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A&P Test 2 > 9/20 > Flashcards

9/20 Flashcards

1
Q

Venous structures in the brain are called

A

sinuses

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2
Q

The walls of the sinuses in the brain are made up of the

A

dura mater

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3
Q

why are most subdural hematomas venous?

A

because the sinus’s are made of the dura mater and if something rips through the dura part of the wall then the venous structures rip too

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4
Q

our brain blood flow rate depends on what?

A

the brain’s metabolic demands

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5
Q

How does the brain prevent under profusion?

A

by vasodilating the blood flow pathways in the brain

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6
Q

How does the brain prevent over profusion?

A

by constricting the blood flow pathways in the brain

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7
Q

Why do we have a circular pathway in the brain?

A

it ensures collateral pathways if we have a blockage in a feed artery

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8
Q

Where do the internal carotid arteries enter into the circle of willis?

A

In the middle, one on each side

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9
Q

Where do the vertebral arteries connect with the circle of willis?

A

they come together to form one artery called the basilar artery

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10
Q

The vertebral arteries come together over what anatomical landmark to make the basilar artery?

A

at the base of the pons

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11
Q

Where does the basilar artery come into the circle of willis?

A

in the middle on the posterior side

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12
Q

What are the 3 large arteries that connect to the circle of willis?

A

Posterior cerebral artery
Middle cerebral artery
Anterior cerebral artery

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13
Q

Of these, which is the largest?
Posterior cerebral artery
Middle cerebral artery
Anterior cerebral artery

A

middle cerebral artery

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14
Q

The middle cerebral artery supplies what area of the brain?

A

The middle and lateral portions

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15
Q

Which part of the brain is supplied by the anterior cerebral artery?

A

the front and midline portions

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16
Q

Which part of the brain is supplied by the posterior cerebral artery?

A

Back and far lateral areas

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17
Q

What are the two parts of the anterior cerebral artery?

A

Early; Pre-communicating A1
Late; Post-communicating A2

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18
Q

Which part of the anterior cerebral artery touches the circle of willis?

A

Early; Pre-communicating A1

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19
Q

Which part of the anterior cerebral artery does not touch the circle of willis?

A

Late; Post-communicating A2

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20
Q

What is the small artery that attaches the two anterior cerebral artery?

A

anterior communicating artery

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21
Q

After the internal carotid’s touch the circle of willis, their names change to

A

middle cerebral artery

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22
Q

Which part of the posterior cerebral artery touches the circle of willis?

A

early; Pre-communicating part P1

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23
Q

Which part of the posterior cerebral artery does not touch the circle of willis?

A

Late; Post-communicating P2

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24
Q

Which artery connects the middle cerebral arterties to the posterior cerebral arteries?

A

The posterior communicating artery

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25
Q

Which artery supplies the front and top of the cerebellum

A

superior cerebellar artery

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26
Q

What artery does the superior cerebellar artery come from

A

the basilar artery

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27
Q

Which artery supplies the middle of the cerebellum

A

anteroinferior cerebellar artery

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28
Q

What artery does the anterioinferior cerebellar artery come from

A

the basilar artery

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29
Q

What supplies the back portion of the cerebellum?

A

posteriorinferior cerebellar artery

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30
Q

What artery does the posteriorinferior cerebellar artery come from

A

vertebral arteries

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31
Q

the anteriorinferior artery comes off of the basilar artery, right over the

A

middle of the pons

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32
Q

the posteriorinferior artery comes off of the vertebral arteries, right over the

A

brainstem

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33
Q

most epidural hematomas are a result of

A

trauma

34
Q

subdural hematomas are a result of

A

tearing the dural walls like a bad wreck and you have whiplash

35
Q

subarachnoid hemorrhage is the most messy, why?

A

because in the other types, the blood typically tends to aggregate into one place which can be solved by a drain or opening the skull there

36
Q

Which type of bleed is associated with aneurysms and hemorrhagic strokes?

A

subarachnoid hemorrhages

37
Q

subarachnoid hemorrhages are typically venous or arterial?

A

arterial

38
Q

what is a cause of hemorrhagic strokes?

A

bad lifestyle choices, alcoholism, long term hypertension

39
Q

When metabolism goes up in the brain, so should

A

blood flow

40
Q

What is the top byproduct of metabolism that is involved in regulation of brain blood flow?

A

CO2

41
Q

why does blood flow increase when metabolic demands increase?

A

CO2 is created as a metabolic byproduct (increased metabolism=increased CO2), and then leaks into the surrounding tissues, blood flow increases to get rid of that excess CO2 as well as replace any nutrients expended in metabolism

42
Q

What is the number 1 regulator of brain blood flow?

A

CO2

43
Q

we need as much cerebral bloodflow as it takes to

A

remove the CO2 that’s being produced

44
Q

Once all of the CO2 is removed from the cerebral blood flow, then blood flow

A

doesn’t increase anymore, it just curtails

45
Q

What is the range of systemic blood pressure (map) that is required for brain blood flow? autoregulation

A

50-150

46
Q

If our cerebral metabolism hasn’t changed, but our blood pressure is increased, than the brain blood flow should

A

stay about the same because the vessels constrict to prevent over profusion

47
Q

Systemic blood pressure is used to drive

A

brain blood flow

48
Q

if there was no autoregulation, what would we see on a graph of brain blood flow and blood pressure?

A

a linear line with low blood flow arising from low blood pressure

49
Q

If we have under profusion of the brain we would have

A

cell death

50
Q

If we have over profusion of the brain we would have

A

bursting of aneurysms

51
Q

More recently they have thought that autoregulation would cut off after the map drops below

A

60-70

52
Q

after about a map of 50, the brain vessels can’t constrict anymore so we would see

A

a reduction in brain blood flow

53
Q

what is the point when the blood vessels in the brain cannot dilate any further?

A

the lower limit autoregulation LLA

54
Q

what is the point when the blood vessels in the brain cannot constrict any further?

A

the upper limit autoregularion ULA

55
Q

if we have a patient who has prolonged HTN, what happens to their lower and upper limits?

A

the system adapts, and the LLA and ULA will shift to the right

56
Q

How do the brain vessels adapt to squeeze tighter than the upper limit when exposed to prolong HTN?

A

The vessels harden
atherosclerosis

57
Q

What will happen when the lower limit is raised d/t atherosclerosis and the patient’s map drops to 50

A

The brain tissue will now be under perfused

58
Q

What is a way that the body adapts to a clot in the vessels?

A

collateral blood flow

59
Q

often times when someone is trying to get a handle on cardiovascular health then they look at

A

the ability of the blood vessels to dilate

60
Q

Collateral blood flow is something that we are

A

born with

61
Q

HTN and diabetes zap the ability to _______ in the blood vessels

A

dilate.
this gives them more serious strokes and MI’s

62
Q

Anesthetic drugs takes some of our _____ ofline

A

autoregulation

63
Q

in an anesthetic that affects autoregulation just a little, you would expect the middle line on the graph to be

A

slightly sloped

64
Q

in An anesthetic that affects autoregulation a lot, you would expect the middle line on the graph to be

A

steeper

65
Q

Most of the textbooks say that anesthetics don’t effect autoregulation, but we know that isn’t really true, and they are simply taking into account the

A

Error bar that arises from variability from testing humans

66
Q

the wider the error bar, they say the data is

A

statistically insignificant, and therefore cannot prove that the anesthetic takes autoregulation offline, even if the graph clearly shows that it does

67
Q

an action protentional moves down an axon d/t

A

fast Na+ channels

68
Q

What is in the axon wall that helps reset the cell after depolarization?

A

Na+/K+ pumps and voltage gated K+ channels

69
Q

When the action potential reaches the end of the neuron, it opens up a second set of voltage gated ion channels specific for

A

Ca++

70
Q

What is another name for the voltage gated Ca++ channel?

A

P-Type voltage gated Ca++ channels

71
Q

When Ca++ floods into the cell after an action potential, what does it do?

A

It binds to VP2 ACh storage vesicles and pushes it to the cell wall for exocytosis

72
Q
A
73
Q

What is the difference between a VP2 ACh storage vesicles and a VP1 ACh storage vesicle?

A

VP2 ACh storage vesicles are at the cell wall, ready to be spilled out into the synapse.
VP1 ACh storage vesicles are either not full or not low enough to the synapse

74
Q

What does VP2 stand for in a ACh storage vesicles?

A

Vesicle pool

75
Q

What shuts off the ACh dumping into the synapse after an action potential?

A

Ca++ pumps using ATP
Na+/K+ pumps
K+ channel
Ca++ sensitive K+ channels

all of these remove + charges

76
Q

What is found on the target skeletal muscle that ACh binds to?

A

nACH receptor

77
Q

nACh receptors function as cylinders that open when 2 ACh molecules bind to it at the same time, and this allows what movement of ions?

A

Na+ floods, some Ca++ comes in, and a tiny but of K+ goes out

78
Q

Why is it that in a healthy muscle cell, an endplate potential will always trigger an action potential?

A

because we have way way way more ACh receptors and ACh neurotransmitters

79
Q

What is an endplate potential?

A

localized depolarization that happens in the muscle d/t ACh receptors opening up

80
Q

Endplate potentials in a healthy muscle is always going to be enough to trigger an

A

an action potential by opening fast sodium channels, which results in a muscle contraction

81
Q

What is the bare minimum end plate potential that is required to create an action potential in the post synaptic cell?

A

500,000 receptors activated

A&P Test 2 (7 decks)

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