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AIIMS Rajkot - 1st MBBS Physiology Paper II - Complete Answers

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SECTION A

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Q.1 - Clinical Case: 55-year-old male with chest pain

a) Most Probable Diagnosis (1 mark)

• Squeezing, central chest pain radiating to the left arm
• Nausea, sweating, diaphoresis
• Risk factors: smoking, hypertension, sedentary lifestyle
• BP 160/100, HR 90, anxious and diaphoretic

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b) ECG Waves and Phases of Cardiac Action Potential (5 marks)

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+20 mV ___
        /   \
       /     \___________  Phase 2 (plateau)
      /                   \
Phase 0                    \  Phase 3
(rapid depol)               \
                             \___  Phase 4 (resting)
-90 mV __________________________|

• Rapid opening of fast Na⁺ channels (voltage-gated)
• Na⁺ rushes into the cell
• Membrane potential rises from -90 mV to +20 mV
• ECG correlation: QRS complex

• Inactivation of fast Na⁺ channels
• Brief opening of transient outward K⁺ (Ito) channels
• Slight repolarization (notch)
• ECG correlation: J point

• Slow L-type Ca²⁺ channels open (Ca²⁺ influx)
• Slow K⁺ efflux balances Ca²⁺ influx
• Membrane potential maintained near 0 mV
• Functionally important: triggers Ca²⁺-induced Ca²⁺ release from SR → contraction
• ECG correlation: ST segment (isoelectric in normal; elevated in STEMI)

• L-type Ca²⁺ channels close
• Rapid K⁺ efflux (IKr, IKs channels open)
• Membrane returns toward resting potential
• ECG correlation: T wave

• Na⁺/K⁺-ATPase pump restores ionic gradients
• Resting potential = -90 mV (maintained by K⁺ leak channels)
• ECG correlation: isoelectric baseline (between T and next P wave)

Key diagram to draw: Draw a ventricular AP (phases 0-4) and below it draw an ECG strip, aligning each phase with its corresponding ECG component. Show the plateau (Phase 2) corresponding to the ST segment.

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c) Inferior Wall MI - ECG Findings and Leads (2+2 = 4 marks)

• ST elevation (convex upward / tombstone shaped) in inferior leads
• Reciprocal ST depression in anterior leads (I, aVL)
• Hyperacute T waves (tall, peaked) - earliest change

• Q waves (pathological: >0.04 sec wide, >1/4 of R wave amplitude) - indicate transmural necrosis
• T wave inversion
• ST elevation gradually resolves

• Persistent Q waves
• T wave may normalize

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Q.2 - Short Notes (5 × 4 = 20 marks)

A. Role of RAAS in Blood Pressure Regulation (4 marks)

1. Decreased renal perfusion pressure (baroreceptor mechanism)
2. Decreased Na⁺ delivery to macula densa
3. Sympathetic stimulation (via β₁ receptors)

Angiotensinogen (liver)
        ↓ [Renin - from JG cells]
Angiotensin I (inactive decapeptide)
        ↓ [ACE - Angiotensin Converting Enzyme, mainly in lungs]
Angiotensin II (active octapeptide)
        ↓
    ┌───────────────────────────────────┐
    ↓                                   ↓
Vasoconstriction              Adrenal Cortex (Zona Glomerulosa)
(↑ TPR → ↑ BP)                        ↓ [Aldosterone release]
    ↓                         Na⁺ reabsorption in DCT/collecting duct
Also: ADH release             H₂O retention → ↑ Blood Volume → ↑ BP
Thirst stimulation
Sympathetic activation

1. Arteriolar vasoconstriction - most potent vasoconstrictor in the body
2. Stimulates aldosterone - Na⁺ and H₂O retention (↑ blood volume)
3. Stimulates ADH (vasopressin) release - water retention
4. Stimulates thirst center in hypothalamus
5. Cardiac hypertrophy and renal mesangial contraction
6. Efferent arteriole constriction - maintains GFR during hypotension

• Short-term: vasoconstriction (↑ TPR)
• Long-term: Na⁺/water retention (↑ blood volume → ↑ cardiac output)

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B. Flowchart of Intrinsic and Extrinsic Pathways of Blood Coagulation (4 marks)

Tissue Damage → Release of Tissue Factor (TF / Factor III)
                         ↓
TF + Factor VII + Ca²⁺ → Factor VIIa-TF complex
                         ↓
                  Activates Factor X → Xa

Contact with collagen/glass → Factor XII activated → XIIa
                         ↓
        XIIa → XI → XIa
                         ↓
        XIa + Ca²⁺ → IX → IXa
                         ↓
        IXa + Factor VIIIa + Ca²⁺ + PF3 → Factor X activated → Xa

Factor Xa + Factor Va + Ca²⁺ + Phospholipid (Prothrombinase complex)
                         ↓
        Prothrombin (Factor II) → Thrombin (IIa)
                         ↓
        Fibrinogen (Factor I) → Fibrin (loose/soluble)
                         ↓
        Factor XIII + Ca²⁺ → Cross-linked Fibrin (stable clot)

• Extrinsic pathway assessed by PT (Prothrombin Time)
• Intrinsic pathway assessed by aPTT (activated Partial Thromboplastin Time)
• Vitamin K-dependent factors: II, VII, IX, X (and Protein C, S)

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C. Counter-Current Multiplier in Kidney (4 marks)

1. Descending limb of Loop of Henle - permeable to water, impermeable to solutes
2. Ascending limb of Loop of Henle - impermeable to water, actively transports NaCl out (thick ascending limb = TAL)

Cortex (300 mOsm)
        ↓ fluid flows DOWN descending limb
Medulla
        ↓ 
At each level:
- TAL pumps NaCl out (active transport via Na⁺-K⁺-2Cl⁻ cotransporter / NKCC2)
- Tubular fluid in descending limb equilibrates with interstitium by losing water
- As fluid descends → becomes more concentrated
- At bend → ~1200 mOsm
- As fluid ascends in TAL → NaCl pumped out without water → fluid becomes dilute
- At cortex → tubular fluid ~100 mOsm (hypotonic)

• At any horizontal level, there is a small gradient (~200 mOsm) between ascending and descending limbs
• The counter-current flow multiplies this small horizontal gradient into a large vertical medullary osmotic gradient (300-1200 mOsm from cortex to papilla)

• Acts as counter-current exchanger (not multiplier)
• Preserves medullary gradient by passive exchange of solutes and water
• Prevents "washout" of the gradient

• In the presence of ADH, collecting duct becomes permeable to water
• Water moves from tubule into hypertonic medullary interstitium (osmosis)
• Concentrated urine (up to 1200 mOsm) is produced

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D. Define Shock - Distributive Types of Shock (4 marks)

• Cause: Gram-negative bacteria (endotoxin/LPS), Gram-positive bacteria, fungi
• Mechanism: LPS → macrophage activation → IL-1, IL-6, TNF-α → iNOS activation → massive NO production → vasodilation
• Features: fever, warm flushed skin, hypotension, ↑ HR, leukocytosis
• Phases: Early (warm/hyperdynamic) → Late (cold/hypodynamic)

• Cause: Type I hypersensitivity reaction (bee sting, drug allergy, food allergy)
• Mechanism: IgE → mast cell degranulation → massive histamine release → vasodilation + ↑ vascular permeability + bronchospasm
• Features: urticaria, angioedema, bronchospasm, hypotension
• Treatment: Adrenaline (epinephrine) IM

• Cause: Spinal cord injury (above T6), severe pain, emotional shock, spinal anesthesia
• Mechanism: Loss of sympathetic tone → uncontrolled vasodilation + bradycardia (loss of cardiac sympathetics)
• Features: hypotension + bradycardia + warm dry skin (unusual triad)
• Distinguishing: bradycardia (not tachycardia as in other shocks)

• Cause: Staphylococcal/Streptococcal exotoxins acting as superantigens
• Leads to massive T-cell activation → cytokine storm → distributive shock

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Q.3 - Short Answer Questions (4 × 2 = 8 marks)

A. Role of Neutrophils in Immune Response (2 marks)

1. Chemotaxis: Respond to chemotactic signals (C5a, IL-8, LTB4, fMLP) and migrate to site of infection/inflammation
2. Phagocytosis:
   • Recognize bacteria via opsonins (IgG, C3b) through Fc receptors and complement receptors
   • Engulf pathogens into phagosomes
   • Phagosome fuses with granules → phagolysosome
3. Killing Mechanisms:
   • Oxygen-dependent (Respiratory burst): NADPH oxidase → superoxide (O₂⁻) → H₂O₂ → HOCl (hypochlorous acid via myeloperoxidase) → kills bacteria
   • Oxygen-independent: Lysozyme (degrades bacterial cell wall), defensins, lactoferrin, elastase, cathepsins
4. Degranulation:
   • Primary (azurophilic) granules: myeloperoxidase, lysozyme, defensins
   • Secondary (specific) granules: lactoferrin, collagenase, B12-binding protein
5. NET formation (Neutrophil Extracellular Traps):
   • Release chromatin + antimicrobial proteins to trap and kill bacteria extracellularly
6. Cytokine Release: IL-1β, TNF-α, IL-6, IL-12 → amplify inflammatory response

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B. Pathophysiological Basis of Erythroblastosis Foetalis (2 marks)

1st Pregnancy:
Rh- mother + Rh+ fetus
→ At delivery (or abortion/trauma): Rh+ fetal RBCs enter maternal circulation
→ Maternal immune system recognizes Rh antigen (D antigen) as foreign
→ Primary immune response → IgM antibodies (don't cross placenta) - No harm to 1st baby

Sensitization occurs (mother becomes anti-D IgG positive)

2nd Pregnancy (Rh+ fetus again):
→ Maternal anti-D IgG antibodies cross placenta (IgG crosses, IgM does not)
→ Anti-D IgG coats fetal Rh+ RBCs
→ Fetal macrophages (spleen) recognize coated RBCs → phagocytosis → HEMOLYSIS

Consequences:
→ Severe hemolytic anemia in fetus
→ Compensatory extramedullary hematopoiesis (liver, spleen, bone marrow)
→ Nucleated RBCs (erythroblasts) in peripheral blood → "Erythroblastosis"
→ Hydrops fetalis (severe cases): generalized edema, ascites, pleural effusion
→ Hyperbilirubinemia → Kernicterus (bilirubin deposition in brain) in neonate

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C. Cushing's Reflex (2 marks)

1. ↑ Blood pressure (marked systolic hypertension) - ischemic vasomotor center fires maximally → intense sympathetic discharge → vasoconstriction and ↑ cardiac output
2. Bradycardia - baroreceptor response to extreme hypertension → vagal activation → bradycardia
3. Irregular/slow respirations (Cheyne-Stokes or agonal breathing) - due to brainstem compression

↑ ICP → ↓ CPP → Brain ischemia → Ischemic vasomotor center fires 
→ Massive sympathetic discharge → ↑ BP
→ Baroreceptors detect ↑ BP → Vagus nerve → Bradycardia

• Cushing's triad (hypertension + bradycardia + irregular breathing) is a late and ominous sign of severely raised ICP (herniation imminent)
• Seen in: head injury, intracranial hemorrhage, brain tumors
• Requires emergency intervention (mannitol, head elevation, neurosurgery)

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D. Wenckebach Phenomenon in Heart Block (2 marks)

• PR interval progressively lengthens beat by beat
• Until one P wave is not followed by a QRS (dropped beat)
• After the dropped beat, PR interval resets to its shortest value
• Cycle repeats (e.g., 3:2 or 4:3 ratio of P:QRS)

• AV node conducts each successive impulse with increasing difficulty (fatigue/decremental conduction)
• Eventually fails to conduct → dropped beat
• During the pause (dropped beat), AV node recovers
• The greatest increment in PR prolongation occurs between the 1st and 2nd beat; subsequent increments are smaller → PP interval shortens before the dropped beat, giving a characteristic "grouped beating" pattern

• Inferior MI (RCA supplies AV node)
• Increased vagal tone (athletes, during sleep)
• Digitalis toxicity
• Myocarditis
• Drug effects (β-blockers, calcium channel blockers)

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SECTION B

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Q.4 - Neural Regulation of Respiration + Cheyne-Stokes + Kussmaul (6+3 = 9 marks)

Neural Regulation of Respiration (6 marks)

• Location: Nucleus tractus solitarius (NTS), dorsal medulla
• Function: Generates the basic rhythm of inspiration (ramp signal)
• Contains mainly inspiratory neurons (I neurons)
• Receives afferents from peripheral chemoreceptors (CN IX, X) and lung stretch receptors
• Sends impulses to phrenic nerve (C3,4,5) → diaphragm

• Location: Nucleus ambiguus + nucleus retroambiguus, ventral medulla
• Contains both inspiratory and expiratory neurons
• Quiet breathing: VRG is relatively inactive (expiration is passive)
• Active breathing/forced expiration: VRG expiratory neurons fire → activate accessory muscles (internal intercostals, abdominals)
• Pre-Botzinger complex (pacemaker of respiratory rhythm) is within the VRG

• Location: Nucleus parabrachialis, upper pons
• Function: Inhibits inspiration → limits inspiratory volume → controls respiratory rate
• Sends inhibitory signals to DRG → turns off inspiration (inspiratory "off-switch")
• When active: rapid, shallow breathing
• When inhibited: slow, deep breathing (apneusis if absent + vagus cut)

• Location: Lower pons
• Function: Prolongs inspiration (sends continuous excitatory drive to DRG)
• Normally inhibited by pneumotaxic center and Hering-Breuer reflex
• If unopposed: produces apneusis (prolonged inspiratory gasps)

• Lung stretch receptors (in bronchial smooth muscle) → activated when lungs inflate sufficiently
• Signals via Vagus nerve to DRG → inhibits inspiration (prevents over-inflation)
• Important in newborns and during tidal volumes >1L in adults

• Location: Ventral surface of medulla (near respiratory centers)
• Sensitive to: CO₂ / [H⁺] in CSF (NOT directly to O₂)
• Mechanism: CO₂ crosses BBB → combines with H₂O → H₂CO₃ → H⁺ + HCO₃⁻ → ↑[H⁺] in CSF → stimulates chemoreceptors → ↑ ventilation
• Main regulator of normal breathing

• Location: Carotid bodies (CN IX) and Aortic bodies (CN X)
• Sensitive to: ↓ PaO₂ (mainly, when <60 mmHg), ↑ PaCO₂, ↓ pH
• Respond to hypoxia, hypercapnia, acidosis
• Important in: hypoxic drive (e.g., COPD patients)

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Cheyne-Stokes Breathing (1.5 marks)

Apnea → gradual ↑ tidal volume (crescendo) → peak → gradual ↓ (decrescendo) → Apnea again
[Each cycle: 30 seconds to 3 minutes]

1. During apnea: PaCO₂ rises, PaO₂ falls
2. When CO₂ rises enough to stimulate respiratory centers → breathing resumes and increases (hyperpnea)
3. Hyperventilation causes PaCO₂ to fall below normal → apnea again
4. The oscillation continues due to delayed feedback (long circulation time from lungs to brain)

• Heart failure (most common in adults) - ↑ circulation time (lung to brain) = delayed CO₂ feedback
• Severe brain damage (stroke, head injury, brain tumors)
• Normal in premature infants and some normal adults during sleep at high altitude
• Uremia, narcotic overdose

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Kussmaul's Breathing (1.5 marks)

• Occurs in severe metabolic acidosis
• ↓ blood pH → stimulates peripheral and central chemoreceptors → hyperventilation
• Goal: to blow off CO₂ (compensatory respiratory alkalosis)
• PaCO₂ falls as compensation for metabolic acidosis (Henderson-Hasselbalch relationship)

• Diabetic Ketoacidosis (DKA) - most classic cause (acetone breath + Kussmaul breathing)
• Lactic acidosis
• Renal failure (uremic acidosis)
• Methanol/salicylate poisoning

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Q.5 - Short Notes (4 × 5 = 20 marks)

A. HCl Secretion in Stomach (5 marks)

1. CO₂ + H₂O → H₂CO₃ (catalyzed by carbonic anhydrase inside parietal cell)
2. H₂CO₃ → H⁺ + HCO₃⁻
3. H⁺ is pumped into gastric lumen by H⁺/K⁺-ATPase (Proton Pump) on the apical membrane (exchange: H⁺ out, K⁺ in)
4. Cl⁻ is secreted into the lumen through Cl⁻ channels → combines with H⁺ → HCl
5. HCO₃⁻ exchanges for Cl⁻ on the basolateral side (via Cl⁻/HCO₃⁻ antiporter) → HCO₃⁻ enters blood ("alkaline tide")

• Cephalic phase (30%): Thought, smell, taste of food → vagal stimulation
• Gastric phase (60%): Food in stomach → gastrin release, distension
• Intestinal phase (10%): Chyme in duodenum (initial stimulation, then inhibition)

• Low pH (<2) in antrum → inhibits gastrin release (local feedback)
• Secretin, GIP, VIP, somatostatin → inhibit acid secretion
• Prostaglandins (E₂) → protect mucosa

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B. Phases of Deglutition (Swallowing) (5 marks)

• Fully voluntary and conscious
• Tongue pushes bolus posteriorly against the hard palate and then to the oropharynx
• Lips sealed, teeth occluded
• Duration: ~1 second
• Triggers the swallowing reflex

• Triggered by touch receptors in posterior pharynx → CN IX → swallowing center in medulla (nucleus tractus solitarius + nucleus ambiguus)
• Entirely reflex and involuntary
• Protective mechanisms occur simultaneously:
  • Soft palate elevates → closes nasopharynx (prevents nasal regurgitation)
  • Larynx elevates and moves anteriorly
  • Epiglottis folds over laryngeal inlet (seals airway)
  • True and false vocal cords adduct (glottis closes)
  • Respiration is inhibited (deglutition apnea)
• Upper esophageal sphincter (UES) relaxes
• Pharyngeal peristaltic waves propel bolus into esophagus
• Duration: 1-2 seconds
• Cranial nerves involved: V (trigeminal), IX (glossopharyngeal), X (vagus), XII (hypoglossal)

• Entirely involuntary
• Primary peristalsis: Continuation of pharyngeal peristaltic wave, propels bolus down esophagus
• Secondary peristalsis: If bolus is not cleared, distension triggers additional peristaltic waves (mediated locally + via vagus)
• Upper 1/3 of esophagus: striated muscle (voluntary)
• Lower 2/3: smooth muscle (involuntary, under Auerbach's plexus)
• Lower Esophageal Sphincter (LES) relaxes ahead of bolus → allows entry into stomach
• LES then contracts to prevent reflux
• Duration: 8-20 seconds (liquids faster, solids slower)
• Gravity assists but is not essential (can swallow upside down)

• Located in medulla oblongata (NTS + nucleus ambiguus)
• Coordinates the sequential contraction/relaxation pattern
• Receives afferents from pharyngeal touch receptors via CN IX

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C. Tubuloglomerular Feedback (5 marks)

• Macula densa: Specialized cells in the wall of the thick ascending limb (TAL) of the loop of Henle, at the point where it abuts its own glomerulus
• Juxtaglomerular (JG) cells: Modified smooth muscle cells in the afferent arteriole wall; produce renin
• Extraglomerular mesangial cells (Lacis cells): Connective tissue cells, may transmit signals

↑ GFR → ↑ tubular flow → ↑ NaCl delivery to macula densa
                ↓
Macula densa cells sense ↑ [NaCl] via NKCC2 transporter
                ↓
Release of adenosine + TXA₂ (vasoconstrictors)
                ↓
Afferent arteriole CONSTRICTS → ↓ GFR (feedback correction)

↓ GFR → ↓ tubular flow → ↓ NaCl delivery to macula densa
                ↓
Macula densa releases prostaglandins (PGI₂, PGE₂) → vasodilator
                ↓
Afferent arteriole DILATES → ↑ GFR (feedback correction)
                ↓
Also: ↓ NaCl → stimulates renin release → RAAS activation

1. Autoregulation of GFR: Maintains constant GFR despite changes in systemic blood pressure (works alongside myogenic mechanism)
2. Matches filtration rate to tubular reabsorptive capacity: Prevents delivery of excess NaCl to distal nephron
3. Links RAAS to tubular NaCl sensing: Low NaCl at macula densa → renin release → Ang II → aldosterone → Na⁺ reabsorption

• TGF is a negative feedback loop
• Sensor: Macula densa (NaCl sensor)
• Effector: Afferent arteriole (changes GFR)
• Mediators: Adenosine (constriction), PGs (dilation), ATP, NO

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D. Role of DCT and Collecting Tubule in Urine Formation (5 marks)

• Via NCC (Na⁺-Cl⁻ cotransporter) on apical membrane (electroneutral)
• Impermeable to water (diluting segment, like TAL)
• Creates dilute tubular fluid
• Regulated by: Thiazide diuretics block NCC (used for hypertension)

• Reabsorbs Na⁺ and Cl⁻ (NCC)
• Reabsorbs Ca²⁺ (via TRPV5 channel, regulated by PTH and Calcitriol)
• Reabsorbs Mg²⁺ (via TRPM6)

• Contains principal cells and intercalated cells (like collecting duct)
• Aldosterone begins to act here

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• Apical: ENaC (epithelial Na⁺ channel) for Na⁺ reabsorption
• Basolateral: Na⁺/K⁺-ATPase
• K⁺ is secreted via ROMK channels (apical)
• Regulated by Aldosterone: ↑ Na⁺ reabsorption + ↑ K⁺ secretion (↑ ENaC and Na⁺/K⁺-ATPase expression)
• Water permeability regulated by ADH (vasopressin):
  • ADH → V2 receptor → ↑ cAMP → PKA → insertion of Aquaporin-2 (AQP2) into apical membrane
  • Water follows osmotic gradient into hypertonic medullary interstitium → concentrated urine

• Type A (alpha) intercalated cells: Secrete H⁺ (via H⁺-ATPase) and reabsorb HCO₃⁻ → acidify urine → important in metabolic acidosis
• Type B (beta) intercalated cells: Secrete HCO₃⁻ → important in metabolic alkalosis

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Q.6 - Short Answer Questions (4 × 2 = 8 marks)

A. Caisson Disease (2 marks)

• At high pressure, gases (especially N₂ - nitrogen) dissolve in blood and tissues in greater amounts (Henry's Law: amount of gas dissolved ∝ partial pressure)
• If pressure is reduced too rapidly (rapid ascent), N₂ comes out of solution as bubbles in blood and tissues before it can be exhaled
• Gas bubbles form in: joints (especially knees, shoulders), muscles, fat, spinal cord, inner ear, blood vessels, lungs

• Type I (mild): Joint pain ("the bends"), skin rash, itching
• Type II (serious):
  • Neurological: paresthesias, paralysis, spinal cord infarction
  • Pulmonary: "the chokes" - chest pain, cough, dyspnea (pulmonary emboli)
  • Inner ear: vertigo, hearing loss (staggers)
  • Cardiovascular: arterial gas embolism

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B. Migrating Motor Complex (MMC) (2 marks)

• Primarily regulated by Motilin (hormone from M cells of duodenum/jejunum)
• Motilin peaks just before Phase III activity front
• Also regulated by intrinsic enteric nervous system
• Abolished by eating (fed pattern replaces the MMC pattern)

1. Clears undigested residues from small intestine
2. Prevents bacterial overgrowth (sweeps bacteria toward colon)
3. Maintains colonic flora in proper location

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C. Effect of Moderate Exercise on Heart Rate and Blood Pressure (2 marks)

• Increases (tachycardia) - from resting ~70 bpm to 120-150 bpm (moderate exercise)
• Mechanisms:
  1. Neural (primary): ↑ sympathetic outflow (via cardiac accelerator nerves) → ↑ SA node firing rate
  2. Withdrawal of vagal tone → further ↑ HR
  3. Bainbridge reflex (atrial reflex): ↑ venous return → atrial stretch → reflex tachycardia
  4. Circulating catecholamines: Epinephrine/norepinephrine from adrenal medulla → β₁ receptor → ↑ HR

• Systolic BP increases (120 mmHg → 160-180 mmHg during moderate exercise)
  • Due to ↑ cardiac output (↑ HR × ↑ stroke volume)
• Diastolic BP remains relatively unchanged or slightly decreases (↑ or ↓ by <10 mmHg)
  • Due to vasodilation in exercising muscles (↓ TPR balances ↑ CO)
• Pulse pressure increases (↑ SBP with stable DBP = widened pulse pressure)
• Mean Arterial Pressure (MAP): Slightly increases
• Total Peripheral Resistance (TPR): Decreases (vasodilation in muscles due to local metabolites: CO₂, H⁺, lactate, adenosine, K⁺, NO)

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D. Heat Stroke (2 marks)

• Classic Heat Stroke: Occurs in elderly, very young, or those with chronic illness during heat waves; due to environmental hyperthermia overwhelming heat dissipation
• Exertional Heat Stroke: Occurs in young, physically active individuals during intense exercise in hot/humid conditions; heat production exceeds dissipation

1. Core temperature rises above the set point
2. Hypothalamus initially triggers sweating, cutaneous vasodilation, ↑ cardiac output
3. When compensatory mechanisms are overwhelmed → temperature continues to rise
4. At >41°C: cellular proteins begin to denature, mitochondrial dysfunction
5. Endothelial damage → inflammatory cascade (cytokines, IL-1, TNF-α)
6. Multiorgan failure: CNS (cerebral edema, hemorrhage), liver, kidneys (ATN), heart, coagulopathy (DIC)
7. Sweating is characteristically absent in classic heat stroke (anhidrosis - sweat glands fail)
8. Exertional type may still have sweating

• Hot, dry, flushed skin (classic type: anhidrotic)
• Core temp >40°C
• CNS dysfunction: confusion, delirium, seizures, coma (key distinguishing feature from heat exhaustion)
• Hypotension, tachycardia
• Nausea, vomiting

• Remove from heat, undress
• Ice packs to neck, axillae, groin (areas of major vessels)
• Evaporative cooling (spraying water + fanning) is most effective
• Cold IV fluids
• Target: cool to <39°C within 30 minutes

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Quick Reference Summary

Paper Structure Covered:

• Section A (38 marks): Q1 + Q2 + Q3
• Section B (37 marks): Q4 + Q5 + Q6

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Key Points to Remember for the Exam:

• Diagnosis = Acute MI (history + risk factors)
• Phase 0 (QRS) = fast Na⁺; Phase 2 (ST segment) = Ca²⁺ plateau; Phase 3 (T wave) = K⁺ efflux
• Inferior MI = ST elevation in II, III, aVF (RCA territory)

• RAAS = Renin → Ang I → ACE → Ang II → vasoconstriction + aldosterone
• Coagulation: Extrinsic (TF + VII) vs Intrinsic (XII→XI→IX→VIII) → common pathway (X→V→prothrombin→thrombin→fibrin)
• Counter-current multiplier = TAL actively pumps NaCl, creates 300-1200 mOsm corticopapillary gradient
• Distributive shock: Septic, Anaphylactic, Neurogenic (all cause ↓ SVR despite ↑/normal CO)

• Neutrophils: Chemotaxis → Phagocytosis → Respiratory burst (NADPH oxidase → O₂⁻ → HOCl via MPO)
• Erythroblastosis: Rh- mother sensitized in 1st pregnancy → anti-D IgG crosses placenta in 2nd pregnancy → fetal hemolysis
• Cushing's Reflex: ↑ ICP → brain ischemia → ↑ BP + bradycardia + irregular breathing (triad = ominous sign)
• Wenckebach = Mobitz I = progressive PR prolongation → dropped beat → reset

• DRG = inspiration rhythm; Pneumotaxic center = limits inspiration; Apneustic center = prolongs inspiration
• Cheyne-Stokes = cyclic apnea-hyperpnea, seen in heart failure (long circulation time)
• Kussmaul = deep, rapid, regular breathing = compensation for metabolic acidosis (DKA)

• HCl: H⁺/K⁺-ATPase (proton pump) on parietal cells; stimulated by ACh, histamine, gastrin
• Deglutition: Oral (voluntary) → Pharyngeal (reflex, glottis closes) → Esophageal (peristalsis, LES relaxes)
• TGF: Macula densa senses NaCl → adenosine → afferent arteriole constriction → ↓ GFR (negative feedback)
• DCT/CD: Na⁺ via ENaC (aldosterone), Water via AQP2 (ADH), H⁺ via intercalated cells

• Caisson disease = rapid ascent → N₂ bubbles → joint pain, neurological deficits; treat with hyperbaric O₂
• MMC: 90-120 min cycles (fasting); Phase III = "housekeeper wave"; regulated by Motilin
• Moderate exercise: ↑ HR, ↑ SBP, DBP unchanged, ↑ CO, ↓ TPR (muscle vasodilation)
• Heat stroke: Core temp >40°C + CNS dysfunction; classic = anhidrotic; treat with rapid cooling