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🩺 MBBS FIRST YEAR — PHYSIOLOGY NOTES

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UNIT 1: GENERAL PHYSIOLOGY (CELLULAR PHYSIOLOGY)

1.1 Body Fluid Compartments

• TBW = 60% of body weight in males; ~50% in females (females have more adipose tissue, which contains less water)
• A 70 kg man has ~42 L of TBW

Major ECF cation = Na⁺; Major ICF cation = K⁺. Osmolarity is equal in both compartments because water crosses freely across cell membranes.

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1.2 Cell Membrane Structure

• Phospholipid bilayer: Hydrophilic heads face aqueous ECF and ICF; hydrophobic tails face inward. Provides a barrier to water-soluble substances.
• Integral (transmembrane) proteins: Span the entire bilayer; include ion channels, receptors (hormone/neurotransmitter), carrier proteins (e.g., Na⁺-K⁺ ATPase), gap junction proteins, G-proteins.
• Peripheral membrane proteins: Loosely attached to intracellular or extracellular face; e.g., ankyrin (anchors RBC cytoskeleton to band 3/Cl⁻-HCO₃⁻ exchanger).

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1.3 Transport Across Cell Membranes

J = PA(C_A − C_B)

• J = flux, P = permeability, A = surface area, C_A − C_B = concentration gradient
• Rate is linearly proportional to concentration gradient (no saturation)

1. Saturation — at high concentrations all carrier sites are occupied → transport maximum (Tm)
2. Stereospecificity — carriers are selective (e.g., D-glucose, not L-glucose)
3. Competition — structurally similar solutes compete for same carrier

• Pumps 3 Na⁺ out and 2 K⁺ in per ATP hydrolyzed
• Maintains the low intracellular [Na⁺] and high intracellular [K⁺]
• The Na⁺ gradient thus created drives all secondary active transport

• Cotransport (symport): Na⁺ and solute move in same direction. Example: Na⁺-glucose cotransporter in renal proximal tubule (SGLT). Failure of saturation → glucosuria (as in diabetes mellitus).
• Countertransport (antiport): Na⁺ and solute move in opposite directions. Example: Na⁺-Ca²⁺ exchanger, Na⁺-H⁺ exchanger

• Movement of water across a semipermeable membrane from low solute → high solute concentration
• Osmolarity = number of osmotically active particles per litre of solution (mOsm/L)
• Osmolality = per kg of solvent
• Osmotic pressure (van't Hoff): π = σgCRT
  • σ = reflection coefficient (0 = freely permeable; 1 = impermeable)
  • Plasma osmolality ≈ 2[Na⁺] + glucose/18 + BUN/2.8 ≈ 290 mOsm/kg
• Tonicity = effective osmolality. Solutions isotonic if same effective osmotic pressure; water flows from hypotonic → hypertonic

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1.4 Membrane Potentials

E_x = (61/z) × log₁₀([X]_out / [X]_in) (at 37°C)

• E_K⁺ ≈ −94 mV (K⁺ wants membrane very negative)
• E_Na⁺ ≈ +66 mV (Na⁺ wants membrane positive)
• E_Cl⁻ ≈ −70 mV (Cl⁻ near resting potential)

• In nerve/skeletal muscle: approximately −70 mV (inside negative)
• At rest, membrane is highly permeable to K⁺ (K⁺ channels open) → K⁺ diffuses out → intracellular negative charge
• RMP is close to E_K⁺ but not equal (small Na⁺ leak keeps it slightly depolarised)
• Goldman Equation accounts for permeabilities of all ions:

Em = 61 × log₁₀ [(P_K[K⁺]_o + P_Na[Na⁺]_o + P_Cl[Cl⁻]_i) / (P_K[K⁺]_i + P_Na[Na⁺]_i + P_Cl[Cl⁻]_o)]

• If negative: cation enters, anion leaves
• If positive: cation leaves, anion enters

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1.5 Action Potential (Nerve & Skeletal Muscle)

• All-or-none: Occurs fully or not at all; once threshold is reached, action potential is inevitable
• Stereotypical: Same size and shape for each cell type
• Non-decremental propagation: Full-sized action potential at every point

• Tetrodotoxin (TTX) from puffer fish — blocks voltage-gated Na⁺ channels → prevents action potentials
• Lidocaine (local anaesthetic) — also blocks Na⁺ channels

• Absolute refractory period (ARP): Na⁺ inactivation gates closed → NO action potential possible regardless of stimulus
• Relative refractory period (RRP): K⁺ channels still open, membrane hyperpolarised → only a very large stimulus can fire

• Faster in large-diameter fibres (lower internal resistance)
• Faster in myelinated fibres → Saltatory conduction — action potentials "jump" from node of Ranvier to node of Ranvier (myelin provides high electrical resistance between nodes)

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1.6 Synaptic & Neuromuscular Transmission

• Electrical synapses: Gap junctions; bidirectional; fast; found in cardiac muscle, smooth muscle (uterus, bladder)
• Chemical synapses: Neurotransmitter-mediated; unidirectional (presynaptic → postsynaptic); involves synaptic delay

1. Action potential arrives at motor nerve terminal
2. Depolarisation opens voltage-gated Ca²⁺ channels → Ca²⁺ influx
3. Ca²⁺ triggers exocytosis of acetylcholine (ACh) from synaptic vesicles
4. ACh diffuses across synaptic cleft, binds to nicotinic ACh receptors (nAChR) on motor end plate
5. nAChR is a ligand-gated ion channel → opens → Na⁺ influx & K⁺ efflux → End Plate Potential (EPP)
6. EPP depolarises adjacent muscle membrane → threshold → muscle action potential
7. ACh is broken down by acetylcholinesterase (AChE) in the cleft

Myasthenia Gravis: Autoimmune — antibodies against nAChR → decreased EPP → muscle weakness, fatigability, ptosis. Treat with AChE inhibitors (pyridostigmine).

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1.7 Skeletal Muscle

• Sarcomere = basic contractile unit (Z-line to Z-line)
• Thick filaments = myosin (has ATPase activity, cross-bridge heads)
• Thin filaments = actin (with tropomyosin + troponin complex)
  • Troponin I — inhibits actin-myosin interaction
  • Troponin T — binds tropomyosin
  • Troponin C — binds Ca²⁺
• A band = thick filaments (dark); includes H zone
• I band = thin filaments only (light)
• H zone = thick only (no overlap); disappears on contraction
• M line = middle of A band

• Thin filaments slide over thick filaments → sarcomere shortens
• Length of filaments does NOT change; overlap increases

1. Muscle action potential travels along sarcolemma → T-tubules
2. T-tubule depolarisation activates dihydropyridine (DHP) receptors (voltage sensors)
3. DHP receptors mechanically activate ryanodine receptors (RyR) on sarcoplasmic reticulum (SR)
4. Ca²⁺ release from SR → intracellular [Ca²⁺] rises from 10⁻⁷ to 10⁻⁵ M
5. Ca²⁺ binds troponin C → conformational change → tropomyosin moves → exposes actin binding sites
6. Myosin cross-bridge binds actin → power stroke (using ATP) → filament sliding
7. Relaxation: Ca²⁺ pumped back into SR by Ca²⁺ ATPase (SERCA)

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1.8 Smooth Muscle

• No troponin — Ca²⁺ regulation via calmodulin
• Ca²⁺ + calmodulin → activates myosin light-chain kinase (MLCK) → phosphorylates myosin → cross-bridge cycling
• Relaxation: myosin light-chain phosphatase dephosphorylates myosin
• Slower, more sustained contractions than skeletal muscle
• Found in blood vessels, GI tract, airways, bladder

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UNIT 2: BLOOD PHYSIOLOGY

2.1 Composition of Blood

• Total blood volume: ~5 L (70 kg adult)
• Haematocrit (PCV): Males 42–52%, Females 36–48%
• Plasma (~55%): Water (91%), proteins (albumin, globulins, fibrinogen), ions, nutrients, hormones
• Formed elements (~45%): RBCs, WBCs, platelets

2.2 Erythrocytes (RBCs)

• Normal count: Male 4.5–6.5 × 10⁶/µL; Female 3.9–5.6 × 10⁶/µL
• Shape: Biconcave disc; increases surface area for O₂ diffusion; highly deformable
• Lifespan: ~120 days
• Destruction: Spleen (extravascular haemolysis) — haemoglobin → bilirubin → conjugated in liver → excreted in bile
• No nucleus or mitochondria — obtain energy by anaerobic glycolysis (Embden-Meyerhof pathway)
• MCV: 80–100 fL; MCH: 27–32 pg; MCHC: 32–36 g/dL

2.3 Haemoglobin (Hb)

• Normal levels: Male 13–17 g/dL; Female 12–15 g/dL
• Structure: 4 subunits — each has a globin chain + haem group (porphyrin ring + Fe²⁺)
• HbA (adult): α₂β₂ — predominant (97%)
• HbA₂: α₂δ₂ — minor (~2.5%); elevated in β-thalassaemia
• HbF (fetal): α₂γ₂ — higher O₂ affinity (reduced 2,3-DPG binding)
• HbS (sickle): β-chain mutation (Glu → Val at position 6) → polymerises when deoxygenated

• Sigmoidal curve (cooperative binding)
• P₅₀ = partial pressure of O₂ at which Hb is 50% saturated ≈ 26 mmHg
• Left shift (↑ O₂ affinity, impaired O₂ release): ↓PCO₂, ↑pH (alkalosis), ↓temperature, ↓2,3-DPG, HbF, CO poisoning
• Right shift (↓ O₂ affinity, enhanced O₂ release to tissues): ↑PCO₂, ↓pH (acidosis = Bohr effect), ↑temperature, ↑2,3-DPG, exercise

2.4 WBCs (Leukocytes)

• Normal count: 4,000–11,000/µL

2.5 Platelets (Thrombocytes)

• Count: 150,000–400,000/µL; Lifespan: 8–12 days; No nucleus; contain granules (ADP, serotonin, thromboxane A₂)
• Functions: Form primary platelet plug; contribute to secondary haemostasis

2.6 Haemostasis & Coagulation

1. Vascular spasm (vasoconstriction)
2. Platelet adhesion (collagen + von Willebrand factor [vWF])
3. Platelet activation → release of ADP, TXA₂ → platelet aggregation → primary platelet plug

• PT (Prothrombin Time): Tests extrinsic + common pathway; INR derived from PT; prolonged in warfarin use
• aPTT: Tests intrinsic + common pathway; prolonged in heparin use, haemophilia A/B

• Heparin: Enhances antithrombin III activity → inactivates thrombin and Xa
• Warfarin: Inhibits Vitamin K–dependent factors (II, VII, IX, X, Protein C & S)

2.7 Blood Groups

• Rh positive: Has D antigen on RBC (~85% of population)
• Rh negative: No D antigen; if exposed to Rh+ blood → forms anti-D antibodies
• Haemolytic Disease of the Newborn (Erythroblastosis Fetalis): Rh− mother sensitised in 1st pregnancy; anti-D IgG crosses placenta in 2nd pregnancy → destroys fetal RBCs. Prevented by anti-D immunoglobulin (Rhogam)

2.8 ESR (Erythrocyte Sedimentation Rate)

• Normal: Males 0–15 mm/hr; Females 0–20 mm/hr (Westergren method)
• ↑ESR: Infections, inflammation, malignancy, pregnancy, anaemia, multiple myeloma (rouleaux formation)
• ↓ESR: Polycythaemia, sickle cell disease, spherocytosis

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UNIT 3: NERVE & MUSCLE PHYSIOLOGY

3.1 Nerve Fiber Classification

Pain fibres: Fast pain = Aδ; Slow/burning pain = C

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UNIT 4: CARDIOVASCULAR PHYSIOLOGY

4.1 Cardiac Cycle

• Systole (~0.3 s): Isovolumetric contraction → Rapid ejection → Reduced ejection
• Diastole (~0.5 s): Isovolumetric relaxation → Rapid filling → Slow filling → Atrial systole

• Aortic systolic: ~120 mmHg; Diastolic: ~80 mmHg
• Left ventricular peak systolic: ~120 mmHg; EDP: ~5–10 mmHg

• S1 ("lub"): Closure of mitral (bicuspid) & tricuspid valves — onset of systole
• S2 ("dub"): Closure of aortic & pulmonary valves — onset of diastole
• S3 (pathological in adults): Rapid ventricular filling; heard in heart failure (ventricular gallop)
• S4: Atrial contraction against stiff ventricle; heard in hypertension, LVH

4.2 ECG (Electrocardiogram)

• ↑PR interval = 1st degree AV block
• ST elevation = STEMI; ST depression = ischaemia/NSTEMI
• Peaked T waves = hyperkalaemia

4.3 Cardiac Output (CO)

CO = HR × Stroke Volume = 5 L/min at rest

• Preload (end-diastolic volume): ↑ preload → ↑ fibre stretch → ↑ force of contraction → ↑ SV
• Afterload (aortic pressure): ↑ afterload → ↓ SV
• Contractility (inotropy): ↑ by sympathetic stimulation, catecholamines, digoxin

4.4 Blood Pressure & Regulation

• Normal BP: 120/80 mmHg; Mean Arterial Pressure (MAP) ≈ DBP + 1/3(PP) ≈ 93 mmHg
• Pulse Pressure (PP) = SBP − DBP = 40 mmHg

• Baroreceptors in carotid sinus (CN IX) and aortic arch (CN X)
• ↑BP → ↑baroreceptor firing → NTS (medulla) → ↑parasympathetic + ↓sympathetic → ↓HR, ↓contractility, vasodilation → ↓BP
• ↓BP → opposite

• ↓BP/↓renal perfusion → renin from juxtaglomerular cells → angiotensin I → ACE → angiotensin II → vasoconstriction + aldosterone secretion → ↑Na⁺ & H₂O retention → ↑blood volume → ↑BP

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UNIT 5: RESPIRATORY PHYSIOLOGY

5.1 Lung Volumes & Capacities

RV cannot be measured by spirometry (air cannot be expelled); measured by helium dilution or body plethysmography

5.2 Mechanics of Breathing

• Compliance = ΔV/ΔP; normal lung compliance = 200 mL/cmH₂O
• ↓ compliance (stiffer lung): fibrosis, pulmonary oedema
• ↑ compliance: emphysema
• Surfactant: Secreted by type II pneumocytes; reduces surface tension in alveoli; prevents alveolar collapse (atelectasis); deficient in Respiratory Distress Syndrome (RDS) of newborns (premature)

5.3 Ventilation-Perfusion (V/Q) Ratio

• Normal V/Q = 0.8
• V/Q = 0 (shunt): alveolus perfused but not ventilated → no O₂ exchange
• V/Q = ∞ (dead space): alveolus ventilated but not perfused → wasted ventilation
• Anatomical dead space: ~150 mL (conducting airways)
• Alveolar ventilation = (TV − Dead space) × RR = (500 − 150) × 12 = 4200 mL/min

5.4 Oxygen Transport

• Dissolved O₂: 0.003 mL/dL/mmHg (small)
• Bound to Hb: Each gram Hb carries 1.34 mL O₂ at full saturation
• O₂ content = (Hb × 1.34 × SaO₂) + (0.003 × PaO₂)

5.5 CO₂ Transport

• 70% as bicarbonate (HCO₃⁻): CO₂ + H₂O ↔ H₂CO₃ ↔ H⁺ + HCO₃⁻ (catalysed by carbonic anhydrase in RBCs)
• 23% bound to Hb as carbaminohaemoglobin
• 7% dissolved in plasma

5.6 Control of Respiration

• Central chemoreceptors (medullary ventral surface): Respond to ↑PCO₂ (via ↓CSF pH); most potent stimulus for ventilation
• Peripheral chemoreceptors (carotid body CN IX, aortic body CN X): Respond to ↓PaO₂ (<60 mmHg), ↑PaCO₂, ↓pH
• Apneustic centre (lower pons): Promotes inspiration
• Pneumotaxic centre (upper pons): Inhibits inspiration, controls rate

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UNIT 6: RENAL PHYSIOLOGY

6.1 Nephron Structure

• ~1.2 million nephrons per kidney
• Cortical nephrons (85%): Short loops of Henle; mainly filtration/reabsorption
• Juxtamedullary nephrons (15%): Long loops of Henle; important for urine concentration

6.2 Glomerular Filtration

• GFR: ~125 mL/min = 180 L/day
• Filtration fraction = GFR/RPF = 125/625 = 0.20 (20%)
• Starling forces govern filtration:
  • Hydrostatic pressure in glomerulus (↑GFR) vs. oncotic pressure of plasma (↓GFR) vs. Bowman's capsule pressure (↓GFR)

• Myogenic mechanism: ↑ renal arterial pressure → afferent arteriole constricts
• Tubuloglomerular feedback (TGF): ↑NaCl delivery to macula densa → constriction of afferent arteriole

6.3 Tubular Reabsorption & Secretion

6.4 Countercurrent Mechanism

• Creates a hypertonic medullary interstitium (up to ~1200 mOsm/L)
• Countercurrent multiplier: Loop of Henle — thick ascending limb pumps NaCl into interstitium; descending limb loses water → urine concentrated
• Countercurrent exchanger: Vasa recta (peritubular capillaries) — preserves medullary hypertonicity

6.5 ADH (Antidiuretic Hormone / Vasopressin)

• Secreted from posterior pituitary in response to ↑plasma osmolality or ↓blood volume
• Acts on V₂ receptors in collecting duct → inserts aquaporin-2 (AQP-2) channels → ↑H₂O reabsorption → concentrated urine
• Diabetes insipidus: Absent/defective ADH (central) or insensitive tubules (nephrogenic) → dilute polyuria

6.6 Renin-Angiotensin-Aldosterone System (RAAS)

1. ↓Renal perfusion / ↓Na⁺ delivery to macula densa / β₁-adrenergic stimulation → Renin from JG cells
2. Renin cleaves angiotensinogen → Angiotensin I
3. ACE (lung) converts Ang I → Angiotensin II
4. Ang II: Vasoconstriction, ↑aldosterone, ↑ADH, ↑thirst
5. Aldosterone (adrenal cortex) → ↑ENaC expression in collecting duct → Na⁺ reabsorption + K⁺ secretion → ↑blood volume

6.7 Renal Clearance

C_x = (U_x × V̇) / P_x (mL/min)

• Inulin clearance = GFR (freely filtered, not reabsorbed or secreted)
• Creatinine clearance ≈ GFR (~125 mL/min)
• PAH clearance = Renal plasma flow (~625 mL/min) — filtered + secreted; completely cleared in one pass

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UNIT 7: GASTROINTESTINAL PHYSIOLOGY

7.1 Salivary Secretion

• Volume: ~1.5 L/day
• Contains: Water, mucus, salivary amylase (ptyalin), lingual lipase, immunoglobulins (IgA), lysozyme
• Parotid (serous, amylase-rich), Submandibular (mixed), Sublingual (mucous)
• Stimulated by: Parasympathetic (VII, IX) — ↑watery saliva; Sympathetic — ↑thick mucous saliva

7.2 Gastric Secretion

• HCl: By parietal cells (oxyntic cells) — via H⁺/K⁺ ATPase (proton pump); stimulated by histamine (H₂), gastrin, ACh; inhibited by prostaglandins, somatostatin; blocked by PPIs (omeprazole) and H₂ blockers (ranitidine)
• Pepsinogen → pepsin (by HCl): By chief (zymogenic) cells; digest proteins
• Intrinsic factor (IF): By parietal cells; essential for vitamin B₁₂ absorption in terminal ileum; absent in pernicious anaemia
• Mucus: By mucus neck cells; protects gastric mucosa
• Gastrin: From G cells (antrum); stimulates HCl and IF secretion

1. Cephalic phase (~30%): Sight/smell/taste of food → vagal stimulation
2. Gastric phase (~60%): Food in stomach → distension + proteins → gastrin
3. Intestinal phase (~10%): Food in duodenum → initially stimulatory then inhibitory (secretin, GIP, CCK)

7.3 Pancreatic Secretion

• Volume: ~1.5 L/day; highly alkaline (HCO₃⁻ rich)
• Stimulated by secretin (↑HCO₃⁻ secretion) and CCK (↑enzyme secretion)
• Enzymes: Trypsinogen (→ trypsin by enterokinase), chymotrypsinogen, elastase, pancreatic lipase, amylase

7.4 Bile

• Produced by hepatocytes; stored/concentrated in gallbladder
• Stimulated by CCK (gallbladder contraction)
• Bile salts (primary: cholic acid, chenodeoxycholic acid; secondary: deoxycholic, lithocholic)
• Functions: Emulsification of fats, micelle formation, aids absorption of fat-soluble vitamins (A, D, E, K)
• Enterohepatic circulation: ~95% of bile salts reabsorbed in terminal ileum

7.5 Digestion & Absorption

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UNIT 8: ENDOCRINE PHYSIOLOGY

8.1 Hypothalamus-Pituitary Axis

• TRH → TSH; CRH → ACTH; GnRH → FSH, LH; GHRH → GH; Somatostatin → inhibits GH, TSH
• Dopamine (PIH) → inhibits prolactin

8.2 Growth Hormone (GH)

• Secreted by somatotrophs; peak secretion during sleep (slow-wave)
• Actions: ↑protein synthesis, ↑lipolysis, ↑blood glucose (anti-insulin), bone growth via IGF-1 (somatomedin C) from liver
• ↑ GH in childhood → gigantism; in adults → acromegaly
• ↓ GH in childhood → dwarfism

8.3 Thyroid Hormones

• T₄ (thyroxine) and T₃ (triiodothyronine; more active)
• Synthesis requires iodine and thyroglobulin; organification by thyroid peroxidase (TPO)
• Transport: mostly bound to TBG (thyroxine-binding globulin)
• Actions: ↑BMR, ↑O₂ consumption, ↑heat production, ↑protein synthesis, essential for normal brain development, ↑heart rate and contractility, ↑gut motility
• Hypothyroidism: ↑TSH, ↓T₄/T₃; myxoedema, cretinism (congenital)
• Hyperthyroidism: ↓TSH, ↑T₄/T₃; Graves' disease (TSH-receptor antibodies)

8.4 Adrenal Cortex & Medulla

• Zona Glomerulosa → Aldosterone (mineralocorticoid); regulated by Ang II, K⁺
• Zona Fasciculata → Cortisol (glucocorticoid); regulated by ACTH
• Zona Reticularis → Androgens (DHEA)

• Cushing's syndrome: ↑cortisol → central obesity, moon face, buffalo hump, striae, hypertension, diabetes
• Addison's disease: ↓cortisol + ↓aldosterone → hypotension, hyperpigmentation, hypoglycaemia

• Secretes adrenaline (epinephrine) ~80% and noradrenaline (norepinephrine) ~20%
• Derived from chromaffin cells (modified sympathetic postganglionic neurons)
• "Fight or flight": ↑HR, ↑BP, ↑blood glucose (glycogenolysis), bronchodilation, ↑lipolysis

8.5 Insulin & Glucagon

• Released in response to ↑blood glucose
• Actions: ↑glucose uptake (GLUT4 in muscle/adipose), ↑glycogen synthesis, ↑protein synthesis, ↑fat synthesis, ↓blood glucose
• Type 1 DM: Autoimmune destruction of β-cells; insulin deficiency; ketoacidosis
• Type 2 DM: Insulin resistance + relative deficiency

• Released in response to ↓blood glucose, exercise, amino acids
• Actions: ↑glycogenolysis, ↑gluconeogenesis → ↑blood glucose; ↑lipolysis, ↑ketogenesis

8.6 Calcium-Regulating Hormones

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UNIT 9: NEUROPHYSIOLOGY

9.1 Sensory Receptors

• Mechanoreceptors: Touch, pressure (Meissner's, Pacinian, Merkel's, Ruffini)
• Thermoreceptors: Temperature
• Nociceptors: Pain (free nerve endings)
• Proprioceptors: Position/movement (muscle spindles, Golgi tendon organs)

• Fast/rapidly adapting: Meissner's, Pacinian corpuscles (respond to change)
• Slow/tonically adapting: Merkel's, Ruffini, muscle spindles (respond to sustained stimulus)

9.2 Spinal Cord Reflexes

• Muscle stretched → muscle spindle (Ia afferents) → monosynaptic → α-motor neuron → muscle contraction
• E.g., knee jerk (patella tendon reflex)

• Painful stimulus → Aδ/C fibres → flexion of ipsilateral limb + extension of contralateral limb (crossed extensor reflex)

• Excessive tension → Ib afferents → inhibit α-motor neuron → muscle relaxation (autogenic inhibition) — prevents muscle injury

9.3 Autonomic Nervous System

9.4 Cerebellum

• Functions: Coordination, balance, fine motor control, smooth voluntary movements
• Does NOT initiate movement, but fine-tunes it
• Lesions: Ipsilateral signs — ataxia, dysmetria (past-pointing), dysdiadochokinesia, intention tremor, nystagmus

9.5 Sleep Physiology

• NREM Sleep: 4 stages; progressively deeper; K complexes and sleep spindles (stage 2); slow delta waves (stages 3–4); growth hormone secreted during stage 3–4
• REM Sleep: Rapid eye movements; vivid dreams; muscle atonia; irregular HR & breathing; occurs ~90 min into sleep; ~25% of sleep time
• REM is controlled by acetylcholine (ACh); suppressed by serotonin and noradrenaline

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UNIT 10: SPECIAL SENSES

10.1 Vision

• Photoreceptors: Rods (dim light/peripheral, rhodopsin) and Cones (colour/central, in fovea — 3 types S/M/L)
• Accommodation: Ciliary muscle contraction → lens becomes more convex → near vision focus
• Pupillary light reflex: Light → retina → CN II → pretectal nucleus → CN III → constriction (direct & consensual)
• Visual pathway: Retina → optic nerve → optic chiasm (nasal fibres cross) → lateral geniculate nucleus (LGN) → primary visual cortex (V1, occipital lobe)
• Defects: Bitemporal hemianopia (chiasm lesion — pituitary tumour); homonymous hemianopia (optic tract lesion)

10.2 Hearing & Vestibular

• Auditory pathway: Sound waves → external ear → tympanic membrane → ossicles (malleus, incus, stapes) → oval window → cochlea → hair cells (organ of Corti) → CN VIII → cochlear nuclei → superior olivary complex → inferior colliculus → medial geniculate nucleus (MGN) → primary auditory cortex (A1, temporal lobe)
• Hair cells: Inner hair cells = actual transducers; outer hair cells = amplification (electromotility via prestin)
• Vestibular system: Semicircular canals (angular acceleration) + utricle & saccule (linear acceleration, gravity)

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KEY VALUES SUMMARY

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