Stroke Part 1 Flashcards

1
Q

Which regions are most affected by an MCA stroke?

A

lateral part of the brain, hand and face most affected

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2
Q

which limbs are most affected by ACA stroke

A

leg structures

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3
Q

key issues you’d find in someone with a PCA stroke

A

PCA= posterior = region where occipital lobe is = All about vision, recgonizing faces, issues with writing sometimes, but mainly Alexia (inability to read because of visual problem)

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4
Q

Stroke to the PICA can cause ____ syndrome

A

wallenburd syndrome/Lateral medullary syndrome: pain and temp loss to ipsilateral face and contralateral body.

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5
Q

A basilar stroke can lead to brainstem ischemia and aamge the pons, which can cause __ ___ syndrome

A

locked in syndrome– complete quadriplegia, can only move the eyes.

A vertebral artery dissection also causes locked in syndrome

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6
Q

Most Neurospells are actually TNAs: __ ___ attacks. Can be mistaken of TIA.

A

Transient neurological attacks \

Benign paroxysmal positional vertigo: crystals in inner ear that throw off vestibular system and can cause dizziness, lasting for <60s.

Often initiated by bump to head, turning in bed, sitting up lying down, etc.

Dx with Hallpike Maneuver.

Migraine Aura: visual phenomenons, diplopia, tingly arm→ can be mistaken for TIA.

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7
Q

T/F TIA’s are caused by acute infarction

A

false.

a transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischemia, without acute infarction.

Mild strokes and TIAs are lower risk.

An acute infarction will cause a full on stroke

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8
Q

Key distinguishing features between central vestibular dysfunction and peripheral vestibular dysfunction

A

centarl: imablance, neurological symptoms/signs, bidirectional nystagmus

PeripheraL: auditory symptoms, unidirectional nystagmus, nausea and vomiting

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9
Q

Risk factors for ischemic stroke

A

hypertension ***, DM, hyperchoelsterolemia, smoking

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10
Q

risk factors for ICH

A

Hypertension ***, alcohol, cocaine, meth

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11
Q

risk factors for SAH:

A

smoking***, family history

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12
Q

risk factors for sinovenous thrombosis:

A

hormonal therapy**** hypercoaguable states like pregnancy or inhertied

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13
Q

CHAD265 score can be used to determine which type of treatment should be used in people with AFib to determine stroke score

A

C; congestive heart failure

hypertension

age

dm

prior stroke or TIA

  • if a lower score, may just need ASA. But if higher score, use DOACS for afib management and carrdioembolic stroke prevention
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14
Q

Primary Prevention of Stroke: Targets

A

Treatment of hypertension→ treating hypertension reduces hemorrhagic and lacunar (ischemic) strokes the best.

Stopping smoking

Treatment of high LDL

Reduce alcohol intake, increase exercise

Anticoagulation in Afib. → use Warfarin or DOACs

  • CHAD265 Score: simple prediction tool for assessing stroke risk:
  • Congestive heart failure
  • Hypertension
  • Age
  • DM
  • Prior stroke or TIA.
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15
Q

Primary Prevention of Atheroscleorosis-related stroke

A

Asymptomatic ICA stenosis; younger males modestly benefit from carotid revascularization.

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16
Q

Primary Prevention of SAH (subarachnoid hemorrhage)

A

recall that SAH is primarily caused by smoking and family history

Unruptured aneurysm; screen families with first degree relatives who have had SAH. MRA preferred. Encourage smoking cessation of entire family (Encourage smoking cessation of the entire family!

>7mm aneurysm warrants consideration for clipping or coiling.

17
Q

Primary Prevention of ICH

A

Limit alcohol intake

Avoid weight loss drugs (PPA, ephredrin)

18
Q

AIS is the main type of stroke. What are the 5 broad categories of acute ischmec storke?

A
  1. large artery atherscloertic stenosis
  2. small artery disase (lacunar stroke)
  3. cryptogenic
  4. cardioembolic stroke
  5. unusual
19
Q

most common cause of acute ischemic stroke

A

large artery atherosclerosis.

Atherosclerosis causes platelet aggregation, which is a lot of active embolization. Therefore atherosclerosis is a bunch of mini emboli, vs cardioembolic is one larger emboli.

Large arteries can harden, MCA stenosis can also happen (intracranial medium sized atherosclerosis)

MCA arteries/Intracranial stenting not safe. Too small.

20
Q

2 revascularization options for large vessel atherosclerosis-stroke.

key non-surg management

A

Two revascularization options:

Carotid endarterectomy CEA

Carotid aortic stent. CAS–> usually done cause less invasive

Non surg management: statins, treatment of comorbid conditions like dyslipidemia, possibly EPA/fish oil derivative. Add Ezetimibe.

Rule of 6: if the dose of a statin is doubled, there is a 6% increase in LDL lowering.

21
Q

Key young adult stroke

A

PFO related stroke: those with a patent foramen ovale (young adult stroke).

Dissections, PFOs and other rare/unusual conditions make up majority cause of strokes in young people under 60.

Treatment of PFO related stroke is to fix the PFO

Larger shunt is a risk factor. There is a clear benefit in stroke prevention with PGO closure overall in patients under 45. The larger the shunt, the more beneficial.

22
Q

Number one cause of a cardioembolic stroke leading to acute ischemic stroke. Treatment?

A

AFIB IS THE NUMBER ONE CAUSE OF CARDIOEMBOLIC STROKE

  • most cardioembolic causes are treated with warfarin, but for afib, use the CHAD265 score to determine ASA/APA vs DOAC! (DOAC USUALLY)
23
Q

Lacunar/ Small Vessel Cause of Ischemia

Often occurs in basal or brainstem penetrating arteries due to __ __.

Most common in _.

__ APA is better than _ _ therapy. Also manage hypertension.

Cholesterol lowering doesn’t have the same benefit as it does in large vessel strokes.

Other→ 5% are unusual presentations like dissections, arteritis.

A

Lacunar/ Small Vessel Cause of Ischemia

Often occurs in basal or brainstem penetrating arteries due to hypertensive arteriolosclerosis.

Most common in ASians.

Aspirin APA is better than dual antiplatelet therapy. Also manage hypertension.

Cholesterol lowering doesn’t have the same benefit as it does in large vessel strokes.

Other→ 5% are unusual presentations like dissections, arteritis.

24
Q

ICH; what sign do you see on CTA

risk factors? management?

A

ICH; can differentiate between other bleeds like SAH because ICHS are lobar and deep, whereas SAHs and epidural hematomas are on the outside. WOuld see a characteristic “spot sign,” which is positive for intracerebral hemorrhage

Risk factor: people on anticoagulants, people with hypertension, cocaine.

Management: correct any coagulopathies/stop any anticoagulants that could be causing them to unnecessarily bleed.

Acute lowering BP <150mmHg (no effect if you lower it more aggressively under 150), Vitamin K, and prothrombin complex concentrate (Clotting factors: FII, VII, IX and X, protein C and S), hemostasis (limited because bleeding occurs very early.

Surgery: indications are superficial lobar hemorrhage, CGS 9-12, volume 20-80ml, worsening status, young patient, high ICP, moderate or large cerebellar ICH.

25
Q

Most common cause of subaracnoid hemorrhage? Key symptom

A

most common cause: berry aneurysm ( most common cause), AVF, dissection. Key risk factor is smoking!

Key symptom: worse head of life/thunderclap, neck stiffness/soreness, nausea/vomiting

26
Q

investigations when suspecting a subarachnoid hemorrhage

Management of SAH?

A

CT head

CSF exam (may see zanthochromia in fluid) due to lysis of RBCs

Berry aneurysm: coils, clips. Smoking cessation**! and BP control.

Manage vasospasms: hypertension, hypervolemia, hemodilution, angioplasty

27
Q

Read about Sinovenous thrombosis:

largest risk factor is hormonal therapies/BCP/ and iron def anemia/ulcerative colitis

A
28
Q

Management in In HIgh risk TIA presentation

A

Management: Although the symptoms of minor stroke may be disabling, intravenous alteplase/TPA should be used within 3 hours of onset.

If there is a mild stroke with NON-DISABLING deficits, DO NOT GIVE THROMBOLYTICS/TPA/ALTEPLASE

: dual antiplatelet therapy: clopidogrel with Aspirin

Continue dual antiplatelet therapy for 3-4 weeks (highest risk of stroke recurrence), then long term ASA.

Bleeding risk overrides the dual anti-platelet therapy after 4 weeks.

*In certain populations, clopidogrel may not activate because of CYP2c19 mutation in Asians. Consider ticagrelor.

29
Q

2 options to restore blood flow in a stroke

A
  1. dissolving the clot within the first 180 minutes with TPA :

Be careful about giving tpa to someone who is on DOACs/anticoagulants– can increase the chance of bleeding.

Make sure you follow closely with PTT/INR, platelet count, clotting and thrombin time. Wait 48 hours after the last anticoagulant dose.

Low dose TPA is better if on antiplatelets.

  1. removing the clot with endovascularr treatment– catheter based mechanical thrombectomy using a stent-retriever. Unlike Tpa which you should give within 180 minutes, there is a benefit of EVT across the entire 24 hour window (but it is still better to do it as early as possible)
30
Q

SECONDARY prevention for large artery atherosclerosis

A
  • short course of ASA/clopidogrel at least
  • high dose statins
  • revascularization if 50% cervical ICA stenosis and early after event
  • intracranial stenosis stenting is NOT safe
31
Q

small vessel disease/lacunar arterioloscloersis secondary prevention: should you use statins?

A

vfalse. avoid high dose statins (unlike large artery atherosclerosis)
- lower the BP/aggressive PB control to target.
- single antiplatelets long term.

32
Q

secondary prevention in people with cardioembolic risk fcators

A
  • antiboafulation for high risk sources (using warfarin)

if AFIB: use doac like apixaban

33
Q

Secondary prevention of unruptured aneurysm

A
  • wanna prevent SAH deterioration. coil any aneursym >7mm. stop smoking. control diabetres
34
Q

Outline the ABCD score for recurrence risk post stroke

A

A: age >60

BP: ober 140

clinical features of tia (unilateral weakness, speech disturbance,)

duration of symptoms: more likely to recurr if over 60 minutes
*H=history of diabetes.

35
Q

top 5 causes of stroke in young patients (dissection would be included here)

A
  1. cervical artery dissection
  2. varicella zoster
  3. carotid web growth
  4. coagulopathies including APLA
36
Q

outline the timeline for stroke recovery

A

80% of all recovery happens in the first 5 weeks, maximum reached within 13 weeks.

Most important recovery in upper extremity first 30 days

Aphasia may continue to improve for months.

Benzodiazepines, phenytoin, phenobarbital, clonidine and haloperidol may hamper stroke recovery.

37
Q

CNS complications of Stroke

The larger the stroke, the worse the outcome.

  • Stroke progression: ICH growth, infarct growth.

Infarct expansion can be minimized by avoiding ___, head position/ambulation early on, ___ __, normoxia/euglycemia/normothermia

Reverse robin hood syndrome.

Recurrent stroke: clot accumulation.active embolization.

Hemorrhagic transformation.

Malignant edema.

  • Durotomy done over entire bony decompression, cruciate or circumferential durotomy acceptable, dural grafting recommended: sewn or overlay.
  • Craniectomy: large diameter (duraplasty), Seizures/Epilepsy

Dementia: very common after stroke– alzheimer’s drugs may also work for mixed dementia

A

CNS complications of Stroke

The larger the stroke, the worse the outcome.

Stroke progression: ICH growth, infarct growth.

Infarct expansion can be minimized by avoiding hypotension, head position/ambulation early on, sleep apnea, normoxia/euglycemia/normothermia

Reverse robin hood syndrome.

Recurrent stroke: clot accumulation.active embolization.

Hemorrhagic transformation.

Malignant edema.

Durotomy done over entire bony decompression, cruciate or circumferential durotomy acceptable, dural grafting recommended: sewn or overlay.

Craniectomy: large diameter (duraplasty),

Seizures/Epilepsy

Dementia: very common after stroke– alzheimer’s drugs may also work for mixed dementia

38
Q

Strokes can cause a malignant infarct, which can cause Malignant edema–> hightened ICP. What must be done to avoid a dangerously high iCP?

A

decompressive surgery must be done.

Durotomy done over entire bony decompression, cruciate or circumferential durotomy acceptable, dural grafting recommended: sewn or overlay.

Craniectomy: large diameter (duraplasty),