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PHYSL 372 > Stroke > Flashcards

Stroke Flashcards

1
Q

What is a stroke?

A

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

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2
Q

What is the difference between stroke and ischemia?

A
  • stroke occurs in the brain
  • ischemia occurs in the vascular system
  • stroke results from brain ischemia
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3
Q

What percentage of strokes are ischemic vs hemorrhagic?

A
  • ischemic = 85%
  • hemorrhagic = 15%
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4
Q

What is a hemorrhagic stroke?

A

rupture of blood vessel in the brain

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5
Q

TRUE or FALSE: hemorrhagic has a higher mortality rate than ischemic stroke

A

TRUE

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6
Q

What are the 2 types of hemorrhagic strokes?

A
  • subarachnoid hemorrhage (SAH)
  • intracerebral hemorrhage (ICH)
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7
Q

What are the symptoms of SAH?

A
  • bleeding in subarachnoid space
  • raised intracranial pressure due to blood trapped in subarachnoid space
  • vasospasm
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8
Q

What can vasospasm due to SAH cause?

A

contraction of vessels to restrict blood flow –> global ischemia –> death

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9
Q

What are symptoms of ICH?

A
  • vessel ruptures leaking blood into parenchyma –> blood toxicity
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10
Q

Which arteries are often affected in ICH?

A

lenticolostriate arteries

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11
Q

Which conditions are ICH common with?

A

hypertension and diabetes

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12
Q

What does global ischemic stroke result from? focal ischemic stroke?

A
  • global results from reduced blood flow to the entire brain –> HEART ATTACK
  • focal results from occlusion of a vessel in the brain - typically MCA –> THROMBUS, EMBOLUS
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13
Q

What do stroke symptoms depend on?

A

size and location, which depends on vasculature: occluded vessel vs collateral blood supply

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14
Q

What is another name for proximal occlusions of the middle cerebral artery? Does it cause cortical or striatal damage? What are some symptoms to look for?

A
  • M1 occlusion
  • cortical and striatal damage
  • symptoms: hemiparalysis, aphasia
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15
Q

What is another name for distal occlusions of the MCA? Does it cause cortical or striatal damage? What are some symptoms to look for?

A
  • M2 occlusion
  • cortical damage only
  • symptoms: more focal neurological signs
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16
Q

Why are the lenticulostriate arteries prone to ruputre?

A

they are very fragile and there is high pressure at M1; therefore a big pressure gradient

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17
Q

What kind of symptoms do lacunar infarcts lead to?

A

silent symptoms

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18
Q

What is the normal perfusion rate? ischemic perfusion rate when cells irreversibly die? ischemic perfusion rate when cells are silent but alive?

A
  • normal: 50 mL/100g/min
  • irreversible ischemia: <10 mL/100g/min
  • silent but alive ischemia: <20 mL/100g/min
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19
Q

TRUE or FALSE: there is better blood flow closer to the occlusion.

A

FALSE: there is better blood flow farther from the occlusion

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20
Q

What kind of arteries maintain partial blood flow in a stroke? Is partial blood flow associated with a stroke core or penumbra?

A

pial collaterals; penumbra

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21
Q

Summarize the ischemic cascade.

A
  1. loss of aerobic metabolism
  2. loss of ATP , acidosis
  3. Na/K-ATPase failure
  4. depolarization
  5. excitotoxicity
  6. increase in intracellular Na+, Ca2+, Cl-
  7. cytotoxic edema
  8. protease activation
  9. free radicals
  10. lipid peroxidation
  11. mitochondrial failure (MPTP)
  12. immune cell infiltration and inflammation
  13. apoptosis
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22
Q

Why do depolarizations cause ischemia?

A
  • ANOXIC (because loss of blood flow)
  • peri-infarct depolarizations increase metabolic demand (stressful for cells)
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23
Q

How is edema cytotoxic?

A

H2O follows ions into the cell –> swelling –> rupture

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24
Q

Describe excitotoxicity in terms of ischemia.

A

release of glutamate, activation of signaling pathways and further depolarization (feedforward mechanism)

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25
Q

In ischemic stroke, which transporter proteins fails, causing loss of Cl- gradient? Does this cause or inhibit inhibition? How does this affect intracellular levels of Na+, Ca2+ and Cl-?

A
  • KCC2 failure
  • impair inhibition
  • increased intracellular levels of Na+, Ca2+, and Cl-
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26
Q

Describe the signaling cascade that results from a change in intracellular ion concentrations and receptor activation?

A
  • protease activation
  • free radical generation
  • lipid peroxidation
  • mitochondrial failure
  • necrosis and apoptosis
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27
Q

damage to which structure of the brain allows infiltration of immune cells? activation of which cells lead to inflammation?

A
  • damage BBB
  • activate glial cells
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28
Q

TRUE or FALSE: panx stops anoxic depolarization

A

FALSE: BLOCKING panx stops anoxic depolarization

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29
Q

Describe extrinsic apoptosis in the peri-infarct.

A
  1. TNF and FasR
  2. Fas-associated protein with Death Domain (FADD)
  3. death inducing signaling complex (DISC = R, FADD, Cas8)
  4. effector caspases (Cas3)
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30
Q

Describe intrinsic apoptosis in the peri-infarct.

A
  1. mitochondrial release of cytochrome C
  2. activate Cas3
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31
Q

Draw a graph demonstrating the growth of infarct over time. Label when the following have the most impact: excitotoxicity, apoptosis, inflammation, peri-infarct depolarizations

A
  • excitotoxicity at minutes
  • peri-infarct depolarizations at minutes
  • inflammation at hours/days
  • apoptosis after days
    (slide 14)
32
Q

After a stroke, asevere M1 occlusion can lead to degeneration in which spinal tract?

A

CST

33
Q

What is diachisis?

A

metabolic dysfunction

34
Q

TRUE or FALSE: focal stroke effects do not extend outside of the core

A

FALSE: focal stroke effects extend outside of the core

35
Q

Why does a cortical stroke lead to diaschisis in the cerebellum?

A

there are strong connections between the cerebellum and the cortex

36
Q

TRUE or FALSE: a corrtical stroke in one area can lead to diaschisis in functionally connected cortical areas

A

TRUE

37
Q

TRUE or FALSE: cell death in the penumbra is immediate, but dell death in the core offers hope for neuroprotection.

A

FALSE: cell death in core is immediate, penumbra offeres hope for neuroprotection

38
Q

What are the 2 main ways to prevent damage due to ischemia? Which is best?

A
  1. restore blood flow (best)
  2. interfere with ischemic cascade
39
Q

What is the mean time to complete a CT scan?

A

less than 1 hour

40
Q

What kind of scan is used to determine if a stroke is ischemic or hemorrhagic?

A

CT

41
Q

What has been the major focus for restoring blood flow after stroke over the last 20 years?

A

thrombolysis / clot busting

42
Q

What is endovascular therapy?

A

catheter used to physically pull out clot

43
Q

What are 3 strategies to restore blood flow after stroke?

A
  • thrombolysis
  • endovascular therapy
  • collateral blood flow therapeutics
44
Q

How does thrombolysis work?

A
  • blood clots are made up primarily of platelets and fibrin
  • recombinant tissue PLASMINOGEN activator (rt-PA) works by cleaving fibrin –> breaking up blood clots (note: PLASMIN cleaves fibrin)
45
Q

What is the only FDA approved clinically proven treatment for acute stroke?

A

rt-PA (thrombolysis)

46
Q

What scale is used to measure functional independence after rtPA tratment of stroke? what score represnets no disability to slight disability?

A

modified Rankin score; 0-2

47
Q

Why does tPA worsen the stroke if it is administered after 4.5 hours?

A

ischemic stroke is verly likely to become hermhorragic

48
Q

should we memorize the limitation fo rt-PA?

A

slide 21

49
Q

What are newer iterations of rt-PA?

A

tenecteplase and desmoteplase

50
Q

What is the window of time for endovascular therapy to be effective?

A

up to 24 hours after stroke

51
Q

What is the window of time for rt-PA to be effective?

A

4.5 hours

52
Q

What substance is used to increase collateral blood flow to treat stroke?

A

nitric oxide dependent vasodilators:
- ACh
- bradykinin
- Substance P
- adenosine

53
Q

L-arginine vs inhaled NO vs NO donors to treat stroke?

A
  • L-arginine: no precursor –> systemic effect
  • inhaled NO: potent vasodilation, some evidence for neuroprotection
  • NO donors: potent but non-selective vasodilators –> systemic effect
54
Q

How does NO treat stroke? mechanism?

A
  • NO increases cGMP cause vasorelaxation
  • dilates all blood vessels in body (incl brain) –> restore blood flow using the collaterals
55
Q

What are some NO donors?

A
  • sodium nitroprusside
  • nitroglycerin
56
Q

What is arguable they best form of NO administration? Why?

A
  • inhaled NO
  • increases CBF during stroke
  • treatment decreases penumbra, increasing normal perfusion
57
Q

What kind of neuroprotective agents have been investigated for stroke treatment? Why have almost all neuroprotective agents failed to treat stroke?

A
  • glutamate antagonists
  • gltamate release inhibitors
  • free radical scavengers
  • Ca2+ chelators
  • GABA agonists
  • rushed trials
58
Q

TRUE or FALSE: pannexins prevent anoxic depolarizations

A

FALSE: pannexins CAUSE anoxic depolarizations and ischemic cell death

59
Q

Which receptor is the key driver of excitation and cell death? Do the channels have to open to cause cell death?

A
  • NMDAR
  • dont have to oepn to drive cell death
60
Q

What are the steps for pannexins and ischemic cell death?

A
  1. NMDAR
  2. Panx
  3. mPTP
61
Q

What leads to cell death cascades?

A

metabotropic coupling of NMDARs to Pannexin-1

62
Q

What are NMDA coupled via?

A

Src family kinases

63
Q

How do we interfere with the cell death siognalling in a stroke?

A
  • blocking the interaction of NMDA with Src
  • block anoxic depolarization
  • prevents panx1 opening and reduces damage and disability due to stroke
64
Q

How is NA1 used to treat stroke?

A
  • NA1 prevents PSD-95 interaction with NMDA and nNOS
  • this leads to generation of NO
  • NO leads to vasodilation/relaxation, notably in the collaterals
65
Q

Label the pathophysiology of stroke over time on a graph. list the bad and good outcomes over minutes, hours, days, weeks

A

BAD:
- minutes: energy failure, excitotoxicity, depolarizations, necrosis
- hours-days: secondary damage (inflammation, programmed cell death)
- weeks: complications

GOOD:
- minutes/hours/days: endogenous brain protection - collaterals, GABA, anti-inflammatory cytokines, trophic factors
- days/weeks: plasticity/regeneration/repair - axonal sprouting, synaptogenesis, neurogenesis, angiogenesis, remyelination, functional remapping

(slide 31)

66
Q

when is the best to to do rehab training after a stroke?

A

immediately after the injury because plasticity is at its peak, but then it decreases with time post-stroke

67
Q

What is the 3 step model for rehabilitative scheduless?

A
  1. IMAGING: determination of the metabolic and PLASTIC status of the brain
  2. APPLICATION OF GROWTH AND PLASTICITY PROMOTING FACTORS: enhancement of the plastic status of the brain and spinal cord –> SPROUTING FIBERS
  3. REHAB TRAINING: selection and STABILIZATION of newly formed functional connections
68
Q

Which protein peaks the most in the post-stroke cervical spinal cord? What is it associated with in terms of stroke recovery?

A
  • Gap43
  • when gap43 increases, axonal sprouting increases (i.e. Gap43 associated with spinal plasticity)
69
Q

after a stroke, at what day does axonal sprouting end? What does this imply about recovery?

A
  • axonal sprouting ends at 28 days
  • this means the window for functional recovery also ends at 28 days
70
Q

TRUE or FALSE: the uninjured side of the brain in a stroke can rewire and cross over at the spinal cord

A

TRUE

71
Q

What is the main barrier for axonal growth after stroke? What is the mechanism?

A

CSPGs - act on receptors NgR1, NgR3, RPTP

(therefore, if we get rid of CSPGs, we can promote axonal sprouting)

72
Q

TRUE or FALSE: CSPGs are downregulated by injury

A

FALSE: upregulated

73
Q

Why does sprouting and plasticity stop at 35 days?

A

bc there is an increase in CSPGs

74
Q

What is one way to get rid of CSPGs?

A
  • Chondroitinase ABC (ChABC) cleaves GAG chains from CSPGs
  • enhances plasticity and plasticity
75
Q

TRUE or FALSE: using only rehab can allow near full recovery after stroke

A

FALSE: both rehab and getting rid of CSPGs is necessary for good recovery –> INDUCES SECOND WAVE OF POST-STROKE RECOVERY

PHYSL 372 (21 decks)

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