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AIIMS Rajkot - MBBS First Professional Examination

PHYSIOLOGY Paper I - Full Model Answers

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SECTION A - 38 Marks

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QUESTION 1 - Structured Long Answer (Case-based) [2+4+4 = 10 Marks]

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(a) What is the likely secondary endocrine problem she has developed? [2 Marks]

• Exogenous glucocorticoids (e.g., prednisolone) mimic cortisol - they stimulate gluconeogenesis in the liver, cause peripheral insulin resistance, and inhibit glucose uptake in muscle and adipose tissue.
• This leads to persistent hyperglycemia (polyuria due to osmotic diuresis, polydipsia - excessive thirst, weight gain from anabolic/fluid-retaining effects of steroids).

• Cushing's syndrome (iatrogenic) - the entire complex: central obesity, moon face, buffalo hump, striae
• Secondary adrenal insufficiency - on stopping steroids abruptly, due to HPA axis suppression
• Hypogonadism - suppression of LH/FSH via feedback
• Hypothyroidism - glucocorticoids suppress TSH

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(b) What are the other clinical features she is likely to have with the endocrine problem? [4 Marks]

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(c) What immunological problems is she likely to develop due to treatment? Explain physiological basis. [4 Marks]

1. Increased susceptibility to infections - bacterial (TB reactivation, staphylococcal), viral (Herpes zoster, CMV), fungal (Candida, Aspergillus), and opportunistic infections
2. Impaired wound healing
3. Reactivation of latent tuberculosis
4. Failure of vaccination response
5. Lymphopenia and eosinopenia

• Glucocorticoids bind to cytosolic glucocorticoid receptors (GR) and translocate to the nucleus.
• They inhibit phospholipase A2 (via annexin/lipocortin), blocking arachidonic acid release, thus preventing synthesis of both prostaglandins and leukotrienes.
• They inhibit NF-kB transcription factor, reducing expression of pro-inflammatory cytokines (IL-1, IL-2, IL-6, TNF-alpha, IFN-gamma).
• They stabilize lysosomal membranes, preventing release of proteolytic enzymes.

• T-lymphocytes: Inhibit proliferation by reducing IL-2 production. Cell-mediated immunity is primarily suppressed.
• B-lymphocytes: Reduce antibody production at high doses.
• Neutrophils: Cause neutrophilia (increased release from bone marrow, decreased margination) - but impair neutrophil function and migration to sites of infection.
• Macrophages: Inhibit monocyte/macrophage function - reduced phagocytosis, antigen presentation, and cytokine secretion.
• Eosinophils/Lymphocytes/Monocytes: Cause lymphopenia, eosinopenia, monocytopenia (sequestration in spleen and lymph nodes).
• Mast cells: Reduced degranulation and histamine release.

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QUESTION 2 - Short Notes [4 × 5 = 20 Marks]

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(a) Explain genesis of resting membrane potential [5 Marks]

• Inside cell: High K+ (140 mEq/L), low Na+ (14 mEq/L), large organic anions (A-)
• Outside cell: Low K+ (4 mEq/L), high Na+ (142 mEq/L), high Cl-

• At rest, the membrane is highly permeable to K+ (via K2P "leak" channels and Kir channels) and relatively impermeable to Na+.
• K+ ions diffuse outward down their concentration gradient, carrying positive charges OUT, leaving behind negatively charged proteins inside.
• This outward K+ movement creates an excess of negative charge inside and positive charge outside.

• As K+ moves outward, a negative electrical potential builds inside, which eventually opposes further K+ efflux.
• The point at which the electrical force inward equals the diffusion force outward is the Nernst (equilibrium) potential for K+, which is approximately -94 mV.

• Nernst potential for K+ = -94 mV (major contributor)
• Nernst potential for Na+ = +61 mV (minor contribution since Na+ permeability is low at rest)
• Small Cl- permeability contributes to the final value.

• This electrogenic pump transports 3 Na+ out and 2 K+ in per cycle.
• Net effect: pumps out 1 extra positive charge per cycle, directly contributing about -4 mV to the RMP.
• More importantly, it maintains the concentration gradients that generate the diffusion potential.

Diagram:
Outside: +  +  +  +  +  +  +  +
         ─────────────────────────  cell membrane
Inside:  -  -  -  -  -  -  -  -
                 -70 mV
K+ leak channels → K+ efflux → creates negativity inside
Na-K ATPase → maintains gradient

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(b) Explain smooth muscle contraction with suitable diagram [5 Marks]

• Stimuli (nerve signals, hormones, stretch, chemicals) trigger Ca2+ entry via voltage-gated Ca2+ channels (L-type) from extracellular fluid AND/OR Ca2+ release from sarcoplasmic reticulum (via IP3-gated channels).
• Intracellular [Ca2+] rises from 10-7 M (resting) to ~10-6 M.

• 4 Ca2+ ions bind to calmodulin (a regulatory protein, since smooth muscle lacks troponin).
• The Ca2+-calmodulin complex is formed.

• The Ca2+-calmodulin complex activates MLCK (myosin light chain kinase).

• MLCK uses ATP to phosphorylate the regulatory light chain of myosin heads.
• This enables myosin heads to bind actin filaments.

• Phosphorylated myosin heads attach to actin at dense bodies (equivalent to Z-discs) and undergo cross-bridge cycling.
• Actin filaments (attached to dense bodies) are pulled inward, shortening the cell.
• Smooth muscle can shorten up to 80% of its length (vs 30% in skeletal muscle).

• Myosin light chain phosphatase dephosphorylates the myosin head → cross-bridges detach → relaxation.

• Dephosphorylated (but still attached) myosin heads form "latch bridges" - allow sustained, energy-efficient contraction with minimal ATP use.

DIAGRAM - Smooth Muscle Contraction:

Stimulus
   ↓
↑ Ca²⁺ (extracellular entry + SR release)
   ↓
Ca²⁺ + Calmodulin → Ca-Calmodulin complex
   ↓
Activates MLCK (Myosin Light Chain Kinase)
   ↓
ATP → ADP + Pi
Myosin light chain phosphorylation
   ↓
Myosin head binds Actin
   ↓
Cross-bridge cycling → CONTRACTION
   ↓ (upon stimulus removal)
Myosin Light Chain Phosphatase
   ↓
Dephosphorylation of myosin → RELAXATION
(or → Latch State = slow sustained contraction)

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(c) Explain the physiological basis of oral contraceptives [5 Marks]

1. Combined OCP - Synthetic estrogen (ethinyl estradiol) + progestin (e.g., levonorgestrel)
2. Progestin-only ("Mini-pill")

• Normally, rising estrogen and progesterone during the luteal phase exert negative feedback on the hypothalamus and anterior pituitary.
• Exogenous estrogen + progestin in OCP maintain continuously elevated steroid levels that suppress GnRH (from hypothalamus), and hence LH and FSH (from anterior pituitary).
• Without LH surge → no ovulation (anovulation) - this is the primary contraceptive effect.
• Without FSH → no follicular development.

• Progestin makes cervical mucus thick, viscous, and hostile to sperm penetration, preventing sperm from reaching the egg.

• The endometrium becomes atrophic, thin, and unreceptive to implantation even if fertilization were to occur.
• Altered endometrial receptivity (changes in pinopodes and adhesion molecules) prevents nidation.

• Alters ciliary activity and tubal peristalsis, affecting transport of the ovum/blastocyst.

HYPOTHALAMUS: GnRH suppressed
        ↓
PITUITARY: FSH ↓ (no follicle), LH surge absent
        ↓
OVARY: No ovulation, no corpus luteum
        ↓
CERVIX: Thick mucus → sperm blocked
        ↓
UTERUS: Atrophic endometrium → no implantation

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(d) Explain iodine trapping with suitable diagram [5 Marks]

• Located on the basolateral membrane of thyroid follicular cells.
• NIS co-transports 2 Na+ and 1 I- into the cell, using the Na+ electrochemical gradient (generated by Na+-K+-ATPase).
• This is a secondary active transport mechanism (energy from Na+ gradient, not directly from ATP).
• The thyroid can concentrate I- to 20-40 times the plasma level (can go up to 250x when TSH is high).

• TSH (from anterior pituitary) is the primary stimulator of NIS expression and activity.
• TSH binds G-protein coupled receptors → ↑ cAMP → upregulates NIS transcription and increases iodine trapping.

• Once inside the cell, I- is transported across the apical membrane into the follicular lumen (colloid) by pendrin (an anion transporter).

• In the colloid, I- is oxidized to I0/I+ by thyroid peroxidase (TPO) in the presence of H2O2.
• Organified iodine is incorporated into thyroglobulin (on tyrosine residues → MIT, DIT → T3, T4).

DIAGRAM - Iodine Trapping:

BLOOD          FOLLICULAR CELL         COLLOID (lumen)
  I- ───NIS──→   I- (intracellular)
  Na+            (TSH stimulates NIS)    ──Pendrin──→ I-
                 Na+-K+-ATPase                           ↓
                 (maintains Na+ gradient)          Thyroid Peroxidase
                                                   + H₂O₂
                                                   Organification
                                                   → MIT, DIT → T3, T4

• Perchlorate (ClO4-) and Thiocyanate (SCN-) competitively inhibit NIS.
• Wolff-Chaikoff effect: High doses of iodine transiently inhibit organification (used in thyroid storm - Lugol's iodine).
• TSH deficit → reduced trapping (secondary hypothyroidism).

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QUESTION 3 - Short Answers [4 × 2 = 8 Marks]

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(a) Capacitation of sperm [2 Marks]

1. Removal of cholesterol from the sperm plasma membrane by albumin and other factors in uterine/tubal fluid → membrane becomes more fluid and permeable to Ca2+.
2. Hyperpolarization then depolarization of sperm membrane - changes in membrane potential.
3. Increased intracellular Ca2+ - activates hyperactivated motility (vigorous, whip-like flagellar movement).
4. cAMP increase - activates tyrosine kinase signaling cascades.
5. Acrosome reaction readiness - the acrosome becomes primed to release hydrolytic enzymes (acrosin, hyaluronidase) upon contact with the zona pellucida of the oocyte.

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(b) Secondary active transport [2 Marks]

• The Na+-K+-ATPase pump (primary active transport) maintains a low intracellular Na+ concentration.
• This Na+ gradient is then used to drive the uphill transport of other molecules.

1. Symport (co-transport): Both Na+ and the solute move in the same direction (e.g., Na+-glucose cotransporter SGLT1 in intestine and kidney proximal tubule - absorbs glucose against gradient using Na+ influx).
2. Antiport (counter-transport/exchange): Na+ moves in one direction and the solute moves in the opposite direction (e.g., Na+-Ca2+ exchanger - 3 Na+ in, 1 Ca2+ out; Na+-H+ exchanger in kidney).

• SGLT1/2: glucose reabsorption in kidney (SGLT2 inhibitors used in diabetes)
• Na+-amino acid cotransporters in intestine
• Na+-K+-2Cl- (NKCC2) cotransporter in loop of Henle

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(c) Differentiate between Dwarfism and Cretinism [2 Marks]

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(d) Explain gain of homeostatic mechanism [2 Marks]

Gain = Correction achieved / Error that remains after correction

• Body temperature regulation: If the body temperature rises by 1°C, and the feedback system corrects 0.9°C (leaving 0.1°C error remaining):
• Gain = 0.9 / 0.1 = 9

• The arterial baroreceptor reflex has a gain of about 2 (moderate effectiveness).
• The long-term body fluid/renal mechanism for blood pressure has a very high gain (approaches infinity) - meaning the kidneys can almost completely correct blood pressure deviations over time.
• Gain of negative feedback systems is always positive.

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SECTION B - 37 Marks

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QUESTION 4 - Structured Long Answer (Case-based) [9 Marks]

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(a) What is this phenomenon? Classify reflexes. [2 Marks]

• Initially after cord transection, spinal shock occurs (all reflexes below the lesion are absent).
• As the spinal cord recovers over weeks-months, reflexes return and become hyperactive (due to denervation supersensitivity).
• Eventually, even a mild cutaneous stimulus (touch/pain) triggers a massive, exaggerated withdrawal reflex involving: limb flexion, bladder emptying (urination), defecation, and sweating - this is the mass reflex.
• It reflects loss of descending inhibitory control from higher centers.

1. Somatic reflexes - receptor in somatic structures (skin, muscle, joint)
2. Visceral reflexes - receptor in viscera

1. Monosynaptic - one synapse (e.g., stretch reflex/knee jerk)
2. Oligosynaptic - few synapses
3. Polysynaptic - many synapses (e.g., withdrawal reflex)

1. Flexor reflexes (protective, e.g., withdrawal)
2. Extensor reflexes (postural, e.g., crossed extensor reflex)
3. Visceral reflexes (e.g., micturition, defecation)

1. Acquired/Conditioned reflexes
2. Unconditioned/Inborn reflexes

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(b) Describe briefly stretch reflex and its higher control with a neat labelled diagram of muscle spindle [5 Marks]

1. Receptor: Muscle spindle (intrafusal fibers with Ia and II afferents)
2. Afferent: Ia (primary - annulospiral) and II (secondary - flower spray) fibers
3. Center: Spinal cord (anterior horn)
4. Efferent: Alpha motor neuron
5. Effector: Extrafusal muscle fibers (contraction)

1. Muscle is stretched → muscle spindle (intrafusal fibers) is also stretched.
2. Ia afferent fibers fire in proportion to stretch.
3. Ia fibers enter the spinal cord via dorsal root and synapse directly on alpha motor neurons in the ventral horn.
4. Alpha motor neurons fire → extrafusal muscle fibers contract → muscle shortens → returns to original length.
5. Simultaneously, via inhibitory interneurons, the antagonist muscle is reciprocally inhibited (Ia inhibitory interneuron - Ia inhibition).

• Dynamic stretch reflex (Ia): responds to RATE of stretch - fast, phasic
• Static stretch reflex (Ia + II): responds to LENGTH of stretch - sustained, tonic

• Gamma motor neurons innervate the polar/contractile ends of intrafusal fibers.
• When gamma neurons fire, intrafusal fibers shorten at their contractile ends → the nuclear bag region is stretched → Ia fibers fire even without overall muscle stretch.
• Alpha-gamma coactivation: Descending pathways simultaneously activate both alpha and gamma neurons, maintaining spindle sensitivity during voluntary contraction.
• Cerebral cortex: Via corticospinal tract - generally inhibitory; lesions cause hyperreflexia.
• Cerebellum: Via fastigiosinal and rubrospinal tracts - modulates gamma neuron activity.
• Reticular formation: Facilitatory (pontine/medullary reticular formation) and inhibitory zones affect gamma neuron discharge.
• Vestibular nuclei: Facilitate gamma discharge to antigravity muscles.

DIAGRAM - Muscle Spindle:

        ┌─────────────────────────────────────────┐
        │        MUSCLE SPINDLE                   │
        │                                         │
 Gamma  │  ┌──────┐   Nuclear   ┌──────┐          │
 motor ─┼→ │Polar │───bag/chain─│Polar │ ←─ Gamma │
 fiber  │  │region│   region    │region│    motor  │
        │  └──────┘  ↑ ↑ ↑    └──────┘            │
        │        Ia (primary)  II (secondary)       │
        │        afferent      afferent              │
        └───────────┼──────────────────────────────┘
                    ↓ (to spinal cord)
       ┌────────────────────────────────┐
       │      SPINAL CORD               │
       │  Ia fiber ──→ α motor neuron   │
       │               ↓               │
       │  Extrafusal muscle contraction │
       │               ↓               │
       │  Ia Inhibitory interneuron     │
       │  → inhibits antagonist muscle  │
       └────────────────────────────────┘

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(c) Enlist general properties of reflexes [2 Marks]

1. Final Common Pathway: All reflexes ultimately act through motor neurons (alpha motor neurons = final common pathway; Sherrington's concept).
2. After-discharge: Even after the stimulus stops, the reflex response may continue for a while due to reverberating circuits.
3. Occlusion: When two afferent inputs that partially share the same motor neuron pool are stimulated together, the combined response is less than the sum of individual responses.
4. Recruitment (Spatial summation): Stronger stimuli activate more motor neurons.
5. Irradiation (Spread): As stimulus intensity increases, the reflex spreads to involve muscles beyond the primary effectors.
6. Rebound: After cessation of an excitatory reflex, a period of inhibition follows, and after inhibition, a rebound excitation occurs.
7. Reciprocal Innervation (Sherrington's law): Contraction of a muscle is associated with inhibition (relaxation) of its antagonist.
8. Reflex Fatigue: A reflex decreases in magnitude if the same stimulus is applied repeatedly.
9. Subliminal fringe: Neurons not directly excited but brought to subthreshold - facilitate subsequent responses.
10. General Inhibition: Strong nociceptive stimuli can inhibit all other reflexes (protective priority).

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QUESTION 5 - Short Notes [4 × 5 = 20 Marks]

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(a) Describe functions of Basal Ganglia. Explain physiological basis of treatment of Parkinson's disease. [3+2]

1. Planning and initiation of voluntary movement: Receive input from cortex, process via thalamus, and return to premotor cortex to facilitate movement initiation.
2. Motor learning and habit formation: Involved in procedural memory (motor skills, habits).
3. Inhibition of unwanted movements: Suppress competing motor programs via direct (D1) and indirect (D2) pathways, ensuring smooth, purposeful movements.
4. Regulation of muscle tone: Basal ganglia normally inhibit excess tone; dysfunction leads to rigidity or hypotonia.
5. Control of movement scaling and velocity: Regulate the speed, force, and amplitude of movements.
6. Cognitive and emotional functions: Caudate nucleus involved in executive function; ventral striatum in reward processing.

• Direct pathway (cortex → striatum → GPi/SNr → thalamus → cortex): Facilitates movement (Go).
• Indirect pathway (cortex → striatum → GPe → STN → GPi/SNr → thalamus → cortex): Inhibits movement (No-go).
• Dopamine from substantia nigra (SNc) activates D1 (facilitates direct) and inhibits D2 receptors (suppresses indirect) → net facilitatory effect on movement.

• Degeneration of dopaminergic neurons in substantia nigra pars compacta (SNc) → dopamine depletion in striatum.
• Loss of D1 activation → direct pathway underactive (less movement facilitation).
• Loss of D2 inhibition → indirect pathway overactive (more movement suppression).
• Net result: excessive inhibition of thalamus → reduced cortical activation → bradykinesia, rigidity, tremor.

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(b) Give physiological basis of following [3+2]:

1. Salivary gland secretion:

• Sympathetic stimulation → thick, mucous saliva (from mucous cells).
• Parasympathetic stimulation → profuse, watery, enzyme-rich saliva.
• Together, they produce complete saliva composition (synergism in quantity and quality).

1. Male sexual function:

• Erection is mediated by the parasympathetic (pelvic nerves → vasodilation of penile arteries via NO/VIP).
• Ejaculation is mediated by the sympathetic (hypogastric nerves → contraction of vas deferens, seminal vesicles, prostate).
• Both are required for complete male sexual response → classic synergism.

1. Pupil:

• Sympathetic → dilator pupillae → mydriasis.
• Parasympathetic → sphincter pupillae → miosis.
• In various conditions, both work together to precisely control pupil diameter.

• Stimulates glycogenolysis (liver) → ↑ blood glucose (via alpha/beta receptors).
• Stimulates lipolysis in adipose tissue → ↑ free fatty acids.
• Increases BMR and thermogenesis.
• Dilates bronchi, increases heart rate and contractility, redirects blood to muscles.
• Inhibits digestion and anabolic processes.
• Overall: breaks down energy stores to meet immediate demand = catabolic.

• Promotes digestion: increases gut motility, gastric acid secretion, pancreatic enzyme secretion.
• Promotes nutrient absorption and storage.
• Promotes insulin secretion (via vagus → pancreas) → facilitates glycogen synthesis.
• Conserves energy, promotes repair and growth processes.
• Overall: builds up energy stores and promotes maintenance = anabolic.

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(c) What is near point? How much is the accommodation at near point? Explain mechanism of accommodation for near point. [5 Marks]

• The eye must change its power (diopters) to focus from infinity to the near point.
• Accommodation at near point = 1/near point distance (in meters).
• For near point = 10 cm = 0.1 m → Accommodation = 1/0.1 = 10 Diopters.
• Normal resting power of eye = ~60 D; at near point = ~70 D.

• When viewing a near object, the parasympathetic fibers (via CN III → ciliary ganglion → short ciliary nerves) stimulate circular ciliary muscle to contract.
• Contraction of the ciliary muscle → the ciliary ring becomes smaller → tension on the zonule fibers (suspensory ligaments) is released.
• The elastic lens, no longer under tension, bulges (especially anteriorly) → increases lens curvature → increases refractive power → near object focused on retina.

• Parasympathetic stimulation → contraction of sphincter pupillae → pupil constricts.
• Increases depth of focus, reduces spherical aberration.

• Both eyes turn medially (via medial rectus - CN III) to maintain binocular vision and prevent diplopia when viewing near objects.

Near Object Viewed
      ↓
Visual Cortex → EW Nucleus (CN III)
      ↓
Short Ciliary Nerve
      ↓
Ciliary Muscle Contracts
→ Zonule tension ↓
→ Lens becomes more convex (↑ power)
→ Image focused on fovea
      +
→ Pupil Constricts (depth of focus ↑)
      +
→ Convergence (both eyes turn inward)

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(d) Draw well labelled diagram explaining Cerebellar circuitry. Explain functions of Spinocerebellum [5 Marks]

CEREBELLAR CIRCUITRY DIAGRAM:

INPUT PATHWAYS:
────────────────────────────────────────────────────────
Mossy fibers         Climbing fibers
(Pontine nuclei,     (Inferior Olive)
Spinal cord,               │
Vestibular)                │
     │                     │
     ↓                     ↓
Granule cells ────→ Parallel fibers → PURKINJE CELL ←────
(Granular layer)      (Molecular layer)        │
                                               │
     ────────────────── also input ────────────┘
     Basket cells, Stellate cells (inhibitory interneurons)
     Golgi cells (inhibitory - feedback to granule cells)

OUTPUT:
     Purkinje Cell (GABAergic - INHIBITORY)
          │
          ↓
     Deep Cerebellar Nuclei:
     - Dentate nucleus (Neocerebellum/Cerebrocerebellum)
     - Emboliform + Globose = Interpositus (Spinocerebellum)
     - Fastigial nucleus (Vestibulocerebellum/Archicerebellum)
          │
          ↓
     Thalamus (VL) → Motor Cortex
     (for voluntary movement modulation)
     OR
     Brainstem (for posture/balance)

1. Compares Motor Command with Actual Performance:

• Receives motor commands "efference copy" from cortex (via corticopontocerebellar fibers) AND sensory feedback from muscles/joints (via spinocerebellar tracts).
• Compares "what was intended" vs "what is happening."
• Error signals used to correct ongoing movements in real time.

1. Regulation of Muscle Tone:

• Vermis and fastigial nucleus: regulate tone in axial/proximal muscles.
• Damage → hypotonia.

1. Gait and Posture Control:

• Controls stepping, walking, and balance (works with vestibular system).
• Lesion → wide-based (truncal) ataxia, decomposition of gait.

1. Correction of Movement During Execution:

• Intermediate zone (paravermal): corrects limb movements.
• Uses feedback from spinocerebellar tracts (DSCT for arm, VSCT for leg).

1. Damping of Movement:

• Prevents oscillatory or over-shooting movements (intention tremor on lesion).

• Dorsal spinocerebellar tract (DSCT): ipsilateral lower limb proprioception.
• Ventral spinocerebellar tract (VSCT): bilateral; carries indirect efferent copy.
• Cuneocerebellar tract: upper limb proprioception.

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QUESTION 6 - Short Answers [4 × 2 = 8 Marks]

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(a) Explain phototransduction in short [2 Marks]

• cGMP is high inside the outer segment.
• cGMP-gated Na+ channels are open → Na+ flows in ("dark current") → rod is relatively depolarized (~-40 mV) → continuous glutamate release onto bipolar cells.

1. Photon absorbed by rhodopsin (opsin + 11-cis retinal) → 11-cis retinal isomerizes to all-trans retinal → rhodopsin is activated (→ metarhodopsin II/activated rhodopsin).
2. Activated rhodopsin activates transducin (a G-protein, Gα subunit binds GTP and becomes active).
3. Activated transducin activates cGMP phosphodiesterase (PDE).
4. PDE catalyzes breakdown of cGMP → 5'-GMP → ↓ cGMP levels.
5. ↓ cGMP → closure of Na+ channels in outer segment membrane.
6. Na+ pump (Na-K-ATPase) continues pumping Na+ out → net hyperpolarization (membrane potential → -70 to -80 mV).
7. Hyperpolarization → reduced glutamate release → signal propagated to bipolar cells → ganglion cells → optic nerve.

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(b) What is cochlear microphonic? How is it different from action potential? [2 Marks]

• A graded electrical potential generated by the outer hair cells of the organ of Corti in response to sound.
• It exactly replicates the waveform and frequency of the acoustic stimulus (like a microphone output - hence the name).
• Results from mechanically-gated K+ channels opening/closing as the stereocilia of hair cells deflect with basilar membrane movement.
• At low sound frequencies, the CM follows the sound wave cycle for cycle.
• Not propagated, has no refractory period, shows no threshold.
• Detected by electrodes near the cochlea (e.g., electrocochleography - ECoG).

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(c) Enlist functions of REM and NREM sleep [2 Marks]

1. Physical restoration and repair - growth hormone (GH) is secreted maximally during slow-wave (N3) NREM sleep → tissue repair and growth.
2. Immune system consolidation - cytokine production (IL-1, TNF) promotes immune function.
3. Energy conservation - metabolic rate and cerebral glucose utilization are reduced.
4. Detoxification - glymphatic system clears brain metabolic waste (beta-amyloid, tau) during NREM.
5. Memory consolidation (declarative/hippocampal memory).
6. Cardiovascular rest - HR, BP, and respiratory rate are at their lowest.

1. Memory consolidation - especially procedural memory, emotional memories, and learning (neural connections are consolidated and pruned).
2. Emotional processing - amygdala highly active; helps process and integrate emotional experiences.
3. Dreams - vivid dreaming occurs; may serve adaptive/psychological functions.
4. Brain development - REM is proportionally greatest in neonates; thought to support synaptic development and neural maturation.
5. Restoration of catecholamine sensitivity - noradrenergic and serotonergic neurons are silent during REM; postulated to restore receptor sensitivity.
6. Creativity and problem-solving - REM fosters non-linear associative thinking.

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(d) A 45-yr-old man was stabbed in the back, MRI shows complete transection of one side of the spinal cord. Which sensory and motor deficits will be seen? [2 Marks]

• Ipsilateral: Motor loss + proprioception/vibration/touch loss
• Contralateral: Pain and temperature loss

• Ipsilateral loss of touch (crude touch is somewhat preserved as it crosses bilaterally).
• Ipsilateral vasomotor changes below lesion.
• No bowel/bladder dysfunction if unilateral (bilateral innervation), though partial dysfunction may occur.

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Note: All answers follow standard MBBS First Year Physiology curriculum as per Medical Council of India (NMC) guidelines and are referenced primarily from Guyton & Hall Textbook of Medical Physiology (14th Ed.) and Ganong's Review of Medical Physiology (26th Ed.) - the standard MBBS textbooks for Physiology. Draw all diagrams in exam with proper labels and arrows for maximum marks.