---

NEET PG Physiology - 8 High-Yield Revision Notes

---

1. RESTING MEMBRANE POTENTIAL (RMP)

Ion concentrations (intracellular vs extracellular):

How RMP is generated:

• Cell membrane at rest is most permeable to K+ (and Cl-), least permeable to Na+
• K+ diffuses OUT down concentration gradient → leaves -ve charge inside
• Equilibrium potential: K+ = -94 mV (Nernst), Na+ = +61 mV, Cl- = -86 mV
• RMP (-70 mV) is close to K+ equilibrium potential because K+ permeability dominates

Na+/K+ ATPase pump:

• Pumps 3 Na+ out and 2 K+ in per cycle (electrogenic - contributes ~-4 mV directly)
• Main role = maintains the concentration gradients (indirect role is bigger)

NEET PG Traps:

• RMP is mainly due to K+ diffusion (not the pump directly)
• Donnan equilibrium: large intracellular anions (proteins) also contribute to -ve interior
• Goldman equation = considers relative permeability of Na+, K+, Cl- together
• Hyperpolarization = more negative than -70 mV; Depolarization = less negative

---

2. ACTION POTENTIAL CURVE

Phases (Nerve fiber):

Key concepts:

• All-or-nothing law: once threshold is reached, AP is full-size regardless of stimulus strength
• Absolute refractory period (ARP): no AP possible - Na+ channels are inactivated (not just closed). ARP = from depolarization to ~2/3 of repolarization
• Relative refractory period (RRP): AP possible only with suprathreshold stimulus - K+ channels still open, membrane is hyperpolarized
• Accommodation: if depolarization is slow/gradual, threshold rises - no AP fires

Cardiac AP differences (vs nerve):

• Phase 0: rapid Na+ influx (upstroke)
• Phase 1: brief repolarization (K+ out, Cl- in)
• Phase 2: Plateau (unique to heart) - L-type Ca2+ channels open = balances K+ efflux
• Phase 3: rapid repolarization - K+ channels (IKr, IKs)
• Phase 4: resting potential (ventricular = -90 mV)
• SA node: NO phase 1 or 2; slow depolarization in phase 4 (pacemaker potential) via If (funny current - Na+/K+), then Ca2+ upstroke (NOT Na+)

NEET PG Traps:

• Drug that blocks Na+ channels = raises threshold = makes membrane less excitable
• Tetrodotoxin (TTX) blocks voltage-gated Na+ channels (puffer fish poison)
• Tetraethylammonium (TEA) blocks K+ channels
• In SA/AV node: AP upstroke is due to Ca2+ (not Na+) - hence Ca2+ channel blockers slow HR

---

3. JVP WAVES

Normal JVP waveform:

Abnormalities (HIGH YIELD):

Normal JVP:

• Measured at 45° with head of patient
• Normal = < 3 cm above sternal angle (< 8 cm above RA)
• Falls on inspiration (intrathoracic pressure drops → blood drains into thorax)

---

4. PACINIAN CORPUSCLE

Structure:

• Large, encapsulated mechanoreceptor - looks like an onion bulb (lamellated capsule of modified Schwann cells)
• Located in: deep dermis, subcutaneous tissue, periosteum, mesentery, joint capsules, external genitalia

Function:

• Detects: vibration (best at 200-300 Hz), deep pressure, rapidly adapting
• Rapidly adapting (phasic): responds at onset and offset of stimulus only - NOT sustained pressure

Classification of sensory receptors (HIGH YIELD):

Fiber types:

• Pacinian corpuscle = Aβ fiber (Group II)
• Fine touch (Meissner's) = Aβ
• Pain = Aδ (sharp, fast) and C fibers (dull, slow/burning)
• Temperature = Aδ (cold/sharp) and C (warm/aching)

---

5. SENSORY FIBRES

Classification (MUST KNOW):

Erlanger-Gasser classification vs Lloyd classification:

• Sensory = A, B, C (Erlanger-Gasser)
• Motor/muscle: Group I (Ia = muscle spindle primary; Ib = GTO), Group II, III, IV (= C fiber for pain)

Order of blockade by local anesthetics:

• Sequence: Aδ → C → Aβ → Aα
• Pain blocked first, motor blocked last ("differential blockade")

NEET PG Traps:

• Fastest fiber = Aα (motor, proprioception)
• Slowest = C fiber
• Local anesthetic blocks pain first (Aδ and C fibers first)
• C fibers most resistant to pressure block (unmyelinated); Aα most resistant to local anesthetic

---

6. GLUT TRANSPORTERS

GLUT family (Facilitative glucose transporters):

SGLT (Sodium-Glucose Linked Transporters):

• SGLT-1: small intestine (glucose + galactose absorption) - 2 Na+ per glucose
• SGLT-2: kidney proximal tubule (reabsorption of 90% filtered glucose) - TARGET of gliflozins

NEET PG Traps:

• GLUT-4 is the insulin-regulated transporter (moves from cytoplasmic vesicles to membrane)
• GLUT-2 is the glucose sensor - low affinity means it only signals when glucose is high
• GLUT-1 deficiency = De Vivo disease (seizures, low CSF glucose with normal blood glucose)
• Fructose uses GLUT-5 in intestine and GLUT-2 in liver (not insulin-dependent)
• SGLT-2 inhibitors (dapagliflozin, empagliflozin) cause glucosuria

---

7. RESPIRATORY DISTRESS SYNDROME (RDS)

Neonatal RDS (Hyaline Membrane Disease):

Surfactant:

• Composition: DPPC (dipalmitoyl phosphatidylcholine) = main component; also SP-A, SP-B, SP-C, SP-D
• Function: reduces surface tension → prevents alveolar collapse at end-expiration
• Produced by: type II pneumocytes (appear at 20 wks, functional by 35 wks)
• L/S ratio: ≥2.0 = lung maturity; < 1.5 = high RDS risk
• Phosphatidylglycerol also indicates lung maturity

Laplace Law: P = 2T/r

• Small alveoli have higher pressure → collapse unless surfactant reduces T
• Surfactant works best at LOW lung volumes (end-expiration) - prevents collapse

ARDS (Adult RDS):

• NOT surfactant deficiency - caused by inflammatory injury to alveolar-capillary membrane
• Criteria (Berlin): acute onset, bilateral infiltrates, PaO2/FiO2 < 300, not fully explained by cardiac failure
• PF ratio: Mild 200-300, Moderate 100-200, Severe < 100
• Treatment: Lung protective ventilation (low tidal volume 6 mL/kg, PEEP, prone positioning)

NEET PG Traps:

• Neonatal RDS = surfactant deficiency; ARDS = inflammation/increased permeability
• Lecithin (L) rises sharply at 35 wks; Sphingomyelin (S) stays constant → L/S ratio rises
• Treatment of neonatal RDS: exogenous surfactant (poractant, calfactant), CPAP, O2
• Corticosteroids given to mother, NOT to baby after birth for RDS prophylaxis

---

8. POST-GASTRECTOMY / ILEAL & JEJUNAL RESECTION SYNDROMES

Dumping Syndrome (Post-Gastrectomy):

• Rapid gastric emptying → hyperosmolar load in small bowel → fluid shift into gut lumen
• Symptoms: bloating, diarrhea, tachycardia, hypotension, flushing
• No hypoglycemia

• Rapid glucose absorption → hyperinsulinemia → reactive hypoglycemia
• Symptoms: sweating, palpitations, confusion, syncope
• Treatment: small frequent meals, high protein/fat/low carbohydrate, avoid liquids with meals; octreotide for refractory cases

Consequences of specific resections:

NEET PG Traps:

• Terminal ileum = only site for B12-IF complex absorption
• Terminal ileum = only site for bile salt reabsorption (enterohepatic circulation)
• After ileal resection: bile salt pool depleted → fat malabsorption + steatorrhea + fat-soluble vitamin deficiency (A, D, E, K)
• Hyperoxaluria after ileal resection: unabsorbed fatty acids bind calcium in colon → free oxalate absorbed → oxalate stones
• Cholesterol gallstones also form after ileal resection (depleted bile salt pool → bile becomes lithogenic)
• Gastric bypass patients: B12 + iron + calcium + vitamin D supplements routinely needed

---

Quick Summary Table

---

---

🧬 NEET PG Physiology - 8 High-Yield Revision Notes

Based on Marrow Notes + Guyton + Costanzo | Dr. Ganga's 180 Predicted Topics

---

1. RESTING MEMBRANE POTENTIAL (RMP)

RMP Values (MUST KNOW):

Why is RMP negative?

• Membrane is most permeable to K+ at rest
• K+ diffuses OUT → leaves -ve charge inside
• Equilibrium potentials (Nernst equation: E = ±61 log Co/Ci):

Role of Na+/K+ ATPase:

• Pumps 3 Na+ OUT : 2 K+ IN (electrogenic)
• Activated by: T3, insulin, aldosterone
• Inhibited by: Ouabain, dopamine
• Direct contribution to RMP: ~-4 mV only
• Main role = maintains K+ gradient (indirect = bigger effect)

Clinical Pearls:

• Hyperkalemia → ↓K+ diffusion out → Depolarized cell → ↑ excitable (arrhythmia risk)
• Hypokalemia → ↑K+ diffusion out → Hyperpolarized cell → ↓ excitable (weakness)
• Gibbs-Donnan effect: intracellular protein anions (non-diffusible) also contribute to negativity

---

2. ACTION POTENTIAL CURVE

Nerve Action Potential Phases:

+30 mV ─── Peak (overshoot)
         /    \
        /      \  Repolarization (K+ efflux)
-55 mV /Threshold \
      /           \_____ Hyperpolarization (-90 mV)
-70 mV (Resting)        ───── return to RMP

Refractory Periods:

Cardiac Action Potential:

• Phase 4 (Prepotential): Na+ funny current (If) + ↓K+ efflux + transient Ca2+ → slow depolarization
• Phase 0: L-type Ca2+ influx (NOT Na+!) → upstroke
• Phase 3: K+ efflux → repolarization
• Slope of Phase 4 ↑ by SNS (↑HR) / ↓ by PNS (↓HR)

NEET PG Traps:

• SA/AV node upstroke = Ca2+ → Ca2+ channel blockers slow HR
• ARP = Na+ channels inactivated (not just closed - cannot be reopened)
• Tetrodotoxin (TTX) = blocks Na+ channels; Tetraethylammonium (TEA) = blocks K+ channels
• Cardiac muscle: No tetany because ARP covers most of systole
• Absence of tetany in heart is due to long ARP, not due to Ca2+

---

3. JVP WAVES

Normal Waveform:

Abnormalities (HIGH YIELD):

Key Rule:

• Tamponade: Absent x AND y descent → only x prominent (x > y)
• Constrictive pericarditis: Both x AND y prominent (x = y or y > x)
• Kussmaul's sign = JVP rises on inspiration (seen in constrictive pericarditis, RV failure) - opposite of normal

---

4. PACINIAN CORPUSCLE

Touch Receptors Comparison Table (MARROW HIGH YIELD):

Pacinian Corpuscle Key Facts:

• Rapidly adapting = responds ONLY at onset and offset of stimulus (detects CHANGE)
• Best frequency = 200-300 Hz
• Fiber type: Aβ (fast, myelinated)
• Structure: Lamellated (onion-skin) capsule of modified Schwann cells around Aβ terminal
• Locations: Deep dermis, subcutaneous tissue, periosteum, mesentery, joint capsules, genitalia

Adaptation Mnemonic:

• Rapid = Pacinian + Meissner's (PaM = Rapid)
• Slow = Merkel + Ruffini (MeRk = Slow)

---

5. SENSORY FIBRES

Erlanger-Gasser Classification (Marrow Table):

Lloyd-Hunt Classification (Only Sensory Fibres):

Susceptibility to:

• Compression (pressure block): Aα > B > C (large fibers blocked first)
• Local anesthetic: Aδ → C → Aβ → Aα (small fibers blocked first → pain gone before motor)
• Hypoxia: Aα > C (large myelinated most susceptible)

NEET PG Traps:

• Fastest conduction = Aα | Slowest = C fiber
• Pain is blocked FIRST by local anesthetics (Aδ and C fibers)
• C fibers are most resistant to pressure block
• Gate control theory: Aβ touch fibers → inhibitory neuron → inhibits pain (substantia gelatinosa = gate)

---

6. GLUT TRANSPORTERS

GLUT Family (Facilitated Diffusion - No ATP):

From Marrow Absorption Table:

• Glucose absorption in gut: SGLT-1 → GLUT-2 (enters blood)
• Fructose absorption in gut: GLUT-5 → GLUT-2 (enters blood)

SGLT (Sodium-Glucose Co-Transporters - Active Transport):

NEET PG Traps:

• GLUT-4 is the only insulin-regulated one → target of exercise and insulin signaling
• GLUT-2 = β-cell glucose sensor (low affinity = only responds when glucose is high)
• GLUT-1 deficiency = De Vivo disease (seizures, low CSF glucose with normal blood glucose)
• SGLT-2 inhibitors (dapagliflozin, empagliflozin, canagliflozin) → glucosuria → weight loss + BP ↓
• SGLT-1 mutation = Congenital glucose-galactose malabsorption (CGGM) - as per Marrow
• ORS works because SGLT-1 cotransports Na+ with glucose → use in diarrhea

---

7. RESPIRATORY DISTRESS SYNDROME (RDS)

Surfactant (from Marrow):

• Lipids: DPPC/Lecithin (major), Sphingomyelin (minor)
• L/S ratio ≥ 2 = Adequate fetal lung maturity
• Proteins: SP-A, SP-D = lung immunity | SP-B, SP-C = surface tension reduction

Neonatal RDS (Hyaline Membrane Disease):

• Cause: Surfactant deficiency (Type II pneumocyte immaturity)
• Risk factors: Prematurity, infant of diabetic mother (insulin ↓ surfactant), male sex, C-section
• Protection: Maternal corticosteroids (betamethasone), PROM, maternal hypertension
• Treatment: Exogenous surfactant replacement + CPAP; Betamethasone = treatment of lung immaturity

Laplace Law: P = 2T/r

• Smaller alveoli → higher pressure → collapse unless surfactant reduces T
• Surfactant works best at low lung volumes (end-expiration)

ARDS vs Neonatal RDS:

NEET PG Traps:

• Surfactant is made by Type II pneumocytes (round, few, = stem cells) - Type I = flat, large surface area
• Infants of diabetic mothers: ↑Insulin → ↓Surfactant → ↑RDS risk (insulin suppresses surfactant)
• L/S ratio: Lecithin rises sharply at 35 weeks; Sphingomyelin stays constant
• Phosphatidylglycerol = additional marker of lung maturity

---

8. POST-GASTRECTOMY / ILEAL & JEJUNAL RESECTION SYNDROMES

Absorption Site Recap (Marrow):

Consequences of Resection:

1. Vitamin B12 malabsorption → megaloblastic anemia (ONLY site for IF-B12 complex)
2. Bile salt malabsorption → bile salt diarrhea (cholerheic enteropathy)
3. Fat malabsorption → steatorrhea (depleted bile salt pool)
4. Fat-soluble vitamin deficiency (A, D, E, K)
5. Hyperoxaluria → oxalate kidney stones (Ca2+ binds to fatty acids → free oxalate absorbed by colon)
6. Cholesterol gallstones (↓bile salt pool → lithogenic bile)

• Note: Ileum compensates for jejunum; jejunum CANNOT compensate for ileum

1. Loss of intrinsic factor → B12 deficiency
2. Loss of HCl → Iron deficiency (Fe3+ → Fe2+ requires acid)
3. Dumping syndrome (see below)

• Iron, folate, calcium, fat-soluble vitamin malabsorption
• Less severe (ileum compensates)

Dumping Syndrome:

Gastric Emptying Rate:

• Fastest: Carbohydrates
• Slowest: Fats
• Decreased by: Enterogastric reflex (fat, acid, carbohydrates in duodenum), CCK, Secretin

NEET PG Traps:

• Terminal ileum = ONLY site for B12 and bile salts - no other site can compensate
• Post-ileal resection: hyperoxaluria because fatty acids "steal" calcium → oxalate freely absorbed
• Post-gastrectomy B12 deficiency: intrinsic factor lost, not B12 itself
• Short bowel syndrome: parenteral nutrition required if <100 cm of small intestine remains
• Gastric bypass patients need: B12, iron, calcium, Vitamin D supplementation

---

⚡ QUICK SUMMARY CHEAT SHEET

---