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PHYSL 372 > Lecture 15 - Stroke > Flashcards

Lecture 15 - Stroke Flashcards

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1
Q

brain damage and dysfunction that results from a reduction in blood flow to the brain

A

stroke

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2
Q

a stroke results from:

A

brain ischemia (reduced blood flow)

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3
Q

injury from stroke starts immediately and is often:

A

permanent

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4
Q

what are the two major types of strokes?

A

hemorrhagic or ischemic (majority - ~85%)

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5
Q

type of stroke caused by a rupture of blood vessels in the brain (can result from trauma, ruptured aneurysms, arteriovenous malformations)

A

hemorrhagic stroke

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6
Q
  • bleeding in the subarachnoid space (puts pressure on the brain)
  • 40-50% early mortality
  • raised intracranial pressure, vasospasm
    these are all characteristics of:
A

subarachnoid hemorrages (SAH)

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7
Q
  • vessel ruptures leaking blood into parenchyma (mechanical disruption and blood toxicity)
  • often occurs in lenticolostriate arteries
  • more common with hypertension and diabetes
  • 30-50% mortality
    these are all characteristics of:
A

intracerebral hemorrhage (ICH)

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8
Q

what is the difference between a global and focal ischemic stroke?

A

global strokes result from reduced blood flow to the entire brain, but focal strokes result from the occlusion of a vessel in the brain (typically the middle cerebral artery)

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9
Q

what causes global ischemic strokes?

A

heart attacks

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10
Q

what causes focal ischemic strokes?

A

a thrombus (blood clot) or embolus (blood clot that originates elsewhere in the body but then travels to the brain)

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11
Q

stroke symptoms depend on _____, which depends on _____

A

size and location, vasculature

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12
Q

where do proximal occlusions occur?

A

in the middle cerebral artery closer to the heart - M1 (brings blood to the brain)

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13
Q

what kind of damage is caused by proximal occlusions?

A

cortical and striatal damade, leads to hemiparalysis and aphasia

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14
Q

where do distal occlusions occur?

A

in the middle cerebral artery further from the heart - M2 (into the cortex)

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15
Q

what kind of damage is caused by distal occlusions?

A

cortical damage, leads to more focal neurological signs

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16
Q

what kind of damage is caused by lenticulostriate artery occlusions?

A

lacunar infarcts, silent or variable neurological signs

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17
Q

fragile arteries prone to rupture

A

lenticulostriate arteries

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18
Q

what is the normal perfusion rate of cerebral blood flow?

A

~50ml/100g/min

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19
Q

what ischemic perfusion rate causes rapid and irreversible cell death?

A

<10ml/100g/min

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20
Q

cannot maintain the cell membrane potential and cells will rupture and die

A

anoxic depolarization

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21
Q

what ischemic perfusion rate where the cells are functionally silent but alive?

A

<20ml/100g/min

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22
Q

what is the difference between the stroke core and the stroke penumbra?

A

the stroke core is the area of the stroke where the brain cells die, the stroke penumbra is the tissue around the core which has the potential to be saved

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23
Q

the size and severity of the stroke penumbra is defined by:

A

collateral circulation

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24
Q

how does having good collaterals help to save brain tissue during a stroke?

A

collaterals maintain partial blood flow

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25
connections between the blood vessels
anastamosis
26
true or false: collateral blood flow to the stroke penumbra is permanent
false
27
collaterals predict _____ and _____
infarct growth, response to therapy
28
the process of restoring flow to or reuniting an interrupted channel of a bodily tube
recanalization
29
stroke patients who undergo recanalization have:
reduced stroke damage
30
there is complete energy failure in the _____ and partial energy failure in the _____
stroke core, stroke penumbra
31
go read slide 392-393
I just have no idea how to write that down
32
acts like a large pore in the cell that is tonically closed
Panx (pannexin 1)
33
during an ischemic stroke, the Panx channels are typically:
open (leads to cellular necrosis)
34
in ischemic conditions, blocking the Panx channels leads to:
prevention of necrosis
35
what are some of the extrinsic conditions that lead to apoptosis?
tumor necrosis factor (TNF) and the death inducing signalling complex (DISC = Fas R, the Fas-associated death domain (FADD), caspase 8)
36
what are some of the intrinsic conditions that lead to apoptosis?
mitochondrial release of cytochrome C
37
changes in structure and function of a brain region connected to an area of injury
diaschisis
38
cell death in the core is immediate, but delayed death in the penumbra offers hope for:
neuroprotection
39
what are the two major paths for neuroprotection during ischemic strokes?
restoring blood flow and interfering with the ischemic cascade
40
what is a major complication with treating strokes?
it takes time to identify and treat strokes, and by then cells have already died (time is brain)
41
what is the best strategy to reduce damage due to stroke?
restoring blood flow (thrombolysis/endovascular therapy)
42
a stroke treatment that focuses on breaking up the blood clot
thrombolysis
43
a stroke treatment where a catheter is inserted into the brain to give rt-PA to the clot to break it up
endovascular therapy
44
blood clots are mostly made up of:
platelets and fibrin
45
how is fibrin made?
generated from fibrinogen by thrombin
46
thrombolysis with recombinant tissue plasminogen activator (rt-PA, altepase) works by:
cleaving fibrin
47
the only FDA approved clinically proven treatment for acute stroke
rt-PA
48
a modified rankin score of 0-2 represents:
no disability to slight disability
49
a modified rankin score of 6 represents:
mortality
50
true or false: rt-PA improves outcomes in some stroke patients even after 3 hours
true
51
historically, the mean time to CT completion can be:
4 hours or more
52
how many patients who are treated within the window of salvagable tissue do NOT benefit?
60%
53
newer iterations of rt-PA treatments
tenecteplase and desmoteplase
54
list two types of intra-arterial therapy
- local thrombolytic delivery - mechanical thrombectomy
55
a type of stroke treatment where you physically grab the clot an pull it out (good for treating proximal middle cerebral artery occlusions)
mechanical thrombectomy (ESCAPE trials)
56
how effective has the ESCAPE trial been?
very (72.4% recanalized)
57
list four nitric oxide dependent vasodilators
- acetylcholine (M3 muscarinic) - bradykinin - substance P - adenosine
58
what is the caveat to using nitric oxide vasodilators as a stroke treatment?
this can reduce blood pressure throughout the body which reduces blood flow to the brain
59
why are nitric oxide depenent vasodilators used as a treatment for strokes?
it selectively dilates arterioles in the ischemic penumbra, thereby increasing collateral blood flow
60
inhaled nitric oxide provides potent vasodilation, and there is some evidence for:
neuroprotection
61
nitric oxide donors act as:
potent but non-selective vasodilators (targets systemic blood flow)
62
list two examples of nitric oxide donors
- sodium nitroprusside - glycerin trinitrate (nitroglycerin)
63
L-Arg acts as a:
nitric oxide precursor
64
how does remote ischemic perconditioning work?
makes another large region of the body ischemic, and some protective factor is released by the body to reduce the effect (vasoactive factors released)
65
is it possible to use remote ischemia to treat brain ischemia?
looks promising
66
collaterals (and collateral therapeutics) can keep tissue alive until recanalization, but futile recanalization still occurs. why?
microcirculatory (capillary bed) failure that prevents restoration of flow at the tissue level may contribute
67
patients with a higher neutrophil:lymphocyte ratio tend to have _____ outcomes than patients with a lower neutrophil:lymphocyte ratio
worse (neutrophils linger in the capillaries and block blood flow)
68
at three hours post-recanalization, young females differentially expressed genes (DEGs) for:
leukocyte activation (25 DEGs related to progesterone)
69
a selective progesterone receptor agonist that causes vasodilation and may reduce neutrophil activation
NTS-104
70
progesterone agonists will improve ____ and reduce ____ after middle cerebral artery occlusion (MCAO) with recanalization
blood flow, neutrophil stalls
71
go review slide 416
good diagram
72
metabotropic coupling of NMDA receptors to Pannexin-1 leads to:
cell death cascades
73
NMDA and Panx-1 are coupled via:
Src family kinases
74
what are the effects of blocking the interaction of NMDA with Src?
blocks anoxic depolarization, and prevents Panx1 opening and reduces damage and disability due to stroke
75
inhibition of the NMDA receptor is associated with:
protein PSD-95
76
PSD-95 binds NMDA receptors and _____ at excitatory synapses
neuronal nitric oxide synthase (nNOS)
77
inhibition of PSD-95 with NA-1 prevents the formation of:
the NMDA-receptor/PSD-95/nNOS complex and generation of nitric oxide
78
are physiological functions of NMDA affected by inhibiting PSD-95?
no
79
how do PSD-95 inhibitors impact strokes in rodents?
reduces infarct in rodent models and exerts neuroprotective properties
80
how do PSD-95 inhibitors impact humans?
protective after small strokes incurred by patients who undergo surgery to repair brain aneurysms (phase II trials)
81
- combined endovascular therapy with NA-1 - moderate-good collaterals - NA-1 prior to EVT within 12h - safe but missed primary efficacy endpoint - however, in patients without tPA there is a suggested benefit these are all characteristics of:
the ESCAPE NA-1 trial
82
go review slide 420
graphs woohoo
83
if you train during teh plastic period, you have a better chance at:
restoring function
84
therapies that can augment neuroplasticity may have a place for:
improving recovery after the damage is done
85
list the three steps for what optimal rehabilitation would look like
1) determine plastic status of the brain (imaging and biomarkers) 2) enhancement of the plastic status of the brain and spinal cord (application of frowth and plasticity promoting factors) 3) selection and stabilization of newly formed functional connections (rehabilitative training)
86
a biomarker of axonal sprouting/growth
Gap 43
87
when does recovery from strokes end?
when the period of heightened plasticity following the stroke ends
88
stabilizes and prevents axonal sprouting and forms a part of the glial scar
chondroitin sulphate proteoglycans (CSPGs)
89
chondroitin sulphate proteoglycans (CSPGs) are upregulated by:
injury (may drive closure of the critical plasciticy period)
90
has an established ability to cleave glycosaminoglycan (GAG) chains from chondroitin sulphate proteoglycans (CSPGs)
chondroitinase ABC (ChABC)
91
digesting chondroitin sulphate proteoglycans (CSPGs) with chondroitinase ABC (ChABC) enhances _____ and _____
structural plasticity, recovery after spinal injury

PHYSL 372 (18 decks)

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