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344 final > Stroke 1 > Flashcards

Stroke 1 Flashcards

1
Q

classification

A

cryptogenic 30%, no risk factors no idea why it happened
cardiac embolism 20%
small vessel disease 25%
atheroscl cerebrovasc disease 20%

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2
Q

Acute Stroke defn

A

An episode of symptomatic neurological
dysfunction caused by focal brain, retinal or spinal cord
ischemia or hemorrhage with evidence of acute
infarction or hemorrhage on imaging (MR, CT, retinal
photomicrographs), and regardless of symptomatic
duration

show damage on ct scan even if symptoms resolve
symtpoms >24 hrs doesnt go away, no stroke seen on ct, still a stroke

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3
Q

Transient Ischemic Attack (TIA)

Hemorrhagic transformation

• Crescendo TIAs

Stroke in evolution

A

A brief episode of
neurological dysfunction caused by focal brain, spinal
cord or retinal ischemia, with clinical symptoms lasting
<24 hours and without imaging evidence of acute
infarction. (see no damage and symp go away)

• Hemorrhagic transformation – bleeding into area of cerebral infarction
• Crescendo TIAs – a series of TIAs separated by periods where blood flow
and neurological function return to normal that occur in succession
• Stroke in evolution – worsening of neurological deficits over minutes or
hours suggesting a widening of the area of brain ischemia

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4
Q

ETIOLOGY

2 typs

A

penetrating artery disease: little arteries are vul to blocking off (small vessel disease), diabetes, smoking, htn
AF
many ways it can happen

hemmoraghic stroke: break off and causes damage
ischemic: decreased blood flow to brain and tissue start to die

An ischemic stroke is when blood vessels to the brain become clogged. A hemorrhagic stroke is when bleeding interferes with the brain’s ability to function.

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5
Q

Stroke Risk Factors

Modifiable

A 
• Hypertension
• Dyslipidemia
• Diabetes
• Smoking
• Homocysteine
• Waist-Hip Ratio
• Diet/Exercise
• Alcohol
• Stress
• Depression
• Cardiac Issues (valvular heart
disease, cardiomyopathy, Afib, PFO,
etc)
• Sleep Apnea
• Illicit drug use (can cause
vasospasm, cardiomyopathy)
• Oral estrogen therapy
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6
Q

Stroke Risk Factors

Non-Modifiable

A 
• Age
• Sex
• Ethnicity
• Family History (Genetic factors)
• Previous TIA or Stroke
• Amyloid angiopathy (increase ICH
risk)
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7
Q

signs of stroke

A

Face - is it drooping
Arms - can you raise both
Speech - is it slurred or jumbled
Time - call 911 right away (activates stroke system, ambulance knows and coordinate hospital)

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8
Q

FIVE cardinal signs and symptoms (patient may have one or

more present):

A

Ø Severe headache (“worst of my life”) - blood vessels hurt
Ø Sudden weakness (paralysis)
Ø Sudden changes in speech (aphasia, dysphasia)
Ø Sudden change in vision (blurred, diplopia double vision, loss)
Ø Sudden dizziness (ataxia)

can have 1 or all symptoms, depending on size and location of stroke

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9
Q

Stroke Mimics

A 
Seizure
• Syncope
• Sepsis
• Migraine
• Space occupying lesions (e.g. tumor)
• Functional disorders
• Metabolic conditions
• Vertigo
• Bell’s Palsy
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10
Q

Sequelae of Stroke

A
  • Hemiparesis/Hemiplegia
  • Aphasia/Dysphasia
  • Altered level of consciousness (LOC)
  • Nausea/Vomiting/Dizziness
  • Disorientation/Confusion
  • Vision changes
  • Dysphagia - swallowing, some ppl need feeding
  • Loss of driving privileges - not to drive for 30 days
  • Inability to return to work
  • Depression
  • Neuropsychiatric dysfunction
  • Seizures
  • Increased susceptibility to infection (catheters, NG tubes)

aspiration pneumonia common

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11
Q

WORK-UP - diagnosis

A

Clinical presentation
ì Neurologic exam (NIHSS) https://www.stroke.nih.gov/documents/NIH_Stroke_Scale_508C.pdf (0 - no problems, 20 - pretty severe)
ì CT scan (or CT angiography) - widely avail
ì MRI (or MR angiography) - harder to get
ì Ultrasound of carotid arteries or angiography - vessels in neck, intracranial vasculature
ì Echocardiography
ì ECG, 24 hour Holter monitor - every pt at emerg, AF high yield
ì Vitals (BP, HR, RR, O2 Sat, Temp)
ì Standard Labs
• Lipid panel, fasting glucose, CBC, lytes, SCr, TSH, PTT, INR, HgA1C, troponin

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12
Q

What lab would you use to RAPIDLY
assess for presence of dabigatran?

1) INR
2) Anti-Xa
3) Thrombin Time
4) PTT
5) Hemoglobin
6) Dabigatran level

A

Tissue plasminogen activator is a protein involved in the breakdown of blood clots.

direct thrombin (factor II?) inhibitor, most sensitive assay is thrombin time (prolonged if on dabig)
Xa (for edoxaban)?

may take a few days to see in CT scan, rule out hemorhage to give TPA

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13
Q

CT scan

MRI scan

A

may take a few days to see in CT scan?, rule out hemorhage to give TPA

MRI more sensitive to pick up ischemia (not blled), not acture (harder to get), see extent of stroke

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14
Q

GOALS OF THERAPY

A
  • Reduce morbidity and mortality
  • Minimize long-term disability
  • Avoid medical complications
  • Prevent stroke recurrence
  • Minimize adverse effects from medications
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15
Q

HYPERTENSION
dyslipidemia
diabetes
smoking

all increases CAD

A

HYPERTENSION
• Increases stroke risk 1-4x baseline
• Decrease of DBP by 6 mmHg ARR 1.3% over 4-5 years

DYSLIPIDEMIA
• Increases stroke risk 1.8-2.6x baseline
• Statin therapy ARR 0.4% over 4 years

DIABETES
• Increases stroke risk 1.8-6x baseline
• Not confirmed if tight control reduces risk

SMOKING
• Increases stroke risk 1.8x baseline
• 50% RRR after 1 year; to baseline after 5 years

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16
Q

diet and exercise

A

DIET
• Fruit and vegetable consumption inversely associated
with risk of stroke
• True for higher fibre, lower GI, lower saturated fat,
higher omega-3 diets as well

• EXERCISE
• Increased physical activity associated with less
morbidity/mortality from stroke
• Moderate 150 min/wk OR vigorous 75 min/wk OR
combo of the two
• Even 20 minutes of walking a day helps!

17
Q

ANTIPLATELETS

A

Three large trials in 2018 studying ASA >47 000 pts
• ARRIVE – Primary prevention of ASCVD in nondiabetic patients at
moderate risk of CVD
• ASCEND – Primary prevention of ASCVD in diabetic patients
• ASPREE – Primary prevention in community-dwelling elderly patients
• Balance potential benefit vs. risk of GI bleed
• For patients with atrial fibrillation ASA or
anticoagulation based on scoring criteria (ex. CHADS2)

Canadian stroke best practice(CSBPR)
“The use of acetylsalicylic acid is not recommended for primary prevention
of a first vascular event (evidence level A)”
“The net benefit of ASA in individuals with asymptomatic atherosclerosis is
uncertain (evidence level B)”

An individual’s risk, benefit, values and preferences should be considered

18
Q

Tools to quantify risk

A 
Need individualized approach
• Patient’s individual risk
• Large NNT
• Side effects of medications
• Patient values
  • Tools to quantify risk
  • Framingham
  • CHADS2/HASBLED for A-fib patients
19
Q

acture issues

flowchart

A

stroke - CT scan - ischemic - evaluate for thrombolysis -> tPa given, not given, endovascular intervention

CT scan - hemorrhagic - surger

20
Q

THROMBOLYSIS

dont need to prove ischeic stroke, just prove no hem

A

• Recanalization limits ischemic infarct size, minimizes
neurologic sequelae
• Many trials evaluated thrombolytics
• NINDS trial first to show benefit > risk (used 3 hour window)
• ECASS III allowed us to expand window (to 4.5 hours)
• t-PA (alteplase) eligibility:
• Ischemic stroke
• Presentation within 4.5 hours
• No contraindications (Of which there are many)
• May benefit highly select patients beyond 4.5 hour window (rare)

21
Q

THROMBOLYSIS CONTRAINDICATIONS

A
  • Blood pressure >185/110 (relative contra)
  • Use of anticoagulants in past 48 hours (INR > 1.7) (they may not be taking it adherent)
  • Intracranial neoplasm or vascular malformation
  • Stroke, intracranial surgery or head injury within 3 months
  • Major surgery within past 14 days
  • Blood glucose <3 or >22 mmol/L
  • Seizures at onset for stroke
  • Other bleeding (ex. GI or GU) within 21 days
  • MI within three weeks
  • Aortic dissection or pericarditis
  • Arterial puncture at a non-compressible site within 7 days
  • Recent lumbar puncture
  • History of intracranial hemorrhage
  • Presentation suggestive of subarachnoid hemorrhage
  • CT evidence of hemorrhage
  • Rapidly improving neurological signs or minimal deficit
  • Pregnancy
22
Q

t-PA (alteplase)
target within 4.5hrs of symptoms
if too late, need to see CT and size to see if you would still get tpa

A
  • Target “door-to-needle” time of 30 minutes
  • Dose
  • Single IV dose of 0.9mg/kg (max 90mg) - always this dose
  • 10% bolus over 1 minute then rest as 60 minute infusion
  • Keep BP < 185/110mmHg
  • Typically delay antiplatelet and DVT prophylaxis until 24 hours post-tPA
  • Repeat CT scan required first to rule out hemorrhage
23
Q

NINDS
• Benefits
risks

A

• At 24 hours:
• Improvement if received tPA at 0-90 minutes
• At 3 months:
• ~12% ARR in number of patients with minimal or no
disability (NNT = 8)
• No significant mortality benefit
• Shorter hospital stay
• Higher proportion discharged home vs. LTC/rehab
• Risks
• 6.4% symptomatic ICH in tPA group (0.64% placebo; NNH = 17)

24
Q

ENDOVASCULAR INTERVENTION

A
  • Mechanical thrombectomy in patients with large artery occlusions presenting within 6 hours (majority of patients) of onset of stroke, proximal large vessels usually
  • Can be done up to 24 hours from onset in highly selected patients
  • May be performed post-tPA
  • Many clinical trials (~10)
  • Improved functional outcomes at 90 days - 5 mins later, they can move and talk
  • 1 trial showed mortality benefit (ESCAPE)
  • Most trials (8) stopped early
25
Q

ANTITHROMBOTICS – General Principles

A
  • Antiplatelets given as soon as possible once hemorrhage is ruled out on initial CT (if no thrombolytics given)
  • Delayed for 24 hours post tPA until repeat CT scan rules out hemorrhage
  • Anticoagulation (IV heparin, LMWH, DOACs, warfarin, etc) is typically avoided in the acute setting as newly infarcted brain tissue is at high risk of hemorrhagic transformation
  • If concurrent medical issues arise in acute stroke setting where anticoagulation is warranted (ex. LV thrombus, PE, DVT, etc), delay of start time for AC is clinically judged on case by case basis; typically the “larger the infarct the longer we wait
26
Q

ANTITHROMBOTICS – Options

A

• ASA (Aspirin)
• Given as 325mg PO/PR initial loading dose then continued at 81/80mg
PO/NG daily (or 325mg PR daily if no gastric access)
• Decreases recurrent ischemic stroke risk
• Decreases number of patients dead or dependent
• Non-significant increase in ICH
• If on ASA pre-stroke…? “ASA failure”

  • Clopidogrel (Plavix)
  • Given as 300mg PO initial loading dose then continued at 75mg PO/NG daily
  • Lack of literature in acute setting (studies focused on secondary prevention)
  • Some clinicians prefer in “ASA failure” patients; no evidence

344 final (16 decks)

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