Stroke Flashcards
includes an assortment of disorders that affect the blood vessels of the CNS; Inadequate blood flow (ischemia) or hemorrage (bleeding) leads to neurologic dysfunction
Cerebrovascualr disease
abrupt-temporary focal neurologic deficit (slurred speech, aphasia, limb paralysis/weakness) that lasts ≤ 24 hours and usually < 30 minutes with complete resolution of symptoms
TIA
bleeding in spaces in or around the brain that results in very similar symptoms as TIA/Infarct and the damage is due to lack of blood flow and direct irritation of blood in contact with brain tissue; blood pools and increases pressure inside the brain
Cerebral hemorrhage
permanent form because the damage is fixed due to neuronal cell death, usually vascular in origin, symptoms last ≥ 24 hours, and can be stable/ improving/ progressive
Stroke (cerebral infarction)
What are the ischemic stroke mechanisms?
- Atherosclerotic (carotid/ cerebral artery)
- Cardiogenic embolism (A.Fib.)
- Penetrating Artery disease (lacunar)
- Cryptogenic (hidden cause)
- Other - Drug abuse, vasospasm, many more
What are the hemorrhagic stroke mechanisms?
- Subarachnoid (blood in CSF) - blood vessel that breaks is usually an artery
- Intracerebral (HTN/ antithrobotic therapy) - blood vessel that breaks is usually an artery
- Subdural (Trauma) - blood vessel that breaks is usually a vein
What are nonmodifiable risk factors for strokes?
- Age (doubles every decade after 55)
- ¾ over age 65
- Men > Women
- African Americans, Asian-Pacific Islanders, Hispanics > Caucasians
- Hereditary
- Geography – SE US
What are modifiable risk factors for strokes?
- HTN – most important
- Smoking 2X
- Heart Disease
- Atrial Fib – 5X
- Diabetes
- Previous TIA – 17% in 90 d
- Dyslipidemia
- Alcohol
- Illicit Drug Use
- Obesity
- Diet
- Physical Activity
accumulation of lipids and inflammatory cells in the arterial wall, combined with hypertrophy of arterial wall smooth muscle, results in plaque formation. It may remain in vessel causing local occlusion or travel distally as an embolism to the cerebral vessels
Carotid Atherosclerosis
- etiologic factor for eschemic stroke
pooling of blood in the atrium/ventricles allows the formation of a clot that can be dislodged and travel to cerebral circulation
Cardiogenic Embolism
- etiologic factor for eschemic stroke
What are the diagnostic strategies for a stroke?
- CT scan- will reveal area of infarct
- MRI- shows if ischemic or hemorrhagic
- Carotid Doppler- determine if patient has a high degree of stenosis in carotid arteries supplying blood to the brain
- ECG- Detects Atrial Fibrillation (Etiologic Factor)
- Transthoracic Echocardiogram (TTE) – determines if there are any valve/wall motion abnormalities
- Transesophageal Echocardiogram (TEE)- test for thrombus in left atrium
- Transcranial Doppler (TCD) – tells if pt is likely to have intracranial arterial sclerosis
- lab tests - hypercoaguable states
What are the desired outcomes of tx for stroke?
- Reduce ongoing neurologic injury
- Decrease mortality and long-term disability
- Prevent complications secondary to immobility and neurologic dysfunction
- Prevent stroke recurrences
What are nonpharmacologic tx of ischemic stroke?
- Craniectomy to release some of the pressure from edema (benefits unclear)
- Carotid endarterectomy of ulcerated/stenotic caroid artery (very effective)
- In patients where carotid endarterectomy is excessive, carotid stenting may be effective
What are nonpharmacologic tx of hemmoragic stroke?
- subarachnoid - surgical intervention to either clip or coil offending vascular abnormality
- intracerebral - not studied well, benefits of surgery to remove hematoma is less documented
- Insertion of extraventricular drain (EVD) and subsequent monitoring of intracranial pressure
- Maint tx is aimed at controlling ICP**
How are ischemic strokes treated acutely?
- Rule out hemorrhage stroke
- tx (tPA, or aspirin w/in 48 hrs if tPA cannot be administered) can be initiated within 3 hours of start of sx
- HTN is not treated initially
Converts plasminogen to plasmin (proteolytic enzyme) that degrades fibrin polymers (meshwork) into degradation products and eventually dissolving the thrombus (clot)
MOA for tissue plasminogen activator (tPA)
- 10% initial dose, then the remainder infused over 60 minutes
- ADR: systemic bleeding, hemorrhagic stroke, most of the contraindications to fibrinolytic therapy involves patients with high risk of hemorrhagic stroke
- pt needs to be monitored closely and should not have antithrombotic for 24 hours
What inclusion criteria needs to be met in order to have tPA administered?
- Age 18 years or older
- Clinical diagnosis of ischemic stroke causing a measurable neurologic deficit
- Time of symptom onset well established to be less than 180 minutes before treatment would begin
Why is aspirin used instead of other NSAIDs as an anticoagulant?
irriversibly binds to COX1 receptors on platelets
- still has risk for GI ulcerations
What are some other drugs used to treat acute ischemic strokes?
- Labetolol IV = 10-20 mg, doubled every 10-20 minutes, to a maximum of 300 mg
- Nicardipine IV= infusion start at 5 mg/hr up to 15 mg/hr
- Nitroprusside IV = Infusion starting at 0.5 mcg/kg/min, with continuous arterial blood pressure monitoring
What antiplateltn agents should non-cardiogenic stroke patients use?
- Aspirin 50-325 mg every day
- Aggrenox (Dipyridamole/ Aspirin) 200/25 mg twice daily
- Plavix (clopidogrel) 75 mg every day
What type of stroke does this pathophysiology describe?
Final outcome = embolism/thrombus formation resulting in arterial occlusion, decreasing CBF (cerebral blood flow)
ischemic stroke
- ischemia occurs distal to the occlusion
- Lack of CBF results in loss of oxygen and nutrients to ischemic cells, depletion of high-energy phosphates needed to maintain cell integrity, and electrolyte imbalances
What type of stroke does this pathophysiology describe?
Presence of blood in the brain parenchyma causes damage to the surrounding tissue by:
- Mechanical Effect (Mass effect)
has fixed volume, normally & when this changes will cause other issues
- Neurotoxicity of the blood components and degradation products
Hemorragic stroke
- Compression of the tissue surrounding the hematoma also may lead to secondary ischemia in some cases
- main tx is aimed at controlling ICP
What is the most important predictor of outcome of a hemorrhagic stroke?
Clot volume
- about 30% hemorrhages enlarge over first 24 hours
What are the following pharmacologic therapies used to treat?
- Tissue Plasminogen Activator (tPA) - best
- Aspirin - antithrombic agent, decrease clotting
- Acute BP lowering (Labetalol, Nicardipine, Nitroprusside, others)
Acute Ischemic stroke
What are the following pharmacologic therapies used to for?
- Antiplatelet Therapy (Aspirin, clopidogrel [Plavix], dipyridamole/aspirin [Aggrenox])
- Antithrombotic (Warfarin [Vitamin K Antagonist])
- BP Lowering (Ace Inhibitors, ARBs, diuretics)
- Statins- Cholesterol Lowering Agents (Atorvastatin, Pravastatin, Lovastatin, Rosuvastatin, Fluvastatin, Stimvastatin)
Secondary prevention of stroke
AKA preventing a second stroke
What are the exclusion criteria for tPA
- Evidence of intracranial hemorrhage
- Only minor or rapidly improving stroke symptoms
- High clinical suspicion of subarachnoid hemorrhage even with normal CT
- Active internal bleeding (GI/GU within 21 days)
- Known bleeding diathesis, including but not limited to platelet count <100,000/ mm3
- Patient has received heparin within 48 hours and had an elevated APTT
- Recent use of anticoagulant and elevated PT/INR
- Intracranial surgery, serious head trauma, or previous stroke within 3 months
- Major surgery or serious trauma within 14 days
- Recent arterial puncture at noncompressible site
- Lumbar puncture within 7 days
- History of intracranial hemorrhage, arteriovenous malformation, or aneurysm
- Witnessed seizure at stroke onset
- Recent AMI
- SBP >185 mm Hg or DBP > 110 mm Hg at time of treatment
What should non-cariogenic stroke patients receive if it’s not contraindicated?
Antiplatelt agent
- Aspirin (if stroke occurs while taking this, switch to stronger prescription)
- Aggrenox - expensive
- Plavix - expensive
What should pts with cardiogenic strokes receive?
Long term oral anticoagulation with warren
- goal = INR of 2-3
MOA: inhibition of ADP dependent [ADP antagonist] expression of Glycoprotein GP 2B/3A receptors which will inhibit platelet aggregation
ADRs: Bleeding risk is additive with other anticoagulants; Muscle Pain, Back Pain, Chest Pain, Hypertension, Headache, Constipation, Diarrhea, Rash, GI Bleed
Plavix
- Monitoring: Routine monitoring of antiplatelet effect is not recommended; Laboratory markers of bleeding should be evaluated and baseline and periodically
MOA: impairs platelet function by inhibiting the activity of adenosine and phosphodiesterase which causes accumulation of adenosine and cAMP; vasodilates coronary arteries
ADRs: Abdominal pain, Diarrhea, Indigestion, Bleeding, Headache
Aggrenox
- Monitoring: coagulation panel, CBC, chemistry profile, blood pressure, fecal occult blood test, liver function
MOA: Vitamin K antagonist that produces its effect by interfering with the interconversion of Vitamin K and its 2,3 epoxide. This leads to the depletion or reduction in activity of vitamin K-dependent coagulation proteins (factors 2,7,9 and 10) produced in the liver. At least 4-5 days of therapy are necessary before a patient is completely anticoagulated.
ADRs: Bleeding- gums, nose, GI tract, urogenital bleeding, Bruising, Teratogenic, Skin Necrosis, MANY DRUG INTERACTION, Many food interactions, Many comorbid disease state interactions
Warfarin
- dosing dependent upon other medications, disease, diet, INR lab values
Why should HTN be addressed at a later time, rather than immediately (first 7 days) with a stroke patient?
May result in decreased cerebral blood flow and worsen stroke symptoms
- HTN should be addressed when pt is out of acute phase, as it lowers risk for stroke recurrence
What are the main categories for HTN medication?
- ACE-Inhibitors - end in “-pril”
- ARB’s - end in “-artan”
- Thiaxide diuretics - end in “-ide” or “-one”
What are recommended for secondary prevention of strokes where the target goal is for lowering clohesteral with CHD or atherosclerotic disease?
Statins
- ischemic stroke or TIA presumed to be due to an atherosclerotic origin
- reduce stroke by 30% in patients with CAD and elevated lipids
MOA: inhibit HMG-CoA reductase which is the enzyme responsible for conversion of HMG-CoA to mevalonate; Mevalonate is an early precursor and a rate-limiting step in cholesterol synthesis. This reduction in liver cholesterol synthesis results in upregulation of liver LDL receptors and increased clearance of LDL from blood
ADRs:Adverse Events; Myopathy due to muscle damage; Myalgia from muscle soreness/ tenderness; Rhabdomyolysis rare, but can cause acute renal failure; stop drug ASAP; Flu-like symptoms; LFT; Contraindicated in Acute or Chronic Liver Disease
Statin therapy
Why does rehabilitation of stroke take time for rehab?
The brain needs to be retrained and it takes time to develop new neuromuscular connections
What tools are used to asses prognosis of stroke patients?
- National Institutes of Health Stroke Scale (Scores 0-42; <3-4 excellent chance of good recovery; > 20 indicates poor outcome)
- Rankin Scale
- Barthel Index
- Glasgow Outcome Scale
