Ischemic Stroke Flashcards

(39 cards)

1
Q

Ischemic Stroke Definition

A

Fixed focal neurological deficit attributable to arterial or venous territory, with evidence of acute infarction.

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2
Q

So what’s a TIA

A

a brief episode of neurological dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction

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3
Q

Large vessel s/s

A

ACA: legs
MCA: “Classic” one sided weakness/numbness
PCA: vision
Basilar: quickly leads to coma and death

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4
Q

tPA! (aka alteplase)

A

Used in the acute stroke setting up to 3 or 4.5 Hours

SHOULD HAVE NORMAL CT SCAN, Abnormal perfusion scan

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5
Q

Catheter Options

A

MERCI/ PENUMBRA (vacuum)

Stent retriever + vacuum (faster)

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6
Q

Clopidogrel

A

Antiplatelet agents that work by a different mechanism than ASA
Effectiveness and tolerability about the same as ASA
Stronger may be good for heart, bad for Brain and GI
Way more expensive (x100)

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7
Q

ASA Therapy and Stroke

A

Effective in secondary prevention of stroke and TIA
Heart and peripheral vascular disease benefits
Well understood / known safety profile
Cheaper than dirt
Underused

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8
Q

metabolic, lifestyle, and structural risk factors for stroke.

A
HTN**
Lipid disorders
Homocysteine elevation 
Smoking 
Obesity 
Physical inactivity 
Diabetes 
Alcohol
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9
Q

non-atherosclerotic causes of stroke in a young patient

General

A
Vasculpothy 
Hematologic 
Inflammatory 
Venous infarction
Vasospasms
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10
Q

non-atherosclerotic causes of stroke in a young patient

Vasculpothy

A

fibromuscular dystrophy, Moya- Moya, arterial dissection

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11
Q

non-atherosclerotic causes of stroke in a young patient

Hematologic-

A

Hematologic- familial deficiency, malignancies, sickle cell, hyperviscoity, birth control, antiphospholipid antibodies

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12
Q

non-atherosclerotic causes of stroke in a young patient

Inflammatory-

A

Inflammatory- vasculitis, migraine

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13
Q

fibromuscular dystrophy

A

F, 30 yo
media layer hypertrophy
dilate arteries to avoid stenosis
acs. w/ intracranial saccular aneurysm

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14
Q

Moya-Moya

A

F, 30-40 (asian/ african)
Middle cerebral artery occlusion
Intimal hyperplasia
acs. w/ intracranial saccular aneurysm & disection

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15
Q

Spontaneous dissection

A

FMD, marfran, coarc, intracranial ansm. Stroke risk

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16
Q

Familial Deficiency

A

Protein C, Protein S, or Antithrombin, or the presence of Factor V Leiden, or Prothrombin Gene

. Treatment for symptomatic individuals is often with anticoagulation.

17
Q

Malignancies

A

can cause a poorly understood hypercoagulable state too. No specific testing is done when this is suspected beyond the search for the malignancy. As above, the peripheral venous events are much more common than any arterial event.

18
Q

Sickle Cell Anemia:

A

SSA responds to transfusion. The Sickle Cell Trait cells can on occasion ‘sickle’ with dehydration or altitude, but this doesn’t seem to impart any additional risk of stroke or CNS hemorrhage.

19
Q

Hyperviscosity States:

A

Protein, elevated hematocrit (60%), thrombocytosis (1,000,000), etc. can generate slowness of flow beyond the pump & pipes ability to compensate.

20
Q

Oral contractive

A

implicated as a cause of stroke or venous thrombosis. This is a concern in patients who smoke, have other risks, or have subtle increases in blood pressure from OCP use.

. Hormone Replacement Therapy can either increase, or decrease your risk depending on the study.

Anecdotally, Neurologists note the triad of Migraine/Smokers/OCP increase risk by 25 times. Bonus if you add Cocaine or Meth, eh?

21
Q

Antiphospholipid antibodies

A

cause a triad of spontaneous miscarriage, thrombocytopenia, and recurrent large vessel thrombosis, arterial or venous. attack of the phospholipid membranes in the platelet, and endothelium.

Rx is directed at the individual problem, and can involve no treatment, any antithrombotics, or even anticoagulation with warfarin.

22
Q

Vasculitis

A

can affect the cns in many ways. T

Vasculitis has traditionally been considered a manifestation of immunological disorders, but over time, infectious causes are emerging. Varicella-Zoster Virus is increasingly being found in CNS vasculitis.

23
Q

Venous Infarction

A

The most common cause is major head trauma. Most non-traumatic venous infarction occurs from dehydration, CNS infections, and hypercoagulable states (transient or genetic). Post-partum Sagittal Sinus Thrombosis around days 3-5 is a popular board question

24
Q

Vasospasm

A

still being better defined to distinguish them from more typical inflammatory causes, but certainly sympathometic drugs, severe hypertension, primary vessel irritation (intrathecal drug, catheter contrast, SAH blood) trigger vasospasm that can cause permanent injury.

25
Reducing the Risk of Stroke
Good health + antiplatelet (aspirin, Thienopyridines (Clopidogrel, Prasurgrel, Ticlopidine) and Anticoagulants )
26
Aspirin
established as the standard antiplatelet agent to prevent recurrent stroke. 81mg or 325mg GI catastrophes occur, and the cost can be increased if an H2 blocker or a proton pump inhibitor is required on a regular basis.
27
Clopidogrel plus aspirin
is quite useful after a catheter based cardiac re-vascularization procedure, may be useful in the first few months after a CNS ischemic event, and longterm may hold an advantage over aspirin alone in arteriopaths
28
_____ are used together in some highest risk patients, but there are no data in stroke to guide such use
. Aspirin and Warfarin
29
Dipyridamole
an extended release 75mg formulation that is available with 25mg of aspirin. This combination in a single pill has generated conflicting data, but overall works as well as any single agent.
30
Warfarin
highly effective in primary prevention of stroke with atrial fibrillation. international normalized ratio (INR) targets for anticoagulation has resulted in lower bleeding complication rates then expected
31
The goal of______________ is to preserve the non-infarcted areas of the brain, prevent progression of infarction, to avoid notorious complications of stroke, and to initiate a rational evaluation to guide future long-term therapy.
ischemic stroke management
32
Resuscitation
Tissue plasminogen activator (TPA) Used within the first three hours after stroke. Therapy carries a significant risk of hemorrhage
33
1. If diastolic BP is >140 mm Hg on two readings 5 minutes apart, then start an infusion of __________ Algorithm for Emergency Antihypertensive Therapy in Acute Stroke
sodium nitroprusside
34
Algorithm for Emergency Antihypertensive Therapy in Acute Stroke If systolic BP is >220 mm Hg and/or diastolic BP is 121-140 mm Hg on two readings 20 minutes apart, them give_________
labetalol dose may be repeated or doubled every 10-20 minutes until a satisfactory BP reduction is achieved
35
Algorithm for Emergency Antihypertensive Therapy in Acute Stroke In acute stroke patients with systolic BP of
usually not indicated
36
TIA
ONSET Instantaneous HEADACHE Rare STUPOR/COMA Rare EXAM Deficit in Vascular Pattern CT/MRI Normal MECHANISM Embolism (thrombus or platelet) Small vessel occlusion, Thrombosis-in-situ EMERGENCY TREATMENT Fluids Anti-thrombotic agent
37
STROKE- ischemic
STROKE ONSET Instantaneous HEADACHE Unusual or mild STUPOR/COMA Rare EXAM Deficit in Vascular Pattern CT/MRI Abnormal after hours MECHANISM Embolism (thrombus or platelet) Small Vessel occlusion Thrombosis-in-situ EMERGENCY TREATMENT TPA Fluids
38
SUBARACHNOID HEMORRHAGE
ONSET Instantaneous HEADACHE Universal & Severe STUPOR/COMA Often at Onset EXAM Normal or Mild to Severe Deficit CT/MRI Abnormal for Days MECHANISM Aneurysm AVM EMERGENCY TREATMENT ICU Support Hyperdynamic Therapy Ventriculostomy Nimodipine
39
INTRACEREBRAL | HEMORRHAGE
ONSET Minutes HEADACHE Common STUPOR/COMA Common by 30-60 minutes EXAM Progressive Hemiparesis CT/MRI Abnormal MECHANISM Hypertension, Coagulation disorder, Vessel degeneration, Stroke (Trauma) EMERGENCY TREATMENT ICU Support, ICP Management Surgery