Spinal Nerves, Membrane Potentials and Action Potentials Flashcards
Spinal Nerves- how many? where do they come from?
Thirty-one pairs of mixed nerves arise from the spinal cord and supply all parts of the body except the head
cervical nerves
8 cervical (C1-C8)
thoracic nerves
12 thoracic (T1-T12) intercostal nerves lumbar enlargement
lumbar nerves
5 Lumbar (L1-L5)
sacral nerves
5 Sacral (S1-S5)
coccygeal
1 Coccygeal (C0)
Brachial Plexus
Formed by C5-C8 and T1 (C4 and T2 may also contribute to this plexus) It gives rise to the nerves that innervate the upper limb
There are four major branches of the brachial plexus
Roots – five ventral rami (C5-T1) Trunks – upper, middle, and lower, which form divisions Divisions – anterior and posterior serve the front and back of the limb Cords – lateral, medial, and posterior fiber bundles Branches
nerve plexuses…where are they found?
All ventral rami except T2-T12 form interlacing nerve networks called plexuses Plexuses are found in the cervical, brachial, lumbar, and sacral regions Each resulting branch of a plexus contains fibers from several spinal nerves Fibers travel to the periphery via several different routes
what happens to damage to one spinal segment?
Damage to one spinal segment cannot completely paralyze a muscle
Brachial plexus
Second most common postop peripheral neuropathy
Axillary
– innervates the deltoid and teres minor
Musculocutaneous
sends fibers to coracobrachialis, biceps brachii and brachialis. Flexion at elbow
Median
branches to most of the flexor muscles of forearm and opponens pollicis Pronation of forearm Flexion of wrist Opposition of thumb Flexion of lateral three fingers
Ulnar
supplies the flexor carpi ulnaris and half of the flexor digitorum profundus Flexion of wrist Adduction of fingers Flexion of medial two fingers **Ulnar nerve- post op compression from the hard operating table**
Radial
Supplies ALL extensors of arm and forearm muscles. Extension at elbow Supination of forearm Extension of wrist and fingers **Radial fracture of the humerus- this nerve can be snapped**
Intercostobrachial nerve
Can be blocked to reduce pain from tourniquet inflation during IV regional neural anesthesia
neuron
Basic building block of CNS ~ 100 billions Integration and transmission of nerve impulses
Schwann cells
produce myelin sheath which wraps around axon, provides insulation
Node of Ranvier
gaps in myelin sheath
Saltatory conduction:
Node to node jumping of depolarization.
where are neurotransmitters synthesized.
Neurotransmitters are synthesized in cell body and transported to synaptic knobs All or none law
Multiple Sclerosis
Demyelination results slow or blocked conduction
Bipolar Neuron
has short axon process from arising from one side of the cell body, and a short dendritic process arising from the opposite side
Special senses neurons
Bipolar neurons- those found in the eyes, ears, and nose are bipolar neurons
Unipolar Neuron:
has single large extension from its cell body. They are found in lower invertebrate ,never in humans.
Pseudounipolar neuron:
Present in dorsal root ganglia
Multipolar Neuron:
comprise one axon and multiple dendritic process. They are the MOST COMMON type in brain and spinal cord.
dorsal root ganglia
Drg cell body lies
Depolarization
Makes the cell membrane potential less negative due to movement of positively charged sodium ions (Na+) into the cell. excitability
Repolarization
Change after depolarization, that returns the membrane potential back to resting potential. Repolarization results from the movement of positively charged potassium ions (K+) out of the cells.
Hyperpolarization
Makes the membrane potential more negative due to movement of negatively charged chloride ions (Cl-) into the cell. excitability
Inward current
Is the flow of positive charge into the cell. Inward current depolarizes the membrane potential.
Outward current
Is the flow of positive charge out of the cell. Outward current hyperpolarizes the membrane potential.
Action potential
Is a property of excitable cells (nerve & muscle) that consists of a rapid depolarization, or upstroke, followed by repolarization of the membrane potential. Action potential have stereotypical size and shape, are propagating and are all-or-none
Threshold
Is the membrane potential at which the action potential is inevitable. At threshold potential, net inward current becomes larger that net outward current. The resulting depolarization becomes self-sustaining and gives rise to upstroke of action potential. If net inward current is less than net outward current, no action potential will occur (i.e. all- or- none response)
Resting membrane potential
is the measured potential difference across the cell membrane in mV (-70 to - 90mV) At rest , the nerve membrane is far more permeable to K+ than to Na+ Leaky K+ channels are responsible for resting membrane potential. The Na+/K+ pump maintains resting membrane potential ( 3Na+ out and 2K+ in)
Action Potential “Nerve Impulse”
is a property of excitable cells (nerve, muscles) that consist of a rapid depolarization (interior becomes less negative) or upstroke , followed by repolarization of membrane potential.
Upstroke of the Action potential (depolarization)
Inward Na+ movement Lidocaine block these voltage sensitive Na+ channels and abolish action potential
Downstroke of the Action potential (repolarization)
Outward K+ movement Inward current (flow of Na+ into the cell) depolarizes the membrane potential , while outward flow of K+ hyperpolarize the membrane potential. Both ions flow by simple diffusion.
Properties of AP Speed? other properties?
Constant size and shape Propagation/ spread ( 60 m/sec ) Myelinated vs. non-myelinated fibers All-or-none Law (no percentage) Threshold is the membrane potential at which the AP is inevitable
Refractory periods
Absolute refractory period: is a period during which another action potential cannot be elicited, no matter how large the stimulus. Due to closure of inactivation gates of Na+
Relative refractory period:
is a period during which an action potential can be elicited only if a larger than usual stimulus is provided. Refractory period protects the cell from over-excitation. It allows a recovery period between the action potentials.
Spread of Depolarization
Opening of Na+ channels generates local current circuit that depolarizes adjacent membrane, opening more Na+ channels…
myelination signal transmission
schwann cells surround the nerve axon forming a myelin sheath Sheath is interrupted every 1-3 mm : node of Ranvier ( Na+/K+ channels)
Action potential occurs where?
AP only occur at the nodes (area rich in Na+/K+ channels) Increased velocity Energy conservation
Multiple Sclerosis. what is it?
MS is an immune-mediated inflammatory selective demyelination of CNS Multiple foci of CNS demyelination of white matter
multiple sclerosis- who does this occur to?
High incidence at higher latitude -About 1 person per 1000 in US is thought to have the disease - The female-to-male ratio is 2:1 - whites of northern European descent have the highest incidence
ms diagnosis/treatment
Dx: MRI Tx: IV steroids to relieve acute symptoms- curable now
ms symptoms
-Numbness, transient sensory deficit; pain -fatigue - H/O remission and relapses - Optic neuritis, hemiparesis, hemisesnory symptoms Bladder/Bowel incontinence Loss of memory, personality changes
MS- MRI symptom free? MRI while sick?
MRI symptom free or crisis looks the same it looks bad. MRI brain images of a patient with multiple sclerosis showing multiple, white matter plaques at the angle of lateral ventricle
MS-Anesthetic Considerations
Avoid elective surgery during relapse Any technique may worsen the symptoms Peripheral nerve blocks with cautions Avoid sux in paresis hyperkalemia Avoid increase in body temperature
Local Anesthetics names? moa? use?
Procaine, cocaine, lidocaine, bupivacaine M/A: Blocks voltage sensitive Na+ channels and inhibit conduction of impulses from periphery to CNS Use: minor surgical procedure, spinal anesthesia
local anesthetics and resting potential
Local anesthetics slow the rate of depolarization of the nerve action potential such that the threshold potential is not reached. As a result, an action potential cannot be propagated in the presence of local anesthetic and conduction blockade results.
No anesthetics and chloride ion channel crossing
binding of gaba causes the chloride ion channel to open, leading to hyper polarization of the cell.
chloride ion channel crossing in the presence of inhaled anesthetic
binding of gaba is enhanced by inhaled anesthetics, resulting in a greater entry of chloride ion. entry of Cl- hyper polarization cell, making it more difficult to depolarize, and therefore reduces neural excitability.
motor neuron action potential
- Motor neuron action potential 2. ca2+ enters voltage-gated channels. 3. acetylcholine releases from the presynaptic terminal 4. Na+ enters the post synaptic terminal 5. Local current between depolarized end plate and adjacent muscle plasma membrane. 6. Muscle fiber action potential initiation. 7. Propagated action potential in muscle plasma membrane 8. Acetylcholine degradation.
Nicotinic Receptor
2 ACh bind to the extracellular nicotinic receptor on the cellular membrane opening the channel and allowing potassium to leave and sodium to come into the cell
the motoneuron-vesicle formation Synaptic vesicles 3 things
- are formed from budding Golgi and are transported to the terminal by axoplasm “streaming” 2. Acetylcholine (Ach) is formed in the cytoplasm and is transported into the vesicles 3. Ach filled vesicles occasionally fuse with the post-synaptic membrane and release their contents. This causes end-plate potentials in the post-synaptic membrane.
The Motoneuron - Ach Release 3 things
AP begins in the ventral horn of spinal cord. Local depolarization opens voltage-gated Ca++ channels. An increase in cytosolic Ca++ triggers the fusion of synaptic vesicles with the pre-synaptic membrane and release of Ach (exocytosis).
Neuromuscular junction
Is the synapse between axons of motoneurons and skeletal muscle The NT released from presynaptic terminal is Ach, and the postsynaptic membrane is nicotinic receptor
what is the most important thing in excitation-contraction coupling
Ca++
first event at neuromuscular junction. synthesis and storage of Ach…
Synthesis and storage of Ach in the presynaptic terminal Acetyl CoA + Choline Acetyl Choline Catalyzed by Choline Acetyltransferase Ach stored in synaptic vesicles
2nd event at neuromuscular junction.
Depolarization of the presynaptic terminal opens Ca++ channels
third event at neuromuscular junction
Ca++ uptake causes release of Ach into synaptic cleft
4th event at neuromuscular junction
Diffusion of Ach to the postsynaptic membrane (muscle end plate) and binding Ach to nicotinic receptor The nicotinic receptor is also a Na+ and K+ ion channel Channels open up and increase Na+ and K+ conductance
5th event neuromuscular junction
Depolarization and AP in muscle end plate
6th event neuromuscular junction
Muscle contraction
7th event neuromuscular junction degradation of each…
Degradation of Ach Ach is degraded by acetyl cholinesterase (AchE) on the muscle end plate Choline is reuptake by presynaptic terminal for recycling AchE inhibitors (neostigmine) blocks the degradation and increases action of Ach Physostigmine is used to reverse neuromuscular blockade
8th event neuromuscular junction hypocalcemia vs hypercalcemia
Hypocalcemia decrease NT release; hypercalcemia increases NT release
9th event neuromuscular junction hypomagnesium vs. hypermagnesium
Hypomagnesemia increases NT release; hypermagnesemia decreases NT release ‘antagonistic actions’
Curare (arrow poison )
action: Competes with Ach for receptor on Motor end plate effect on NM transmission: Decrease EPP; paralysis of resp. muscles and death
Neostigmine
Action: Inhibit acetyl cholinesterase effect on NM transmission: Prolongs and enhance action of Ach at muscle end plate
Hemicholinium
action: Blocks re-uptake of choline into presynaptic terminal effect on NM transmission: Depletes Ach stores from presynaptic terminals
Aminoglycosides and Lambort Eaton syndrome (neomysine- side effect of the abx)
action: Antibodies block Ca++ channels effect NM transmission: No release of Ach
Black widow spider
action: Excessive release of Ach effect on NM transmission: convulsions.
MG
Myasthenia gravis“Grave muscle weakness”
MG mechanism of action
Antibodies to Ach receptors Reduce number of Ach receptors (Ach cannot attach leading to no muscle contraction) Double vision, difficulty in swallowing and speaking, skeletal muscle weakness and fatigue
MG improvement
I/V edrophonium; a short acting cholinesterase inhibitor, causes a temporary improvement
MG symptoms
Double vision, difficulty in swallowing and speaking, skeletal muscle weakness and fatigue
Lambert-Eaton myasthenic disease:
Antibodies against calcium channels markedly reduce release of Ach. Associated with underlying malignancy, such as small cell lung cancer Repetitive nerve stimulation demonstrate an increase in the motor action potential (contrasted with the decrease response in patient with true myasthenia gravis) Why?
MG- mechanism of action
Acetylcholine released at the nerve ending by the nerve impulse normally binds with acetylcholine receptors. This evokes the action potential in the muscle. In myasthenia gravis, antiacetylcholine receptor antibody binds to the acetylcholine receptor and inhibits the action of acetylcholine. Bound antibody evokes immune-mediated destruction of the end plate
Posterior Horn
Receives Sensory information
Anterior Horn
contains motor neuron that supply axial muscles
Excitatory postsynaptic potentials (EPSP)
Depolarize the postsynaptic cell Opening of Na+channels
Inhibitory postsynaptic potentials (IPSP)
Hyperpolarize the postsynaptic cell Opening of K+ or Cl- channels
Excitatory postsynaptic potentials (EPSP) examples
Include Ach, norepinephrine, epinephrine, dopamine, glutamate and serotonin
Inhibitory postsynaptic potentials (IPSP)
Include - amino butyric acid (GABA)& glycine
Facilitation, augmentation and post-tetanic potentiation
Occurs after tetanic stimulation Due to accumulation of Ca++
norepinephrine Metabliolized by?
metabolized by MAO &COMT
Small Molecule, Rapidly acting Transmitters
Ach, Norepi, Epi, Dopamine, Serotonin, Histamine, GABA, Glycine, Glutamate, Aspartate, Nitric oxide (NO)
Neuropeptides, slowly acting Transmitters
Hypothalamic hormones, Pituitary hormones, Peptides (Substance P, gastrin, insulin, glucagon) Angiotensin II , Bradykinin
NE
increase In anxiety; Decrease in depression
Dopamine
increase in schizophrenia decrease in parkinson’s and depression
Serotonin 5 hydroxytryplamine
decrease in anxiety and depression
Ach
decrease in alzheimers, huntington’s, REM sleep
GABA
decrease in anxiety huntingtons
MAGNESIUM SLIDE 22
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Mechanoreceptor
Pacinian corpuscles Joint receptors Stretch receptors in muscle Hair cells in auditory and vestibular system
Photoreceptor
Rods and cones of retina
Chemoreceptor
Olfactory receptors Taste receptors Osmoreceptors Carotid body O2 receptors
Extreme of temperature and pain
Nocireceptors
A-alpha
Large alpha motor neuron
a beta
touch pressure
a gamma
motor neuron to muscle spindle
a delta
touch pressure temp pain MOST SENSITIVE TO LA
b
preganglionic autonomic fibers
C
slow pain temp unmyelinated resistant to LA
Slowly adapting or tonic receptors
(muscle spindle; pressure; slow pain) - respond repetitively to a prolonged stimulus
Rapidly adapting receptor
(Pacinian corpuscle ; light touch)- show a decline in AP frequency with time in response to constant stimulus
Limbic System
Structures located on the medial aspects of cerebral hemispheres and diencephalon Includes the rhinencephalon, amygdala, hypothalamus, and anterior nucleus of the thalamus Parts especially important in emotions: Amygdala – deals with anger, danger, and fear responses Cingulate gyrus – plays a role in expressing emotions via gestures, and resolves mental conflict Puts emotional responses to odors – e.g., skunks smell bad Responsible for ‘F’ activities : Feeding, Fleeing, Fighting, Feeling and sex
Reticular Activating System (RAS)
Dorsal column tract is a ‘direct’ rout whereas RAS is an indirect route for sensory information reaching to sensory strip Maintains alert/awake state RAS is OFF when sleeping Complete loss of RAS activity is coma GA produces sedation and hypnosis by depressing RAS
Thalamus
Thalamus has some ability to discriminate tactile sensation. Thalamus has an important role in the perception of pain and temperature. Information from different parts of the body is arranged somatotopically. Destruction of thalamic nuclei results in loss sensation on the contralateral side of the body
Hypothalamus
Located below the thalamus, it caps the brainstem and forms the inferolateral walls of the third ventricle Mammillary bodies Small, paired nuclei bulging anteriorly from the hypothalamus Relay station for olfactory pathways Infundibulum – stalk of the hypothalamus; connects to the pituitary gland Main visceral control center of the body
Headache
Non-neurological causes Sinus infection, glaucoma, oral infection, TMJ disease, cervical spine problems esp. C1 and C2 Potentially fatal causes Intracranial mass, subarachnoid hemorrhage “worst headache of my life” Migraine headache Aura in classical type Cluster headache Give 100% oxygen Tension headache Hangover irritation of the meninges by alcohol breakdown products and additives Eye strain Excessive contraction of ciliary muscles to focus
Raynaud’s disease
Recurrent vasospasm after cold exposure Triphasic color response “ white, blue, red” Commonly occur in young women
Raynaud’s phenomenon
Similar to Raynaud’s disease but is always secondary to an underlying disorder e.g. SLE Treatment: Sympathectomy
