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Ana/Phys/Patho I > Unit 2 + Unit 3: spinal anatomy > Flashcards

Unit 2 + Unit 3: spinal anatomy Flashcards

1
Q

what other ion channel is similar in structure to a VG Na+ channel?

A

VG Ca2+ channel
also termed SLOW calcium channels

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2
Q

slow VG Ca2+ channels are blocked by:

A

dihydropyridine calcium channel antagnoists

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3
Q

Cl- permeability is adjusted to _____ or _____ electrical activity in excitable cells

A

hyperpolarize; suppress

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4
Q

these receptors typically open up Cl- channels in neurons

A

GABA receptors

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5
Q

Cl- influx typically makes the cell membrane more ____ and more ____ to excite

A

negative; difficult

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6
Q

permeability of Na+ _____ via opening of membrane Na+ channels; membrane potential becomes closer to nernst for Na+ during ______

A

increases; depolarization

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7
Q

why would a 2-way signaling process for depolarization along a cell be considered beneficial

A

if the AP can move in both directions, there would be a shorter time required to excite a cell

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8
Q

how is propogation of an AP in a VG Na+ channel considered a positive feedback loop?

A

the initial stimulus causes Na+ to come in, which then activates fast Na+ channels to allow more Na+ to come in until repolarization initiates

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9
Q

how does the motor neuron communicate with skeletal muscle if there is a “gap” between the two structures?

A

neurotransmitters

the gap is termed the neuromuscular junction (NMJ)

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10
Q

nicotinic-ACh receptor

A

found on skeletal muscles
(also on brain; think nicotine)

receptor has 2 binding sites

NT: ACh released from motor neurons and 1 receptor needs 2 ACh to bind

the inside of the receptor is negatively charged but the channel is specific for positively charged ions

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11
Q

which type of ions can pass through the nicotinic-ACh receptor?

A

the majority of the current is Na+ current; this means there is more Na+ influxing vs K+ effluxing (and Ca2+ influxing)

Ca2+ can also influx and depolarize the cell, but the majority of the influx is Na+

Ca2+ is a larger ion, which is why there isn’t as much Ca2+ influxing through the channel as there is Na+

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12
Q

aside from the n-ACh receptors found on skeletal muscle, how else do the skeletal muscles cells become more positively charged during depolarization?

A

after the initial depolarization through n-ACh receptors, nearby fast Na+ channels can open up to allow more Na+ to influx into the cell

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13
Q

paralytics work here

A

the neuromuscular junction

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14
Q

list out the steps to “excite” a nerve cell to cause skeletal contraction

A
  1. the brain sends “signal” to motor neuron to communicate with skeletal muscle cell
  2. the signaling molecules are the ACh neurotransmitters
  3. 2 ACh NTs bind to the nicotinic-ACh receptors
  4. the postively charged ion selective channel allows an influx of Na+ to flow into the cell
  5. depolarization occurs and activates nearby fast VG Na+ channels nearby to help propogate the AP across the skeletal cell leading to muscle contraction
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15
Q

which receptor types cause hyperpolarization in cardiac cells?

A

hyperpolarization makes cells more NEGATIVELY charged; this will suppress electrical activity in the cell

ex) muscarinic-ACh receptors
muscarine stimulates muscarinic-ACh receptors

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16
Q

where are m-ACh receptors found on the heart?

A

the “pacing centers”
SA and AV nodes

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17
Q

the RIGHT vagus nerve communicates with the ____ node

A

SA

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18
Q

the LEFT vagus nerve primarily communicates with the ____ node

A

AV

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19
Q

the vagus nerves communicate with the SA/AV nodes via this NT

A

ACh

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20
Q

the mACH-R has this type of protein structure

A

7TM (GPCR)

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21
Q

list out the mechanism of hyperpolarization in cardiac cells

A
  1. ACh binds to 7TM m-ACh-R
  2. alpha subunit and communicates with potassium channels (the effector protein) in the cell wall
  3. K+ channels now activated and effluxes K+ out of the cell
  4. increased EN makes the cell much more difficult to excite
  5. hyperpolarization (making the cell more negative past vrm) will make it so that it takes longer for the cell to become excited enough to fire off another AP
  6. this in turn will “keep the pace” of the heart (“70-72” BPM)
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22
Q

how does a vagal response cause a bradycardic response?

A

massive vagal stimulation causes potassium permeability to INCREASE, causing more K+ to efflux, causing hyperpolarization of pacemaker cells and causing the HR to slow down

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23
Q

describe what happens when an antimuscarinic drug inhibits pacemaker cell hyperpolarization

A
  1. antimuscarinic (antagonist) binds to active site of m-ACh-R
  2. alpha subunit is not active
  3. potassium channels close and cause cell to become more POSITIVE
  4. vrm is now more positive, and since our vrm has approached the threshold potential, it will take a SHORTER time to fire an AP
  5. shorter time to fire an AP means more APs fired AKA an elevated HR
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24
Q

give an example of a muscarinic-ACh-R antagonist

A

atropine

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25
Q

these two GPCRs antagonize each other in terms of keeping pace of the HR

A

m-ACh-R and beta receptors

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26
Q

how does physical pressure activate a neuron

A
  1. a stimulus causes a change in electrical activity
  2. once pressure (stimulus) is applied pressure sensitive Na+ channels will elongate the walls of the channels
  3. Na+ influx will be even greater (because the Na+ channel walls are wider)
  4. if there is enough Na+ current through the cell, an AP is depolarized and propogated through the neuron to the brain
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27
Q

nernst potential and ohm’s law

A

the nernst potential gives us polarity of the cell

ohm’s law states that if you have current going over some kind of resistance, you should have VOLTAGE

ex) if you have a bunch of Na+ channels open, there is a lot of Na+ current coming in, the current changes the resting membrane potential

you don’t have to have current; you just need POTENTIAL to influence the resting membrane potential

ex) 9V battery has stored voltage but doesn’t have any current going across the electrodes

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28
Q

what is the difference in a weak stimulus vs a very strong stimulus on an action potential graph

A

a weak stimulus barely gets over the threshold and it takes longer to fire an AP vs a very strong strong stimulus will fire an AP almost immediately

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29
Q

why is an AP sustained in the heart

A

it will give the heart time to contract and for the heart to fill

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30
Q

what are the effects of Cl- on a cell’s permeability

A

chloride “pumps the breaks”; the nervous system uses Cl- to control electrical activity in the heart

Cl- will hyperpolarize the cell and will make the cell much more difficult to excite

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31
Q

what are the extracellular effects of Ca2+

A

if ECF Ca2+ is increased, Ca2+ can block Na+ leaky channels, which will limit resting Na+ permeability

Ca2+ is a very large ion compared to Na+, so it will block Na+ from entering the cell

this is why Ca2+ is useful in treating hpERkalemic patients – hyperkalemia causes the cell to become more POSITIVE by not leaking out as much K+ and Ca2+ will esentially counteract this by making the cell more NEGATIVE by blocking Na+ channels

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32
Q

how are Mg2+ and Ca2+ dissimilar? how are they alike?

A

Mg2+ will function in the same way as Ca2+ will in terms of decreasing cell electrical excitability (Mg2+ is more specific to the heart); however, Mg2+ is a smaller ion than Ca2+

ICF/ECF Mg2+ can influence cell membrane potential vs ECF Ca2+

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33
Q

how does muscular tetany develop in a patient? (Trousseau/Chvostek’s sign)

A

hypocalcemia –

this will cause increased electrical activity at the motor neuron because hypocalcemia will allow much more leaky Na+ channels to diffuse more Na+ into the cell, making the cell much more excitable

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34
Q

rate of AP propogation in nerve dependent on:

A
  1. length of nerve (shorter = faster)
  2. diameter of nerve (wider = faster)
  3. insulation of the nerve (myelin sheath) – more insulation = faster AP
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35
Q

how does a Schwann cell (comprised of Schwann cell cytoplasm) end up myelinating an axon on a nerve fiber?

A

over time the Schwann cell will spiral around the nucleus, wrapping its lipid body around the axon, and will “squeeze” out the water, which it will then become a good insulator of the neuron

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36
Q

4 benefits to an insulated/myelinated neuron

A
  1. helps speed up AP
  2. reduces amt of energy consumed by cell (covering over more Na+/K+/ATPase pumps)
  3. less prone to ischemia
  4. prevents Na+ from leaking out neuron during AP
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37
Q

how do the Nodes of Ranvier assist with AP conduction?

A

they have a high density of Fast VG Na+ pumps localized in the node to ensure that there’s enough Na+ influx to propogate the AP futher along the axon

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38
Q

what is meant by “saltatory conduction”?

A

the AP is quickly “jumping/leaping” across a myelinated neuron

“saltatory” means to “jumping or leaping”

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39
Q

name 3 demyelinating disease and list their characteristics

A

1. multiple sclerosis
+autoimmune attacking of the myelin sheaths; causes issues with AP conduction
+lifelong/chronic disease
2. optic neuritis
+loss of vision d/t inflammation of optic nerve; associated with MS
+acute or chronic
3. Guillain-Barré Syndrome
+prevalent s/p COVID; autoimmune disease attacking myelin sheaths originating s/p viral infection/immunization/etc.
+acute

all can lead to progressive loss of function
all can be associated with genetics, infection, autoimmune hyperreactivity, polyneuropathies

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40
Q

explain the mechanism of demyelinated areas and how it affects AP conduction

A

demyelinated areas of the axon will not be able to regenreate ion channels, BUT, Na+/K+/ATPase pumps can remain in these areas

if the Nodes of Ranvier are intact close to these demyelinated areas, the INFLUX of Na+ from the fast VG Na+ channels will ultimately get EFFLUXED out of these remaining Na+/K+/ATPase pumps in the demyleinated areas, causing issues with AP conduction

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41
Q

why would an area with myelinated neurons require a higher than normal dose of local anesthetic?

A

harder to “block” because of the high density VG Na+ channels at the nodes

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42
Q

what makes up a gap junction?

A

6 connexin proteins = 1 connexon
2 connexons = 1 gap junction

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43
Q

how do gap junctions depolarize neighboring cells?

A

one cell can be depolarized via sodium influx and that sodium can travel into a neighboring cell to depolarize that cell via a gap junction; gap junctions allow small ions to pass through very easily and very quickly to a neighboring cell

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44
Q

what determines the signal resistance associated with electrical synapses?

A

the signal resistance is dependent on how many gap junctions are present
+the higher the # of gap junctions, the least amount of resistance there is to send ions across, thus creating a very fast current flow

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45
Q

where are gap junctions located in the body?

A

myocardium
smooth muscles
a few neurons

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46
Q

how can the bidirectionality of gap junctions cause issues in a tissue?

A

in the heart, if there is a “rogue” AP floating around, this can cause electrical disturbance on the tissue since there will be current flowing across the tissue much more quickly due to its bidirectionality, versus if there was a chemical synapse where it is a bit more controlled in signal conduction

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47
Q

in the heart, where would there be less amounts of gap junctions?

A

at the SA/AV nodes

these pacing areas of the heart have a built in system to cause delays to incorporate the “functional pause” needed for the heart to pump correctly

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48
Q

what are glial cells?
where are these glial cells located?

A

glial cells are the “support cells” in the nervous system

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49
Q

oligodenrocytes: location and characteristics

A

located in the CNS
are not good at regenerating myelin

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50
Q

the CNS is comprised of?

A

brain
spinal cord
CN II
retinas

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51
Q

Schwann cells: location and characteristics

A

located in the PNS (everything outside of the spinal cord)
can usually regenerate myelin if its not extensively damaged

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52
Q

how do chemical synapses assist in cell to cell communication?

A

presynaptic terminal will release chemicals (NTs) to bind to post-synaptic terminal to elicit communication

ex) ACh release to communicate between cells

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53
Q

where in the body is ACh inhibitory towards its target tissue?

A

the heart

54
Q

where in the body can ACh be excitatory towards its target tissue?

A

skeletal muscle

55
Q

differntiate A vs B and C nerve fibers

A

A: myelinated
B: lightly myelinated
C: non-myelinated

56
Q

what are the largest nerve fibers measured to be? the smallest?

A

largest: 20 micrometers
smallest: 0.5 micrometers

57
Q

differentiate the various motor functions and sensory functions in terms of nerve fiber size and myelination

A

the largest/myelinated nerve fibers will send messages the quickest; the smallest/unmyelinated nerve fibers send messages the slowest

large AND myelinated nerve fibers primarily are associated with MOTOR function
(i.e. brain decides you need to run away from a predator, motor neurons will get the message right away)

small and unmyelinated nerve fibers may be associated with SENSORY functioning such as: crude touch, tickle, aching pain, cold/warmth, etc.

58
Q

what are the 4 subdivisions of the group A nerve fiber classification?

A

α > β > γ > δ

where alpha is the largest and delta is the smallest

59
Q

what is comprised of generalized neuron structure?

A

cell body (soma)
dendrites
axon
axon hillock
myelin
node of ranvier
pre/post synaptic terminals

60
Q

what makes up the postsynpatic terminal?

A
  1. soma
  2. axon hillock
  3. the dendritic ends:
    +excitatory post-synaptic connections (EPSP/e) excitatory connections
    have more positive membrane potential than vrm
    +inhibitory post-synaptic connections (IPSP/i)
    more negative membrane potential than normal vrm (hyperpolarizing)

can make over 10,000 connections/inputs at postsynaptic terminal end

61
Q

what is special about the axon hillock in terms of synapse connections

A

there are no excitatory connections here; only inhibitory

GABA receptors on the axon hillock increase Cl- permeability – which will lead to more inhibition of the cell

62
Q

what would happen if ALL GABA receptors were blocked at the axon hillock?

A

if all GABA was removed, all electrical activity inhibition properties would be gone, thus, causing seizures

ex) chronic ETOHer (GABA receptor AGONIST) suddenly stops drinking > body isn’t producing its own GABA > seizures

63
Q

why does the axon hillock not have any excitatory inputs?

A

if (e) inputs were on the axon hillock, it would bypass all of the soma/dendrites, AKA, the decision making part of propogating an AP

64
Q

what are 4 supporting cells in the NS? which ones are MACROglia?

A

astrocytes
ependymal cells
oligodendrocytes/Schwann
(these are all macroglia^)

microglia

65
Q

what do astrocytes do

A

most abundant type of glial cell

has appendages that connect and wrap around the outside of the endothelial cells/capillaries of the NS

maintains electrolyte balance in the CSF; buffers the pH of the CSF

66
Q

ependymal cells

A

has cilia projecting on the surface of the cells

produces CSF
and moves/circulates around the brain

67
Q

oligodendrocytes

A

myelin producing cells in the CNS

(Schwann cells produce myelin in PNS)

68
Q

microglia

A

the “immune system” of the CSF

digests worn out cells in the CSF/functions as “macrophages”

keeps CSF clean and free of debris

69
Q

what are 3 different neuron types found in humans

A

multipolar
pseudounipolar
bipolar
(true unipolar: found in lower life forms)

70
Q

multipolar

A

decision making cells
intakes information and makes a decision to fire an AP or not

ex) pain sensory> decision to pull away from pain stimulus = motor neuron (multipolar neuron)

71
Q

bipolar

A

“bi” - two projections
used in special organs
ex) photoreceptors in retina > sends messages to optic nerve

“bipolar” ppl are “special”

72
Q

pseudounipolar

A

the majority of the sensory cells in the spinal cord or immediately outside of it

good for sensory function

non-decision making; meant to just relay information to the rest of NS

the soma of the pseudounipolar makes proteins, replaces things that need to be maintained in the neuron; supports the rest of the structures in the neuron

73
Q

true unipolar

A

found in “lower life forms”; not in humans

74
Q

somatic sensory receptors: define and give examples

A

somatic = consciously discernible (“sensible”)

free nerve endings = pain receptors = nociceptors

pressure/stretch sensors:
+pacinian corpuscle
+meissner’s corpuscle
+golgi tendon apparatus
+muscle spindle

75
Q

give an example of how somatic sensory receptors can adapt

A

baroreceptors will** adapt** to the prolonged stretch in vasculature; they become desensitized after prolonged HTN

ex) pt’s MAP is normally 100 mmHg; after 1 week of HTN @ 150 mmHg, baroreceptors have ability to respond to changes from normal > adaptation

if the baroreceptors were unable to adapt, prolonged HTN would cause baroreceptors to keep firing and they may not be able to fire any faster at some point, limiting ability of the brain to gather information on BP changes

76
Q

what is meant by “reverse adaptation”

A

some sensors that are stimulated for a very long time might become MORE sensitized to stimulus

ex) nociceptors are prone to reverse adaptation if pain is not controlled

77
Q

why is it important to have many fast adapting sensory receptors in our nervous system?

A

the NS is only concerned about changes that are happening NOW; the nervous system needs to adapt to changes quickly and efficiently

ex) you grab a ball with your hand and you keep your grip on the ball; the NS will cut down on the amount of sensory signals that are sent to your brain so you’re not continuously stimulated about the ball being in your hand; the NS is efficient in this way

78
Q

which receptors are prone to reverse adaptation?

A

pain/nociceptors

this is why tackling pain early is key! you want to treat pain early before the receptors get too stimulated for too long and become MORE sensitized to stimulus

79
Q

what are two different ways to prevent reverse adaptation in nociceptors?

A
  1. treat pain early
  2. create a nerve block in area
80
Q

directional nomenclature:

head+feet

A

superior
inferior

81
Q

directional nomenclature:

back+front

A

dorsal
ventral

or

posterior
anterior

82
Q

directional nomenclature:

medial+lateral

A

medial: “more towards midline”
lateral: “more towards side”

83
Q

directional nomenclature:

rostral/caudal

A

rostral: front upper portion
“beak”
caudal: lower and to the rear
“tail end”

84
Q

directional nomenclature:

distal+proximal

A

in reference to NS:

distal: further away from NS
proximal: closer to NS

85
Q

directional nomenclature:

superficial+deep

A

superficial
deep

86
Q

saggital plane

A

separates L + R sides of the body

think of splitting a brain down the central sulcus

87
Q

coronal plane

A

separates front and back of the body

think of separating your face from your ass

88
Q

horizontal plane

A

separates superior from inferior

“a magician’s saw”

89
Q

oblique plane

A

an odd angle view

90
Q

what are the 4 CNS divisions?

A

telencephalon
diencephalon
brain stem
spinal cord
(+optic nerve is also part of the CNS)

91
Q

name 4 structures of the telencephalon

A
  1. cerebral cortex
  2. subcortical white matter
  3. commisures
  4. basal ganglia
92
Q

name 4 structures of the diencephalon

A
  1. thalamus: relay center of the brain for communication
  2. hypothalamus: hypo-below the thalamus; vital functions and sensory info control center
  3. epithalamus
  4. subthalamus
93
Q

name the 3 structures that make up the brain stem

A
  1. midbrain (mesencephalon)
  2. pons
  3. medulla oblongata
94
Q

sulcus

A

a “groove” in the brain

95
Q

gyrus

A

a “lump” in the brain
pleural: gyri

96
Q

fissure

A

“deep groove” in the brain

97
Q

name the 4 lobes of the brain and what their functions are

A
  1. frontal - premotor (planning)/motor
  2. parietal - somatosensory cortex
  3. occipital - vision
  4. temporal - hearing
98
Q

where is the central sulcus located on the brain

A

at the very end of the frontal lobe, right before the parietal lobe

99
Q

where is the temporal/temporolateral fissure?

A

this is distinctly found in between the frontal lobe and the temporal lobe

100
Q

where is the longtiudinal fissure?

A

this is located right down the center line between the left and right hemispheres of the brain

101
Q

what is the structure that allows communication between the L and R hemisphere called?

A

corpus callosum

102
Q

differentiate Broca’s Area from Wernicke’s Area

A

Broca’s Area: located in the FRONTAL lobe – word formation/speech is more of a MOTOR function

Wernicke’s Area: located in the TEMPORAL lobe – deals with language comprehension and this is more of an auditory processing function

103
Q

differentiate premotor cortex, motor cortex, and primary motor cortex

A

premotor cortex: most anterior portion of the frontal lobe; deals with planning complex movements and elaboration of thoughts

motor cortex: deals with motor function

primary motor cortex: deals with execution of motor function – this is located at the most posterior part of the motor cortex/anterior to the central sulcus

104
Q

explain how the limbic system might intensify a painful experience

A

prolonged pain associated with the limbic system (behaviors/emotions/motivation) will be perceived as a much worse experience than without having emotions involved

105
Q

what is the difference between brain matter in terms of its color

A

white matter: myelinated – used to transmit the “decisions” to target organs

gray matter: unmyelinated; many cell bodies are located here – decision makers

in the spinal cord, the gray matter is more central/in the core of the cord; white matter is superficial to the gray matter

106
Q

differentiate lamina X vs the anterior white commisure

A

lamina X is where L and R divisions of the GREY MATTER communicate in the spinal cord

anterior white commisure is where the L and R divisions of the WHITE MATTER communicate in the spinal cord

107
Q

differentiate the dorsal and ventral horns of the spinal cord

A

dorsal horns have sensory input and relay the info to the brain

ventral horns of the spinal cord take motor function output from the brain to the rest of the body

108
Q

why is the anterior median fissure deeper/have a wider gap than the posterior median sulcus

A

the anterior median fissure is deeper to accomodate the blood vessels

109
Q

which arteries feed into the spinal cord

A

intercostal arteries
also the top of the cord/brain stem/base of neck feeds the spinal arteries

110
Q

how many posterior spinal arteries are there? how many anterior spinal arteries?

A

2 posterior spinal arteries
1 anterior

111
Q

how does sensory information travel through the spinal cord?

A

sensory information will come in thru the posterior rootlets > travel from gray matter > HORIZONTALLY > to white matter > then it will travel up an ASCENDING COLUMN to the brain

112
Q

what 2 structures meet to make the spinal nerve?

A

anterior spinal root + posterior spinal root

the spinal nerve is comprised of a mixture of sensory pathways and motor output

113
Q

what makes up the spinal ganglion of the posterior root of the spinal nerves?

A

many pseudounipolar (sensory) cell bodies makes up the spinal ganglion (bulging part of the posterior root)

114
Q

why doesn’t the anterior spinal root not have a spinal ganglion?

A

the anterior root deals with motor output; the cell bodies would be located in the ventral/anterior horns

115
Q

how does motor output get relayed through the spinal cord?

A

lateral/anterior spinal cord deals with motor output

motor output would come from the brain, down the spinal cord, through the descending columns, from the WHITE MATTER > horiztonally > to the GREY MATTER > through the anterior rootlets, to the anterior root, to the spinal nerve > to effector target

116
Q

how many cervical vertebrae are there? how many cervical spinal nerve pairs are there?

A

C1-C7 vertebrae
8 c. spinal nerve pairs

C1 spinal nerve pair is ABOVE C1 vertebra; C2-C8 spinal nerve pairs are below previous vertebrae

117
Q

how many thoracic vertebrae are there?
how many thoracic spinal nerve pairs are there?

A

T1-T12
12 t. spinal nerve pairs
these nerves exit BELOW the vertebrae

118
Q

how many lumbar vertebrae are there?
how many lumbar spinal nerve pairs are there?

A

L1-L5 vertebrae
5 l. spinal nerve pairs
these nerves exit BELOW the vertebrae

119
Q

how many sacral vertebrae are there?
how many sacral spinal nerve pairs are there?

A

S1-S5 vertebrae
5 s. spinal nerve pairs
these nerves exit BELOW the vertebrae

120
Q

how many coccygeal vertebrae are there?
how many coccygeal spinal nerve pairs are there?

A

(4 coccygeal vertebrae at BIRTH)
2 coccygeal vertebrae when fused after birth
1 pair of coccygeal spinal nerves

121
Q

describe the “dermatome man”

A

dermatome man illustrates a man bent over and differentiates areas of where the cervical, thoracic, lumbar, and sacral spinal nerves innervate

c spinal nerves: head/neck/anterior arms
t spinal nerves: thoracic cavity, posterior arms
l spinal nerves: anterior legs/hips
s spinal nerves: posterior legs/butt

122
Q

how does our spine provide our body support?

A

“shock absorbing” properties

123
Q

describe the spinal curvature in the different areas of the spine

A

c-spine & lumbar spine: lordosis/”convex” curvature if looking from the front of the body

t-spine and & sacral spine: kyphosis/”concave” curvature if looking from the front of the body

“concave: “bear clawing” > )”
concave: opposite

the generalized curvature is “front to back” curvature

124
Q

what is a type of abnormal spinal curvature that might develop with age

A

thoracic kyphosis
“hunchback”

125
Q

what type of curvature is an abnormal LATERAL spine curvature?

A

scoliosis
“think S shape, but laterally”

126
Q

what is the most common type of abnormal combination spinal curvature?

A

kypho-scoliosis

127
Q

what type of curvature does the body have at birth?

A

kyphotic curvature

128
Q

where would the verterbral body of the vertebrae be largest? smallest?

A

largest near the trunk of the spinal cord; smallest near the head/neck

smaller near the top because it is not supporting as much weight as the lower spinal cord

129
Q

what makes up 1 (generic) vertebrae?

A
  1. vertebral body
  2. the vertebral arch
    +pedicle
    +lamina
  3. spinous process
  4. tranverse processes (2)
  5. inferior articular processes (2)
  6. superior articular processes (2)
  7. inferior/superior vertebral notch
  8. inferior/superior articular facet
  9. verterbral foramen
130
Q

where does the cartilage lie on the vertebra?

A

cartilage lies in the articular facets

Ana/Phys/Patho I (6 decks)

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