seminar 3 physiology
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SEMINARPRESENTED BY- Dr NIKHIL SRIVASTAVAMODERATED BY- Dr. DEEPIKA KENKERE
NERVOUS SYSTEM- PHYSIOLOGY
CONTENTS INTRODUCTION CELL MEMBRANE POTENTIAL NERVE PHYSIOLOGY PAIN PATHWAY PARASYMPATHETIC SYSTEM SYMPATHETIC SYSTEM MECHANISM OF CONTROL OF BODY TEMPERATURE NERVE INJURIES BIBLIOGRAPHY
INTRODUCTIONThe nervous system is composed of -1. NEURONS transmit nerve impulses along
nerve fibers to other neurons. Neurons typically have a cell body, axons and
dendrites.2. NERVES are made up of bundles of nerve
fibers.3. NEUROGLIA carry out a variety of
functions to aid and protect components of the nervous system.
Dendrites
Myelin sheath
Schwann cell Nucleus of Schwann cell
Axon
Nodes of Ranvier
Terminal dendrites
Organs of the nervous system can be divided into CENTRAL NERVOUS SYSTEM (CNS) PERIPHERAL NERVOUS SYSTEM (PNS) The nervous system provides sensory, integrative, and
motor functions to the body. Motor functions can be divided into the SOMATIC NERVOUS SYSTEM AUTONOMIC SYSTEM
A. SENSORY RECEPTORS
B. INTEGRATIVE FUNCTIONS
C. EFFECTOR ORGANS
GENERAL OUTLINE OF MEMBRANE PHYSIOLOGY DIFFUSION FACILITATED DIFFUSION ACTIVE TRANSPORT
PASSIVE TRANSPORT
The concentration gradient: causing the ions to diffuse down their concentration gradient
The electrical potential: causing ions to be attracted to the opposite charge to the one they carry
FACILITATED DIFFUSION
ACTIVE TRANSPORT
PRIMARY
SECONDARY
SODIUM & POTASSIUM IONS`The two important ions in a nerve cell are K+ and Na+
Both are cations Na+ ions move more slowly across the membrane than K+ or Cl- ionsThis is because although the Na+ ion is smaller than the K+ ionNa+ has a larger coating of water molecules giving it a bigger diameterThis makes the plasma membrane 25 times more permeable to K+ than Na+
In addition to this K+ ions leak out of K+ ion pores when the nerve cell is at rest
So to maintain the high concentration of K+ inside the cell, it has to be actively pumped inwards a bit when the cell is at rest
The result is that the resting potential of the neurone is almost at the equilibrium for K+ ions
K+ leak out a bit and need pumping in Na+ ions, however, are actively pumped
out and kept out
A COUPLED NA+-K+ PUMP
coupled ion pump
plasma membrane
K+
Na+
K+
Na+
Cytoplasm ECF
© 2008 Paul Billiet ODWS
NERVE PHYSIOLOGY Are capable of generating rapidly changing
electrochemical impulses at their membranes.
Resting membrane potential -90 mV
Na+ (outside)-142mEq/L Na+ (inside)- 14 mEq/L K+ (outside)-4 mEq/L K+ (inside)-140 mEq/L Ratio Na+inside/Na+outside=0.1 K+inside/K+outside=35.0
NERVE IMPULSE An electrochemical event that occurs in
nerve cells following proper stimulation. An all-or-none process which is fast acting
and quick to recover. An event that is described by a voltage curve
that is called an action potential. The nerve impulse can be conducted the
entire length of a nerve cell without diminishment (“domino effect”).
OVERVIEW OF NERVE IMPULSE
RESTING STAGE Sodium/Potassium pump
continuously and actively pumps (3) Na+ out of the cell and (2) K+ into the cell.
Na+ channels are closed so Na+ are not able to move into the cell.
K+ channels are open so K+ can diffuse out of the cell.
This generates a separation of charges so that the inside of the cell is relatively – and the outside is relatively +.
The cell will remain in this state (at rest) until it is stimulated.
DEPOLARIZATION STAGE Permeable to Na+
ions “polarized” state
neutralized Depolarization
occurs Widening of
transmembrane channels
Threshold potential
REPOLARIZATION STAGE Na+ channels close K+ Channels open
more Rapid diffusion of K+
ions to the exterior Voltage gated Na+ &
K+ channels
MECHANISMS OF ACTION OF L.A.
Fig.
MECHANISMS OF ACTION
Inhibiting excitation of nerve endings or blocking conduction in peripheral nerves.
Binding to and inactivating sodium channels.
MECHANISMS OF ACTION
Sodium influx through these channels is necessary for the depolarization of nerve cell membranes and subsequent propagation of impulses along the course of the nerve.
when a nerve loses depolarization and capacity to propagate an impulse, the individual loses sensation in the area supplied by the nerve
block nerve fiber conduction by acting on nerve membranes
inhibit sodium ion activity
blocks depolarization--> blocks nerve conduction
PAIN
CLASSIFICATION OF PAIN
PAIN
Somatic(somasthetic)
Visceral (from viscera)e.g. angina pectoris, peptic ulcer, intestinal colic, renal colic, etc.
Superficial (from skin & subcutaneous tissue) e.g. superficial cuts/burns, etc.
Deep (from muscles/bones/fascia/periosteum) e.g. fractures/arthritis/fibrositis, rupture of muscle belly
DEFINITIONThe International Association for the Study of Pain
Pain is "an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage“
Monheim : “An unpleasant emotional experience usually initiated by noxious stimulus and transmitted over a specialized neural network to the CNS where it is interpreted as such.”
TYPES OF PAIN
Allodynia Hyperalgesia & hypoalgesia Hyperesthesia & hypoesthesia Hyperpathia Causalgia Neuralgia
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Neurovascular Blood Vessels Throbbing, pulsing or pounding
Neuropathic Sensory nervous system
Shooting, sharp, burning pain
Causalgic Sympathetic nervous system
Burning
Muscular Muscles Deep aching, tight
CHARACTERSTICS TYPE SYSTEM AFFECTED CHARACTER
Sensory Receptors :
Sensory input from various external stimuli is thought to be received by specific peripheral receptors that act as transducers and transmit by nerve action potentials along specific nerve pathways toward the central nervous system.
Termed first–order afferents, these peripheral terminals of afferent nerve fibers differ in the form of energy to which they respond at their respective lowest stimulus intensity, that is, are differentially sensitive.
The impulse interpreted is nociceptive (causing pain) if it exceeds the pain threshold
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TYPES OF RECEPTORS
SENSORY RECEPTORS
GENERAL
SENSES
SPECIAL
SOMATIC VISCERAL
SUPERFICIAL DEEPTouch-pressureThermalPain
Pain Proprioception
PainBaroreceptionChemoreception
VisualAuditionOlfactionGustation
Cutaneous Receptors:
Distinguished morphologically as corpuscular and noncorpuscular.
The pacinian corpuscles, in particular, are highly sensitive mechanoreceptors
Other mechanoreceptors are the Meissner corpuscles, Golgi – Mazzoni corpuscles, Ruffini’s ending and Krause bulb.
Functionally three categories of cutaneous receptors are thought to exist: mechanoreceptors, thermo receptors, and nociceptors.
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A nerve ending that responds to noxious stimuli that can actually or potentially produce tissue damage.
Free nerve endings i.e., they are not enclosed in a capsule. The receptors for fast pain are sensitive to mechanical or thermal stimuli of noxious strength.
The receptors for slow pain are sensitive not only to noxious mechanical and thermal stimuli but also to a wide variety of chemicals associated with inflammation.
NOCICEPTORS
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Since pain receptors respond to a wide variety of stimuli, they are called polymodal.
Types of nociceptors : Aδ Mechanical NociceptorsC Polymodal NociceptorsC fibre mechanical nociceptorsHigh threshold cold nociceptors
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MECHANORECEPTORS
Mechanoreceptors, which respond to tactile non painful stimuli.
Divided into two functional groups (rapidly or slowly adapting) depending on their response during stimuli.
Rapidly adapting mechanoreceptors respond at the onset and offset of the stimuli
Slowly adapting mechanoreceptors respond throughout the stimuli duration.
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C – FIBRE MECHANO HEAT SENSITIVE NOCICEPTORS
These fibres are considered polymodal, as they respond to mechanical, heat, cold and chemical stimuli.
Their monotonic increase in activity evokes a burning pain sensation at the thermal threshold in humans (41–49°C).
Subject to fatigue and sensitization modulation.
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A-FIBRE MECHANO-HEAT-SENSITIVE NOCICEPTORS
Activation of these receptors is interpreted as sharp prickling or aching pain.
Owing to their relatively rapid conduction velocities (5–36 m/s), they are responsible for first pain.
Two subclasses of AMHs exist: types I and II. Type I fibres respond to high magnitude heat, mechanical and
chemical stimuli and are termed polymodal AMHs. They are found in both hairy and glabrous skin.
Type II nociceptors are found exclusively in hairy skin. They are mechanically insensitive and respond to thermal stimulation.
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DEEP TISSUE NOCICEPTORS
Unlike cutaneous pain, deep pain is diffuse and difficult to localize, with no discernable fast (first pain) and slow (second pain) components.
In many cases deep tissue pain is associated with autonomic reflexes (e.g. sweating, hypertension and tachypnoea).
Units that do not respond to mechanical stimuli have been termed silent nociceptors. Silent nociceptors are also present within the viscera.
Silent visceral afferents fail to respond to innocuous or noxious stimuli, but become responsive under inflammatory conditions.
Visceral afferents are mostly polymodal C- and A-fibres.
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Aß - fibres Aδ - fibres C- fibres
Threshold Low Medium High
Axon diameter 6-14μm 1-6μm 0.2-1μm
Myelination Yes Thinly No
Velocity 36-90 5-36 0.2-1
Receptor types Mechanoreceptor Mechano/Nociceptor
Nociceptor
Receptive field Small Small Large
Quality Touch Sharp/first pain Dull/second pain
Summary of receptor types
Gate Control Theory
This theory proposed by Melzack and Wall in 1965 This theory of pain takes into account the relative in put
of neural impulses along large and small fibers, the small nerve fibers reach the dorsal horn of spinal cord and relay impulses to further cells which transmit them to higher levels.
The large nerve fibers have collateral branches, which carry impulses to substantia gelatinosa where they stimulate secondary neurons.
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The substantia gelatinosa cells terminate on the smaller nerve fibers just as the latter are about to synapse, thus reducing activity, the result is, ongoing activity is reduced or stopped –gate is closed.
The theory also proposes that large diameter fiber input has ability to modulate synaptic transmission of small diameter fibers within the dorsal horn.
Large diameter fibers transmit signals that are initiated by pressure, vibration and temperature; small diameter fibers transmit painful sensations.
Activation of large fiber system inhibits small fiber synaptic transmission, which closes the gate to central progression of impulse carried by small fibers.
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SENSORY NEURONS
First Order Second Order Third Order
FIRST ORDER NEURON
Each sensory receptor is attached to a first order primary afferent neuron that carries the impulses to the CNS.
The axons of these first-order neurons are found to have varying thickness.
The larger fibers conduct impulses more rapidly than smaller fibers.
Type A fibers Alpha fibers: size - 13 to 20 µm, velocity - 70 to 120 m/ s. Beta fibers: size – 6 to 13 µm, velocity – 40 to 70 m/s. Gamma fibers: size – 3 to 8 µm, velocity – 15 to 40 m/s. Delta fibers: size – 1 to 5 µm, velocity – 5 to 15 m/s.
Type C fibers Size – 0.5 to 1 µm, velocity – 0.5 to 2 m/s.
SECOND ORDER NEURON The primary afferent neuron carries impulse into the
CNS and synapses with the second-order neuron. This second-order neuron is sometimes called a
transmission neuron since it transfers the impulse on to the higher centers.
The synapse of the primary afferent and the second-order neuron occurs in the dorsal horn of the spinal cord.
THIRD ORDER NEURON
Cell bodies of third order neurons of the nociception-relaying pathway are housed in: the ventral posterior lateral, the ventral posterior inferior, and the intralaminar thalamic nuclei
Third order neuron fibers from the thalamus relay thermal sensory information to the somesthetic cortex.
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FAST PAIN & SLOW PAIN Fast Pain Also known as Sharp pain, pricking pain or acute pain. Easily localized. Not felt in the deep visceral organs. Slow Pain Also known throbbing pain, aching pain or chronic pain.It can occur both in skin and in almost any deep tissue or
organ.
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PAIN PATHWAYS AND MEDICATIONS
Pain Pathways Medications
Peripherally (at the nociceptor) Cannabinoids, NSAIDs, Opioids, Tramadol, Vanilloid receptor antagonists (i.e., capsaicin)
Peripherally(along the nociceptive nerve)
Local anaesthetics, Anticonvulsants (except the gabapentinoids)
Centrally(various parts of the brain)
Acetaminophen, Anticonvulsants (except the gabapentinoids), Cannabinoids, Opioids, Tramadol
Descending inhibitory pathwayin the spinal cord
Cannabinoids, Opioids, Tramadol, Tricyclic antidepressants, SNRIs
Dorsal horn of the spinal cord Anticonvulsants, Cannabinoids, Gabapentinoids, NMDA receptorantagonists, Opioids, Tramadol, Tricyclic antidepressants, SNRIs
AUTONOMIC NERVOUS SYSTEM
AUTONOMIC NERVOUS SYSTEM Controls most visceral functions of the body Rapidity & intensity with which it changes
functions Activated by centres located in spinal cord,
brain stem, & hypothalamus 2 major subdivisions-PARASYMPATHETICSYMPATHETIC
SYNAPSE
SYMPATHETIC SYSTEM
SYMPATHETIC SYSTEM Also called thoracolumbar system:
all its neurons are in lateral horn of gray matter from T1-L2
Lead to every part of the body (unlike parasymp.)
Norepinephrine ( noradrenaline) is neurotransmitter released by most postganglionic fibers (acetylcholine in preganglionic) “adrenergic”
PARASYMPATHETIC SYSTEM
PARASYMPATHETIC SYSTEM
Also called the craniosacral system because all its preganglionic neurons are in the brain stem or sacral levels of the spinal cord Cranial nerves III,VII, IX and X In lateral horn of gray matter from S2-S4
Only innervate internal organs (not skin) Acetylcholine is neurotransmitter at end
organ as well as at preganglionic synapse “cholinergic”
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ADRENAL GLAND
On top of kidneys
Adrenal medulla (inside part) is a major organ of the sympathetic nervous system
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ADRENAL GLAND Synapse in gland Can cause body-wide
release of epinephrine/adrenaline and norepinephrine in an extreme emergency(adrenaline “rush” or surge)
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Summary
HOMOEOSTASIS
CORE TEMPERATURE
The core temperature of the human body is 37°C The core of the human body includes the organs
of the thorax, abdomen and the head This is where the vital organs are located Their enzyme systems must operate in optimum
conditions The periphery of the body can withstand some
deviation from the core temperature
HEAT LOSS AND HEAT GAINThe body must balance its heat budgetHeat is gained: by conduction from warm air surrounding the body by the body’s metabolic activity which generates heat
e.g. when muscle moveHeat is lost: by conduction and radiation to cold air (or water) by evaporation of sweat from the body surface
(c.f. properties of water) Humans can also affect their body temperature by
changing their behavioure.g. wearing different clothes, seeking shade
MAINTAINING THE BODY TEMPERATURE
Keeping warm Staying cool
Increased insulation, subcutaneous fat reduces the conduction of heat from the body
Increase blood flow to skin, increases conduction and radiation of heat from the body
Reduced sweating decreases evaporation
Increased sweat secretion, increases evaporation
Increased shivering, increases heat produced by muscle tissue 2 to 5 times
Reduced activity
© 2008 Paul Billiet ODWS
nerves
Less heat generated
More water covers the skin.
More evaporation
Skin arteries dilateMore blood to the
skin. More radiation & conduction of heat
Muscles of skin arteriole
walls relaxSweat glands
increase secretion
Musclesreduce activity
Core body temperature
>37°C
Hypothalamus
Thermoreceptors
Thermoreceptors
Return to 37°C
Muscles of skin
arteriole walls relax
Core body temperature
>37°CHypothalamus
Sweat glands
increase secretion
nerves
Musclesreduce activity
Thermoreceptors
NEGATIVE FEEDBACK
Blood temperature
Body loses heat
nerves
More heat generated
Less water covers the skin.
Less evaporation
Skin arteries constrict
Less blood to the skin.
Less radiation & conduction of heat
Muscles of skin arteriole
walls constrict
Sweat glands
decrease secretion
Musclesshivering
nerves
Core body temperature
<37°C
Thermoreceptors
Hypothalamus
Thermoreceptors
Return to 37°C
NEGATIVE FEEDBACK
Blood temperature
Body loses less heat
Body gains heat
Muscles of skin
arteriole walls
constrict
Core body temperature
<37°C
Sweat glands
decrease secretion
nerves
Musclesshivering
Thermoreceptors Hypothalamus
nerves
OVERVIEW -TEMPERATURE HOMEOSTASIS
IN HUMANS
NERVE INJURIES
Epineurium
Perineurium
Endoneurium
Fascicles
Nerve fiber
Node of Ranvier
Schwann cellMyelin
Axon
TRAUMA TO PERIPHERAL NERVES Interruption of nerve trunk (neurotmesis) Interruption of axons (axonotmesis) Total conduction failure (neurapraxia) Impaired conduction (no morphologic
change)
CAUSES OF INJURY TO PERIPHERAL NERVES Trauma Compression (entrapment) Irritation Metabolic disorders Inflammatory (neuritis) Virus Age related changes
Axon
EpineuriumPerineuriumEndoneurium
Neurapraxia
NEURAPRAXIA Caused by pressure for a short period Axon not destroyed No function loss Recovers spontaneously over days or weeks
(when the cause is resolved) Results of spontaneous recovery are almost
always good
AXONOTMESIS
Severe prolonged pressure Wallerian degeneration Nerve may regenerate from injured location away
from the cell body Regeneration: 1 mm per day (approx. 1 inch per
month) Results of spontaneous recovery are good to
moderate depending on distance
NEUROTMESIS
Does not regenerate spontaneously Grafting is necessary to restore function Results of grating are good to moderate to failures Of three types- 3rd degree- endoneurium interrupted 4th degree- epineurium and perineurium also
interrupted 5th degree-complete transection of the nerve trunk
Injured nerves
Axon interrupted(Wallerian degeneration)
Interruption of axon andendoneurial sheet
Interruption ofperineurial sheet
Interruption of nerve trunk
INTERRUPTED AXONS
Degenerate distally (away from cell body) Wallerian degeneration Interrupted axons regenerate from injury, provided
that endoneural tube is intact
BIBLIOGRAPHY GUYTON’S TEXTBOOK OF PHYSIOLOGE MALAMED’S LOCAL ANAESTHESIA MONHEIM’S LOCAL ANAESTHESIA ROWE & WILLIAMS VOLUME 2
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