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Physiology 3% exam weight

General Physiology and Cell Biology

Part of the NEET PG study roadmap. Physiology topic physio-001 of Physiology.

General Physiology and Cell Biology

🟢 Lite — Quick Review (1h–1d)

Rapid summary for last-minute revision before your exam.

General Physiology and Cell Biology — Key Facts for NEET PG

  • Cell membrane is a fluid mosaic model (phospholipid bilayer + proteins)
  • Resting membrane potential ≈ −70 mV (inside negative); maintained by Na⁺/K⁺-ATPase
  • Homeostasis — internal environment maintained constant despite external changes
  • Active transport uses ATP; Passive transport (diffusion, osmosis, facilitated diffusion) does not
  • Exam tip: Na⁺/K⁺-ATPase pumps 3 Na⁺ out, 2 K⁺ in per ATP — this 3:2 ratio is frequently tested

🟡 Standard — Regular Study (2d–2mo)

Standard content for students with a few days to months.

General Physiology and Cell Biology — NEET PG Study Guide

Cell Membrane Structure

Fluid Mosaic Model (Singer-Nicolson, 1972):

  • Phospholipid bilayer: Amphipathic molecules — hydrophilic heads outward, hydrophobic tails inward
  • Proteins: Integral (span bilayer) or peripheral (attach to surface)
  • Cholesterol: Regulates membrane fluidity
  • Carbohydrates: Glycocalyx — cell recognition, adhesion

Functions of Membrane Proteins:

TypeFunction
Channel proteinsPassive diffusion of ions
Carrier proteinsActive/facilitated transport
Receptor proteinsSignal transduction
Enzyme proteinsCatalyze reactions at membrane
Cell adhesion moleculesIntercellular adhesion

Transport Across Cell Membrane

Passive Processes:

  1. Simple diffusion: Non-polar molecules (O₂, CO₂, N₂) move along concentration gradient
  2. Facilitated diffusion: Glucose, amino acids via carrier/channels (saturation kinetics)
  3. Osmosis: Water movement across semipermeable membrane toward higher solute concentration

Active Processes:

  1. Primary active transport: Direct ATP use — Na⁺/K⁺-ATPase, Ca²⁺-ATPase, H⁺-ATPase
  2. Secondary active transport: Coupled transport (symport/antiport) — uses electrochemical gradient
    • Example: Na⁺/glucose cotransporter (SGLT) in proximal tubule

Bulk Transport:

  • Endocytosis: Phagocytosis (solid), pinocytosis (fluid), receptor-mediated
  • Exocytosis: Release of secretions, neurotransmitters

Resting Membrane Potential

Key Points:

  • Resting potential = −70 mV (inside negative relative to outside)
  • Maintained by Na⁺/K⁺-ATPase (pumps 3 Na⁺ out, 2 K⁺ in)
  • K⁺ leaks through leak channels (high permeability to K⁺)
  • Na⁺ and protein anions also contribute
  • Nernst equation calculates equilibrium potential for each ion
IonExtracellular (mEq/L)Intracellular (mEq/L)Equilibrium Potential
Na⁺14512+60 mV
K⁺4140−90 mV
Cl⁻1034−70 mV

Exam tip: Changes in membrane potential depend on ion permeability and concentration gradients

Body Fluid Compartments

Total Body Water (TBW): ~60% of body weight in adult males (~50% in females)

CompartmentPercentage of TBWApproximate Volume
Intracellular fluid (ICF)40%25 L
Extracellular fluid (ECF)20%12 L
→ Plasma5%3 L
→ Interstitial fluid12%7 L
→ Transcellular3%1.5 L

Exam tip: ECF includes plasma and interstitial fluid; transcellular includes CSF, pleural fluid, etc.

Homeostasis

Definition: Maintenance of internal constancy despite external changes

Control Systems:

  • Receptors: Sense changes (afferent pathway)
  • Control center: Integrates information (brain/spinal cord)
  • Effectors: Produce responses (efferent pathway)

Feedback Mechanisms:

TypeResponseExample
Negative feedbackOpposes change, restores set pointThermoregulation, blood glucose
Positive feedbackAmplifies changeChildbirth, blood clotting

Exam tip: Most physiological systems use negative feedback; positive feedback is less common and typically pathological

Cell Junctions

JunctionStructureFunction
Tight junctionsSeal between cellsPrevent paracellular transport
Adherens junctionsCadherin-mediatedCell-cell adhesion, mechanical support
DesmosomesIntermediate filamentsMechanical strength
HemidesmosomesIntegrins to basement membraneCell-basement membrane adhesion
Gap junctionsConnexons (channels)Direct cell-cell communication (ions, small molecules)

Exam tip: Gap junctions are abundant in cardiac muscle and smooth muscle for coordinated contraction


🔴 Extended — Deep Study (3mo+)

Comprehensive coverage for students on a longer study timeline.

General Physiology and Cell Biology — Comprehensive NEET PG Notes

Detailed Cell Membrane Physiology

Phospholipid Bilayer Properties

  • Amphipathic nature: Polar head + nonpolar tail
  • Asymmetric distribution: Phosphatidylcholine and sphingomyelin on outer leaflet; phosphatidylethanolamine and PS on inner leaflet
  • Fluidity: Depends on fatty acid saturation and cholesterol content
  • Saturated fats → more rigid membrane
  • Unsaturated fats → more fluid membrane
  • Cholesterol: Increases stability but reduces fluidity at high temperatures

Membrane Protein Dynamics

Integral Proteins:

  • Span the lipid bilayer (transmembrane proteins)
  • Usually have α-helical regions for transmembrane domains
  • Functions: Transport, receptors, enzymes

Peripheral Proteins:

  • Attached to membrane surface via electrostatic interactions
  • Can be removed without disrupting membrane integrity
  • Functions: Signaling, structural support, enzymes

Membrane Protein Classes:

  1. Type I: Single transmembrane domain, N-terminus outside
  2. Type II: Single transmembrane domain, N-terminus inside
  3. Multi-pass: Multiple transmembrane domains (GPCRs)
  4. Lipid-anchored: Covalently attached to lipid tails

Ion Channels

Gating mechanisms:

TypeTrigger
Voltage-gatedChanges in membrane potential
Ligand-gatedNeurotransmitter binding
Mechanically-gatedPhysical stretch
Leak channelsAlways open

Key Channels for Exam:

  • Na⁺ channels: Voltage-gated (nerve, muscle excitability)
  • K⁺ channels: Voltage-gated and leak channels
  • Ca²⁺ channels: Voltage-gated (muscle contraction, neurotransmitter release)
  • Cl⁻ channels: Maintains electrical neutrality

Exam tip: Tetrodotoxin (puffer fish) blocks voltage-gated Na⁺ channels → local anesthesia

Second Messenger Systems

cAMP Pathway:

  • Gs protein activates adenylyl cyclase → ↑ cAMP → activates PKA
  • Example: Glucagon, epinephrine (β-receptors)

IP₃/DAG Pathway:

  • Gq protein activates phospholipase C → IP₃ + DAG
  • IP₃ → Ca²⁺ release from ER; DAG → activates PKC
  • Example: α₁-receptors, vasopressin

cGMP Pathway:

  • NO activates guanylyl cyclase → ↑ cGMP → smooth muscle relaxation
  • Example: Nitroglycerin for angina

Tyrosine Kinase Pathway:

  • Insulin receptors, growth factor receptors
  • Receptor autophosphorylation activates intracellular cascades

Transport Kinetics

Michaelis-Menten Kinetics for Carrier-Mediated Transport:

  • Vmax: Maximum transport rate
  • Km: Substrate concentration at half Vmax
  • Saturation: Unlike simple diffusion, carrier transport saturates at high substrate concentrations
  • Specificity: Carriers are specific for particular molecules
  • Competition: Similar molecules compete for same carrier

Active Transport Stoichiometry:

  • Na⁺/K⁺-ATPase: 3 Na⁺ out, 2 K⁺ in, 1 ATP per cycle
  • Creates electrochemical gradient (Na⁺ gradient used for secondary active transport)
  • Ca²⁺-ATPase (SERCA): 2 Ca²⁺ per ATP, pumps Ca²⁺ into ER/sarcoplasmic reticulum
  • H⁺-ATPase: Gastric parietal cells (secretion) and renal tubule cells

Exam tip: Cardiac glycosides (digoxin) inhibit Na⁺/K⁺-ATPase → ↑ intracellular Na⁺ → ↓ Na⁺/Ca²⁺ exchange → ↑ Ca²⁺ in cardiac myocytes → positive inotropy

Detailed Body Fluid Physiology

Measurement of Body Fluid Compartments

Indicator Dilution Method:

  • TBW: Radioactive water (³H₂O) or antipyrine
  • ECF: Inulin, radioactive bromide, sodium thiosulfate
  • ICF: Calculated as TBW − ECF
  • Plasma volume: Radioactive iodine (¹³¹I) labeled albumin (RISA)
  • Blood volume: Plasma volume + RBC volume (measured with ⁵¹Cr)

Derangements:

CompartmentDecreaseIncrease
PlasmaDehydration, hemorrhageFluid overload
InterstitialSevere dehydrationEdema, inflammation
ICFCellular dehydrationWater intoxication

Fluid Shifts Across Capillaries

Starling Forces:

ForceNormal Direction
Capillary hydrostatic pressure (Pc)Outward
Interstitial hydrostatic pressure (Pif)Variable
Plasma oncotic pressure (πc)Inward
Interstitial oncotic pressure (πif)Variable

Net filtration pressure = (Pc − Pif) − (πc − πif)

  • Normally: Net filtration at arterial end, reabsorption at venous end
  • Edema when net filtration exceeds lymphatic drainage

Cellular Communication

Autocrine: Cell acts on itself Paracrine: Cell acts on nearby neighbors Endocrine: Hormones via bloodstream Neurocrine: Neurotransmitters Neuroendocrine: Combination (e.g., hypothalamic releasing hormones) Juxtacrine: Direct cell-cell contact

G Protein-Coupled Receptors (GPCRs):

  • 7 transmembrane domains
  • Activate heterotrimeric G proteins (Gα, Gβγ)
  • Examples: Adrenergic, muscarinic, dopamine, serotonin receptors

Receptor Tyrosine Kinases (RTKs):

  • Insulin, IGF, EGF, PDGF receptors
  • Dimerization → autophosphorylation → signaling cascade

Cell Physiology Special Topics

Cell Volume Regulation:

  • Hypertonic stress: K⁺ and Cl⁻ exit via channels; organic osmolytes accumulate
  • Hypotonic stress: Water enters cell → swelling; regulatory volume decrease (RVD)

Apoptosis vs Necrosis:

FeatureApoptosisNecrosis
EnergyATP-dependentNo ATP
MorphologyBlebbing, chromatin condensationCell swelling
MembraneIntactRuptured
InflammationMinimalSignificant
RegulationProgrammedUncontrolled

Exam tip: Bcl-2 (anti-apoptotic), Bax/Bak (pro-apoptotic), Caspases (executioners)

Practice Questions for NEET PG

  1. Describe the fluid mosaic model of cell membrane. What role does cholesterol play?
  2. Compare simple diffusion, facilitated diffusion, and active transport.
  3. Explain how Na⁺/K⁺-ATPase maintains resting membrane potential.
  4. Calculate the net filtration pressure given specific Starling forces.
  5. Differentiate between negative and positive feedback with physiological examples.
  6. What happens to cell volume in hypotonic solution? How does the cell compensate?
  7. Describe the mechanism of receptor-mediated endocytosis using LDL as an example.

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