Physiology
Medical physiology for MBBS: cell and body fluids, blood, nerve and muscle, and the cardiovascular, respiratory, gastrointestinal, renal, endocrine, reproductive and nervous systems, special senses and integrative physiology.
Definition
An action potential (AP) is a rapid, transient, self-propagating reversal of membrane potential in an excitable cell (nerve/muscle), obeying the all-or-none law.
Phases
- Resting — −70 mV (polarised)
- Depolarisation — Na⁺ influx → +30 mV
- Repolarisation — K⁺ efflux → back to negative
- Hyperpolarisation — brief dip below resting
Ionic Basis
- Stimulus → reaches threshold (−55 mV)
- Voltage-gated Na⁺ channels open → Na⁺ in (depolarisation)
- Na⁺ channels close, K⁺ channels open → K⁺ out (repolarisation)
- Na⁺–K⁺ pump restores the gradients
Properties
- All-or-none law
- Refractory period (absolute + relative)
- Non-decremental (self-propagating) conduction
- Needs a threshold stimulus
Na⁺ entry depolarises, then K⁺ exit repolarises — an all-or-none spike. Phase Ion movement Potential Resting — −70 mV Depolarisation Na⁺ in +30 mV Repolarisation K⁺ out → −70 mV Hyperpolarisation K⁺ out (excess) < −70 mV Applied
- Local anaesthetics block Na⁺ channels
- Hyperkalaemia alters excitability
- Basis of nerve conduction, ECG and EMG
🔑KEY POINTS TO REMEMBER- AP = all-or-none reversal of membrane potential.
- Depolarisation = Na⁺ in; repolarisation = K⁺ out.
- Threshold −55 mV; peak +30 mV.
- Refractory period ensures one-way conduction.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
A nerve fibre is the axon of a neuron that conducts impulses; conduction is continuous in unmyelinated and saltatory in myelinated fibres.
Structure of a Neuron
- Cell body (soma), dendrites, axon
- Axon covered by a myelin sheath (Schwann cells)
- Gaps in myelin = nodes of Ranvier
Classification of Nerve Fibres
- Type A — thick, myelinated, fastest (motor, touch)
- Type B — medium, myelinated (autonomic preganglionic)
- Type C — thin, unmyelinated, slowest (pain, postganglionic)
Conduction of the Impulse
- Local current depolarises the next segment
- Myelinated → jumps node to node (saltatory) — fast
- Unmyelinated → continuous — slow
- Speed ↑ with fibre diameter and myelination
Thicker, more myelinated fibres conduct faster. Type Myelin Speed Function A Yes Fastest Motor, touch B Yes Medium Autonomic C No Slowest Pain Applied
- Demyelination (MS, Guillain–Barré) slows conduction
- Nerve conduction velocity is a diagnostic test
🔑KEY POINTS TO REMEMBER- Nerve fibre = axon; myelinated (saltatory) vs unmyelinated (continuous).
- Fibres: A (fast, motor), B (autonomic), C (slow, pain).
- Speed ↑ with diameter and myelination.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
The neuromuscular junction (NMJ) is the synapse between a motor nerve terminal and a skeletal muscle fibre, using acetylcholine (ACh) as the transmitter.
Structure
- Presynaptic nerve terminal (ACh vesicles)
- Synaptic cleft
- Postsynaptic motor end-plate (nicotinic ACh receptors)
- Acetylcholinesterase in the cleft
Sequence of Transmission
- Nerve impulse → Ca²⁺ enters the terminal
- ACh released into the cleft
- ACh binds nicotinic receptors
- End-plate potential → muscle action potential
- Acetylcholinesterase breaks down ACh
Calcium → ACh release → receptor → end-plate potential → muscle contracts. Drug / Disease Effect at NMJ Myasthenia gravis ↓ ACh receptors Curare Blocks receptor (relaxant) Neostigmine Inhibits AChE (↑ ACh) Botulinum toxin Blocks ACh release Applied
- Myasthenia gravis — receptor antibodies
- Organophosphates — inhibit acetylcholinesterase
- Muscle relaxants act at the NMJ
🔑KEY POINTS TO REMEMBER- NMJ transmitter = acetylcholine (nicotinic receptor).
- Sequence: Ca²⁺ → ACh → receptor → end-plate potential → AP.
- AChE terminates the signal.
- Myasthenia = receptor antibodies; curare blocks receptor.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Skeletal muscle is voluntary, striated muscle that contracts by the sliding-filament mechanism, in which actin and myosin filaments slide over one another.
Structure — the Sarcomere
- Functional unit = sarcomere (Z line to Z line)
- Thick filament = myosin; thin filament = actin
- A band (dark), I band (light), H zone
- Triad = T-tubule + 2 SR cisternae
Sliding-Filament Mechanism
- Ca²⁺ binds troponin → exposes actin sites
- Myosin head binds actin (cross-bridge)
- Power stroke → filaments slide, sarcomere shortens
- ATP detaches the head → cycle repeats
The cross-bridge cycle repeatedly pulls actin inward — needing Ca²⁺ and ATP. Band / Zone On contraction Sarcomere Shortens I band Shortens H zone Shortens A band Unchanged Energy Sources
- Creatine phosphate (immediate)
- Anaerobic glycolysis (short bursts)
- Aerobic respiration (sustained)
Applied
- Rigor mortis — no ATP to detach heads
- Muscle fatigue — ATP depletion, lactate
- Muscular dystrophy — defective muscle proteins
🔑KEY POINTS TO REMEMBER- Sarcomere = functional unit; sliding-filament mechanism.
- Ca²⁺ + ATP needed; A band unchanged, I band & H zone shorten.
- Cross-bridge cycle: bind → power stroke → detach (ATP).
- No ATP → rigor mortis.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
The body has three muscle types — skeletal, cardiac and smooth — differing in structure, control and function.
Skeletal Muscle
- Voluntary, striated, multinucleated
- Fast, powerful, tires easily
- Attached to bones → movement
Cardiac Muscle
- Involuntary, striated, branched
- Intercalated discs with gap junctions
- Rhythmic and tireless (heart)
Smooth Muscle
- Involuntary, non-striated, spindle-shaped
- Slow, sustained, uses little energy
- In walls of viscera and vessels
Properties of Muscle
- Excitability and contractility
- Extensibility and elasticity
- Tone (partial sustained contraction)
Structure matches function — movement, pumping, or slow squeezing. Feature Skeletal Cardiac Smooth Control Voluntary Involuntary Involuntary Striations Yes Yes No Fatigue Yes No No Applied
- Cardiac muscle cannot be tetanised (long refractory period)
- Smooth muscle shows plasticity (stress-relaxation)
🔑KEY POINTS TO REMEMBER- Three types: skeletal (voluntary, striated), cardiac, smooth.
- Cardiac = branched, intercalated discs, tireless.
- Smooth = non-striated, slow, sustained.
- Muscle properties: excitability, contractility, extensibility, elasticity, tone.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
A synapse is the junction where an impulse passes from one neuron to another (or to an effector), usually chemically via a neurotransmitter.
Types
- Chemical — via neurotransmitter (common)
- Electrical — via gap junctions (very fast)
Chemical Transmission
- Impulse → Ca²⁺ enters the terminal
- Neurotransmitter released
- Binds postsynaptic receptor
- EPSP (excite) or IPSP (inhibit)
Properties
- One-way conduction; synaptic delay
- Summation and facilitation
- Fatigue
A chemical synapse transmits one way and lets neurons sum their inputs. Feature EPSP IPSP Effect Excitatory Inhibitory Change Depolarise Hyperpolarise Applied
- Site of action of many drugs and poisons
- Basis of learning and memory
🔑KEY POINTS TO REMEMBER- Synapse = neuron-to-neuron junction; mostly chemical.
- Transmission: Ca²⁺ → neurotransmitter → receptor → EPSP/IPSP.
- Properties: one-way, delay, summation, fatigue.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Saltatory conduction is the propagation of an impulse in myelinated fibres by jumping from one node of Ranvier to the next.
Mechanism
- Myelin insulates the internodes (no ion flow there)
- AP regenerates only at nodes of Ranvier
- Impulse leaps node to node
Advantages
- Much faster conduction (up to ~120 m/s)
- Energy-efficient (fewer ion pumps needed)
- Less membrane to depolarise
Insulation forces the impulse to jump between nodes, speeding conduction. Feature Myelinated Unmyelinated Conduction Saltatory Continuous Speed Fast Slow Energy Efficient More Applied
- Demyelination (MS) slows or blocks conduction
🔑KEY POINTS TO REMEMBER- Saltatory = impulse jumps node to node in myelinated fibres.
- Faster and more energy-efficient than continuous conduction.
- Lost in demyelination (MS).
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Excitation–contraction coupling links the muscle action potential (excitation) to contraction, through calcium release from the sarcoplasmic reticulum.
Sequence
- Muscle AP travels down the T-tubule
- Triggers Ca²⁺ release from the sarcoplasmic reticulum
- Ca²⁺ binds troponin C
- Tropomyosin shifts → actin sites exposed
- Cross-bridge cycling → contraction
- Ca²⁺ pumped back → relaxation
Calcium is the coupling ion linking the electrical signal to contraction. Key Points
- Calcium is the coupling ion
- Relaxation also needs ATP (Ca²⁺ pump)
Applied
- Dantrolene blocks SR Ca²⁺ release (malignant hyperthermia)
Process Requirement Contraction Ca²⁺ + ATP Relaxation ATP (Ca²⁺ pump) Coupling ion Calcium Ca²⁺ store Sarcoplasmic reticulum 🔑KEY POINTS TO REMEMBER- E-C coupling links AP to contraction via Ca²⁺.
- AP → T-tubule → SR Ca²⁺ → troponin → contraction.
- Relaxation needs Ca²⁺ pumped back (ATP).
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Myasthenia gravis is an autoimmune disease in which antibodies against acetylcholine receptors at the NMJ cause fatigable muscle weakness.
Mechanism
- Autoantibodies vs nicotinic ACh receptors
- ↓ Functional receptors at the end-plate
- Weak neuromuscular transmission
Clinical Features
- Fatigable weakness (worse with use, better with rest)
- Ptosis and diplopia (eye muscles first)
- Worse in the evening
- Myasthenic crisis — respiratory failure (emergency)
Receptor loss makes transmission fail with use — giving fatigable weakness. Diagnosis & Treatment
- Anti-AChR antibodies; repetitive nerve stimulation
- Neostigmine / pyridostigmine (AChE inhibitors)
- Immunosuppression; thymectomy
Feature Myasthenia gravis Nature Autoimmune Target ACh receptors Weakness Fatigable First muscles Eye (ptosis, diplopia) Treatment AChE inhibitors, thymectomy 🔑KEY POINTS TO REMEMBER- Myasthenia gravis = autoimmune loss of ACh receptors.
- Fatigable weakness, ptosis, diplopia; worse in evening.
- Treat with AChE inhibitors, immunosuppression, thymectomy.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
A muscle twitch is a single contraction–relaxation to one stimulus; tetanus is a sustained maximal contraction from rapidly repeated stimuli.
Phases of a Twitch
- Latent period
- Contraction period
- Relaxation period
Summation → Tetanus
- Rapid stimuli → no full relaxation between them
- Contractions add up (summation)
- Fuse into a sustained maximal contraction = tetanus
Rapid repeated stimuli summate and fuse into a smooth, forceful contraction. Note
- Physiological tetanus ≠ disease tetanus (lockjaw)
- Normal movement uses tetanic contraction
Type Stimulus Result Twitch Single Contract + relax Summation Rapid Contractions add up Tetanus Very rapid Sustained maximal 🔑KEY POINTS TO REMEMBER- Twitch = single response (latent, contraction, relaxation).
- Rapid stimuli → summation → tetanus (sustained).
- Physiological tetanus is normal, unlike the disease.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
A motor unit is a single motor neuron together with all the muscle fibres it supplies — the functional unit of muscle contraction.
Features
- All fibres of a unit contract together (all-or-none)
- Small units (few fibres) → fine control (eye)
- Large units (many fibres) → power (limb)
Grading of Force
- Recruitment — activate more units
- Rate coding — fire units faster
- Size principle — small units recruited first
Force is graded by recruiting more units and firing them faster. Unit size Control Example Small Fine Extraocular muscle Large Powerful Gastrocnemius Applied
- Motor neuron disease → loss of units → weakness, wasting
- EMG measures motor-unit activity
🔑KEY POINTS TO REMEMBER- Motor unit = one motor neuron + all fibres it supplies.
- Small units = fine control; large units = power.
- Force graded by recruitment + rate coding (size principle).
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Rigor mortis is the stiffening of muscles after death due to lack of ATP, which is needed to detach myosin from actin.
Mechanism
- Death → ATP production stops
- Ca²⁺ leaks → myosin binds actin
- No ATP → cross-bridges cannot detach
- Muscle stays stiff and contracted
Time Course
- Onset 2–4 hr after death
- Complete by ~12 hr
- Passes off in 24–48 hr (protein breakdown)
Without ATP the cross-bridges stay locked, so the muscle stiffens until proteins break down. Applied (Forensic)
- Helps estimate the time of death
- Read with algor mortis (cooling) and livor mortis (staining)
Stage Time after death Onset 2–4 hr Complete ~12 hr Passes off 24–48 hr 🔑KEY POINTS TO REMEMBER- Rigor mortis = post-death stiffening from lack of ATP.
- Onset 2–4 hr, complete ~12 hr, resolves 24–48 hr.
- Used forensically to estimate time of death.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).