Therapeutics Neuro/psych Exam 2- Stroke

Front 1

stroke definition paragraph

Back 1

--

Front 2

TIA definition

Back 2

Transient episode of neurological dysfunction caused by focal brain, spinal
cord, or retinal ischemia, without acute infarction
i. Revised definition which takes time out of the equation

Front 3

TIA: thought of as..
damage done
duration
risk of stroke afterwards

Back 3

Thought of as temporary strokes that reverse themselves (“ministrokes”)
ii. By definition, these do not leave a permanent deficit
iii. Majority last less than one hour with a median duration of ~8 minutes
iv. Patients who experience TIAs are at increased risk for stroke

Front 4

TIA

Back 4

clinically useflu...

Front 5

Risk of stroke after TIA: ABCD score components

how to interpret score

Back 5

age of pt (60+ or not)
blood pressure at assessment SBP > 140 or DBP 90+
Clinical features (unilateral weakness, speach disturbance with no weakness)
duration of TIA (60+ minutes, 10-59, less than 10)


• Total score of 6 suggests 30%+ risk of stroke in the first 7 days after the TIA

Front 6

is stroke a major cause of mortality?

Back 6

no.

biggest issue is the disability (morbidity)

Front 7

disabilities (4)

Back 7

a. 48% have hemiparesis
b. 22% cannot walk
c. 12-28% are aphasic
d. 32% are clinically depressed

Front 8

“Stroke belt” (3)

Back 8

. Based on epidemiologic data, the Southeastern United States has been coined the
“stroke belt” because of higher mortality from stroke across all ethnic groups
a. Georgia, North Carolina, South Carolina had the highest stroke mortality than
any state in the country and was labeled the “stroke buckle”
b. Reasons for this are unknown however may be tied into lifestyle, higher
percentage of African Americans, or lower socioeconomic status

Front 9

stroke pathophys

Back 9

1. Abrupt disruption of blood flow to areas of the cerebrum (more common) and
cerebellum resulting in sudden, nonconvulsive, focal neurological deficits

Front 10

The significance of the stroke will depend on (2)

Back 10

a. The location and length of time in which blood flow is disrupted
b. Collateral blood flow

Front 11

collateral blood flow in brain (2)

lack of it is going to cause what?
what does collateral blood flow allow for

Back 11

i. Lack of collateral blood flow will result in irreversible damage to brain cells within minutes

ii. Some degree of collateral flow will allow for possible survival of brain cells and potential reversal of neurological damage

Front 12

what is the penumbra (2) and what is it's significance

Back 12

a. Area surrounding the ischemic core (necrotic tissue)
b. Blood flow is sufficient to maintain viable tissues however these tissues are not
able to survive for long periods of time unless reperfused in reasonable timeframe
c. Limiting the penumbra and salvaging the viable tissue has been a targeted area
for pharmacotherapy (aka neuroprotection

Front 13

Classification of cerebrovascular disease (there are a variety of pathophysiologic processes
which involve the blood vessels in the brain) (4 processess/types)

Back 13

1. A process that is intrinsic to the vessels whereby there is a disruption of blood flow
a. Examples include: atherosclerosis, inflammation, arterial dissection,
developmental malformations, venous thrombosis
2. A process originating remotely whereby an embolus from the heart or extracranial
ciculation becomes lodged in the intracranial vessels
3. A process resulting from inadequate cerebral blood flow secondary to decreased
perfusion pressure or an increase in blood viscosity
4. A process that results from a rupture of a vessel

Front 14

largest prevalanece type of stroke

Back 14

ishemic

Front 15

4 causes of ischemic stroke

Back 15

1. Large artery atheroslcerosis
2. embolic stroke
3. lacunar
4. unknown origin

Front 16

Large artery atheroslcerosis (2)

Back 16

a. A thrombus formation in an artery produces a stroke by reducing blood
flow distal to the occlusion; generally, the arterial obstruction is local however
there may be emboli that become lead to an obstruction

Front 17

embolic stroke (2)

Back 17

a. Embolism will refer to particles of debris that originate elsewhere, dislodge,
travel “downstream”, and become lodged in smaller arterial vessels thus blocking
the flow of blood
b. In contrast to thrombosis, the embolic process is not local

Front 18

causes of embolic stroke (known cardiac sources) (6)

also 3 potential cardiac sources

Back 18

• Atrial fibrillation
• Mitral valve stenosis
• Rheumatic valvular disease
• Dilated cardiomyopathy (venous stasis)
• AMI
• Infectious endocarditis
--

• Left ventricular wall motion abnormalities
• Arterial septal aneurysm
• Mitral valve prolapse

Front 19

lacunar stroke (2)

Back 19

a. Subtype of stroke involving occlusion of small arteries (defined as lesion
<1.5 cm)
b. Will not affect cortical function

Front 20

strokes of other or unknown etiology

Back 20

Stokes due to other causes such as vascular diseases, hypercoagulable states, etc

Front 21

hemorrhagic strok eincidnece

Back 21

--Accounts for ~10% of strokes and is associated with a poorer prognosis than ischemic
strokes  30 day mortality is between 40-50%

Front 22

Intracerebral hemorrhage (3)

derived from where?
where does bleeding occur/what happens (2)

Back 22

i. Derived from arterioles or small arteries
ii. The bleeding occurs directly into the brain and forms a localized
hematoma that spreads along the white matter pathways
iii. Blood will accumulate over minutes or hours and will gradually
enlarge (some have described it as a snowball rolling downhill)

Front 23

causes of intracerebral hemm stroke (4)

Back 23

: hypertension, trauma, illicit drug use (amphetamines and
cocaine), and vascular abnormalities

Front 24

2 types of hemorrhagic stroke

Back 24

intracerebral hemorrhage
Subarachnoid hemorrhage (SAH)

Front 25

SAH (2) secondary to what? what happens?

Back 25

i. This is secondary to a rupture of arterial aneurysms which will release
blood directly into the cerebrospinal fluid
ii. Blood will spread quickly within the CSF causing a rapid increase
in intracranial pressure followed by deep coma or death if the bleeding
continues

Front 26

primary sx of SAH

Back 26

The primary symptom is a sudden and severe headache (described
as “the worst headache of my life”)

Front 27

what is nimodipine and what is it used for (theoretically- not really used)

Back 27

. Calcium channel blocker which theoretically decreases cerebral vasospasm following SAH

Front 28

nimodipine indication

Back 28

Indication is for improvement of neurological outcome by reducing the
incidence and severity of ischemic deficits in patient with subarachnoid
hemorrhage

Front 29

drug induced stroke- drugs (4)

Back 29

. Includes hormonal therapies (HRT, oral contraceptives), COX-2’s, NSAIDs, and
recreational drugs such as cocaine (usually illicit drugs tho)

Front 30

link b/t hormones and stroke

Back 30

Link between hormones and stroke is less clear however there is an associated risk
for ischemic stroke among oral contraceptive users compared to non-users

Front 31

RF for stroke- single vs. multiple

Back 31

A. Single risk factors will place people at increased risk of ischemic stroke
B. Multiple risk factors will increase the risk of stroke severalfold and plays a role in the
aggressiveness of management

Front 32

RFs for stroke (non modifiable) (5

Back 32

Age (doubles each decade after 55)
Gender (men > women)
Race/ethnicity (blacks/mexicans higher)
Low birth weight (double for those with BW less than 2500 g)
Genetic factors (lots- family hx of stroke/TIA especially)

Front 33

RFs for stroke (modifiable) and goals (6)

Back 33

htn (goal: less than 140 over 90)- isolated systolic HTN needs to be treated
smoking
diabetes- AiC less than 7 (or less than 8 if old and dying; a little grey area)
Asymptomatic carotid stenosis
Afib
hyperlipidemia

Front 34

details for modifiable risk factors

Back 34

some shit about taking asa

Front 35

Potentially modifiable risk factors and approach to stroke prevention

Back 35

obesity (BMI 30+)- wt reduction rec'd/associated with other factors that contribute to stroke

physical inactivity- regular exercise 30+ min/day
poor diet
alcohol abuse (no more than 2 drinks/day for men, 1 drink/day for women)

hyperhomocysteinemia
drug abuse
metabolic syndrome
sleep disordered breathing

Front 36

details for potentially modifiable risk factors

Back 36

--

Front 37

s/sx of stroke (6)

Back 37

depends on where stroke is


contralateral muscle weakness
sensory disturbance
decreased coordination
language dysfunction
memory disturbance
confusion
vessels and where they go to

know the BOLDED symptoms - don't have to know OH HE HAS THIS SX SO THIS PART OF BRAin

Front 38

hem stroke sx (5)

Back 38

. Any of the focal signs/symptoms that occur in ischemic stroke may also occur
in hemorrhagic stroke with stupor and coma dominating the picture
i. Severe headache with sudden onset
ii. Lethargy or decrease in level of consciousness
iii. Nausea and vomiting
iv. Severe hypertension

Front 39

National Institutes of Health Stroke Scale (NIHSS)- used for what?

scale ranges from...

scores that indicate poor/good outcome

Back 39

for risk factor assessment

a. Primary scales used combining level of consciousness, motor function, sensory function, and language ability
b. Scale ranges from 0 to 42
i. Scores less than 3-4 indicate excellent change for complete recovery
ii. Scores 20+ indicate a poor outcome

Front 40

Other scales used for risk assessment for stroke (3)

Back 40

. Modified Rankin Scale (0 = no disability; 6 = dead)
b. Barthel Index (0 = complete dependence; 100 = complete independence)
c. Glasgow Outcome Scale (1 = dead; 5 = good recovery)

Front 41

Outcome goals for stroke (3)
2 predominae outcome indicators
predicted by?

Back 41

1. Stroke recurrence and death are the two predominate outcome indicators
a. Many times, these are predicted by the size and location of the infarcted area
2. Risk factor modification
a. Any risk factor that increases the risk for subsequent strokes should be targeted
3. Extent of disability will be determined by the severity of the injury, location, and cause
of the stroke

Front 42

Complications of stroke (3)

Back 42

1) edema/increased ICP
2) hemorrhagic transformation
3) seizure

Front 43

brain edema/ICP (2)
primary cause of...
more common to have this issue wiht what type of stroke

Back 43

a. Primary causes of neurologic deterioration and death within the first week of
a stroke
b. More common to have this problem with trauma or hemorrhagic strokes

Front 44

hemorrhagic transformation (2) may occur when

linked to what

Back 44

a. May occur spontaneously in those with AIS
b. Linked to those receiving anticoagulation and thrombolytics

Front 45

seizure (2) incidence

ppx?

Back 45

a. May occur in 4-6% of stroke victims and typically happens within the 1st
24 hours of stroke onset
b. Prophylactic therapy is not recommended

Front 46

ER triage times

door to doc?

door to stroke team
door to CT initiation
door to CT interpretation
door to drug
door to stroke unit admission

Back 46

Door to physician less than 10 minutes
Door to stroke team less than 15 minutes
Door to CT initiation less than 25 minutes
Door to CT interpretation less than 45 minutes
Door to drug (less than 80% complaince) less than 60 minutes
Door to stroke unit admission less than 3 hours

Front 47

importance of CT

Back 47

won't show ischemia til later

IMPORTANT due to r/o hemorrhage

Front 48

single most important piece of patient history

Back 48

The single most important piece of historical information is the time of
symptom onset- won't be TPA candidate if can't pinpoint time

Front 49

For ABCs/Physical exams- encourage use of..

Back 49

Encourage the use of stroke scales and standardized neurological exam

Front 50

immediate dx studies for ALL patients (often will start tx before labs come back) (9)

Back 50

• Noncontrast brain CT or MRI
• Blood glucose
• Oxygen saturation
• Serum electrolytes/renal function tests
• CBC
• Markers of cardiac ischemia
• PT/INR
• aPTT - for bleeding risk and whatnot
• EKG

Front 51

optional tests in select patients (9)

Back 51

• Hepatic function tests
• Toxicology screen
• Blood alcohol level- if appears intoxicated
• Pregnancy test
• ABG’s
• Chest x-ray
• Lumbar punction
• EEG

Front 52

Elevated blood pressure and how this ties to fibrinolytic therapy: BP lowering, goal BP to be able to use

Back 52

• Blood pressure should be carefully lowered to SBP less than 185 and DBP less than 110 mm Hg (will worsen stroke if you drop it too fast- not enough blood flow)
• If BP is not maintained lower than 185/110 mm Hg, do not administer tPA

Front 53

how often to monitor BP when giving TPA

Back 53

Frequent blood pressure monitoring is required (every 15 minutes for 2 hours from the start of tPA, then every 30 minutes for 6 hours, then every hour for 16 hours)

Front 54

Agents commonly used to lower BP for TPA include (4)

Back 54

labetalol, nicardipine, hydralazine, and rarely nitroprusside

Front 55

If patient is not candidate for fibrinolytic therapy: how to lower BP

Back 55

• Reasonable to lower BP by 15% during the first 24 hours after stroke onset

Front 56

BP at which you would not withhold antihypertensive meds? (it says "medications")

Back 56

Consensus exists that medications should be withheld unless SBP is greater than 220 or the DBP is greater than 120 mm Hg

Antihypertensive treatment should initially be withheld in acute ischemic stroke patients NOT candidates for TPA unless the diastolic blood pressure is >120 or systolic blood pressure is >220. (1) Many of these patients may decrease their blood pressure spontaneously.

Front 57

brain imaging (2)

Back 57

Computerized tomography (CT) scan
MRI

Front 58

use of TPA- what does it do and not do

Back 58

does NOT decrease mortality

mainly there to help decrease the morbidity issues with stroke

Front 59

primary complication of TPA

Back 59

symptomatic ICH

Front 60

Predictors of ICH from rt-PA administration (from NINDS trial) (3)

Back 60

• NIHSS score 20+
• History of anticoagulation
• Cerebral edema on CT

Front 61

predictors of ICH from t-PA from Community-based studies (3)

Back 61

• teatment beyond 3 hour window
• Antithrombotic drugs given within 24 hours of rt-PA
• Blood pressure greater than 185/110 mm Hg

Front 62

Criteria for Intravenous rt-PA Therapy inclusion (3)

Back 62

o Diagnosis of ischemic stroke causing measurable neurological deficit
o Onset of symptoms less than 3 hours before beginning treatment
age 18+

Front 63

Criteria for Intravenous rt-PA Therapy in the time period of 3-4.5 hours after ischemic stroke: exclusion (4)

Back 63

o Aged 80+ years
o Severe stroke (NIHSS more than 35)
o Taking an oral anticoagulant regardless of INR
o History of both diabetes and prior ischemic stroke

Front 64

Other pharmacologic therapies in the treatment of acute ischemic stroke besides TPA

Back 64

Anticoag (e.g. used to give HIT, LMWH and shit)- no clinical benefit of urgent anticoagulation with the goal of
improving neurological outcomes in patients who present with acute ischemic strokes. only benefit is DVT prevention

Front 65

If unfractionated heparin, low-molecular weight heparins, or heparinoids are used,
the recommendations are as follows: (3)

Back 65

• The use of these agents may be considered for DVT prophylaxis in at-risk individuals presenting with acute ischemic stroke
• Initiation should not be within 24 hours of receiving rt-PA
• Do not prescribe until brain imaging has excluded the possibility of an intracranial hemorrhage

Front 66

Antiplatelet medications in stroke recommendation (4) ACUTE- can you use other agents?

Back 66

• Oral administration of aspirin (initial dose of 325 mg) within 24-48 hours after stroke onset is recommended for treatment of most patients
• Use of aspirin as an adjunctive therapy within 24 hours of receiving r-tPA is not recommended
• Aspirin should not be used as a substitute for other acute interventions for the treatment of AIS
• No recommendation can be made about the use of other antiplatelet agents in the acute situation

Front 67

merci retriever- what is it? what does it do?

Back 67

Device approved by the FDA for removal of thrombi from the cerebral vasculature

allows use within 6 hours of onset of symptoms

Front 68

Secondary Prevention of Ischemic Stroke

Back 68

1) antiplatelet meds- only reduces like 25% of strokes (secondary prevention)

Front 69

Class I recs for antiplatelets (2) what to use, etc.

Back 69

• For patients with noncardioembolic stroke or TIA, antiplatelet agents rather than oral anticoagulation are recommended to reduce the risk of recurrent stroke and other cardiovascular events
• Aspirin (50-325 mg/d) monotherapy, the combination of aspirin and extended-release dipyridamole, and clopidogrel monotherapy are all acceptable options for initial therapy-->usually 81 mg

Front 70

class II recs for antiplatelets- alternatives to asa, increasing asa dose if you have a stroke while on ASA

Back 70

• For patients allergic to aspirin, clopidogrel is reasonable
• For patients who have an ischemic stroke while taking aspirin, there is no evidence that increasing the aspirin dose provides additional benefit; alternative antiplatelet agents are often considered; no single agent or combination has been studied in patients who have had an event while receiving aspirin

Front 71

class III recs- adding ASA to plavix'
specific indication

Back 71

• The addition of aspirin to clopidogrel increases the risk of hemorrhage. Combination therapy of aspirin and clopidogrel is not routinely recommended for ischemic stroke or TIA patients unless they have a specific indication for this therapy (i.e. – coronary stent or acute coronary syndrome)

Front 72

CHADS2

Back 72

C Congestive heart failure
H Hypertension (SBP>160 mm Hg)
A Age 75+ years
D Diabetes
S Prior TIA or stroke

Front 73

how to tie CHADS2 into antiplatelet therapy

Back 73

if anyone has had prior TIA/stroke- need warfarin regardless of score?
0- ASA (low risk)
1-2- asa or warfarin (moderate)
3+ high risk - warfarin

Front 74

issues with CHADS2 (2)

Back 74

• The main criticism of the CHADS scoring system is someone with a previous history of TIA/stroke but no other risk factors is considered to be at moderate risk when in fact they are at high risk for another stroke
• A second issue are those who fall into the “moderate” risk category; should they be anticoagulated or not

Front 75

Recommendations for Atrial Fibrillation in those with Stroke or TIA: Class I (2)

Back 75

• Adjusted-dose warfarin (INR 2-3) is recommended for all patients with nonvalvular AF deemed to be at high risk and many deemed to be at moderate risk for stroke who can receive it safely
• Antiplatelet therapy with aspirin is recommended for low-risk and some moderate-risk patients with AF on the basis of patient preference, estimated bleeding risk if anticoagulated, and access to high quality anticoagulation monitoring

Front 76

Recommendations for Atrial Fibrillation in those with Stroke or TIA: Class II (2) if high risk with afib and can't take warfarn (not due to hemorrhagic reasons)...

bridging

Back 76

• For high-risk patients with AF deemed unsuitable for anticoagulation, dual-antiplatelet therapy with clopidogrel and aspirin offers more protection against stroke than aspirin alone but with an increased risk of major bleeding and might be reasonable
• Bridging with a LMWH is reasonable in those at high risk for stroke who require temporary interruption of oral anticoagulation (though hardly ever do this- and have to make sure you don't use ppx dosing- use therapeutic dosing)

Front 77

Recommendations for Atrial Fibrillation in those with Stroke or TIA: Class III; for pt unable to take oral anticoagulants due to hemorrhage risk

Back 77

• For patients unable to take oral anticoagulants, aspirin alone is recommended. The combination of clopidogrel plus aspirin carries a risk of bleeding similar to that of warfarin and therefore is not recommended for patients with a hemorrhagic contraindication to warfarin

Front 78

Recommendations for Use of Newer Anticoagulants: Class I recommendations

Back 78

• Warfarin, dabigatran, apixaban, and rivaroxaban are all indicated for the prevention of first and recurrent stroke in patients with nonvalvular AF. The selection of an antithrombotic agent should be individualized on the basis of risk factors, cost, tolerability, patient preference, potential for drug interactions, and other clinical characteristics, including time in INR therapeutic range if the patient has been taking warfarin

BASICALLY there are options.

Front 79

Recommendations for Use of Newer Anticoagulants: Class II recommendations- safety/efficacy

Back 79

• The safety and efficacy of combining dabigatran, rivaroxaban, or apixaban with an antiplatelet agent have not been established

Front 80

Risk factor modification in stroke (3)

Back 80

1. Modification of modifiable risk factors will aid in reducing stroke risk
2. Smoking cessation, lifestyle modification, exercise as directed
3. Hypertension management typically with thiazides and ACE inhibitors

Front 81

things to educate pt on (3)

Back 81

good modification of RFs!

warnings signs/stroke sx

stroke info/phone numbers

Front 82

2 things to educate pt on regarding RF management

Back 82

1. Education on general good health is essential for patients at increased risk of stroke
2. Management of modifiable risk factors should be pursued

Front 83

2 things to educate pt on regarding stroke sx

Back 83

1. Timing is very important for treatment of stroke
2. Warning signs

Front 84

warning signs for stroke (5)

Back 84

a. Sudden numbness or weakness of the face, arm or leg, especially on one side
of the body
b. Sudden confusion, trouble speaking or understanding
c. Sudden trouble seeing in one or both eyes
d. Sudden trouble walking, dizziness, loss of balance or coordination
e. Sudden, severe headache with no known cause

Front 85

definition of stroke

Back 85

rapidly developing clinical signs of focal and global disturbances in cerebral function with symptoms lasting 24 hours or longer with no
apparent cause other than vascular origin

Front 86

purpose of weight reduction in stroke

associated with what in stroke

Back 86

o Weight reduction is recommended as a means to lower blood pressure
o Weight reduction is associated with an increase in comorbid conditions associated with increased risks of stroke

Front 87

how to prevent homocysteingiwnowng

Back 87

o Adequate intake of folic acid, vitamin B6 and B12 are encouraged; these may be obtained through increased intake of fruits and vegetables

Front 88

3 abused drugs that increase risk of stroke

Back 88

o Amphetamines, cocaine, and heroin have all been linked to increasing the riskof stroke

Front 89

o The effectiveness of agents that ameliorate aspects of insulin resistance for reducing stroke is

Back 89

unknown

Front 90

tx sleep apnea?

Back 90

o Treatment of sleep apnea to reduce risk of stroke might be reasonable although the effectiveness is unknown

Front 91

efficacy of CT scan in differentiating ischemic from hemorrhage

Back 91

The CT scan can miss subtle subarachnoid hemorrhages however the
yield of a CT in differentiating hemorrhage from ischemia is close to 100%

Front 92

MRI (2)

Back 92

i. More sensitive than CT but not as readily available
ii. May replace CT as the initial screening tool for hemorrhage in the future

Front 93

National Institute of Neurological Disorders and Stroke (NINDS) rt-PA Stroke Study

Back 93

study that forms basis of who can/can't use tpa

Front 94

what did NINDS trial show (4)

Back 94

1) TPA better than placebo at 24 hours for clinical improvement (not significant??)
2) more likely to have full recovery or have minimal disability vs. placebo
3) mortality- no difference
4) increased risk of hemorrhage with TPA

Front 95

estimated benefit of TPA (3)

Back 95

a. For every three patients receiving IV rt-PA, one will have a favorable outcome
b. For every 30 patients receiving IV rt-PA, one will have an adverse event
c. Despite this, it is estimated that rt-PA is only used in 1-3% of all AIS

Front 96

inclusion criteria for giving people TPA if 3-4.5 hours after stroke (2)

Back 96

o Diagnosis of ischemic stroke causing measurable neurological deficit
o Onset of symptoms within 3-4.5 hours before beginning treatment

Front 97

a few exclusions factors for using TPA (3)

Back 97

o Recent intracranial or intraspinal surgery
o Current use of anticoagulant with INR >1.7 or PT >15 seconds
o Current use of direct thrombin inhibitors or direct factor Xa inhibitors with elevated sensitive laboratory tests

Front 98

• Relative exclusion criteria: might still get it if benefit more than risk (2)

Back 98

o Only minor or rapidly improving stroke symptoms (clearing spontaneously)** mentioned these people tend not to get TPA when they need it
o Pregnancy

Front 99

dosing of TPA

Back 99

• Infuse 0.9 mg/kg (maximum dose of 90 mg) over 60 minutes with 10% of the dose given as a bolus over 1 minute

Front 100

after TPA...what do you do?

Back 100

• Admit patient to intensive care or stroke unit for monitoring

Front 101

neuro monitoring after TPA

Back 101

• Perform neurologic assessments every 15 minutes during infusion and every 30 minutes thereafter for the next 6 hours, then hourly until 24 hours after treatment

Front 102

• If patient develops which 4 sx, discontinue the infusion (if rt-PA is being administered) and obtain emergency CT head scan

Back 102

severe headache, acute hypertension, nausea, or vomiting, (hemorrhage)

Front 103

delay placement of...(4) after TPA

Back 103

• Delay placement of nasogastric tubes, indwelling bladder catheters, or inta-arterial pressure catheters (bleeding)

Front 104

what must you do before starting anticoagulants or antiplatelets

Back 104

• Obtain follow-up CT scan at 24 hours before starting anticoagulants or antiplatelet agents

Front 105

ASA usage in early AIS - 2 trials
NNT

Back 105

International stroke trial- 300 mg ASA
chinese acute stroke trial (CAST)- 150 mg ASA
NNT- 100

Front 106

first line therapy for secondary stroke prevention

why is it first line

rec'd dose range

major AE and how to prvent

Back 106

o Recommendation is 50-325 mg per day

less GI irritation as it has been shown that the higher the dose of ASA, the increased risk for GI side effects (so use babby aspirin?)
o Considered 1st line therapy based on cost

Front 107

plavix moa

Back 107

o Inhibit adenosine diphosphate (ADP) which is responsible for stimulating platelet aggregation

Front 108

plavix efficacy in secondary prevention vs. asa

why is it second line

Back 108

o Slightly more effective than aspirin but cost of these medications places them as second line for those who have failed aspirin

Front 109

aggrenox dosing

Back 109

o Dose: 1 capsule (25 mg aspirin/100 mg dipyridamole) BID

Front 110

what is dipyridamole?

Back 110

o Platelet adhesion inhibitor in aggrenox

Front 111

. CHA2DS2-VASc - benefit


what is difference from CHADS2

Back 111

considered better than CHADS2 for the moderate types

Vasc = Vascular Disease History (previous MI, PAD, aortic plaque)

age split into 3 groups (75+ is +2)

Front 112

• On the basis of the SPARCL trial...what to do with statin

Back 112

administration of statin therapy with intensive lipid-lowering effects is recommended for patients with atherosclerotic ischemic stroke or TIA and without known CHD to reduce the risk of stroke and cardiovascular events

Front 113

• Ischemic stroke or TIA patients with low HDL cholesterol may be considered for

Back 113

treatment with niacin or gemfibrozil