is important for maintaining gradients, the immediate and primary cause of the resting potential is K⁺ permeability.

❌ Chloride ion distribution

• Cl⁻ does contribute to overall potential in some neurons, but it is not the main determinant of the resting potential.

❌ Equilibrium of sodium and potassium ions

• Resting potential is not a simple equilibrium between Na⁺ and K⁺.
• Instead, it is closer to the K⁺ equilibrium potential because the membrane is more permeable to K⁺.

❌ Neurotransmitter release

• Neurotransmitters affect postsynaptic potentials (EPSPs/IPSPs), not the intrinsic resting potential of a neuron.

❌ Sodium-potassium pump activity

• The pump (3 Na⁺ out, 2 K⁺ in) is essential to maintain ion gradients.
• Without it, the gradients would collapse over time, but the pump is not the direct primary cause of the –70 mV RMP.
• It contributes a small electrogenic effect (~ –5 mV).

✅ Correct Answer:

Somatic lateral plate mesoderm

Explanation:

• Bones of the appendicular skeleton (pectoral girdle, pelvic girdle, and limb bones) are derived from the somatic (parietal) layer of lateral plate mesoderm.
• The scapula, being part of the pectoral girdle, is therefore mesodermal in origin from this layer.
• These mesodermal cells undergo chondrification first and later ossify through endochondral ossification.

❌ Neural crest cells

• Give rise to craniofacial bones, cartilage, and connective tissue, especially in the head and neck region.
• They do not contribute to scapula formation.

❌ Splanchnic lateral plate mesoderm

• Forms the heart, blood vessels, and connective tissue of the gut and viscera.
• Not involved in scapula development.

❌ Axial mesoderm

• This refers to the notochord, which induces neural tube development and forms the nucleus pulposus of intervertebral discs.
• Not related to bone formation.

❌ Somatic mesoderm (without specifying lateral plate)

• A vague option, but embryologically, “somatic” in bone context refers specifically to the somatic layer of lateral plate mesoderm.
• To be precise, the correct term is somatic lateral plate mesoderm.

✅ Correct Answer:

Paraxial mesoderm

Explanation:

• During embryonic development, the intraembryonic mesoderm organizes into three main parts on either side of the notochord:
  • Paraxial mesoderm → forms somites
  • Intermediate mesoderm → forms urogenital system
  • Lateral plate mesoderm → splits into somatic and splanchnic layers (body wall, heart, vessels, etc.)
• The paraxial mesoderm segments into somites → which later differentiate into:
  • Sclerotome → vertebrae & ribs
  • Myotome → skeletal muscles of trunk & limbs
  • Dermatome → dermis of the back

Thus, somites are the foundation of the segmental organization of the body.

❌ Endoderm

• Forms epithelial lining of GI tract, lungs, liver, pancreas, etc.
• Not musculoskeletal structures.

❌ Ectoderm

• Forms epidermis, nervous system, neural crest cells.
• No somites.

❌ Lateral plate mesoderm

• Forms body wall, heart, blood vessels, connective tissues of viscera.
• Not segmental, and not somites.

❌ Neural crest

• Migratory cells from ectoderm.
• Give rise to melanocytes, sensory ganglia, Schwann cells, adrenal medulla, craniofacial cartilage.
• Not somites.

The digits would be connected by webbing, and would not be separated

• Apoptosis (programmed cell death) plays a crucial role in sculpting developing structures.
• In the limb bud, apoptosis occurs in the interdigital mesenchyme → this allows separation of the digits.
• If apoptosis fails, the digits remain fused by soft tissue → a condition known as syndactyly.
• Thus, failure of apoptosis doesn’t stop bone or muscle formation, but it prevents proper separation of structures that need sculpting.

❌ Bone and muscle would not form

• Formation of bone (via endochondral ossification) and muscle (from myoblasts) does not depend on apoptosis.
• These rely on mesodermal differentiation.

❌ Overlying epidermis would not form

• Epidermis is derived from ectoderm, not apoptosis-dependent.

❌ Proximal-distal patterning would not occur normally

• Proximal-distal patterning is regulated by the AER (Apical Ectodermal Ridge) and FGF signals, not apoptosis.

❌ All bones would form as the same structure

• Bone identity (humerus vs radius/ulna vs digits) is determined by HOX genes and limb bud signaling (AER, ZPA), not apoptosis.

✅ Correct Answer:

Formation of structures proximal to apical ridge, no formation of new distal structures

Explanation:

• The Apical Ectodermal Ridge (AER) is a thickened ectoderm at the tip of the limb bud.
• It secretes FGF (Fibroblast Growth Factors), which maintain the progress zone of mesenchymal cells in an undifferentiated, proliferative state.
• As long as the AER is present, mesenchymal cells keep proliferating and contribute to distal limb structures (e.g., fingers, toes).
• If the AER is removed:
  • Proximal structures (e.g., humerus, femur) that already began development will still form.
  • But new distal structures cannot form, leading to truncated limbs.

❌ Degeneration of limb bud

• Removal of AER does not cause complete degeneration of the limb bud.
• Proximal parts still develop normally.

❌ Regeneration of entire limb bud from underlying mesoderm

• Mammals cannot regenerate an entire limb from mesoderm once AER is removed.
• Proximal structures already specified will continue to develop, but distal regeneration does not occur.

❌ Regeneration of new AER

• In mammals, a lost AER does not regenerate.
• Some regeneration is possible in lower vertebrates (like salamanders), but not in humans.

❌ Continued development in progress zone

• The progress zone requires signals from the AER.
• Without the AER, progress zone mesenchyme differentiates prematurely, halting distal outgrowth.

• Long bones increase in length through the epiphyseal (growth) plate, which is made of hyaline cartilage.
• The cartilage here undergoes interstitial growth (growth from within) by proliferation of chondrocytes.
• This provides a scaffold that is then replaced by bone via endochondral ossification.
• Important distinction: bone itself cannot grow interstitially because of its rigid mineralized matrix. Growth in length therefore depends on cartilage.

❌ Removal of calcified cartilage

• This is part of endochondral ossification, but removal alone does not account for bone lengthening.
• It is a step in remodeling, not the primary growth mechanism.

❌ Endochondral deposition of bone tissue

• Endochondral ossification is indeed how cartilage is replaced by bone, but the increase in length comes first from cartilage proliferation (interstitial growth), not from bone deposition itself.

❌ Appositional deposition of bone tissue

• Appositional growth = addition of new bone layers to the outer surface (beneath periosteum).
• This increases the thickness (diameter) of bone, not its length.

❌ Interstitial growth of bone tissue

• Bone cannot grow interstitially because its matrix is calcified and rigid.
• Only cartilage is capable of interstitial growth.

✅ Correct Answer:

Osteoblasts

• Osteoblasts are the bone-forming cells derived from osteoprogenitor cells.
• They are found lining the bone surfaces, especially in areas of active bone formation.
• Their main roles are:
  • Secreting osteoid (unmineralized bone matrix).
  • Initiating mineralization.
• Once surrounded by matrix, osteoblasts differentiate into osteocytes.

❌ Osteoclast

• Large multinucleated cells involved in bone resorption.
• Found in Howship’s lacunae (resorption pits), not simply along intact bone surfaces.

❌ Osteon

• Not a cell, but a structural unit of compact bone (Haversian system).
• Composed of concentric lamellae around a central canal.
• Therefore, this is a histological structure, not a cell.

❌ Lymphocytes

• White blood cells involved in immune responses.
• Not part of normal bone histology unless there’s pathology (e.g., inflammation, infection, marrow involvement).

❌ Chondrocytes

• Cells of cartilage, found in lacunae within cartilage matrix.
• Not present in bone tissue.

• T-tubules (transverse tubules) are invaginations of the sarcolemma (the muscle cell membrane).
• They extend deep into the muscle fiber, allowing the action potential to travel quickly into the interior of the cell.
• This ensures synchronous contraction of all myofibrils by triggering the sarcoplasmic reticulum to release calcium.
• So, while the T-tubules are closely associated with the sarcoplasmic reticulum (forming the triad in skeletal muscle: T-tubule + 2 terminal cisternae), structurally they are derived from the sarcolemma, not the SR.

❌ Nucleus

• The nuclei of skeletal muscle are peripheral, multinucleated, but they do not form tubular extensions.

❌ Rough Endoplasmic Reticulum

• RER is mainly involved in protein synthesis.
• In muscle, the specialized ER is the sarcoplasmic reticulum (SR), not the T-tubules.

❌ Sarcoplasmic Reticulum

• The SR stores and releases calcium for contraction.
• It lies adjacent to the T-tubules, but T-tubules are not extensions of the SR—they are separate but functionally linked.

❌ Sarcoplasm

• The sarcoplasm is simply the cytoplasm of the muscle cell (contains mitochondria, glycogen, myoglobin).
• It is not structurally continuous with T-tubules.

• The prepatellar bursa lies between the patella and the skin.
• It is prone to inflammation in people who kneel for long periods → classically known as “housemaid’s knee.”
• Clinical features:
  • Pain localized to the front of the knee.
  • Worse with kneeling or climbing stairs (because of patellofemoral stress).
  • Usually normal range of motion since the joint itself is not involved.

❌ Anserine bursa

• Located between the pes anserinus tendons (gracilis, sartorius, semitendinosus) and the tibia.
• Pain is usually medial to the tibial tuberosity, not directly anterior over the patella.
• More common in obese middle-aged women or athletes with overuse injuries.

❌ Popliteal (Baker’s cyst)

• Located in the popliteal fossa at the back of the knee.
• Causes posterior knee swelling and tightness, especially with knee extension.
• Not related to kneeling.

❌ Suprapatellar bursa

• Lies above the patella, beneath the quadriceps tendon.
• Inflammation here is usually linked to joint effusion/infection (suprapatellar pouch communicates with knee joint).
• Would cause restricted motion rather than preserved ROM.

❌ Gastrocnemius bursa

• Lies between the medial head of gastrocnemius and joint capsule.
• Pain is posterior-medial, not anterior.
• Rarely involved compared to prepatellar bursitis.

• The rotator cuff (supraspinatus, infraspinatus, teres minor, subscapularis) stabilizes the shoulder joint and allows lifting and rotation of the arm.
• Key features of a rotator cuff tear:
  • Night pain, especially when lying on the affected shoulder, is very characteristic.
  • Weakness in abduction and external rotation due to involvement of supraspinatus or infraspinatus.
  • Often seen in overhead athletes like tennis players.
• The combination of night pain + weakness in lifting/rotation points strongly toward a rotator cuff tear rather than just inflammation.

❌ Tendinopathy

• This is an overuse injury of tendons (often supraspinatus tendon).
• Causes pain on activity, especially overhead movement, but weakness is less pronounced compared to a tear.
• Night pain is less typical unless it progresses to a tear.

❌ Bursitis (Subacromial)

• Presents with painful arc syndrome (pain between 60–120° abduction).
• Pain is often inflammatory and aggravated with motion, but muscle weakness is not a key feature.
• Night pain is less specific compared to rotator cuff tears.

❌ Frozen shoulder (Adhesive capsulitis)

• Involves capsular fibrosis, leading to global restriction of movement (active AND passive).
• Patients struggle with both abduction and external rotation, but pain at night is not the main hallmark.
• More common in diabetics, not necessarily in athletes.

❌ Acromioclavicular (AC) joint injury

• Causes localized pain and tenderness at the AC joint.
• Pain is worse with cross-body adduction of the arm.
• Does not cause generalized weakness in lifting or rotation like a rotator cuff tear.

✅ Correct Answer: 

Pectoral (Anterior) group of axillary lymph nodes

Explanation:

• The lateral thoracic artery runs along the lateral border of the pectoralis minor and supplies the serratus anterior and the breast.
• The pectoral (anterior) group of axillary nodes lies along the inferolateral border of the pectoralis minor, close to where the lateral thoracic vessels are located.
• These nodes mainly drain the anterior thoracic wall, including most of the breast, which explains their surgical importance during mastectomy.

❌ Apical nodes

• Located at the apex of the axilla, near the first rib and clavicle.
• Associated more with the axillary vein and cephalic vein tributaries, not the lateral thoracic artery.

❌ Lateral nodes

• Found along the axillary vein on the lateral wall of the axilla.
• They drain most of the upper limb, not directly related to the lateral thoracic artery.

❌ Central nodes

• Situated in the center of the axilla within the adipose tissue.
• Receive lymph from pectoral, lateral, and posterior groups, but they are not anatomically related to the lateral thoracic artery.

❌ Posterior nodes (Subscapular)

• Lie along the subscapular vessels at the posterior axillary fold.
• They drain the posterior thoracic wall and scapular region, not the area supplied by the lateral thoracic artery.

Step 1: Pathophysiology in severe MG

• MG causes progressive weakness of skeletal muscles, including respiratory muscles (diaphragm, intercostals).

• In severe or untreated cases, this leads to a myasthenic crisis, which can cause acute respiratory failure due to hypoventilation.

• This is the most feared complication and a medical emergency requiring ventilatory support.

Step 2: Evaluate each option

• Acute respiratory failure ✅
  The classical and life-threatening complication of severe myasthenia gravis.

• Cardiomyopathy ❌
  Not a typical complication; MG affects skeletal, not cardiac muscle.

• Chronic kidney disease ❌
  Not associated with MG directly.

• Deep vein thrombosis ❌
  Possible in immobilized patients but not a direct MG complication.

• Pulmonary embolism ❌
  Same reasoning — not a direct MG complication.

Step 1: Why chest CT?

• In myasthenia gravis, there is a strong association with thymic pathology:

  • Thymic hyperplasia in most younger patients.

  • Thymoma in some, especially older patients.

• Because the thymus sits in the anterior mediastinum, a chest CT scan is performed to evaluate for these abnormalities.

Step 2: Evaluate options

• To assess diaphragm weakness ❌
  Diaphragm weakness is tested with spirometry (vital capacity, NIF), not CT scan.

• To detect lung metastasis ❌
  Not the purpose in MG — no link to lung metastasis.

• To evaluate pulmonary function ❌
  Done by pulmonary function tests, not imaging.

• Identify thymic abnormalities ✅
  This is the primary reason for ordering a chest CT in MG.

• To rule out cardiac involvement ❌
  MG doesn’t primarily involve the heart, so not the purpose of imaging.

Step 1: Symptomatic treatment focus

• The goal in symptomatic therapy is to improve neuromuscular transmission.

• This is achieved with acetylcholinesterase inhibitors, which prevent breakdown of acetylcholine at the NMJ → more ACh available to bind to the few remaining receptors.

• The drug of choice: Pyridostigmine.

Step 2: Evaluate each option

• Albuterol ❌
  A β₂-agonist used for asthma/COPD. Not used in MG.

• Atropine ❌
  A muscarinic antagonist — in fact, it would worsen MG symptoms by blocking acetylcholine action.

• Diazepam ❌
  A benzodiazepine used for anxiety, seizures, and muscle relaxation. Not part of MG therapy.

• Prednisone ❌
  This is used as an immunosuppressant for long-term disease control, but it’s not the first-line symptomatic treatment.

• Pyridostigmine ✅
  An acetylcholinesterase inhibitor that provides symptomatic relief by prolonging acetylcholine activity at the neuromuscular junction.

Step 1: Recall the association

• Around 65–75% of patients with myasthenia gravis have an associated thymic abnormality.

• These may include:

  • Thymic hyperplasia (most common)

  • Thymoma (in a smaller percentage, often older patients)

This explains why chest imaging is always recommended in MG cases.

Step 2: Evaluate each option

• Adrenal hyperplasia ❌
  Associated with congenital adrenal hyperplasia (endocrine disorders), not MG.

• Parathyroid hyperplasia ❌
  Seen in primary hyperparathyroidism, not MG.

• Pineal gland calcification ❌
  A normal aging phenomenon, not related to MG.

• Pituitary adenoma ❌
  Causes endocrine syndromes (acromegaly, Cushing’s, etc.), not MG.

• Thymic hyperplasia ✅
  The most common anatomical abnormality in myasthenia gravis.

Step 1: Recall the disease mechanism

• Myasthenia gravis is an autoimmune disease.

• Autoantibodies are directed against the postsynaptic acetylcholine receptors (AChR) at the neuromuscular junction.

• This blocks transmission, reduces the number of functioning receptors, and leads to fatigable weakness.

Step 2: Evaluate each option

• Autoimmune attack on the neuromuscular junction ✅
  Broad but correct description — the disease is autoimmune and targets the NMJ.

• Degeneration of muscle fibres ❌
  Seen in muscular dystrophies, not MG.

• Demyelination of motor neurons ❌
  Seen in Guillain-Barré syndrome or multiple sclerosis, not MG.

• Destruction of acetylcholine receptors ✅ (More specific and best answer)
  This is the primary mechanism — autoantibodies bind to and destroy/block ACh receptors at the postsynaptic membrane.

• Excessive release of acetylcholine ❌
  Not true — in fact, the problem is failure of transmission, not excess release.

Step 1: Key Features in the Case

• Fatigable weakness → arms weaken while writing on blackboard, improves with rest.

• Ocular involvement → drooping eyelids (ptosis), double vision (diplopia).

• Bulbar involvement → difficulty swallowing, slurred speech.

• Examination → weakness increases with repetition, improves with rest.

• Investigations:

  • Serum positive for acetylcholine receptor antibodies.

  • Decremental response on EMG.

  • Chest CT shows thymic hyperplasia.

Step 2: Evaluate Each Option

• Amyotrophic lateral sclerosis (ALS) ❌
  Progressive weakness with both upper and lower motor neuron signs, but not fatigable and no association with thymus or ACh receptor antibodies.

• Guillain-Barré syndrome ❌
  Acute ascending paralysis, areflexia, often post-infectious. No fatigability, no ocular involvement.

• Lambert-Eaton myasthenic syndrome ❌
  Paraneoplastic (often small cell lung cancer), antibodies against presynaptic calcium channels. Improves with exercise (opposite of myasthenia gravis). No ptosis as a main feature.

• Multiple sclerosis ❌
  Demyelinating CNS disease with visual, sensory, and motor deficits. Not fatigable weakness, and not linked to ACh receptor antibodies.

• Myasthenia gravis ✅
  Classical presentation: fatigable weakness, ptosis, diplopia, bulbar symptoms, ACh receptor antibodies, decremental EMG, thymic hyperplasia.

Step 1: Recall the joint

The radiocarpal (wrist) joint is formed between:

• Distal end of radius and its articular disc

• Proximal row of carpal bones (scaphoid, lunate, and triquetrum)
  ⚠️ Ulna does not articulate directly with the carpal bones because the articular disc of the distal radioulnar joint intervenes.

Step 2: Evaluate options

• Radius and proximal carpal bones ❌
  Incomplete, because it misses the articular disc that separates ulna from carpals.

• Radius and Ulna ❌
  That forms the radioulnar joint, not the wrist joint.

• Radius articular disc and proximal carpal bones ✅
  Correct — this describes the radiocarpal joint.

• Ulna articular and proximal carpal bones ❌
  The ulna does not directly articulate with carpals (disc intervenes).

• Ulna and proximal carpal bones ❌
  Same reason — no direct articulation between ulna and carpals.

Step 1: Identify the movement at the wrist

From your earlier clinical scenario, the movement mentioned at the wrist joint was wrist flexion.

• Main wrist flexors:

  • Flexor carpi radialis → supplied by median nerve

  • Flexor carpi ulnaris → supplied by ulnar nerve

  • Palmaris longus → supplied by median nerve

• Median nerve is the chief supplier of wrist flexors.

Step 2: Analyze each option

• Anterior interosseous nerve ❌
  Branch of median nerve, but it supplies deep flexors (flexor pollicis longus, pronator quadratus, lateral half of FDP). These aren’t primary wrist flexors.

• Median nerve ✅
  Supplies flexor carpi radialis and palmaris longus — the prime movers for wrist flexion. This is the correct choice.

• Posterior interosseous nerve ❌
  Branch of radial nerve, supplies extensors — responsible for wrist extension, not flexion.

• Radial nerve ❌
  Extensor supply, not wrist flexion.

• Ulnar nerve ❌
  Does supply flexor carpi ulnaris (a wrist flexor), but the main nerve classically tested for wrist flexion is the median nerve.

Step 1: Identify the reflex

The reflex tested at the cubital fossa is the biceps jerk.

• The examiner places a finger/thumb over the biceps tendon in the cubital fossa and strikes it with a hammer.

• This elicits contraction of the biceps brachii muscle, producing flexion at the elbow.

Step 2: Nerve and root value

• The biceps brachii is supplied by the musculocutaneous nerve.

• Its spinal root values are C5 and C6.

• Of these, C5 is the dominant root tested.

Step 3: Evaluate options

• C4 – C5 ❌ → C4 not involved; biceps is C5–C6.

• C4 – C5 – C6 ❌ → includes C4 unnecessarily.

• C5 – C6 ✅ → correct root values for the biceps jerk.

• C6 – C7 ❌ → this corresponds more to the triceps and brachioradialis reflexes.

• C7 – C8 ❌ → triceps (C7) and finger flexor reflexes, not biceps.

Step 1: Clinical background

The patient clearly has myasthenia gravis (fatigable weakness, ptosis, diplopia, dysphagia, positive ACh receptor antibodies, decremental EMG, thymic hyperplasia).

But the question is specifically asking: Which muscle is tested when a patient is asked to raise the arm?

Step 2: Movements of arm elevation

• Initial 0–15° abduction → supraspinatus

• 15–90° abduction → deltoid

• Above 90° elevation → requires serratus anterior (scapular rotation) and trapezius (scapular rotation)

The question states: “asked to raise the arm” (to 90°). This specifically tests the deltoid.

Step 3: Evaluate each option

• Deltoid ✅
  Responsible for abduction of the arm from 15° to 90°. This is the muscle being tested when asking a patient to raise the arm to shoulder level.

• Serratus anterior ❌
  Important for raising the arm above 90°, by rotating the scapula upward. Supplied by the long thoracic nerve.

• Subscapularis ❌
  Medial rotator of the arm, part of rotator cuff, not responsible for elevation.

• Teres major ❌
  Assists in adduction and medial rotation, not abduction.

• Trapezius ❌
  Elevates and rotates the scapula to assist abduction above 90°, but not the primary muscle for raising to 90°.

Step 1: Location of “C”

In the lateral view of the leg, the label “C” points to a muscle on the outer (lateral) side of the leg, running downward behind the lateral malleolus toward the foot.

That position corresponds to the peroneus (fibularis) longus muscle.

Step 2: Function and Confirmation

• Peroneus longus originates from the upper lateral fibula.

• Its tendon passes behind the lateral malleolus, crosses the sole, and inserts at the base of the 1st metatarsal and medial cuneiform.

• Main action: eversion of the foot and weak plantarflexion.

• Supplied by the superficial peroneal nerve.

Correct Answer

Peroneus longus ✅

Explanation of Other Options

• Extensor digitorum longus ❌ → lies anterior, not lateral; extends toes and dorsiflexes.

• Gastrocnemius ❌ → posterior calf, not lateral.

• Soleus ❌ → deep to gastrocnemius, posterior side.

• Tibialis anterior ❌ → located on the anterior leg, dorsiflexes and inverts the foot.