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PHYSIOLOGY VIVA - COMPREHENSIVE ANSWERS

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SECTION 1: PHYSIOLOGY OF EXCITABLE TISSUES

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• Phospholipid bilayer: hydrophilic heads face outward, hydrophobic tails face inward (~7-10 nm thick)
• Proteins: integral (transmembrane - channels, pumps, receptors) and peripheral (attached to surface)
• Cholesterol: embedded between phospholipids, regulates fluidity
• Glycocalyx: glycoproteins/glycolipids on the outer surface - cell recognition, adhesion

• Resting state: Na+/K+-ATPase pumps 3 Na+ out for every 2 K+ in (electrogenic)
• Ionic concentrations: Na+ outside 142 mEq/L, inside 14 mEq/L; K+ outside 4 mEq/L, inside 140 mEq/L
• At rest, membrane is highly permeable to K+ (via leak channels) but poorly permeable to Na+
• K+ diffuses out down its concentration gradient, leaving negative charges behind
• This creates the resting membrane potential (RMP) of about -70 mV (Guyton & Hall)
• Nernst equation calculates equilibrium potential for each ion; Goldman equation accounts for multiple ions
• Biopotentials arise from selective permeability changes to ions

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• Correlation - coordinated interaction between organs/systems; types: humoral, nervous, immune
• Regulation - nervous (fast, precise), humoral (slow, widespread), immune (defense)
• Self-regulation - the ability of a system to maintain homeostasis without external input (e.g., heart automatism, baroreceptor reflex)
• Reflex - stereotyped response to a stimulus via the nervous system; requires intact reflex arc
• Functional system (P.K. Anokhin) - dynamic self-regulating organization of elements whose joint activity achieves a useful adaptive result; key components: afferent synthesis, decision-making, efferent program, result, back-afferentation (feedback)

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• Irritant - any agent that causes a response; types:
  • By origin: physical (mechanical, thermal, electrical), chemical, biological
  • By adequacy: adequate (naturally suited to receptor), inadequate
  • By strength: subthreshold, threshold, suprathreshold, maximal, supramaximal
• Irritability - property of all living cells to respond to any stimulus (metabolic change); broader concept
• Excitability - property of specialized cells (nerve, muscle, gland) to generate an action potential in response to adequate stimulation; measured by threshold

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• Threshold law - minimum stimulus strength needed to elicit a response
• Law of force (strength) - stronger stimulus = stronger response (applies to whole muscle/nerve, not single fiber)
• Law of "all or nothing" - a single excitable cell either responds maximally or not at all (applies to single fiber, heart muscle, single axon)
• Law of force-time (strength-duration) - to produce excitation, a stimulus must exceed a minimum strength AND act for a minimum duration; relationship expressed by the rheobase-chronaxie curve:
  • Rheobase = minimum effective current of unlimited duration
  • Chronaxie = time needed for a current of 2× rheobase to produce excitation (measure of excitability)

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• Accommodation - increase in threshold during slow-rising stimulus; Na+ channels partially inactivate before threshold is reached
• Polar law (Du Bois-Reymond) - at make (closing) of circuit, excitation occurs at cathode; at break (opening), excitation at anode
• Repeated responses (Pflüger's law) - make of DC current excites at cathode; break excites at anode; with AC, both make and break cause cathode excitation
• Lability (N.E. Vvedensky) - maximum frequency of impulses a tissue can reproduce without distortion; nerve ~1000/sec, skeletal muscle ~200/sec, synapse ~100/sec; determined by duration of refractory period
• Adaptation - gradual decrease in response to a maintained stimulus; receptor adaptation (fast vs. slow adapting receptors)

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• Excitability - capacity to generate AP; inversely proportional to threshold
• Measurement: rheobase and chronaxie (electrophysiologically); also galvanic-tetanic ratio
• Threshold = minimum stimulus intensity to produce AP; at threshold, enough Na+ channels open to cause regenerative depolarization
• Functional lability (Vvedensky) - number of excitation cycles per unit time; higher lability = faster response capability
• Optimum of frequency - frequency of stimuli producing maximal response (tetanus); below this, responses summate; above = pessimum
• Pessimum of frequency - too-high frequency causes each stimulus to fall in the relative refractory period, giving a paradoxical DECREASE in response (weak tetanus)
• Optimum of strength - stimulus intensity giving maximum response
• Pessimum of strength - supramaximal stimulus that falls in refractory period of previous response

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• Parabiosis = reversible functional block created by applying a local damaging agent (narcotic, heat, pressure) to a segment of nerve
• The damaged segment has reduced lability
• Three phases (as stimulation frequency increases):
  1. Equalizing phase - strong and weak stimuli give equal responses (the parabiotic segment equalizes response amplitude)
  2. Paradoxical (inhibitory) phase - weak stimuli give larger responses than strong ones (strong stimuli fall in relative refractory period of the damaged zone more)
  3. Inhibitory phase - no stimuli produce responses; complete block
• Significance: explains mechanisms of narcosis and some CNS inhibition

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• RMP = -70 mV in large neurons and myelinated nerve fibers (Guyton & Hall)
• Inside of cell is negative relative to outside
• Maintained by: Na+/K+-ATPase pump + selective K+ permeability (leak channels)
• Concentration gradients: K+ 35:1 (in:out), Na+ 1:10 (in:out)
• K+ Nernst potential = -94 mV; Na+ Nernst potential = +61 mV
• Actual RMP (-70 mV) is close to K+ equilibrium because resting membrane is ~100× more permeable to K+ than Na+
• Goldman (constant field) equation accounts for multiple ions and their permeabilities

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1. Depolarization (rising phase) - stimulus opens voltage-gated Na+ channels; Na+ rushes in; membrane depolarizes from -70 mV to +30 mV (overshoot)
2. Repolarization (falling phase) - Na+ channels inactivate; voltage-gated K+ channels open; K+ rushes out; membrane repolarizes
3. Hyperpolarization (after-potential) - K+ channels close slowly; brief undershoot below RMP (-80 to -90 mV)
4. Return to RMP via Na+/K+ pump

• Absolute refractory period (ARP) - during depolarization and early repolarization; Na+ channels are inactivated (h-gate closed); NO stimulus can produce another AP; ensures unidirectional propagation and limits maximum firing rate; lasts ~1-2 ms in nerve
• Relative refractory period (RRP) - during repolarization/hyperpolarization; only supranormal stimulus can excite; Na+ channels recovering; K+ channels still partially open
• Supranormal period - slight decrease in threshold transiently after full recovery
• Significance of ARP: limits impulse frequency; ensures one-way conduction; prevents cardiac tetanus (ARP of cardiomyocyte lasts entire systole)

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• Receptor = specialized structure that transduces stimulus energy into graded receptor potential
• Types:
  • By location: exteroceptors (skin), interoceptors (viscera), proprioceptors (muscle/joint)
  • By modality: mechanoreceptors, chemoreceptors, thermoreceptors, photoreceptors, nociceptors
  • By adaptation: rapidly adapting (phasic - signal change), slowly adapting (tonic - signal sustained)
  • By structure: free nerve endings, encapsulated (Meissner, Pacinian, Ruffini, Krause)

1. Stimulus energy absorbed by receptor
2. Receptor (generator) potential generated - graded, local, decremental; proportional to stimulus intensity; no refractory period
3. When receptor potential reaches threshold → AP in afferent fiber (frequency coding)
4. AP propagated to CNS

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• Cell body (soma) - contains nucleus, Nissl substance (rough ER), metabolic center
• Dendrites - receive input; short, branching; graded potentials
• Axon (1 per neuron) - output; myelinated or unmyelinated; nodes of Ranvier; axon hillock = AP initiation zone (lowest threshold)
• Axon terminals (boutons) - presynaptic

• By function: sensory (afferent), motor (efferent), interneurons (association)
• By polarity: unipolar, bipolar, multipolar, pseudounipolar

• Spatial and temporal summation of EPSPs and IPSPs at axon hillock
• When net depolarization at hillock reaches -55 mV (threshold) → AP fires (all-or-nothing)
• Propagation along axon: unmyelinated = continuous propagation; myelinated = saltatory conduction (faster, more energy efficient)

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• Make up ~50% of CNS volume; do not generate APs
• Types and functions:
  • Astrocytes - structural support, blood-brain barrier (BBB) maintenance, K+ buffering (spatial buffering), neurotransmitter recycling, metabolic support to neurons
  • Oligodendrocytes (CNS) / Schwann cells (PNS) - produce myelin sheath; increase conduction velocity
  • Microglia - CNS immune cells; phagocytosis; activated in injury/infection
  • Ependymal cells - line ventricles and central canal; produce and circulate CSF

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• Unmyelinated fibers - local circuit currents between active and adjacent resting membrane; continuous, slow
• Myelinated fibers - saltatory conduction (current jumps from node to node); faster, energy efficient

1. Bilateral conduction (physiologically unidirectional due to synaptic polarity)
2. Isolated conduction (no lateral spread between fibers)
3. Anatomical and physiological integrity required
4. Fatigability of nerve is negligible (virtually non-fatiguable compared to muscle/synapse)

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• Definition - specialized junction for transmission of signals between neurons, or neuron-effector cell
• Structure: presynaptic terminal (mitochondria + vesicles of NT), synaptic cleft (20-40 nm), postsynaptic membrane (receptors)

• By location: axo-dendritic, axo-somatic, axo-axonic, dendro-dendritic
• By effect: excitatory (EPSP), inhibitory (IPSP)
• By mechanism: chemical (most common), electrical (gap junctions - fast, bidirectional)
• By NT: cholinergic, adrenergic, dopaminergic, serotonergic, GABAergic, glutamatergic, glycinergic

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1. AP arrives at presynaptic terminal
2. Depolarization opens voltage-gated Ca2+ channels → Ca2+ influx
3. Ca2+ triggers vesicle fusion (SNARE proteins) → exocytosis of NT into cleft
4. NT diffuses across cleft and binds postsynaptic receptors
5. Receptor activation → ion channel opening (ionotropic) or second messenger cascade (metabotropic)
6. EPSP (Na+/Ca2+ entry) or IPSP (Cl- entry or K+ exit) generated
7. NT removed: reuptake, enzymatic degradation (e.g., acetylcholinesterase), diffusion

• Presynaptic: tetrodotoxin (blocks Na+ channels), botulinum toxin (blocks vesicle release)
• Postsynaptic: curare (nicotinic ACh receptor block), atropine (muscarinic block)
• Enzymatic: organophosphates (inhibit AChE → accumulation of ACh)

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• Extensibility, elasticity, plasticity

• Excitability, conductivity, contractility
• Skeletal muscle: striated, voluntary, multinucleated, fast, fatigable, all-or-nothing per fiber but graded response in muscle (motor unit recruitment + rate coding)

• Single twitch - response to one suprathreshold stimulus; latent period → contraction phase → relaxation
• Summation - second stimulus during relaxation phase → summation of twitches
• Incomplete tetanus - rapid stimuli during relaxation phase; saw-tooth pattern
• Complete tetanus - stimuli during contraction phase; smooth sustained contraction (max force ~4× single twitch)
• Isotonic - length changes, constant tension (movement)
• Isometric - tension changes, constant length (posture)
• Auxotonic - mixed (most physiological)

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SECTION 2: PHYSIOLOGY OF THE CENTRAL NERVOUS SYSTEM

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• Definition - group of neurons in the CNS functionally united for regulation of a specific function
• Classification:
  • By location: spinal, brainstem, diencephalic, cortical
  • By function: respiratory, cardiovascular, swallowing, etc.

• One-way (unilateral) conduction - due to synaptic polarity
• Synaptic delay - 0.3-0.5 ms per synapse; nerve centers with many synapses have long latency
• Summation - spatial (many inputs simultaneously) and temporal (repeated from same source)
• Transformation of rhythm - output frequency ≠ input frequency
• Post-tetanic potentiation - enhanced response after high-frequency stimulation
• Low lability (~100/sec vs 1000/sec for nerve)
• Fatigue - due to NT depletion and receptor desensitization
• Tone - baseline activity at rest
• High sensitivity to hypoxia and drugs
• Plasticity - ability to reorganize after damage

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• Between neurons: via synapses; divergence (one neuron excites many) and convergence (many neurons onto one)
• Circuits of propagation:
  • Serial (chain): simple linear relay
  • Divergent: one input → multiple outputs; amplification
  • Convergent: multiple inputs → one neuron; integration
  • Recurrent (reverberating): collateral from output neuron feeds back to input; basis for sustained activity and short-term memory
  • Parallel with feedback: stable oscillatory circuits
• Between structures: ascending and descending tracts; crossed and uncrossed pathways; commissures (corpus callosum)

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• Postsynaptic inhibition - IPSPs generated at postsynaptic membrane by inhibitory interneurons (via GABA/glycine → Cl- influx → hyperpolarization)
  • Direct (feed-forward): inhibitory interneuron activated by collateral of afferent fiber
  • Renshaw (recurrent) inhibition: motor neuron axon collateral activates Renshaw cell → inhibits same motor neuron; prevents overexcitation
• Presynaptic inhibition - axo-axonic synapse depolarizes presynaptic terminal → reduces NT release from it; does not affect postsynaptic neuron directly; longer duration; important in sensory gating
• Pessimum inhibition (Vvedensky) - at very high stimulation frequencies, response paradoxically decreases

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• Destruction (ablation/lesion) - surgical/chemical removal; identify function by what is lost; limitation: compensatory reorganization
• Stimulation (irritation) - electrical/chemical/light (optogenetics); identify function by what is produced
• Electroencephalography (EEG) - records spontaneous electrical activity of cortex via scalp electrodes; rhythms: δ (0.5-4 Hz, deep sleep), θ (4-8 Hz, drowsy/children), α (8-13 Hz, relaxed wakefulness), β (13-30 Hz, active thought), γ (>30 Hz, complex cognition)
• Evoked potentials (EP) - EEG response to specific stimulus; visual EP, auditory EP, somatosensory EP; test sensory pathway integrity
• Microelectrode methods - record single-unit activity (intracellular or extracellular); highest resolution
• Other: fMRI, PET, transcranial magnetic stimulation (TMS), pharmacological methods

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• R. Descartes (17th c.) - concept of reflex as mechanical response; animal spirits in nerve tubes
• I.M. Sechenov (1863) - "Reflexes of the Brain": all acts of conscious and unconscious life are reflexes; cerebral inhibition; laid basis for objective study of behavior
• I.P. Pavlov (1890s-1930s) - conditioned reflex (CR) vs. unconditioned reflex (UCR); higher nervous activity; GNI types; experimental neurosis
• P.K. Anokhin (20th c.) - functional system theory; introduced concept of afferent synthesis, action acceptor, back-afferentation; replaced linear reflex arc with dynamic self-regulating system

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• Reflex = stereotyped, genetically determined response of the organism to a stimulus, carried out with the obligatory participation of the CNS

• By origin: conditioned (acquired) / unconditioned (innate)
• By biological significance: defensive, food, sexual, orienting
• By receptor type: exteroceptive, interoceptive, proprioceptive
• By effector: somatic (motor), autonomic (visceral)
• By number of synapses: monosynaptic (stretch reflex), polysynaptic

1. Receptor
2. Afferent (sensory) nerve
3. Nerve center (CNS)
4. Efferent (motor) nerve
5. Effector (muscle/gland)

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1. Afferent synthesis (dominant motivation + memory + situation + trigger stimulus)
2. Decision making
3. Action acceptor (efferent copy) - model of expected result; compared with actual result
4. Efferent synthesis - commands to effectors
5. Action and result
6. Back-afferentation - sensory signals from result → compared to action acceptor
7. If match: stops behavior; if mismatch: behavior continues/modifies

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1. Reflex function - executes somatic and autonomic reflexes
2. Conduction function - ascending (sensory) and descending (motor) pathways

• Stretch reflex (myotatic) - monosynaptic; Ia fiber from muscle spindle → α motor neuron → muscle contraction (e.g., knee jerk); Ia reciprocal inhibition of antagonist
• Golgi tendon reflex - Ib fiber from tendon organ → inhibitory interneuron → inhibits agonist (protects against overload)
• Flexor (withdrawal) reflex - polysynaptic; nociceptive stimulus → flexion of limb + contralateral extension (crossed extensor reflex)
• Rhythmic reflexes - stepping, scratching
• Autonomic reflexes - defecation, micturition, erection (sacral centers)
• Spinal shock - after transection: loss of all reflexes below lesion; gradually return (spinal animal)

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• Spatial summation - simultaneous weak stimuli from different presynaptic neurons summate to reach threshold
• Temporal summation - repeated subthreshold stimuli from same source summate over time
• Transformation of rhythm - output ≠ input frequency (can be increased via reverberating circuits, or decreased by inhibitory circuits)
• Post-tetanic potentiation - increased response after tetanic stimulation; increased Ca2+ in terminal, increased NT release; lasts minutes; basis for short-term plasticity
• Low lability - max ~100/sec due to synaptic delay; contrast with nerve fiber at 1000/sec
• Fatigue - decreasing response to repeated stimulation; NT depletion, receptor desensitization, accumulation of metabolites
• Sensitivity to neurotropic drugs and hypoxia - nerve centers exhaust O2 supply quickly; damaged by anesthetics, narcotics

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• Vital centers: vasomotor center (blood pressure), cardiac center, respiratory center (DRG and VRG)
• Reflex centers: vomiting, swallowing, coughing, sneezing, hiccupping, sucking
• Cranial nerves: IX (glossopharyngeal), X (vagus), XI (accessory), XII (hypoglossal)
• Conduction: all ascending and descending tracts pass through
• Pyramidal decussation occurs here

• Pneumotaxic center (limits inspiration) and apneustic center (prolongs inspiration) - respiratory rhythm modulation
• Cranial nerves: V (trigeminal), VI (abducens), VII (facial), VIII (vestibulocochlear)
• Conduction: cerebellar peduncles; pontine nuclei relay cortical signals to cerebellum

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• Superior colliculi - visual reflexes; orientation to light, pupillary light reflex (with CN III nucleus)
• Inferior colliculi - auditory reflexes; startle response
• Red nucleus - rubrospinal tract; fine motor control of distal limbs
• Substantia nigra - dopaminergic; nigrostriatal pathway; motor control (basal ganglia input)
• Periaqueductal gray (PAG) - endogenous analgesia; descending inhibitory control
• Oculomotor reflexes - via CN III (oculomotor), CN IV (trochlear)
• Decerebrate rigidity - if section between midbrain and hindbrain → release of reticular facilitatory area → extensor rigidity
• Righting reflexes - via midbrain (labyrinthine and optical righting)

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• Motor: coordinates voluntary movement, timing, sequencing; compares intended vs. actual movement (compares efferent copy with proprioceptive feedback)
• Muscle tone: modulates via vestibulocerebellum → vestibulospinal tract
• Balance and posture (archicerebellum)
• Fine voluntary movement (neocerebellum - via dentate nucleus → thalamus → motor cortex)
• Autonomic functions: heart rate, blood pressure modulation
• Learning of motor skills (procedural memory)

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• Reticular formation (RF) - diffuse network of neurons throughout brainstem core
• Descending influence:
  • Facilitatory area (pontine RF, lateral hypothalamus) → reticulospinal tracts → increase muscle tone, facilitate reflexes; tonically active
  • Inhibitory area (medullary RF - Magoun & Rhines) → inhibit motor neurons; reduce tone
  • Balance between facilitatory and inhibitory determines spinal cord motor output
  • RF modulates sensory input via presynaptic inhibition (sensory gating)
  • Controls autonomic reflexes of spinal cord

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• RF sends diffuse projections to thalamus → non-specific thalamic nuclei → widespread cortical arousal
• Maintains wakefulness and consciousness
• Damage to ARAS → coma
• Stimulated by: pain, sensory stimuli, emotions; inhibited by: sleep mechanisms, barbiturates

• Located in diencephalon; ~4 g; major homeostatic center
• Nuclear groups: anterior (preoptic), tuberal (arcuate, ventromedial, dorsomedial, lateral), posterior, mammillary
• Functions:
  • Autonomic integration: sympathetic activation (posterior), parasympathetic (anterior)
  • Endocrine control: hypophysiotrophic hormones → pituitary (CRH, TRH, GnRH, GHRH, somatostatin)
  • Thermoregulation: anterior hypothalamus = heat dissipation center; posterior = heat conservation
  • Feeding: lateral area = hunger (feeding) center; ventromedial = satiety center
  • Water balance/thirst: osmoreceptors; AVP (ADH) from posterior pituitary
  • Circadian rhythms: suprachiasmatic nucleus (SCN) - master clock
  • Emotions and stress: connects limbic system to autonomic and endocrine
  • Sleep-wake cycles, sexual behavior, fear, rage

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• Components: hippocampus, amygdala, cingulate gyrus, parahippocampal gyrus, septal nuclei, olfactory areas, fornix, mammillary bodies; Papez circuit
• Functions:
  • Emotion: amygdala - fear conditioning, emotional memory; damage → Kluver-Bucy syndrome
  • Memory: hippocampus - consolidation of declarative (explicit) memory; damage → anterograde amnesia (H.M. case)
  • Motivation: integration of internal drives (hunger, sex, thirst) with behavior
  • Olfaction: primary olfactory cortex is part of limbic system (only sensory system not relayed through thalamus)
  • Autonomic regulation: visceral responses to emotions (fear → tachycardia, etc.)
  • Papez circuit (1937): hippocampus → fornix → mammillary bodies → anterior thalamus → cingulate gyrus → hippocampus; circuit of emotional experience

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• ~2200 cm² surface area; 6 layers (I-VI) in neocortex; Brodmann's 52 areas
• Layer I (molecular), II (external granular), III (external pyramidal), IV (internal granular), V (internal pyramidal - Betz cells), VI (multiform)
• Columns as functional units

• Primary motor cortex (area 4, precentral gyrus) - voluntary movement; somatotopic map (homunculus)
• Primary somatosensory (areas 3,1,2, postcentral gyrus) - tactile sensation; somatotopic
• Primary visual (area 17, occipital lobe) - retinotopic map
• Primary auditory (areas 41,42, temporal lobe) - tonotopic map
• Broca's area (44, 45, left inferior frontal) - motor speech production
• Wernicke's area (22, left superior temporal) - language comprehension
• Prefrontal cortex - executive function, planning, working memory, personality
• Association areas - higher cognitive functions, integration

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SECTION 3: PHYSIOLOGY OF THE ANS

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• D1, D5 (Gs-coupled) - striatum, cortex, limbic; stimulation → adenylate cyclase activation → ↑cAMP; renal vasodilation
• D2, D3, D4 (Gi-coupled) - striatum, limbic (mesolimbic), pituitary; stimulation → ↓cAMP; inhibit prolactin; basis for antipsychotic drug targets

• Motor control (nigrostriatal pathway)
• Reward/pleasure (mesolimbic)
• Prolactin inhibition (tuberoinfundibular)
• Renal: D1 activation → vasodilation, natriuresis

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• Nm (muscle type) - NMJ → muscle contraction
• Nn (neuronal type) - all autonomic ganglia, adrenal medulla, CNS → ganglionic transmission
• Blocked by: curare (Nm), hexamethonium (Nn), succinylcholine

• Blocked by atropine (all M types)

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SECTION 4: PHYSIOLOGY OF THE HEART AND CIRCULATION

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1. Automatism (chronotropy) - ability to generate spontaneous rhythmic impulses without external neural input; due to pacemaker cells with unstable RMP (funny current If, slow Ca2+ channels)
2. Excitability - can generate AP; ARP covers entire systole → absolute tetanus impossible (protective)
3. Conductivity (dromotrophy) - specialized conduction system
4. Contractility (inotrophy) - sliding filament mechanism; Ca2+ regulated via troponin C; "all or nothing" for whole heart (functional syncytium via gap junctions)
5. Rhythmicity - regular pacemaker activity
6. Refractoriness - very long ARP (~250 ms) = duration of systole; prevents tetanus; essential for pump function

• SA node: 60-80/min (dominant pacemaker; fastest spontaneous depolarization)
• AV node: 40-60/min
• Bundle of His: 30-40/min
• Purkinje fibers: 20-30/min
• Ventricular muscle: 15-20/min

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1. Isovolumetric contraction (0.05 s) - all valves closed; pressure rises rapidly; no volume change
2. Rapid ejection (0.1 s) - aortic/pulmonary valves open; rapid pressure rise; rapid outflow
3. Slow ejection (0.15 s) - pressure falling; continued outflow

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• P wave - atrial depolarization (SA node → AV node spread through atria); 80-100 ms, <2.5 mm
• PR interval - AV nodal delay + atrial activation; 120-200 ms; prolonged in heart block
• QRS complex - ventricular depolarization; <120 ms; widened in bundle branch block
• ST segment - entire ventricle depolarized; isoelectric; elevated in STEMI, depressed in ischemia
• T wave - ventricular repolarization (base to apex, epicardium to endocardium)
• QT interval - total ventricular electrical systole; corrected QTc <440 ms

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• During depolarization and systole: absolute refractory period (ARP) - no new AP possible regardless of stimulus strength; lasts ~200-250 ms (entire systole)
• During repolarization: relative refractory period (RRP) - supranormal stimulus can cause AP; may produce premature ventricular contraction (PVC); dangerous if R-on-T phenomenon
• Vulnerable period - portion of RRP where stimulus can trigger ventricular fibrillation (R-on-T)
• Supranormal period - brief period just before full recovery; slightly lower threshold
• The long ARP ensures heart cannot undergo sustained tetanic contraction (would be fatal as it prevents ventricular filling)

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• Cardiomyocytes: branched, uninucleate, striated, ~100 µm long, ~20 µm diameter
• Intercalated discs - connect cardiomyocytes end-to-end:
  • Mechanical connections: fascia adherens (actin attachment), desmosomes
  • Gap junctions (nexuses) - electrical coupling; allow AP to spread freely → functional syncytium
• T-tubules - deep invaginations at Z-lines; bring Ca2+ signal to interior
• Sarcoplasmic reticulum (SR) - Ca2+ store; less developed than skeletal muscle
• Ca2+-induced Ca2+ release (CICR): L-type Ca2+ channels (DHPR) in T-tubule → small Ca2+ influx → triggers ryanodine receptors (RyR2) on SR → large Ca2+ release → troponin C activation → cross-bridge cycling
• Staircase phenomenon (Treppe): force increases with increasing rate (unlike skeletal)
• Bathmotropy: responsiveness to stimuli

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• Phase 4 spontaneous depolarization in SA node: starts at ~-60 mV
  1. Slow inward Na+/K+ current (If or "funny" current) - activated by hyperpolarization; depolarizes membrane
  2. Decreased K+ conductance (IK channels gradually close)
  3. Slow Ca2+ influx (T-type Ca2+ channels) - brings membrane toward threshold
  4. At ~-40 mV: L-type Ca2+ channels open → rapid depolarization (SA node AP has no fast Na+ component)

• SA node (Keith & Flack node) - right atrium
• Internodal tracts (Bachmann, Wenckebach, Thorel)
• AV node (Aschoff-Tawara) - AV junction; main delay node; decremental conduction
• Bundle of His - only electrical connection between atria and ventricles
• Right and Left bundle branches
• Purkinje fiber network → ventricular muscle
• Velocities: SA node 0.05 m/s; atrial 1 m/s; AV node 0.05 m/s; Bundle of His 1.5 m/s; Purkinje 4 m/s; ventricular 1 m/s

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• Phase 0 (depolarization) - rapid Na+ influx via fast Na+ channels; upstroke from -85 mV to +20 mV
• Phase 1 (early rapid repolarization) - transient K+ outflow (Ito channels); partial repolarization
• Phase 2 (plateau) - hallmark of cardiac AP; L-type Ca2+ influx balances K+ efflux (IKr, IKs); maintained at ~0 mV for 200-250 ms; maintains contraction and prevents tetanus
• Phase 3 (rapid repolarization) - K+ efflux via IKr, IKs dominates as Ca2+ channels inactivate; repolarization to RMP
• Phase 4 (resting) - -85 to -90 mV in contractile cells; stable (unlike pacemaker); maintained by IK1 channels

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• Myogenic autoregulation (Frank-Starling law) - increased preload → increased EDV → increased sarcomere stretch → increased force of contraction (heterometric regulation); up to optimal sarcomere length of 2.2 µm
• Homeometric regulation (Anrep effect) - increased afterload → increased contractility without length change
• Chronotropic regulation (SA node automatism)

• Nervous (reflex): sympathetic and parasympathetic; intracardiac ganglia; extracardiac reflexes
• Humoral: adrenaline, acetylcholine, thyroid hormones, electrolytes, pH, temperature

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• Equalizes output of left and right ventricles
• Explains why increased venous return → increased stroke volume
• Basis of Starling curves; cardiac function curves
• Operates via increased Ca2+ sensitivity at longer sarcomere length (titin-mediated)

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• Bainbridge reflex - ↑venous return → stretch right atrium → reflex tachycardia (opposes pooling)
• Bezold-Jarisch reflex - chemical stimulation of left ventricular receptors → bradycardia + vasodilation + apnea (protective in ischemia)
• Baroreceptor reflex (aortic arch, carotid sinus) - ↑BP → vagal activation → ↓HR
• Oculocardiac reflex - pressure on eyes → vagal bradycardia
• Goldflam reflex - pressure on carotid sinus → bradycardia (hypersensitive sinus syndrome)
• Cardiac reflexes from chest, abdomen (pericarditis, cholecystitis → referred cardiac pain)

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• Adrenaline/noradrenaline (sympathomimetic) - ↑HR, ↑contractility, ↑automatism via β1 receptors
• ACh (parasympathomimetic) - ↓HR, ↓AV conduction, ↓automatism
• Thyroid hormones - chronotropic and inotropic (↑β receptor expression)
• Glucocorticoids - potentiate catecholamines
• Glucagon - positive inotropic and chronotropic
• Electrolytes: ↑K+ → bradycardia, ↓conduction, arrest; ↑Ca2+ → ↑contractility, shortened QT; ↓Ca2+ → ↓contractility
• Hypoxia - initially ↑HR (via chemoreceptors) → later depression
• pH - acidosis depresses cardiac function

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SECTION 5: CARDIOVASCULAR STUDY METHODS & VASCULAR BED

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• Standard leads: I, II, III (bipolar limb); aVR, aVL, aVF (unipolar augmented); V1-V6 (precordial)
• Normal axis: 0° to +90°
• Rate: 60-100/min; regularity; P-QRS relationship
• Intervals: PR 120-200 ms; QRS <120 ms; QTc <440 ms
• ST changes: elevation ≥1 mm = ischemia/injury

• S1 - closure of mitral and tricuspid (AV) valves; beginning of systole; "lub"
• S2 - closure of aortic and pulmonary (semilunar) valves; end of systole; "dub"
• S3 - rapid filling of ventricle; low frequency; normal in children/young adults; pathological in heart failure (gallop)
• S4 - atrial contraction against stiff ventricle; always pathological; suggests decreased ventricular compliance

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• Cuff inflated above systolic pressure → compresses brachial artery
• Slowly deflate → at systolic pressure: first Korotkoff sounds appear (turbulent flow)
• Sounds change through phases I-IV
• Disappearance of sounds = diastolic pressure
• Normal: 120/80 mmHg

• Windkessel vessels (elastic arteries - aorta, pulmonary artery): dampen pulsatile flow
• Resistance vessels (arterioles): main determinant of peripheral vascular resistance; regulate organ blood flow
• Exchange vessels (capillaries): gas/nutrient exchange
• Capacitance vessels (veins): contain ~70% of blood volume; venous reservoir

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• Filtration at arterial end (hydrostatic pressure > oncotic): ~0.5 mmHg net outward
• Reabsorption at venous end (oncotic > hydrostatic)
• Net filtration exceeds reabsorption slightly; excess drained by lymphatics
• Transcapillary exchange also via vesicular transport (transcytosis), diffusion, pores

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• Sympathetic vasoconstrictor fibers (NA → α1): most arterioles, veins; main tonic control
• Sympathetic vasodilator (ACh or adrenaline → β2): skeletal muscle vessels (during exercise)
• Parasympathetic vasodilator (ACh): limited (salivary glands, external genitalia)
• Vasomotor center (medulla): pressor area (lateral) and depressor area (medial)

• Vasoconstrictors: NA, adrenaline (α), angiotensin II, ADH, endothelin-1, thromboxane A2
• Vasodilators: adrenaline (β2, low dose), nitric oxide (NO), bradykinin, histamine, prostacyclin, atrial natriuretic peptide (ANP), CO2
• RAAS: Renin (kidney) → Angiotensin I → ACE → Angiotensin II → vasoconstriction + aldosterone secretion → Na+/water retention → ↑BP

• Mechanoreceptors; active at 60-180 mmHg; signal via CN IX (carotid) and CN X (aortic) to NTS in medulla
• ↑BP → ↑baroreceptor firing → inhibit pressor center → ↓sympathetic → vasodilation + ↓HR
• Short-term buffer; reset to new BP in hypertension

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SECTION 6: RESPIRATORY PHYSIOLOGY

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1. External respiration (ventilation + diffusion across alveolar membrane)
2. Transport of gases by blood
3. Internal respiration (tissue gas exchange)

• Inspiration (active): Diaphragm contracts → descends (~1.5 cm normal, up to 10 cm maximum) → ↑thoracic volume; external intercostals → ↑AP diameter; accessory muscles (scalene, sternocleidomastoid) in deep inspiration
• Expiration (passive at rest): Elastic recoil of lungs + chest wall → ↓thoracic volume; forced: internal intercostals + abdominals

• Tidal volume (TV): ~500 ml (quiet breathing)
• Inspiratory reserve volume (IRV): ~3000 ml
• Expiratory reserve volume (ERV): ~1100 ml
• Residual volume (RV): ~1200 ml
• Vital capacity (VC) = TV + IRV + ERV = ~4600 ml
• Total lung capacity (TLC): ~5800 ml
• FEV1/FVC ratio: >0.7 normal; <0.7 = obstructive pattern; normal FEV1/FVC with ↓TLC = restrictive

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• Dorsal respiratory group (DRG) - mainly inspiratory neurons; receives input from vagus and glossopharyngeal; sends to phrenic nerve motor neurons
• Ventral respiratory group (VRG) - both inspiratory and expiratory neurons (Bötzinger and pre-Bötzinger complex); active in forced breathing; VRG contains the rhythm generator
• Pneumotaxic center (pons, parabrachial nucleus) - limits inspiration duration; promotes smooth inspiratory-expiratory switching
• Apneustic center (lower pons) - prolongs inspiration; normally inhibited by pneumotaxic center

• Pre-Bötzinger complex (Smith et al., 1991) - kernel of respiratory rhythm; pacemaker neurons with intrinsic bursting properties; generates ~12-20 breaths/min
• Hering-Breuer reflex - lung stretch receptors (pulmonary vagal afferents) → active at large volumes → inhibit inspiration (prevents over-inflation); mainly active in neonates and during large tidal volumes

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• Dissolved in plasma: ~0.3 ml O2/100 ml blood (negligible)
• Bound to hemoglobin: ~20 ml O2/100 ml blood (main transport)
• O2 capacity of blood: 1 g Hb binds 1.34 ml O2; normal Hb ~15 g/dl → capacity ~20 ml/dl

• Tetramer: 2α + 2β chains (HbA adult); each with one heme group (Fe2+)
• HbA2 (2α+2δ), HbF (2α+2γ - fetal, ↑O2 affinity)
• Cooperative binding: each O2 increases affinity for the next (sigmoid curve)

• Sigmoidal shape (cooperativity)
• P50 = PO2 at which Hb is 50% saturated = ~26.6 mmHg
• Right shift (↓affinity, ↑O2 delivery to tissues): ↑PCO2, ↓pH (Bohr effect), ↑temperature, ↑2,3-BPG
• Left shift (↑affinity): ↓PCO2, ↑pH, ↓temperature, ↓2,3-BPG, HbF, CO poisoning

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• Intrapleural (intrathoracic) pressure: ~-5 cmH₂O at end-expiration; ~-10 cmH₂O at end-inspiration
• Origin: Lung elastic recoil pulling inward + chest wall elastic recoil pulling outward; balance creates subatmospheric pressure in sealed pleural space
• Significance: Keeps lungs expanded; aids venous return; maintains airway patency
• Pneumothorax: Air enters pleural space (trauma, ruptured bleb)
  • Simple: lung collapses to ~40% volume; mediastinum stable
  • Tension pneumothorax: one-way valve mechanism; air accumulates under pressure → mediastinal shift → compression of contralateral lung and great veins → life-threatening emergency; treat with needle decompression

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• Gas moves by diffusion down partial pressure gradient
• Alveolar-arterial O2 gradient (A-a gradient): normally <15 mmHg; ↑in V/Q mismatch, shunt, diffusion limitation

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• Dissolved: 7% of total CO2
• Carbamino compounds (CO2 + Hb → carbaminoHb): 23%
• Bicarbonate (main form, 70%): CO2 + H2O → H2CO3 → H+ + HCO3- (catalyzed by carbonic anhydrase in RBCs; ~5000× faster than uncatalyzed); HCO3- moves out of RBC via chloride-bicarbonate exchanger (Band 3 protein); H+ buffered by Hb (Haldane effect)
• Carbonic anhydrase: zinc metalloenzyme; also in kidney proximal tubule (HCO3- reabsorption), stomach (H+ secretion)
• Haldane effect: Deoxygenated Hb binds more CO2 (as carbamino) and more H+ (better buffer) → facilitates CO2 loading in tissues; at lungs, oxygenation unloads CO2

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• CO2 is the main chemical drive: ↑PCO2 → ↑H+ in CSF → stimulates central chemoreceptors (ventral medullary surface) → hyperventilation; most sensitive controller
• O2: peripheral chemoreceptors (carotid and aortic bodies - glomus cells); respond to ↓PaO2 (<60 mmHg) and ↑PCO2 and ↓pH; IX nerve (carotid) and X nerve (aortic)
• pH: ↓pH (acidosis) → ↑ventilation; independent of CO2 via peripheral chemoreceptors

• Fetus: lung fluid-filled; no breathing; PO2 ~25 mmHg; umbilical vessels oxygenate
• Birth: umbilical cord cut → ↑PCO2, ↓PO2, ↓pH → strong chemoreceptor stimulation
• Cooling of skin (cold receptors) → additional reflex stimulus
• Accumulation of proprioceptive stimuli during delivery
• These combined stimuli activate medullary respiratory center → first breath; negative intrathoracic pressure (-40 to -60 cmH₂O) opens alveoli; surfactant (DPPC) prevents collapse

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SECTION 7: PHYSIOLOGY OF BLOOD

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• Blood = liquid connective tissue; ~5-6 L (M), 4-5 L (F); ~7-8% of body weight
• Properties: viscosity 3-5× water (plasma 1.7×); specific gravity 1.055-1.065; pH 7.35-7.45; temperature 37-38°C; osmolarity ~290-310 mOsm/L
• Functions:
  • Transport: O2, CO2, nutrients, metabolites, hormones, drugs
  • Regulatory: thermoregulation, pH, osmolarity, blood volume
  • Protective: hemostasis, immunity (leukocytes, antibodies, complement)
  • Integrative: hormonal communication

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• Plasma (55%): water (91%), proteins (7-8%), electrolytes, nutrients, hormones, wastes
• Formed elements (45% = hematocrit): Erythrocytes, leukocytes, platelets

• Hematocrit: 40-54% (M), 37-47% (F)
• Hb: 130-175 g/L (M), 120-160 g/L (F)
• RBC: 4.5-5.5 × 10¹²/L (M), 4.0-5.0 × 10¹²/L (F)
• WBC: 4.0-9.0 × 10⁹/L
• Platelets: 150-400 × 10⁹/L
• pH: 7.35-7.45
• Osmolarity: 285-295 mOsm/L

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• Albumin (60%): 35-50 g/L; made in liver; maintains oncotic pressure; transport protein (fatty acids, bilirubin, Ca2+, drugs)
• Globulins (36%): α1, α2 (e.g., α2-macroglobulin, ceruloplasmin), β (transferrin, LDL), γ (IgG, IgM, IgA, IgE, IgD)
• Fibrinogen (4%): 2-4 g/L; clotting factor I; converted to fibrin by thrombin

• ~25-28 mmHg; created mainly by albumin (~80%)
• Keeps fluid in vascular compartment (opposes hydrostatic pressure at capillary)
• ↓Albumin (malnutrition, liver disease, nephrotic syndrome) → ↓oncotic pressure → edema

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• O2 transport (Hb)
• CO2 transport (carbaminoHb, bicarbonate via CA)
• Buffer function (HbH system)
• Biconcave disc shape: ↑surface area, ↓diffusion distance, ↑deformability for capillary passage

• HbA (α2β2) - 97% adult
• HbA2 (α2δ2) - 2.5%; ↑in β-thalassemia
• HbF (α2γ2) - fetal; ↑O2 affinity (↓interaction with 2,3-BPG)
• HbS - valine replaces glutamate at β6; polymerizes when deoxygenated → sickle cell disease

• Oxyhemoglobin (HbO2) - reversible O2 binding
• Deoxyhemoglobin (reduced Hb)
• Carboxyhemoglobin (HbCO) - CO binds 240× stronger than O2; left-shifts ODC → tissue hypoxia
• Methemoglobin (MetHb) - Fe3+; cannot bind O2; oxidizing agents; treated with methylene blue
• Carbaminohemoglobin - CO2 binding

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1. Vascular spasm - immediate vasoconstriction (myogenic + neurogenic + endothelin)
2. Platelet (primary) hemostasis - platelet plug; VWF bridges collagen and GpIb; ADP, TXA2 amplify activation; GpIIb/IIIa binds fibrinogen linking platelets
3. Coagulation (secondary hemostasis) - fibrin clot formation

• Extrinsic pathway: tissue damage → Tissue Factor (TF/FIII) + FVIIa → activates FX
• Intrinsic pathway: contact with collagen → FXII → FXIa → FIXa + FVIIIa → activates FX
• Common pathway: FXa + FVa (prothrombinase complex) → Prothrombin → Thrombin → Fibrinogen → Fibrin monomer → (FXIIIa) → cross-linked fibrin
• Phases: vascular (0-30 sec), platelet (1-3 min), coagulation (3-10 min), fibrinolysis (hours-days)

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• Group A: A antigens on RBC; anti-B antibodies in plasma
• Group B: B antigens; anti-A antibodies
• Group AB: A+B antigens; no antibodies (universal recipient)
• Group O: no antigens; anti-A + anti-B antibodies (universal donor)
• Antibodies are IgM (naturally occurring); activate complement → severe hemolytic transfusion reaction

• D antigen most immunogenic; Rh+ if present (85% population), Rh- if absent
• No natural anti-D antibodies; formed after sensitization (transfusion or pregnancy)
• HDN (Hemolytic Disease of Newborn): Rh- mother + Rh+ fetus; prevented with RhoGAM (anti-D immunoglobulin) within 72h of delivery

• Match ABO and Rh; crossmatch before transfusion
• Donor RBCs must be compatible with recipient plasma (major crossmatch)
• Emergency: O Rh- packed RBCs

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• 2-4 µm, anucleate (no nucleus), lifespan 7-10 days; produced by megakaryocytes in bone marrow; ~150-400×10⁹/L
• Granules: α-granules (fibrinogen, vWF, P-selectin, platelet factor 4), dense granules (ADP, ATP, serotonin, Ca2+), lysosomes
• Activation sequence: adhesion (vWF-GpIb) → shape change → degranulation → aggregation (GpIIb/IIIa-fibrinogen)
• Arachidonic acid pathway: collagen/thrombin → phospholipase A2 → arachidonic acid → COX → TXA2 → vasoconstriction + platelet aggregation (aspirin irreversibly inhibits COX)
• Role: Primary hemostatic plug; provide phospholipid surface for coagulation (platelet factor 3)

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• B lymphocytes - humoral immunity; differentiate into plasma cells (antibody production) and memory B cells; antibodies: IgG (most abundant, crosses placenta), IgM (primary response, pentamer, ABO), IgA (secretory, mucosal), IgE (allergy, parasites), IgD (B cell receptor)
• T lymphocytes - cell-mediated immunity:
  • CD4+ T helper (Th1: macrophage activation; Th2: B cell help; Th17: neutrophil recruitment; Treg: suppress immune response)
  • CD8+ Cytotoxic T cells (CTL): kill virus-infected/tumor cells via perforin and granzymes
• NK cells - innate; kill cells lacking MHC I (virus-infected, tumor cells); ADCC

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SECTION 8: PHYSIOLOGY OF HORMONES

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• Gs-coupled (adenylate cyclase pathway): ACTH, FSH, LH, TSH, glucagon, PTH, adrenaline (β) → ↑cAMP → PKA activation → phosphorylation of target proteins
• Gi-coupled: somatostatin, α2-adrenergic → ↓cAMP
• Gq-coupled: oxytocin, angiotensin II, TRH, α1-adrenergic → PLC → IP3 + DAG → ↑Ca2+ + PKC
• Tyrosine kinase receptors: insulin, IGF, EGF, GH → autophosphorylation → cascade (MAPK, PI3K/Akt)
• JAK-STAT pathway: cytokines, GH, prolactin

• Hormones diffuse through cell membrane → bind cytoplasmic or nuclear receptor → hormone-receptor complex → binds hormone response elements (HRE) on DNA → changes gene transcription
• Steroid hormones (cortisol, aldosterone, estrogen, progesterone, testosterone, vitamin D)
• T3/T4: nuclear receptor; regulates basal metabolic rate, protein synthesis, organ development

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• hCG (human chorionic gonadotropin): detected from day 8-10 post-fertilization; maintains corpus luteum → continued progesterone production; basis of pregnancy test; ↑in Down syndrome, molar pregnancy
• Progesterone: produced by corpus luteum → placenta after 8-10 weeks; maintains endometrium; inhibits uterine contractions; stimulates breast development
• Estrogens (estriol E3): mainly estriol from placenta (requires fetal adrenal DHEAS); stimulates uterine growth; prepares breast for lactation
• hPL (human placental lactogen/chorionic somatomammotropin): ↑insulin resistance → ↑glucose to fetus; lipolysis; mammary gland development
• Relaxin: softens cervix and pubic symphysis; inhibits myometrial contractions in early pregnancy
• CRH (placental): timing of parturition

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• ADH (vasopressin): ↑water reabsorption in collecting duct (via AQP2); vasoconstriction; deficiency = diabetes insipidus
• Oxytocin: uterine contraction (labor); milk ejection (let-down reflex); social bonding

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• Hypothalamus → releasing hormones (TRH, CRH, GnRH, GHRH) → anterior pituitary portal system → tropic hormones → target gland → end-organ hormones

• Long-loop negative feedback: end-organ hormone (e.g., cortisol) inhibits both hypothalamus and pituitary; most important
• Short-loop negative feedback: anterior pituitary hormone feeds back to inhibit hypothalamus
• Ultra-short loop: hypothalamic hormone inhibits its own secretion
• Positive feedback: estrogen surge at mid-cycle → triggers LH surge → ovulation (exception to negative feedback)
• Clinical: Loss of feedback → ↑tropic hormones (e.g., Addison's → ↑ACTH)

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• Days 1-14 (follicular/proliferative): FSH → follicle growth → ↑estrogen → endometrial proliferation
• Day 14: LH surge (triggered by ↑estrogen positive feedback) → ovulation
• Days 14-28 (luteal/secretory): LH → corpus luteum → progesterone + estrogen → endometrial secretory changes; if no pregnancy: corpus luteum regresses → ↓P + E → menstruation
• If pregnancy: hCG maintains corpus luteum

• FSH → Sertoli cells → support spermatogenesis; inhibin B → negative feedback on FSH
• LH → Leydig cells → testosterone (2°sexual characteristics, libido, spermatogenesis)
• Stages: spermatogonia → (mitosis) → spermatocytes → (meiosis) → spermatids → (spermiogenesis) → spermatozoa; ~72-74 days

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• T4 (thyroxine) and T3 (triiodothyronine); T3 is more active (~10× potency); peripheral T4 → T3 conversion by deiodinases
• Synthesis: iodide trapping → organification (TPO + H2O2) → coupling → stored as thyroglobulin → TSH → proteolysis → T3/T4 released
• Transport: >99% bound to TBG, albumin, transthyretin

• Metabolic: ↑BMR (↑O2 consumption, ↑heat production); calorigenic effect
• Cardiovascular: ↑HR, ↑cardiac output, ↑β-receptor sensitivity
• CNS development: essential for brain maturation (cretinism if deficient in early life)
• Growth: permissive for GH; required for skeletal maturation
• Protein synthesis (physiological doses); catabolism at excess
• GI: ↑gut motility
• Hematopoiesis: ↑erythropoietin
• Hyperthyroid: ↑BMR, weight loss, tachycardia, heat intolerance, exophthalmos (Graves')
• Hypothyroid: ↓BMR, weight gain, bradycardia, cold intolerance, myxedema

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• Zona Glomerulosa → Mineralocorticoids (aldosterone): ↑Na+ reabsorption, ↑K+ secretion in collecting duct; regulated by RAAS and K+; ↑blood volume and BP
• Zona Fasciculata → Glucocorticoids (cortisol): anti-inflammatory; ↑gluconeogenesis; protein catabolism; lipolysis; immunosuppression; regulated by ACTH/CRH; circadian rhythm (peaks early AM)
• Zona Reticularis → Androgens (DHEA, androstenedione): weak; converted to testosterone/estrogen peripherally

• Adrenaline (epinephrine, 80%) and Noradrenaline (20%): fight-or-flight; ↑HR, ↑BP, bronchodilation, ↑glucose (glycogenolysis, gluconeogenesis), lipolysis; released in stress via splanchnic nerve (preganglionic cholinergic)

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• β-cells (70%) → Insulin
• α-cells (20%) → Glucagon
• δ-cells → Somatostatin (inhibits both)
• PP-cells → Pancreatic polypeptide

• Released by ↑blood glucose, ↑amino acids, GIP, GLP-1, vagal stimulation; inhibited by adrenaline, somatostatin
• Mechanism: glucose enters β-cell → KATP channel closes → depolarization → Ca2+ influx → exocytosis
• Actions: ↑glucose uptake (GLUT4 in muscle/fat), ↑glycogenesis, ↓gluconeogenesis, ↑protein synthesis, ↑lipogenesis, ↓lipolysis
• Deficiency → diabetes mellitus

• Released by ↓blood glucose, ↑amino acids, stress; inhibited by insulin, glucose, somatostatin
• Actions: ↑glycogenolysis, ↑gluconeogenesis, ↑lipolysis, ↑ketogenesis (liver); counter-regulatory hormone

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• PTH: 84-amino acid peptide; released by ↓Ca2+; rapid response
• Actions (all ↑serum Ca2+, ↓serum phosphate):
  • Bone: ↑osteoclast activity → bone resorption → ↑Ca2+ + phosphate release
  • Kidney: ↑Ca2+ reabsorption (distal tubule); ↑phosphate excretion (proximal tubule); ↑1α-hydroxylase → ↑vitamin D activation
  • Gut: indirectly via calcitriol → ↑Ca2+ and phosphate absorption
• Calcitonin (C-cells of thyroid): opposes PTH; released by ↑Ca2+; ↓bone resorption; less physiologically important in adults
• Vitamin D (calcitriol): ↑intestinal Ca2+ and phosphate absorption; ↑renal reabsorption; permissive for PTH on bone

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SECTION 9: METABOLISM AND THERMOREGULATION

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• Metabolism = sum of all chemical reactions in the body
• Anabolism = synthesis of complex molecules from simple ones; energy-consuming; biosynthesis
• Catabolism = breakdown of complex molecules; energy-releasing; fuels ATP production
• Plastic role: proteins/fats/carbohydrates as building materials
• Energetic role: primarily carbohydrates (quick energy), fats (major energy store)
• ATP is the universal energy currency; ~38 ATP per glucose (aerobic glycolysis + Krebs + ETC)

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• RDA ~0.8 g/kg/day; essential amino acids (His, Ile, Leu, Lys, Met, Phe, Thr, Trp, Val)
• Nitrogen balance: intake = excretion (adults); positive (growth, pregnancy); negative (starvation, burns)
• Catabolism: deamination → urea cycle (liver) → urea excreted by kidneys

• 9 kcal/g; major energy store; essential fatty acids: linoleic (ω-6), linolenic (ω-3)
• β-oxidation in mitochondria; ketone bodies in liver during starvation → fuel for brain
• Lipogenesis when caloric excess

• 4 kcal/g; main fuel for brain (glucose); blood glucose 3.9-6.1 mmol/L (70-110 mg/dl)
• Glycolysis → pyruvate → (aerobic) acetyl-CoA → Krebs cycle; (anaerobic) lactate
• Glycogen storage: liver (glucostat) and muscle (local fuel)

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• Direct calorimetry: measure heat production directly in insulated chamber (calorimeter); accurate but impractical
• Indirect calorimetry (respiratory calorimetry): measure O2 consumption (VO2) and CO2 production (VCO2)
  • Respiratory quotient (RQ) = VCO2/VO2: carbohydrates = 1.0; fats = 0.7; proteins = 0.8; mixed diet = ~0.85
  • Caloric equivalent of O2: 1 L O2 ≈ 4.8-5 kcal
• Douglas bag method: collect expired air, analyze composition, calculate

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• Definition: Energy expenditure under standard conditions: lying at rest, fasting ≥12h, thermoneutral environment, mentally relaxed
• Normal: 1600-1800 kcal/day (M), 1300-1500 kcal/day (F); ~35-40 kcal/m²/h
• Factors affecting BMR:
  • ↑BMR: thyroid hormones, sympathetic activity, fever (+10% per 1°C rise), pregnancy, growth, exercise training, cold, male sex, younger age
  • ↓BMR: hypothyroidism, starvation, aging, female sex, sleep

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• Core: 36.5-37.5°C; oral ~36.8°C; rectal ~37.3°C (0.5°C higher)
• Diurnal variation: lowest at 4-6 AM, highest at 6-8 PM (circadian rhythm via SCN)
• Shell temperature (skin): 30-34°C; varies with environment
• Thermoreceptors: peripheral (skin cold receptors at 10-15°C activate, warm at 30-45°C); central (hypothalamic - most important for thermoregulation)

• Shivering thermogenesis: skeletal muscle contraction without movement; ↑heat
• Non-shivering thermogenesis: brown adipose tissue (BAT) - uncoupling protein-1 (UCP-1) uncouples oxidative phosphorylation → heat; important in neonates and cold-adapted adults

• Radiation: ~60% heat loss at rest (infrared); not possible when environment > skin temp
• Conduction: direct contact; enhanced by conductivity of water
• Convection: air movement carries heat away
• Evaporation: ~25%; insensible perspiration + sweating; only mechanism when environment > skin temp; 1 L sweat = 580 kcal

• Anterior hypothalamus = heat dissipation center (sweating, vasodilation)
• Posterior hypothalamus = heat conservation + shivering (via descending sympathetic pathways)
• Set point normally ~37°C; elevated in fever (by pyrogens → IL-1, IL-6, TNF → COX → PGE2 → hypothalamus)

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SECTION 10: EXCRETION PHYSIOLOGY

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• Daily water intake: ~2500 ml (drink 1200 + food 1000 + metabolic water 300)
• Daily water output: urine ~1500 ml, insensible perspiration ~900 ml, feces ~100 ml
• Excretory organs: kidneys (main), skin (sweat, insensible), lungs (CO2 + water vapor), intestine (feces, bile)
• Kidneys maintain: osmolarity, pH, volume, electrolyte balance, excrete waste products, produce hormones (EPO, renin, calcitriol)

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• Renal corpuscle: Bowman's capsule + glomerulus (fenestrated capillaries + podocytes)
• Proximal convoluted tubule (PCT): reabsorbs ~65% of filtered water, Na+, all glucose, amino acids; secretes H+, drugs; high metabolic activity
• Loop of Henle: thin descending (water permeable), thin ascending (impermeable to water, permeable to ions), thick ascending (active NaCl transport - NKCC2 cotransporter, site of furosemide action); creates medullary concentration gradient
• Distal convoluted tubule (DCT): NaCl reabsorption (thiazide site), Ca2+ reabsorption (PTH-regulated), dilution segment
• Collecting duct: final adjustment; water permeability regulated by ADH (AQP2); Na+/K+ exchange regulated by aldosterone

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• GFR: ~125 ml/min (180 L/day); only ~1.5 L/day excreted → 99% reabsorption
• Filtration membrane: fenestrated endothelium + glomerular basement membrane + podocyte slit diaphragm; size cutoff ~70 kDa; negative charge repels albumin
• Driving forces (Starling): Glomerular hydrostatic pressure (60 mmHg) - Bowman's oncotic pressure (0) - Bowman's hydrostatic (15 mmHg) - Capillary oncotic (32 mmHg) = net filtration pressure ~13 mmHg
• Primary urine composition: same as plasma but no large proteins or cells; glucose, urea, creatinine, electrolytes
• Regulation of GFR:
  • Autoregulation (myogenic + tubuloglomerular feedback via macula densa)
  • Neural: sympathetic → ↓GFR (↓RBF)
  • Hormonal: angiotensin II → ↓GFR; prostaglandins → ↑GFR; ANP → ↑GFR

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• PCT: Na+ by Na+/K+-ATPase (secondary active transport drives everything else); glucose via SGLT2 (cotransport); amino acids; bicarbonate; 65% water (osmotic)
• Loop of Henle: countercurrent multiplier creates medullary hyperosmolarity (up to 1200 mOsm at papilla)
• DCT: Aldosterone acts on principal cells → ↑ENaC expression → ↑Na+ reabsorption, ↑K+ secretion
• Collecting duct: ADH → inserts AQP2 water channels → facultative water reabsorption (produces concentrated urine up to 1200 mOsm)
• Without ADH → dilute urine (50-100 mOsm); maximum water excretion

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• ADH: collecting duct AQP2 → water reabsorption
• Aldosterone: DCT/CD principal cells → ↑Na+ reabsorption, ↑K+ secretion, ↑H+ secretion
• PTH: DCT → ↑Ca2+ reabsorption; PCT → ↓phosphate reabsorption; ↑calcitriol
• ANP/BNP: ↑GFR, ↑Na+ excretion (natriuresis), inhibit renin and aldosterone
• Angiotensin II: ↑Na+ reabsorption (PCT), ↑aldosterone

• H+ (acid-base balance)
• K+ (in exchange for Na+ under aldosterone)
• Organic acids: urate, drugs (penicillin, aspirin, probenecid inhibits)
• Creatinine (minor), PAH (used to measure RPF)
• Clinical urine analysis: color, transparency, pH (5-8), specific gravity, protein (negative), glucose (negative), ketones, cells, casts, bacteria

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• Osmometric thirst: ↑plasma osmolarity (detected by osmoreceptors in anterior hypothalamus, organum vasculosum of lamina terminalis) → thirst + ADH release; ~2% rise sufficient
• Volumetric thirst: ↓plasma volume (detected by low-pressure receptors in atria and veins; baroreceptors) → RAAS activation → angiotensin II stimulates subfornical organ and OVLT → thirst
• Thirst center: lateral hypothalamus, subfornical organ
• Satisfied by drinking BEFORE enough absorption to normalize osmolarity (oropharyngeal metering)

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SECTION 11: DIGESTIVE PHYSIOLOGY

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• Result: constant nutrient level in blood (glucose, amino acids, fatty acids)
• Components: digestive system (digestion/absorption), liver (metabolism/storage), pancreas (insulin/glucagon), hypothalamus (hunger/satiety), ANS regulation

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• Salivary glands: parotid (serous, amylase), submandibular (mixed), sublingual (mucous)
• Saliva composition: water (99%), amylase (α-amylase - starch digestion), mucin (lubrication), lysozyme (antibacterial), IgA (immunity), lingual lipase, bicarbonate (buffer), 1-1.5 L/day
• Functions: moistens food, initiates carbohydrate digestion, antibacterial, taste dissolution, speech
• Regulation: unconditioned reflex (chemo/mechanoreceptors in mouth → salivary nuclei in medulla → CN VII, IX, X), conditioned reflex (sight/smell of food → Pavlov); parasympathetic: ↑watery saliva; sympathetic: ↑viscous saliva (mucin)

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• Pancreatic juice: ~1.5-2 L/day; pH 7.5-8.3 (HCO3- rich); enzymes:
  • Proteases: trypsinogen, chymotrypsinogen, proelastase (inactive; activated by enteropeptidase → trypsin → activates all); trypsin + chymotrypsin cleave proteins
  • Lipase (with colipase): emulsified fat → fatty acids + monoglycerides; requires bile
  • Amylase: starch → maltose
  • Nucleases: DNAase, RNAase
• Regulation:
  • Secretin (S-cells, duodenum): released by acid (low pH) → ↑HCO3- secretion from pancreatic ductal cells
  • CCK (I-cells, duodenum): released by fat + protein → ↑enzyme secretion + ↑bile release; also causes satiety
  • Vagal (cephalic phase): ↑enzyme secretion
• Clinical: pancreatitis → autoactivation of proteases → self-digestion

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• Bile production: liver continuously ~600-800 ml/day; stored/concentrated in gallbladder (5-10× concentration)
• Composition: bile salts, phospholipids (lecithin), cholesterol, bilirubin, bicarbonate, water
• Bile salts (primary: cholic/chenodeoxycholic; secondary: deoxycholic/lithocholic after bacterial modification)
• Functions:
  • Emulsification of fats → ↑surface area for lipase
  • Micelle formation → solubilize fatty acids + fat-soluble vitamins (A,D,E,K) for absorption
  • Enterohepatic circulation: bile salts reabsorbed in terminal ileum → portal vein → liver (recycled 6-10×/day)
• Regulation: CCK → gallbladder contraction + Oddi sphincter relaxation → bile release; secretin → ↑bile water/HCO3-; vagus → ↑bile secretion

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• Gastric juice: ~2-3 L/day; pH 1-2
  • HCl (parietal cells): activates pepsinogen → pepsin; kills bacteria; facilitates Fe2+ absorption; regulated by: ACh (M3), gastrin (CCK2), histamine (H2) - all ↑; somatostatin, prostaglandins - ↓
  • Pepsinogen (chief cells): activated by HCl → pepsin; cleaves proteins at aromatic amino acids
  • Intrinsic factor (parietal cells): essential for vitamin B12 absorption in terminal ileum; deficiency → pernicious anemia
  • Mucus + HCO3- (mucous cells): protective gastric mucosal barrier

• Converts pepsinogen to pepsin
• Denatures proteins (unfolding)
• Bactericidal
• Activates intrinsic factor-B12 complex
• Stimulates secretin release from duodenum

1. Cephalic phase (~30%): sight/smell/taste/thought of food → vagal (ACh) → gastric secretion; anticipatory
2. Gastric phase (~60%)**: food in stomach → distension (vagal reflex) + proteins + peptides → gastrin (G-cells, antrum) → ↑HCl + pepsinogen
3. Intestinal phase (~10%)**: chyme in duodenum → initially stimulates then inhibits (enterogastrones: secretin, GIP, CCK) → ↓gastric secretion

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• Motility: segmentation (mixing) + peristalsis; MMC (migrating motor complex) between meals - "intestinal housekeeper"
• Brush border enzymes (parietal/contact digestion):
  • Disaccharidases: maltase, sucrase, lactase
  • Peptidases: aminopeptidase, dipeptidase
• Absorption mechanisms:
  • Glucose, galactose: SGLT1 (secondary active, Na+ cotransport) → GLUT2 (basolateral)
  • Fructose: GLUT5 (facilitated) → GLUT2
  • Amino acids: Na+-cotransporters; dipeptides via PepT1
  • Fatty acids + monoglycerides: passive into enterocyte → reassembled into triglycerides → chylomicrons → lymphatics (lacteals) → thoracic duct
  • Fat-soluble vitamins: with fat in micelles
  • Vitamin B12: bound to IF → receptor (cubilin) in terminal ileum
  • Iron: Fe2+ via DMT1 in duodenum; Fe3+ reduced by vitamin C; stored as ferritin or transported as transferrin
  • Calcium: active (calbindin, regulated by calcitriol) in duodenum; passive in jejunum/ileum

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• Esophagus: primary peristalsis (swallowing) + secondary (clearance); LES (lower esophageal sphincter) - tonic contraction, relaxes with swallowing
• Stomach: receptive relaxation (vagal, VIP); mixing waves; peristaltic waves push chyme to pylorus; pyloric sphincter regulates gastric emptying (fats delay: CCK; acid delays: secretin)
• Small intestine: segmentation (mixing, 11-12/min in duodenum) + peristalsis; MMC every 90-120 min
• Large intestine: haustration; mass movements 1-3×/day (after meals - gastrocolic reflex); defecation reflex (rectal distension → internal anal sphincter relaxes; external = voluntary)

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SECTION 12: ANALYZER (SENSORY SYSTEM) PHYSIOLOGY

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1. Peripheral part (receptor)
2. Conducting paths (afferent nerve)
3. Cortical projection area (brain)

• Specificity (adequate stimulus)
• Threshold (minimal detectable stimulus)
• Adaptation (rapid = Meissner, Pacinian; slow = Merkel, Ruffini, nociceptors, muscle spindle)
• Receptor (generator) potential (graded, proportional to stimulus intensity)
• Transduction (stimulus energy → electrical signal)

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• Cornea → aqueous humor → lens (accommodation via ciliary muscle/zonule) → vitreous → retina
• Retina: rods (~120 million, periphery, low light, no color) and cones (~6 million, fovea, color, acuity)
  • Photoreceptors: outer segment contains photopigment stacked discs
  • Rods: rhodopsin (opsin + 11-cis-retinal); bleached by light → all-trans-retinal → hyperpolarization (Gt → ↓cGMP → CSPNG closes → no Na+ entry → hyperpolarized)
  • Cones: photopsins (S - blue 420 nm; M - green 530 nm; L - red 560 nm)
• Neural pathway: photoreceptors → bipolar cells → ganglion cells → optic nerve (CN II) → optic chiasm (nasal fibers cross) → optic tract → LGN (thalamus) → optic radiation → primary visual cortex (area 17, calcarine sulcus)
• Pupillary light reflex: CN II (afferent) → pretectal area → EW nucleus → CN III (efferent) → sphincter pupillae

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• Air conduction: pinna → EAC → tympanic membrane → ossicles (malleus → incus → stapes) → oval window → cochlea (scala vestibuli/tympani/media)
• Bone conduction: vibration transmitted directly via skull bones

• Basilar membrane vibrates; different frequencies → different locations (tonotopy): high frequency at base, low at apex
• Hair cells (inner = signal, outer = amplification): stereocilia deflection → K+ channels (tip links open) → depolarization → glutamate release → spiral ganglion (CN VIII)

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• Semicircular canals (3, orthogonal): detect angular acceleration; ampullary crest with cupula; hair cells detect endolymph movement
• Utricle and Saccule: detect linear acceleration and gravity; macula with otoliths (calcium carbonate crystals)

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• Aδ fibers (sharp, fast, well-localized pain - "first pain")
• C fibers (dull, burning, slow, diffuse - "second pain")

• Periaqueductal gray (PAG) + raphe nuclei + locus coeruleus → descending inhibition via serotonin and noradrenaline → inhibit dorsal horn neurons
• Endogenous opioids: β-endorphin (hypothalamus/pituitary), enkephalins (spinal cord, widespread), dynorphins; activate μ, δ, κ receptors → presynaptic inhibition of substance P release + postsynaptic hyperpolarization
• Stimulated by: exercise, acupuncture, stress, TENS, laughter

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SECTION 13: PHYSIOLOGY OF HIGHER NERVOUS ACTIVITY (GNI)

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• Descartes: mechanistic reflex (spinal reflexes are mechanical; soul only in brain - interactionist dualism)
• Sechenov (1863): "Reflexes of the Brain" - all acts of brain are reflex; external inhibition of spinal reflexes from brain (Sechenov inhibition); proposed objective study of psychic phenomena
• Pavlov: developed method of conditional reflexes in chronic experiments; described conditioned and unconditioned reflexes; types of inhibition; GNI types; signal systems; laws of GNI; Nobel Prize 1904

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1. Conditioned stimulus (CS) must precede unconditioned stimulus (US)
2. CS must be repeated with US (reinforcement)
3. CS must be neutral initially
4. No distracting strong stimuli
5. Animal must be awake and alert

• Classical (Pavlovian): CS → CR (involuntary); stimulus substitution
• Trace vs. delay CR
• 1st order, 2nd order, 3rd order CRs (higher order conditioning)
• Natural vs. artificial

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• External inhibition - new strong stimulus → orienting reflex → inhibits ongoing CR
• Transcendent inhibition (protective) - very strong/prolonged stimulation → inhibition (protects neurons from overexcitation)

• Extinction - CS without reinforcement → gradual extinction of CR; not permanent (spontaneous recovery)
• Differentiation - distinguish similar stimuli; non-reinforced variant extinguishes
• Conditioned inhibitor - stimulus paired with absence of reinforcement → becomes signal for no-CR
• Delayed inhibition - long delay between CS and US → animal inhibits early response

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1. Strength (strong/weak)
2. Balance (balanced/unbalanced)
3. Mobility (mobile/inert)

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1. Afferent synthesis: integrates 4 components:
   • Dominant motivation (internal need)
   • Memory (past experience)
   • Situational afferentation (current environment)
   • Trigger afferentation (specific trigger stimulus)
2. Decision making: selects one behavior from multiple alternatives
3. Efferent synthesis: formation of action program
4. Action (result)
5. Action acceptor (of results): neural model of expected result; formed before action; evaluates back-afferentation
6. Back-afferentation (feedback): sensory signals from result → compared with action acceptor
   • Match → behavior stops
   • Mismatch → afferent synthesis continues → new action

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• Motivation = emotional and physiological state driving goal-directed behavior; created by dominant need
• Mechanism (P.K. Anokhin): biological need (internal homeostatic imbalance) → hypothalamus activates → ARAS → cortical arousal → motivational state
• Types:
  • Biological (primary): hunger, thirst, sex, pain avoidance, sleep
  • Social: achievement, affiliation, dominance
  • Ideal: curiosity, justice
• Hunger: lateral hypothalamus (hunger center) + blood glucose ↓ + ghrelin ↑ + absence of stomach stretch
• Satiety: ventromedial hypothalamus + blood glucose ↑ + leptin ↑ + GLP-1 + CCK + gastric stretch
• Role: organizes behavior toward specific goal; selects from behavioral repertoire

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• Emotions = subjective states reflecting the biological significance of stimuli and situations; have motivational, evaluative, communicative functions
• Neurophysiological substrate: limbic system (amygdala for fear/negative emotions; nucleus accumbens for pleasure/reward), hypothalamus, prefrontal cortex
• Types: positive (joy, pleasure) / negative (fear, anger, sadness); primary / secondary; sthenic (mobilizing) / asthenic (paralyzing)
• James-Lange theory: emotion is perception of bodily changes
• Cannon-Bard theory: emotion and physiological response occur simultaneously from thalamus
• Role: motivation, evaluation, communication, memory consolidation (emotional enhancement of memory via amygdala-hippocampus interaction)

• Prolonged negative emotions → activation of sympatho-adrenal axis + HPA axis
• Catecholamines + cortisol elevation → cardiovascular strain, immunosuppression, metabolic changes
• Prevention: relaxation, social support, cognitive reframing, exercise, adequate sleep

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• Definition: non-specific response of the organism to any demand placed upon it
• Eustress (positive) vs. Distress (negative/harmful)

1. Alarm reaction (hours-days): initial exposure to stressor; hypothalamus → sympatho-adrenal activation → adrenaline, cortisol; "fight or flight"; temporary ↓resistance
2. Stage of resistance (days-weeks): adaptation; cortisol dominant; maintained HPA axis activation; ↑resistance to original stressor; cross-adaptation to other stressors
3. Stage of exhaustion (if stress continues): adrenal exhaustion; ↓cortisol; loss of adaptation; disease, damage, death

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• Declarative (explicit): hippocampus-dependent; episodic (personal events) + semantic (facts)
• Non-declarative (implicit): cerebellum (motor skills), basal ganglia (habits), amygdala (emotional), brainstem (reflexes)
• Working memory (seconds): prefrontal cortex; limited capacity (~7±2 items)

1. Short-term memory (STM): seconds-minutes; reverberating neuronal circuits; labile (disrupted by concussion); limited capacity
2. Long-term memory (LTM): days-years; structural synaptic changes; unlimited capacity
3. Consolidation: conversion STM → LTM; requires protein synthesis; sleep-dependent

• LTP (Long-Term Potentiation): NMDA receptors (require coincident pre+post synaptic activity); Ca2+ influx → AMPA receptor insertion + spine enlargement; basis of synaptic strengthening
• Molecular: CREB transcription factor activation → new protein synthesis → structural synaptic change
• Hippocampus critical for consolidation (not storage); damage → anterograde amnesia

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• NREM (Non-REM) / Slow-wave sleep:
  • Stage N1 (dozing): θ waves (4-8 Hz), vertex sharp waves
  • Stage N2: sleep spindles (12-16 Hz bursts), K-complexes; ~50% total sleep
  • Stage N3 (deep/slow-wave): δ waves (0.5-4 Hz, >20%); most restorative; GH peak; memory consolidation; ↓HR, ↓BP, ↓temperature
• REM (Rapid Eye Movement) / Fast sleep:
  • EEG resembles wakefulness (desynchronized, β-like); paradoxical sleep
  • Rapid eye movements, complete atonia of skeletal muscles (except diaphragm, eye muscles)
  • Dreams (vivid)
  • ↑HR, ↑BP, ↑RR variability
  • Important for emotional memory processing, learning, creativity
  • Penile/clitoral tumescence

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• Awareness of self and environment; requires intact ARAS + thalamo-cortical circuits + prefrontal cortex
• EEG: β/γ activity in wakefulness; different patterns in different states
• Disorders: coma (no arousal, no awareness), vegetative state (arousal without awareness), minimally conscious state

• Freudian concept: contains repressed memories, drives, conflicts
• Psychophysiological correlates: implicit memory, priming, procedural learning, subliminal processing
• Unconscious emotional processing: amygdala can respond to stimuli below conscious awareness
• Neurophysiology: most CNS processing is unconscious; only ~5% of neural activity reaches consciousness; prefrontal cortex as "global workspace" for conscious access (Global Workspace Theory, Baars/Dehaene)

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What's included: