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Neuro 1 > CVA Intro and Patho > Flashcards

CVA Intro and Patho Flashcards

1
Q

Modifiable risk factors for CVA:

A

i. HTN
ii. Diabetes
iii. CV Disease
iv. Obesity (connected with obstructive sleep apnea)
v. Obstructive Sleep Apnea (hypoxia during sleep)
vi. Physical inactivity
vii. Diet
viii. Blood disorders
ix. Arrhythmias (Atrial fib)
x. Hyperglycemia
xi. Smoking
xii. Alcohol
xiii. Recreational drug use

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2
Q

How can Obstructive Sleep Apnea lead to stroke?

A

hypoxia during sleep can lead to morning strokes

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3
Q

Non-modifiable risk factors for CVA:

A 
W>M
Age: >55yrs
Race (black/hispanic)
Prior stroke, TIA, and or MI
Genetics
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4
Q

Cause of ischemic stroke -

A

Gradual worsening of fatty deposits lining arterial walls (atherosclerosis)

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5
Q

Two types of ischemic strokes -

A
  1. Thrombotic

2. Embolic

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6
Q

Most common type of ischemic stroke -

A

Thrombotic

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7
Q

Thrombotic stroke caused by what?

A

Blockage caused by clot form within involved artery

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8
Q

Embolic stroke caused by what?

A

Blockage caused by clot that travels from elsewhere in circulatory system

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9
Q

Common origins of embolic strokes?

A
  1. Heart

2. Larger arteries of upper chest and neck

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10
Q

Embolic ischemic strokes more commonly found in what type of arteries?

A

Distal and smaller arteries

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11
Q

Cause of hemorrhagic stroke?

A
  • Rupture of artery due to weakening of vessel wall

- atraumatic – spontaneous event

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12
Q

Primary cause of Intracerebral hemorrhage (ICH)?

A

HTN

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13
Q

Primary causes of subarachnoid hemorrhage (SAH)?

A 
Aneurysm 
Arteriovenous Malformation (AVM)
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14
Q

Aneurysm -

A
  • enlargement/ballooning of weakened vessel wall

- Typically asymptomatic until rupture

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15
Q

Arteriovenous Malformation (AVM) -

A
  • tangle of abnormal blood vessels connecting arteries and veins (brain and spinal cord most often)
  • Congenital: symptoms don’t show up till late teens-30 yrs and some don’t even have symptoms
  • Symptoms: seizures, HA, weakness, speech and vision, or can be asymptomatic
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16
Q

What is a Transient Ischemic attack (TIA)?

A

mini/warning stroke

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17
Q

Causes of Transient Ischemic attack (TIA) -

A

Not entirely understood:

  1. Leading hypothesis: temporary blockage that dissolves on its own or gets dislodged naturally
  2. Cerebral vasospasm and transient systemic arterial hypotension
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18
Q

T/F 10x increased chance for full blown CVA with history of TIA

A

True, highest risk for stroke in first 90 days post TIA

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19
Q

Describe the steps of ischemic cascade:

A
  1. Loss ATP production (loss of aerobic metabolism) followed by increased lactic acid in brain (change in ph)
  2. Stoppage of Na/K pump
  3. Excess intracellular Na -> influx H2O = cytotoxic edema (deadly swelling)
  4. Excess intracellular Ca -> excess glutamate release at axon terminal
    - Hyper-excitability cycle transpires throughout nearby neurons =“Excitotoxicity”
    - Activates degradative enzymes that breakdown proteins in neuron and cell membrane
    - release of free radicals -> neuronal death via necrosis
  5. Breakdown of mitochondria in response to toxins and unstable cell membrane
    - Neuronal death via apoptosis (nearby neurons die on purpose)
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20
Q

Infarct core? Time frame?

A
  • primary blood supply (necrosis)
  • irreversible damage
  • Within minutes
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21
Q

Penumbra? Time frame?

A
  • area surrounding ischemic event
  • increase area of cell death -> leads to greater stroke (apoptosis)
  • potentially salvageable
  • Within hours
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22
Q

History of present illness (HPI) includes what aspects?

A
  1. Past medical history/systems review

2. Description of symptoms (onset, type)

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23
Q

Onset of symptoms for thrombotic stroke -

A

gradual onset, days to weeks

- Most common in late PM or first thing AM, may see “wake up strokes”

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24
Q

Onset of symptoms for embolic stroke -

A

more abrupt than thrombotic, minutes to hours

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25
Onset of symptoms for hemorrhagic stroke -
immediate, severe Aneurysm: asymptomatic until rupture AVM: may have preceding symptoms (seizures, etc)
26
Common complaints of stroke symptoms -
- imbalance, paraesthesias, weakness, blurry or double vision, - “Worse HA of my my life” common with hemorrhages, particularly aneurysms
27
National Institutes of Health Stroke Scale (NIHSS) -
- Quantitative measure of symptoms associated with - Most commonly used in acute phases of CVA - Diagnostic power strong
28
``` Cutoff scores for NIHSS and where patient will be discharged: >25 15-24 5-14 1-5 ```
>25 very severe - long-term skilled care 15-24 severe - long-term skilled care 5-14 mild-moderate severe - acute patient rehab 1-5 mild - 80% discharged home from acute hospital
29
CT preferred for patients in these situations:
1. Head trauma 2. Financial concerns 3. Acute hemorrhage 4. Speed needed 5. Skull fracture 6. Calcified lesion 7. Claustrophobic patient 8. Pacemaker/other metallic implant
30
MRI preferred for patients in these situations:
1. Subtle areas of tumor, infarct, demyelination 2. Brainstem lesion 3. Ischemia 4. Subacute/chronic hemorrhage 5. Anatomy detail needed
31
Cerebral edema -
swelling in the brain
32
Cerebral edema can cause increased intracranial pressure (ICP) What is ICP? Pt considerations?
ICP: pressure exerted by fluids in brain (CSF, interstitial fluid) - If elevated, can lead to further damage to brain tissue - PT Considerations: monitor for S&S of ↑ ICP, avoid activity that may exacerbate, mobility usually contraindicated if >20mmHg
33
Cerebral edema can cause midline shift: What is midline shift? Pt considerations?
Shifting of structures into contralateral hemispheric space due to fluid buildup - Poor prognostic indicator for functional recovery - PT Considerations: evaluate for bilateral symptoms, monitor closely for neurological decline
34
Cerebral edema can cause brain herniation: What is brain herniation? Pt considerations?
Protrusion of brain tissue through rigid intracranial barrier (ex: foramen magnum - Very poor prognostic indicator, typically leads to mortality - PT Considerations: PT usually not indicated
35
What is a vasospasm?
Persistent vasoconstriction and dilation of the blood vessels Typically asymptomatic, but can be highly dangerous
36
When is a vasospasm most commonly seen? When greatest risk?
Most commonly seen post SAH (subarachnoid hemorrhage) | Great risk: 7 days post bleed
37
How monitor vasospasms?
Transcranial Doppler (TCD)
38
How treat vasospams?
Permissive HTN – cause HTN that opens the vessel
39
Pt considerations vasospasm?
Mobility contraindicated with moderate to severe vasospasm – consult MD prior to mobility
40
Seizures are most commonly seen after what type of hemorrhage? When greatest risk?
Most commonly seen post ICH (intracerebral hemorrhage) | Greatest risk: first 48 hours post ICH
41
How monitor seizures post-stroke?
Electroencephalogram (EEG)
42
How treat seizures post-stroke?
Anti-seizure medication, surgery rare
43
Pt considerations for seizures post-stroke?
Mobility usually deferred until >24hr after quiet EEG. Monitor closely for seizure activity
44
Other acute CVA complications: (6)
Hypertension, Infection, Fever, Pneumonia, Pressure ulcers, Hyperglycemia
45
Major goal of acute management of ischemic stroke?
Revascularization
46
Medication (general) used for acute management of ischemic stroke?
Tissue plasminogen activator (tPA) 1. Clot buster into blood stream 2. 3-8 hour window of opportunity
47
What is permissive HTN used for acute management of ischemic stroke?
1. < 220/110 | 2. Increase pressure to force blood through vessel
48
Major goal of acute management of hemorrhagic stroke?
Reduce intracranial pressure (ICP) - Sedation - hyperosmolar agents - hyperventilation (hypocapnia -> vasoconstriction -> slow down blood flow)
49
Medication (general) used for acute management of hemorrhagic stroke?
Anti-hypertensives for BP control | - Strict BP parameters (< 130/80)
50
Prognostic considerations of hemorrhagic stroke?
higher mortality rates acutely, but better prognosis for neuro-recovery long-term
51
Prognostic considerations of ischemic stroke?
lower mortality rate, but tend to demonstrate slower and less recovery
52
T/F First 1 month is crucial period for rehabilitation and neuro recovery
False, first 3 months
53
T/F Evidence supports possibility of significant neuro recovery up to 18 months post injury
True
54
Functional Outcomes by Vascular Territory: (most disability to least)
1. Multiple vascular territories 2. MCA 3. ACA 4. PCA 5. Brainstem 6. Small vessel stroke 7. cerebellar
55
Common impairments of UE post stroke:
paresis, loss of isolated movement, abnormal muscle tone, and sensory changes.
56
More involvement seen in (UE/LE) post stroke:
UE
57
Positive prognostic Indicators for UE recovery (4 weeks post injury):
1. Early active finger extension, grasp release, shoulder shrug, and shoulder abduction observed 2. Absence of additional non-motor impairments, such as somatosensory loss, visual field loss and/or neglect 3. Presence of a measurable grip strength or active shoulder flexion
58
Positive prognostic indicators for return to ambulation post stroke:
1. Ambulation on evaluation 2. Balance scores on evaluation (BBS, Romberg, DGI) 3. Minimal loss of LE strength and somatosensory function 4. No evidence of perceptual, visual, or cognitive deficits 5. Healthy BMI 6. <65
59
Gait speed:
60
Additional prognostic considerations:
1. Cognitive deficits 2. Activity intolerance - leads to secondary complications 3. cardiac disease 4. Depression 5. Fatigue - may predict mortality

Neuro 1 (5 decks)

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