Exam 2 Flashcards

1
Q

What is Ohm’s Law?

A

I = V/R or in words, current equals voltage (membrane potential) over resistance (cell membrane)

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2
Q

Describe how nicotinic ACh receptors work

A

2 ACh bind the nACh-R sites on a negatively charged ion pore in the cell membrane. Positive ions flow in (mostly Na+) and depolarize the cell. This initial current can then open adjacent VG fast Na channels.

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3
Q

Where are nicotinic ACh receptors found? What is significant about this site?

A

Mainly in the skeletal muscles at the neuromuscular junction (NMJ). This is where our paralytics work.

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4
Q

Describe how muscarinic ACh receptors work…

A

ACh released from the vagus nerve binds a mACh receptor site on a GPCR. This activates the alpha protein which goes on to open the coupled K channel. This allows more K+ to leave the cell hyperpolarizing the cell.

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5
Q

Where are muscarinic ACh receptors found?

A

mACh-R are found in the SA and AV node of the heart. The right vagus nerve sends ACh to the SA node and the left vagus nerve sends ACh to the AV node.

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6
Q

How does atropine work to increase our heart rates?

A

It blocks mACh-R and inhibits them, which increases our heart rate as ACh inhibits our pacemaker cells.

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7
Q

Describe how pressure sensors in the vascular system relay the message ^MAP to the CNS

A

Pressure sensors on our smooth muscle cells in the vascular system are compressed and Na leak channels on these cell walls widen. This allows more Na into the cell and can generate an action potential to the CNS for processing.

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8
Q

How is VG Na channel opening an example of positive feedback when generating an action potential?

A

An initial stimulus/action potential causes fast NA channels to open in a resting cell. Na enters the cell, this depolarization leads to activation of adjacent VG Na channels. The signal is propagated along the length of the cell and can be bidirectional allowing for faster conduction of the signal.

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9
Q

What three things would decrease the rate of action potential propagation? (What about increase?)

A
  1. Narrow neuron (wide)
  2. Longer neuron (short)
  3. Less insulation or myelin (more myelination)
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10
Q

What’s the precursor to myelin again? Where is it found?

A

Sphingomyelin, in the cell wall

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11
Q

How does myelin insulate the neuron?

A

It wraps around the neuron and squeezes all the water out between layers. All lipid, makes an excellent insulator.

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12
Q

Where are most of the fast Na channels found in the myelinated neuron?

A

At the nodes of ranvier

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13
Q

How does saltatory conduction work?

A

The action potential spreads from one node to the next via myelin, which prevents leakage of the Na as it “covers up” Na/K ATPase pumps. This helps propagate action potentials really quickly.

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14
Q

What makes myelin? In the CNS? The PNS?

A

Glial cells. In the CNS oligodendrocytes specifically and schwann cells in the peripheral nervous system.

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15
Q

Which cells can generate more myelin in adults?

A

Schwann cells in the PNS. Oligodendrocytes are not good at doing this in adulthood!

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16
Q

How do diseases like Guillain Barre and Multiple Sclerosis lead to paralysis?

A

These are demyelinating diseases. There is a progressive loss of myelin from the neurons. This “uncovers” the Na/K pumps and lots of Na gets pumped out. The action potential will not be able to propagate to the next node.

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17
Q

What are connexins, where are they located.

A

These are proteins that form a tube with 6 connexins. They form at gap junctions and create a conduit between cells for Na current to flow through. This allows for rapid conduction of a signal.

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18
Q

Where is ACh excitatory and where is ACh inhibitory?

A

It is excitatory at skeletal muscle cells and inhibitory at pacemaker cells in the heart.

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19
Q

How does calcium impact membrane potential?

A

Ca is larger and positively charged and hangs out near sodium leak channels. It gets “in the way” and inhibits Na leakiness, which makes the inside of the cell more negative (decreases excitability).

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20
Q

What effect does hypocalcemia have on the ICF?

A

Low serum calcium makes the inside of the cell more positive as there is less to block Na leak channels and more Na gets into the cells.

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21
Q

Why would we give calcium to someone with hyperkalemia?

A

With hyperkalemia, less K wants to leave the cell (lower concentration gradient). By adding more Ca one could block more Na leak channels, lowering the membrane potential, which would “hold on to” k more

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22
Q

Describe how hypocalcemia leads to Trousseau’s tetany

A

Less calcium means more Na can “leak” into the cell, which increases the membrane potential, making the cell more excitable. This causes overactivity of the motor neuron which leads to increased contraction of the skeletal muscles

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23
Q

What are the three classes of neurons and what’s special about them?

A

A neurons are myelinated. B, lightly myelinated and C non-myelinated neurons.

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24
Q

What does a inhibitory post-synaptic potential do?

A

It makes the membrane potential more negative than normal.

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25
Q

What does an excitatory post-synaptic potential do?

A

It makes the membrane potential more positive than normal.

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26
Q

What occurs at the axon hillock?

A

There are four inhibitory connections here. Usually these are GABA receptors that increase Chloride permeability.

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27
Q

How does alcohol withdrawal lead to seizures?

A

Alcohol is a GABA1 agonist and therefore inhibits the neurons so the body doesn’t need to make as much of it’s own GABA. If one stops drinking the GABA receptors are no longer inhibited and there is not enough endogenous GABA left and the nervous system is overexcited

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28
Q

Where are Astrocytes located and what are they good at?

A

They are wrapped around capillaries in the NS to help maintain the BBB and are good at maintaining an electrolyte balance in the CNS

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29
Q

What are ependymal cells?

A

These are concentrated in the 3rd and 4th ventricles and form the choroid plexus which produces CSF.

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30
Q

What do Oligodendrocytes do?

A

They make myelin in the CNS

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31
Q

What do Schwann cells do?

A

They form myelin in the PNS

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32
Q

What are microglia responsible for?

A

Cleaning up debris, they are macrophages.

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33
Q

What are multipolar neurons and give an example

A

These are the “decision makers” an example are motor neurons

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34
Q

What are pseudounipolar neurons

A

These are typically found near the spinal cord. They are good at sensing.

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35
Q

What are bipolar neurons?

A

These are neurons that can send bidirectional messages. They are in the retina and optic nerve and are primarily for sensing

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36
Q

An example of nociceptors? Two examples of pressure receptors or “bend” receptors?

A

Free nerve endings (pain)
Pacinian corpuscle (pressure)
Meissner’s corpuscle (pressure)

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37
Q

What are some examples of stretch/pressure sensing receptors?

A

Golgi tendon apparatus
muscle spindles

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38
Q

How do pressure receptors sense?

A

They respond to pressure changes with edema caused by sodium shifts (which is followed by water)

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39
Q

How do nociceptors undergo adaptation?

A

They go through reverse adaptation. They become sensitized each time there is a pain response

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40
Q

Which sensory receptors undergo fast adaptation?

A

All of them, except free nerve endings

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41
Q

What does the sagittal plane bisect?

A

Left from right

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42
Q

What does the coronal plane bisect?

A

anterior from posterior

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43
Q

what does the horizontal plane bisect?

A

superior from inferior

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44
Q

What structures are in the telencephalon?

A

The outer portion of the brain, cerebral cortex and basal ganglia

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45
Q

What structures are in the diencephalon?

A

inner part of the brain (thalamus, hypothalamus) and 3rd ventricle

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46
Q

What structures are in the mesencephalon?

A

Midbrain

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47
Q

What part of the brain is responsible for speech?

A

Broca’s area

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48
Q

Which part of the brain is responsible for language comprehension?

A

Wernicke’s area

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49
Q

where is the somatosensory cortex?

A

in the anterior part of the parietal lobe

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50
Q

Where is the primary motor cortex?

A

in the posterior part of the frontal lobe

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51
Q

What makes up the white matter?

A

usually axons, myelinated axons, does the sending and receiving of messages

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52
Q

What is in the grey matter?

A

Cell bodies, axons, and dendrites. Is the decision-making center

53
Q

What is the lamina X, and the anterior white commissure?

A

The lamina ten is the grey matter area that connects the left and right sides of the cord, the AWC is the area of white matter right in front of lamina X where crossover in the spinal cord happens.

54
Q

Which areas of the spine have lordotic curvature

A

cervical spine and lumbar spine

55
Q

Which areas of the spine kyphotic?

A

thoracic spine and the sacral spine

56
Q

What is the clinical significance of fats in the epidural space?

A

Lipophilic pain medicine can get taken up by the adipose tissue and should last awhile

57
Q

Where does the spinal cord terminate in the spinal column?

A

The conus medullaris at L1 in adults and L3 in newborns

58
Q

What anchors the cord in place in the dural sac?

A

The filum terminale ligament

59
Q

When doing a lumbar puncture where is the CSF coming from?

A

The lumbar cistern which extends all the way to S2

60
Q

What considerations do we need to take into account when sampling CSF from lower down in the lumbar region?

A

CSF gets turned over three times per day, but the choroid plexus is in the spinal cord, after the cord terminates, less of that CSF gets “turned over” and could be a bit more “stale”

61
Q

there are two enlargements in the spinal cord, where are they?

A

The cervical enlargement: C3-C6 and the lumbar enlargement T11-L1

62
Q

What is the significance of these two spinal enlargements?

A

The cervical enlargement is due to innervations r/t the upper limbs. The lumbar enlargement is due to all the motor and sensory innervations of the lower limbs.

63
Q

Where does the cervical enlargement feed into? The lumbar enlargement?

A

The brachial plexus. The lumbar plexus and the sciatic nerve.

64
Q

Why do we want to take a slightly off midline approach (15 degree angle) when doing a lumbar puncture or block?

A

Many people have incomplete fusion of the ligamentum flava. If you take a midline approach you may not find the resistance you are looking for from ligaments and accidentally go too deep damaging the cord/nerve roots.

65
Q

where do the spinal nerves and arteries live?

A

in the transverse foramen

66
Q

How many vertebrae are there in each section of the spine? Nerves?

A

Cervical: 7 and 8
Thoracic: 12
Lumbar: 5
Sacral: 5
Coccygeal: 2 and 1

67
Q

What is unique about the cervical vertebrae?

A

These have wide foramen, smaller bodies, and bifid processes (C2-C5 bifid) C6 is bifid 50% of the time and C7 rarely bifid. They also have transverse processes with sulci for spinal nerves.

68
Q

What is the name of the vertebrae connecting the skull to the spine and what is special about it?

A

Atlas (C1). It does not have a vertebral body. It has both a posterior and anterior arch and tubercle. The anterior arch houses a facet and the dens from C2. No spinous process. It has superior articular facets for the base (occipital condyles) of the skull to rest.

69
Q

What is unique about the Axis (C2)

A

It has a dens, or a spinous process that projects upwards and articulates with the atlas. There is an anterior articular facet on it which allows us to turn our heads from side to side (swivel motion).

70
Q

Which ligaments hold the vertebrae together?

A

interspinous ligaments

71
Q

What is special about the ligamentum flava?

A

It connects the anterior vertebral arches together and has more collagen, so it is more stretchy.

72
Q

What is the bump at the lower back of the skull called and what attaches to it?

A

The External occipital protuberance. The nuchal ligaments attach to it.

73
Q

What is the small bump you can palpate at the back of the neck?

A

Vertebral prominance (C7 according to textbooks T1 according to Schmidt)

74
Q

How many ribs do we have? How many are true ribs? False ribs?

A

12 total ribs. Ribs 1-7 are “true ribs” they connect to costal cartilage. Ribs 8,9,10 “false ribs” connect to the costal cartilage of rib 7. Ribs 11 and 12 are “floaters” not cartilaginous connections.

75
Q

What’s unique about thoracic vertebrae?

A

These vertebrae articulate with our ribs at two spots the superior costal facet and the costal facet of the transverse process. The spinous process is also very slanted.

76
Q

What’s unique about the vertebral bodies of the thoracic vertebrae?

A

The L side of the vertebral body is straighter and flatter for the aorta and the R side is more rounded.

77
Q

What’s unique about the lumbar region of the spine?

A

Large vertebral bodies. Larger intervertebral foramen (good for access).

78
Q

What is unique about the sacrum?

A

There is a promontory and base where it meets the lumbar spine. There are transverse lines and sacral crests where it has fused as adults. There is a sacral canal and hiatus where the cauda equina resides and the filum terminale terminates at the coccyx.

79
Q

What are the two little indents at the small of the back? What is clinically relevant about these?

A

Posterior iliac spines. If you go down 1 cm and inward 1 cm from them you can access the posterior sacral foramen of S2. Useful for blocks as you can aim for this location with a perpendicular angle.

80
Q

What two bones does the inguinal ligament connect?

A

The iliac spine to the pubic tubercle.

81
Q

what are the two components of the intervertebral disks?

A
  1. Anulus fibrosus
  2. Nucleus pulposus
82
Q

Why do we see more wear and tear on the posterior part of the spine?

A

The anterior portion of the anulus fibrosus is cross-hatched (much stronger) the posterior portion is not. This is why when we see herniated discs, we tend to see the nucleus pulposus leak into the spinal canal, where is presses on our spinal nerves.

83
Q

What do the arachnoid trabeculae do?

A

These maintain the structural integrity of the space between the arachnoid mater and the pia mater. It ensures that there is enough room for CSF and blood vessels.

84
Q

What controls CSF composition?

A

the astrocytes

85
Q

What is unique about the composition of CSF compared to blood?

A

pH: 7.31 (more acidic d/t less bicarb and more CO2)
Cl: is higher (matches Na levels ~140mEq)
K: is about 40% lower
Mg: higher
glucose: 60 mg/dL

86
Q

What is significant about more Cl, Mg and less K?

A

These all increase the “brakes” on cell excitability.

87
Q

What is the normal volume of CSF? How much do we make per day?

A

150 mL of CSF is contained in the ventricular system. We make 500mL per day, so the CSF gets “changed out” 3x per day.

88
Q

How would we slow down CSF production?

A

via suppression of Na/K ATPase pumps

89
Q

What cells are responsible for making CSF in the choroid plexus?

A

The ependymal cells.

90
Q

What do the arachnoid granulations (arachnoid villi) do and where are they?

A

They are above the cranial meninges and just inferior to the superior sagittal sinus. These are pressure “blow off” valves to help maintain stable ICP.

91
Q

Describe the movement of CSF through the ventricular system…

A

CSF can go from R to L lateral ventricles and to the 3rd ventricle via the intraventricular foramen (or foramen of Monro). From the 3rd ventricle to the 4th ventricle via the cerebral aqueduct (or foramen of Sylvius)

92
Q

How does CSF get to the cerebellum? And the spinal cord?

A

The central canal to the spinal cord. The median aperture (foramen of Magendie) to the cerebellum.

93
Q

What is hydrocephalus? What is the difference between communicating and noncommunicating hydrocephalus?

A

Hydrocephalus is the build up of CSF in the brain. Communicating is where CSF can freely flow throughout the ventricular system but is overproduced or cannot exit the bloodstream. Non-communicating (obstructive) is when there is a blockage in one of these foramens or aqueducts. The later can cause ventricular enlargement.

94
Q

What is the falx cerebri and where does it partition the brain? How about the tentorium cerebrii?

A

Its connective tissue between the superior sagittal sinus and the inferior sagittal sinus that separates the R from the L hemisphere. T.C. goes to the back of the brain and provides a shelf for the occipital lobe and overlies the cerebellum

95
Q

Name the 7 venous sinuses of the brain we need to know?

A
  1. superior sagittal sinus
  2. inferior sagittal sinus
  3. straight sinus
  4. sinus confluence
  5. transverse sinus
  6. sigmoid sinus
  7. cavernous sinus
96
Q

What major arteries make up the circle of willis?

A
  1. Anterior communicating
  2. Anterior cerebral
  3. Middle cerebral (from the internal carotid arteries)
  4. Posterior cerebral
  5. Posterior communicating
  6. Basilar (from the vertebral arteries)
97
Q

Name the 3 sets of cerebellar arteries

A
  1. Superior cerebellar arteries (from basilar art.)
  2. Anterior inferior cerebellar arteries (from basilar artery)
  3. Posterior inferior cerebellar arteries (from vertebral arteries)
98
Q

Which 3 arteries supply the superficial portion of the cerebrum?

A
  1. Anterior cerebral arteries
  2. Middle cerebral arteries
  3. Posterior cerebral arteries
99
Q

Where and how are epidural hematomas formed?

A

Above the dura beneath the skull. Usually due to a skull fracture (trauma) and are fast arterial bleeds.

100
Q

Where and how are subdural hematomas formed?

A

These are usually venous bleeds in the superior sagittal sinus caused by a rip in the dura from impact injuries. These are slower to develop.

101
Q

Where and what causes subarachnoid hemorrhages?

A

These are arterial bleeds in the arachnoid space usually caused by ruptured aneurysms. These are especially bad because the blood irritates the neurons and glial cells (there is no dura layer or arachnoid layer to protect the brain from the blood)

102
Q

What are two ways motor neurons can be stimulated?

A
  1. via the descending pathways
  2. via a reflex arc
103
Q

How do action potentials traverse across thick muscle fibers?

A

via transverse tubules

104
Q

What breaks down ACh at the NMJ?

A

acetylcholinesterase breaks down ACh via hydrolysis into choline and acetate

105
Q

How many ACh-R are at each NMJ? How many get opened? How much ACh does each neuron release into the synaptic cleft?

A

5 million ACh-R at each NMJ. 500,000 are opened (about 10%). 2 million ACh Nt’s get released at each synaptic cleft.

106
Q

Describe skeletal muscle calcium signaling…

A

An action potential travels down a T tubule. This depolarization stimulates voltage sensors (DHP receptors) lining the T tubule. These can open Ca release channels on the sarcoplasmic reticulum via a tether and Ca gets released into the skeletal muscle.

107
Q

Why not have Ca channels lining the T tubule instead?

A

This would allow extracellular Ca in. The concentration gradient is so large that WAY too much ca would flood the muscle, which is why we use ca from the sarcoplasmic reticulum.

108
Q

What are SERCA pumps?

A

Sarcoplasmic Endoplasmic Reticulum Calcium ATP pumps. These help pump Ca from the muscle back into the sarcoplasmic reticulum.

109
Q

What two disease processes are the result of things “going wrong” at the NMJ?

A
  1. Myasthenia gravis
  2. LEMS (Lambert-Eaton Myasthenic syndrome)
110
Q

What causes myasthenia gravis?

A

Antibodies generated to ACh-R that bind to and block these receptors. Over time the immune system attacks and destroys these receptors. Scar tissue formed from the immune response causes flattened infoldings of the muscle cells and leave less surface area for receptors to respond to ACh. This is progressive and gets worse throughout the day.

111
Q

What are three treatments we talked about for MG?

A
  1. Remove the thymus gland
  2. Plasmaphoresis
  3. drugs ending in -stigmine (AChesterase inhibitors)
112
Q

What causes LEMS?

A

This is a paraneoplastic syndrome (develops in conjunction with a cancer). The body develops antibodies to P type Ca channels. This results in a Ca deficiency.

113
Q

In class, we talked about drugs that target VG K channels as a treatment for LEMS, describe how these work? Why are they so dangerous?

A

Drugs that target closing VG K channels results in sustained depolarization. This allows more time for Ca to get into the cell. These are very dangerous and should only be used as a last resort because they are cardiotoxic.

114
Q

What are two substances the mitochondria can make of use to the motor neuron?

A
  1. acetate (for ACh synthesis)
  2. ATP
115
Q

How does the body recycle choline?

A
  1. Via a choline ATPase pump
  2. Secondary active cotransport coupling choline to Na
116
Q

Where can we store choline?

A

In the cell wall as phosphatidylcholine

117
Q

Give an example of a disease that impacts muscle function by acting post-synaptically? How about a pre-synaptic disease?

A

Myasthenia gravis (post-synaptic). LEMS/ELMS (pre-synaptic).

118
Q

How much blood flow does the brain get per minute? How much per 100g of tissue?

A

750 mL. 50mL/min per 100g of tissue.

119
Q

How much blood goes to the white matter? To the grey matter?

A

80% to the grey matter and 20% to the white matter

120
Q

What percent of the blood of the total CO goes to the brain?

A

15%

121
Q

What are the 4 major arteries that supply the cerebral arteries?

A

R and L vertebral arteries and the R and L internal carotid arteries

122
Q

What are the two types of paralytics we discussed in class?

A

Non-depolarizing ACh antagonists and depolarizing ACh agonists (succinylcholine)

123
Q

How does Succinylcholine work?

A

It is made up of two ACh molecules that are bound together (this cannot be broken down by AChesterase). They bind to the nACh-R and hold it open. This depolarizes the cell and lasts about 10 minutes.

124
Q

What does the influx of Na through the nACh-R do to the fast Na channels?

A

This depolarization, keeps the fast Na channels from resetting. The inactivation gate stays shut. This keeps that area of the cell depolarized for an even longer period of time

125
Q

How does succinylcholine cause hyperkalemia and how much could we expect to see K+ levels rise in the blood?

A

The muscle cell at the NMJ stays depolarized for a longer period of time. Thus the membrane potential becomes more positive pushing K+ out of the cell. This can lead to an increase in plasm K+ levels up to 0.5mOsm/L

126
Q

The hyperkalemia caused by succinylcholine is considered minor in a normal healthy human being. In what scenario can Succ’s cause pathologic hyperkalemia and elaborate why?

A

In paralyzed patients or stroke patients (also with hemiparesis). These patients tend to have more nACh-R throughout their bodies as a result of muscular atrophy. The effects of Succ’s is therefore much greater in these patients and can cause even higher levels of plasma potassium levels.

127
Q

Give an example of a nACh-R antagonist? An agonist?

A

Antagonist: Curare
Agonist: Succinylcholine

128
Q

Which foramina allows for CSF to pass directly from the ventricular system into the subarachnoid space?

A

The foramen of Luschka and the foramen of Magendie.