Neurosciences > Exam3Lecture8Stroke > Flashcards

Exam3Lecture8Stroke Flashcards

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1
Q

What are modifiable risk factors of stroke?

A
  • high BP
  • High Body mass index
  • high fasting glucose
  • poor diet
  • high LDL
  • Kidney dyfunction
  • air pollution
  • alcohol use
  • smoking
  • low physical activity
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2
Q

What are Unmodifiable risk factors of stroke?

A
  • Age
  • Gender
  • Genetics
  • Head/ Neck Injuries
  • Pregnancy
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3
Q

What is a stroke?

A
  • Sudden loss of blood supply to brain tissue as a result of either a blocked or burst blood vessel
  • Loss of oxygen and nutrients leads to neural cell death (infarction)
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4
Q

What are the two types of strokes?

A
  • Hemorrhagic stroke (15%)
  • Ischemic stroke (85%)
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5
Q

What are the two types of hemorrhagic strokes?

A
  • intracerebral hemorrhage: in brain tissue
  • subarachnoid hemorrhage: btw pia layer and arachnoid layer-> bleeding in the space that surrounds the brain-> MOST DEADLY
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6
Q

What are the two types of ischemic stroke?

A
  • Thrombotic strokes: caused by a blood clot that develops in the blood vessels inside the brain.
  • Embolic strokes: Ouside of CNS-> when a blood clot or debris (embolus) travels from one part of the body and lodges in a narrower brain artery
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7
Q

What are the two types of ischemic stroke?

A
  • Thrombotic strokes: caused by a blood clot that develops in the blood vessels inside the brain.
  • Embolic strokes: Ouside of CNS-> when a blood clot or debris (embolus) travels from one part of the body and lodges in a narrower brain artery
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8
Q

Where do 65% of strokes occur in?

A

territory of the middle cerebral artery

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9
Q

Where do 15-25% of strokes occur? 10%?

A

15-25% occur in posterior circulation
* Otherwise effects not as severe
* Occlusion supplying the brainstem (basilar artery) often leads to death

10% of strokes occur in watershed areas (near capillary beds)

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10
Q

After MCAO, regions which sustain damage include:

A
  • Dorsolateral Striatum (usually damaged)
  • Neocortex (usually damaged)
  • Hippocampus (caused by larger strokes)
  • Thalamus (secondary injury)
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11
Q

Is middle cerebral artery or posterior ciculation stroke worse? explain?

A

posterior ciculation stroke because there no no other way to get blood around the brain since all the arteries come together at basilar artery -> EITHER MAJOR EFFECT OF NO EFFECT

Middle cerebral has another side to supply the brain

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12
Q

External carotid supplies what? which sends collaterals to the brain via what? (2)

A
  • External Carotid supplies facial artery which sends collaterals to the brain via the internal carotid
  • External Carotid supplies superficial artery which also sends collaterals to the brain via the internal carotid

Bold: how we connect the two

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13
Q

External to vertebral artery connects through what?

A

External Carotid supplies the occipital artery which sends collaterals into the vertebral artery

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14
Q

External to internal
1. external->
2. external->

A
  1. Facial
  2. superficial
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15
Q

External to Vertebral
* External->

A

occipatial

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16
Q

what are the leptomeningeal branches/anastomoses

A

watershed areas
* Anterior cerebral artery
* middle cerebral artery
* posterior cerebral artery

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17
Q

What are all the collateral blood flow?

A
  1. External -> facial
  2. External -> superficial
    1. External -> occipital
  4. Circle of Willis
  5. Leptomeningeal-> anterior, middle, posterior
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18
Q

What is unique about the cicle of willis?

A

If you get damage on your right side, flow on the left may compensate for losses on the right side

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19
Q

What is the importance of collateral flow in recannulation?

A

When you have high collateral flow, the infarct will not be as bad because blood will reach there

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20
Q

What are the regions that are damage after MCAO?

A
  • NeoCortex , Dorsal-lateral striatum, corpus callsum, Hippocampus
  • Thalamus-> considered a 2nd injury
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21
Q

The types and degrees of disability that follow a stroke depend upon what?

A

area of the brain is damage and how much damage is there

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22
Q

What are the five types of disabilities?

A
  • paralysis or problems controlling movement sensory disturbances including pain
  • problems using or understanding language
  • problems with thinking and memory
  • emotional disturbances
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23
Q

What are the sensory distrubances after stroke?

A
  • lose the ability to feel touch, pain, temperature, or position
  • neuropathic pain-> nothing will stop it completely
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24
Q

What are problems using or understanding language after stroke?

A
  • One-fourth of all stroke survivors experience language impairments
  • Broca’s area, causes expressive aphasia (can understand words but cannot respond to them)
  • Wernicke’s area, results in receptive aphasia (cannot understand but can talk)
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25
What are the problems with thinking and memory after stroke?
shortened attention spans or may experience deficits in short- term memory
26
What are the emotional distrubances after stroke?
* fear, anxiety, frustration, anger, sadness, and a sense of grief -> depends on what area you damage * clinical depression is common-> not sure if it is damage or just dealing with the stroke
27
What is the core of a stroke?
* the region that lost direct vascularization * Cells within this region usually die within minutes and create an infarct * Place that loses vascularization
28
What is the area surrounding the core?
Penumbra
29
What is happening in the penumbra from a stroke?
Although this area did not directly lose blood flow, the damage caused at the core leads to inflammation and apoptosis. Compensatory reactions such as acidosis, decreases in protein synthesis, and selective gene expression within this region intensify inflammation and can eventually lead to cell death if left untreated.
30
What happens in the immediate phase?
* Vascular thrombosis * Platelet embolization * BBB permeability * **Metabolic stres -> Increase lactate, decrease ATP** * **Ionic perturbations (Ca++, Na+, K+)** * **Anoxic depolarization (cortical spreading depression)-> no O2 so trouble firing APs** * Cytokine release
31
What happens in the acute phase?
* **Selective neuronal damage (necrosis)** * **Inflammation (PMNLs, Macrophages, lymphocytes, microglia)** * Vascular reactivity abnormalities * glial swelling * secondary axotomy | Phase II
32
What happens in the subacute phase?
* **Apoptosis** * **Protein Aggregation** * Cell signaling perturbations * Gene expression (HSP, Growth factors) * Axonal Damage (permanent, transient, delayed) * Axonal transport abnormalities * Wallerian degeneration | phase III
33
What happens in the ultimate outcome
* **Infaract formation** * **progressive tissue loss (atrophy)** * Functional deficits (behavioral and electrophysiological) | Phase 4
34
What is happens in the brain after a stroke?
35
What does neuropatholgy affect?
all cell populations in the CNS
36
What are happens to neurons, astrocytes, oligodendrocytes?
* Necrotic & Apoptotic cell death Cellular inclusions * Vaculoation of neurons/neuropil Binucleated * Neurofibrillary tangles * Neuronal storage disorder * Edema (axon, astrocyte processes | some degen casude as alz
37
What are two ways neurons die after stroke?
* Necrosis-> no going back and happen quickly * Apoptosis ->affects the penumbra layer
38
What is the difference of necrosis and apoptosis? | hy
## Footnote hy
39
What are two ways of visualizingdying neurons?
TTC and Fluorojade
40
How does TTC work?
Vital dye * Dye used to detect vitality of tissue shortly after stroke/trauma-> Good for early on detection * If cells are alive they take up red dye and white areas are dead cells
41
How does fluorojade work? ⭐️
good for later on * Basic dye that is attracted to acidified cells (dt to lacate acid+glutamate) * More sensitive than most other histochemical methods * Easy to use and can see individal population unlike TTC
42
What are the glial response to brain injury?
oligodendrocytes. astrocytes and microglia respond
43
What happens to glial cells?
* Nuclear hypertrophy * Scar forming
44
How does astrocytes react to injury?
* React to injury becoming hypertrophic (enlarged) and expressing increased **glial fibrillary acidic protein (GFAP)** * Wall off injured area
45
What happens to oligodendroglials after stroke? What can we use to help?
* oligo lose myelin basic protein and the production of neuronal myelin sheath. Decreased AP propagation * Can use HUCBC (cord blood cells) to lessen the damage
46
How does microglial resposne to stroke?
Increase after stroke * React to injury becoming phagocytic and releasing inflammatory cytokines * Responsible for **delayed neuronal death**
47
* When do you want microglia present? * When do you not want them present?
* You want them early on at the site of damage to get rid of all the debris for repair * You do not want them 48-72 hours after when perpherial immune cells come in
48
What is the unifying pathophysiolic mechanisms of CNS injury
49
What is inflammation?
a protective response occurring in the vascularized connective tissue in response to an insult
50
What does inflammation response to?
* Bacteria * Virus * Tissue Injury * Pattern Recognition Receptor on antigen presenting cells respond to PAMPs (bacteria) or DAMPs (tissue damage) that binds to toll like receptors
51
What does inflammation remove +result?
* Removes noxious agents, thereby limiting their detrimental effects * Becomes dysregulated with age * uncontrolled inflammation may be harmful and may underlie the pathogenesis of many acute and chronic diseases
52
In stroke pts . what is inflammation cascade triggered by?
In stroke patients, inflammatory cascades are triggered by the release of endogenous molecules by damaged tissue and necrotic cells. These endogenous molecules will bind to pattern recognition receptors (i.e. DAMPs) which illicit the NFkB pathway.
53
Why is inflammation a double edged sword?
During instances of neuronal injury, microgliosis can have two effects: tissue repair and recovery OR chronic disease progression. * Tissue repair and recovery is mediated by timely and well-regulated inflammation which can remove noxious agents and limit their detrimental effects. * Uncontrolled inflammation, however, may be harmful and an underlie the pathogenesis of many acute and chronic diseases
54
look at slide 22
55
What is the function of neurotrophic factors?
secrete proteins that modulate neuronal growth, differentiation, repair, and survival; some have additional functions, including roles in Neurotransmission and in the synaptic reorganization involved in learning and memory
56
What are the different neurotrophins and their corralating receptors
* TrkA receptor: NGF * TrkB receptro: BDNF, NT-4/5, NT-3 * TrkC receptor: NT3 * p75 receptor: all of them above
57
Explain the signal cascade for trk receptor
58
What does the signal cascade for p75 receptor lead to
decr in neural cell survival (cell death)
59
What are the other neurotrophic factor families
60
What does BDNF do?
central role in neuronal survive because have repairative affects in brain
61
Explain the structural organization of NF-KB, IKB, IKK
62
Explain the activation of the canonical NF-KB pathway
Activation of the canonical NF-kB pathway culminates in the translocation of NF-kB dimers (p65/cRel + p50) into the cell nucleus. This activates gene transcription of pro-inflammatory mediators.
63
Explain the activation of the alternative NF-B pathway
64
What happens when there is a lack of p50?
increase vulnerability to neurotoxic insult
65
What are questions about research models?
66
What is 1,3-Di-O-Tolylfuanidine (DTG)? Function?
Selective Sigma 1 and Sigma 2 receptor ligand **Neuroprotective** * Inhibits ischemia induced cell death * Regulates Ca2+ homeostasis and membrane excitability * Upregulates neuroprotective genes **Anti-inflammatory** * Inhibits microglial inflammatory responses
67
What does DTG do?
Decreases Neurodegeneration as Indicated by Fluoro
68
How was DTG short term and long term?
Very good short term but long term results (5 weeks) there was no improvement of behavior and tissue
69
What is important about therapeutic targets for strokes
need to focus on more than one effect
70
What is the preclinical STAIR Criteria to enhance translation of stroke therapies?
Neurosciences
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