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Spring '20/ L. A&P > Spinal Nerves, Membrane Potentials and Action Potentials > Flashcards

Spinal Nerves, Membrane Potentials and Action Potentials Flashcards

1
Q

Spinal Nerves- how many? where do they come from?

A

Thirty-one pairs of mixed nerves arise from the spinal cord and supply all parts of the body except the head

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2
Q

cervical nerves

A

8 cervical (C1-C8)

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3
Q

thoracic nerves

A

12 thoracic (T1-T12) intercostal nerves lumbar enlargement

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4
Q

lumbar nerves

A

5 Lumbar (L1-L5)

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5
Q

sacral nerves

A

5 Sacral (S1-S5)

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6
Q

coccygeal

A

1 Coccygeal (C0)

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7
Q

Brachial Plexus

A

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

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8
Q

There are four major branches of the brachial plexus

A

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

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9
Q

nerve plexuses…where are they found?

A

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

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10
Q

what happens to damage to one spinal segment?

A

Damage to one spinal segment cannot completely paralyze a muscle

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11
Q

Brachial plexus

A

Second most common postop peripheral neuropathy

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12
Q

Axillary

A

– innervates the deltoid and teres minor

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13
Q

Musculocutaneous

A

sends fibers to coracobrachialis, biceps brachii and brachialis. Flexion at elbow

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14
Q

Median

A

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

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15
Q

Ulnar

A

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**

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16
Q

Radial

A

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**

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17
Q

Intercostobrachial nerve

A

Can be blocked to reduce pain from tourniquet inflation during IV regional neural anesthesia

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18
Q

neuron

A

Basic building block of CNS ~ 100 billions Integration and transmission of nerve impulses

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19
Q

Schwann cells

A

produce myelin sheath which wraps around axon, provides insulation

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20
Q

Node of Ranvier

A

gaps in myelin sheath

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21
Q

Saltatory conduction:

A

Node to node jumping of depolarization.

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22
Q

where are neurotransmitters synthesized.

A

Neurotransmitters are synthesized in cell body and transported to synaptic knobs All or none law

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23
Q

Multiple Sclerosis

A

Demyelination results slow or blocked conduction

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24
Q

Bipolar Neuron

A

has short axon process from arising from one side of the cell body, and a short dendritic process arising from the opposite side

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25
Q

Special senses neurons

A

Bipolar neurons- those found in the eyes, ears, and nose are bipolar neurons

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26
Q

Unipolar Neuron:

A

has single large extension from its cell body. They are found in lower invertebrate ,never in humans.

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27
Q

Pseudounipolar neuron:

A

Present in dorsal root ganglia

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28
Q

Multipolar Neuron:

A

comprise one axon and multiple dendritic process. They are the MOST COMMON type in brain and spinal cord.

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29
Q

dorsal root ganglia

A

Drg cell body lies

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30
Q

Depolarization

A

Makes the cell membrane potential less negative due to movement of positively charged sodium ions (Na+) into the cell.  excitability

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31
Q

Repolarization

A

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.

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32
Q

Hyperpolarization

A

Makes the membrane potential more negative due to movement of negatively charged chloride ions (Cl-) into the cell.  excitability

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33
Q

Inward current

A

Is the flow of positive charge into the cell. Inward current depolarizes the membrane potential.

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34
Q

Outward current

A

Is the flow of positive charge out of the cell. Outward current hyperpolarizes the membrane potential.

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35
Q

Action potential

A

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

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36
Q

Threshold

A

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)

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37
Q

Resting membrane potential

A

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)

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38
Q

Action Potential “Nerve Impulse”

A

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.

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39
Q

Upstroke of the Action potential (depolarization)

A

Inward Na+ movement Lidocaine block these voltage sensitive Na+ channels and abolish action potential

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40
Q

Downstroke of the Action potential (repolarization)

A

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.

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41
Q

Properties of AP Speed? other properties?

A

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

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42
Q

Refractory periods

A

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+

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43
Q

Relative refractory period:

A

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.

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44
Q

Spread of Depolarization

A

Opening of Na+ channels generates local current circuit that depolarizes adjacent membrane, opening more Na+ channels…

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45
Q

myelination signal transmission

A

schwann cells surround the nerve axon forming a myelin sheath Sheath is interrupted every 1-3 mm : node of Ranvier ( Na+/K+ channels)

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46
Q

Action potential occurs where?

A

AP only occur at the nodes (area rich in Na+/K+ channels) Increased velocity Energy conservation

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47
Q

Multiple Sclerosis. what is it?

A

MS is an immune-mediated inflammatory selective demyelination of CNS Multiple foci of CNS demyelination of white matter

48
Q

multiple sclerosis- who does this occur to?

A

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

49
Q

ms diagnosis/treatment

A

Dx: MRI Tx: IV steroids to relieve acute symptoms- curable now

50
Q

ms symptoms

A

-Numbness, transient sensory deficit; pain -fatigue - H/O remission and relapses - Optic neuritis, hemiparesis, hemisesnory symptoms Bladder/Bowel incontinence Loss of memory, personality changes

51
Q

MS- MRI symptom free? MRI while sick?

A

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

52
Q

MS-Anesthetic Considerations

A

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

53
Q

Local Anesthetics names? moa? use?

A

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

54
Q

local anesthetics and resting potential

A

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.

55
Q

No anesthetics and chloride ion channel crossing

A

binding of gaba causes the chloride ion channel to open, leading to hyper polarization of the cell.

56
Q

chloride ion channel crossing in the presence of inhaled anesthetic

A

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.

57
Q

motor neuron action potential

A
  1. 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.
58
Q

Nicotinic Receptor

A

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

59
Q

the motoneuron-vesicle formation Synaptic vesicles 3 things

A
  1. 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.
60
Q

The Motoneuron - Ach Release 3 things

A

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).

61
Q

Neuromuscular junction

A

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

62
Q

what is the most important thing in excitation-contraction coupling

A

Ca++

63
Q

first event at neuromuscular junction. synthesis and storage of Ach…

A

Synthesis and storage of Ach in the presynaptic terminal Acetyl CoA + Choline  Acetyl Choline Catalyzed by Choline Acetyltransferase Ach stored in synaptic vesicles

64
Q

2nd event at neuromuscular junction.

A

Depolarization of the presynaptic terminal opens Ca++ channels

65
Q

third event at neuromuscular junction

A

Ca++ uptake causes release of Ach into synaptic cleft

66
Q

4th event at neuromuscular junction

A

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

67
Q

5th event neuromuscular junction

A

Depolarization and AP in muscle end plate

68
Q

6th event neuromuscular junction

A

Muscle contraction

69
Q

7th event neuromuscular junction degradation of each…

A

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

70
Q

8th event neuromuscular junction hypocalcemia vs hypercalcemia

A

Hypocalcemia decrease NT release; hypercalcemia increases NT release

71
Q

9th event neuromuscular junction hypomagnesium vs. hypermagnesium

A

Hypomagnesemia increases NT release; hypermagnesemia decreases NT release ‘antagonistic actions’

72
Q

Curare (arrow poison )

A

action: Competes with Ach for receptor on Motor end plate effect on NM transmission: Decrease EPP; paralysis of resp. muscles and death

73
Q

Neostigmine

A

Action: Inhibit acetyl cholinesterase effect on NM transmission: Prolongs and enhance action of Ach at muscle end plate

74
Q

Hemicholinium

A

action: Blocks re-uptake of choline into presynaptic terminal effect on NM transmission: Depletes Ach stores from presynaptic terminals

75
Q

Aminoglycosides and Lambort Eaton syndrome (neomysine- side effect of the abx)

A

action: Antibodies block Ca++ channels effect NM transmission: No release of Ach

76
Q

Black widow spider

A

action: Excessive release of Ach effect on NM transmission: convulsions.

77
Q

MG

A

Myasthenia gravis“Grave muscle weakness”

78
Q

MG mechanism of action

A

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

79
Q

MG improvement

A

I/V edrophonium; a short acting cholinesterase inhibitor, causes a temporary improvement

80
Q

MG symptoms

A

Double vision, difficulty in swallowing and speaking, skeletal muscle weakness and fatigue

81
Q

Lambert-Eaton myasthenic disease:

A

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?

82
Q

MG- mechanism of action

A

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

83
Q

Posterior Horn

A

Receives Sensory information

84
Q

Anterior Horn

A

contains motor neuron that supply axial muscles

85
Q

Excitatory postsynaptic potentials (EPSP)

A

Depolarize the postsynaptic cell Opening of Na+channels

86
Q

Inhibitory postsynaptic potentials (IPSP)

A

Hyperpolarize the postsynaptic cell Opening of K+ or Cl- channels

87
Q

Excitatory postsynaptic potentials (EPSP) examples

A

Include Ach, norepinephrine, epinephrine, dopamine, glutamate and serotonin

88
Q

Inhibitory postsynaptic potentials (IPSP)

A

Include  - amino butyric acid (GABA)& glycine

89
Q

Facilitation, augmentation and post-tetanic potentiation

A

Occurs after tetanic stimulation Due to accumulation of Ca++

90
Q

norepinephrine Metabliolized by?

A

metabolized by MAO &COMT

91
Q

Small Molecule, Rapidly acting Transmitters

A

Ach, Norepi, Epi, Dopamine, Serotonin, Histamine, GABA, Glycine, Glutamate, Aspartate, Nitric oxide (NO)

92
Q

Neuropeptides, slowly acting Transmitters

A

Hypothalamic hormones, Pituitary hormones, Peptides (Substance P, gastrin, insulin, glucagon) Angiotensin II , Bradykinin

93
Q

NE

A

increase In anxiety; Decrease in depression

94
Q

Dopamine

A

increase in schizophrenia decrease in parkinson’s and depression

95
Q

Serotonin 5 hydroxytryplamine

A

decrease in anxiety and depression

96
Q

Ach

A

decrease in alzheimers, huntington’s, REM sleep

97
Q

GABA

A

decrease in anxiety huntingtons

98
Q

MAGNESIUM SLIDE 22

A

….

99
Q

Mechanoreceptor

A

Pacinian corpuscles Joint receptors Stretch receptors in muscle Hair cells in auditory and vestibular system

100
Q

Photoreceptor

A

Rods and cones of retina

101
Q

Chemoreceptor

A

Olfactory receptors Taste receptors Osmoreceptors Carotid body O2 receptors

102
Q

Extreme of temperature and pain

A

Nocireceptors

103
Q

A-alpha

A

Large alpha motor neuron

104
Q

a beta

A

touch pressure

105
Q

a gamma

A

motor neuron to muscle spindle

106
Q

a delta

A

touch pressure temp pain MOST SENSITIVE TO LA

107
Q

b

A

preganglionic autonomic fibers

108
Q

C

A

slow pain temp unmyelinated resistant to LA

109
Q

Slowly adapting or tonic receptors

A

(muscle spindle; pressure; slow pain) - respond repetitively to a prolonged stimulus

110
Q

Rapidly adapting receptor

A

(Pacinian corpuscle ; light touch)- show a decline in AP frequency with time in response to constant stimulus

111
Q

Limbic System

A

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

112
Q

Reticular Activating System (RAS)

A

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

113
Q

Thalamus

A

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

114
Q

Hypothalamus

A

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

115
Q

Headache

A

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

116
Q

Raynaud’s disease

A

Recurrent vasospasm after cold exposure Triphasic color response “ white, blue, red” Commonly occur in young women

117
Q

Raynaud’s phenomenon

A

Similar to Raynaud’s disease but is always secondary to an underlying disorder e.g. SLE Treatment: Sympathectomy

Spring '20/ L. A&P (21 decks)

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