CVA primary care Flashcards
(38 cards)
PE of pt with CVA
Neurological examination notable for expressive aphasia and mild weakness on Rt side of face and arm. CV examination: S4 gallop and dorsalis pedis pulses diminished bilaterally. ECG shows NSR. CBC and BMP show glucose normal. Spouse wants to know what else to do.
ABCD2 score
Score (Age, BP, uinlateral weakness, duration 10-59 min
two types of stroke
Ischemic (occlusive) vs hemorrhagic
ischemic is seen with occlusions 80% of stroke are ischemic 8/10 chance of ischemia seen with a fibb
(permanent brain infarction) –>accounts for 80% of all CVA.
o 3 main subtypes: thrombosis (49%), embolism (31%), systemic hypoperfusion
hemorrhagic strokes are caused by
usually derived from arterioles or small arteries –> causes bleeding directly into the brain, forming a localized hematoma which spreads along white matter pathways. Hematoma gradually enlarges
o Causes: HTN, trauma, bleeding diatheses: unusual susceptibility to bleed, amyloid angiopathy, illicit drug use (i.e. amphetamines, cocaine), vascular malformations
o Accounts for 20% of all CVA
why do we see thrombis
when ever an artery forks it is turbulent
susceptible to more damange
TIA
ischemia (transient ischemic attack TIA): transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, WITHOUT acute infarction
intrinsic pathophysiology of CVA
i.e. atherosclerosis, lipohyalinosis, inflammation, amyloid deposition, arterial dissection, developmental malformation, aneurysmal dilation, venous thrombosis
remote origin of cva
) The process may originate REMOTELY, as occurs when an embolus from the heart or extracranial circulation lodges in an intracranial vessel
describe inadequacy that leads to CVA
The process may result from INADEQUATE (CBF) cerebral blood flow 2˚ ↓ perfusion pressure or ↑ blood viscosity
statins don’t do anything about
that fats you ingest
they only effect the biosynthesis of cholesterol in the liver
you will get a better effect with lifestyle modfications
when does the liver biosynthesize cholesterol
at night
take statins at night
doesn’t have a great half life need to take at night when the liver is productive
what did the SPRACL trial find about the effects of CVA with statins
- ” Reduced CVA risk 3.4-2.7%
atorvastatin: reduces risk of recurrent stroke & major event over 5 years
Some concern about more hemorrhagic strokes in treatment group (55 vs 33)
but benefits outweight the risks
looking at lipid reductions with medications
what do you see with atorvastatin
35-39% reductions with 10 mg
40mg (53%)
10 mmHg reduction in SBP decreases risk by ___
regardless of whether or not you are HTN
10 mmHg reduction in SBP decreases risk by 1/3
but we are worried about people over 60 have perfusion of coronary arteries (occurs in diastole so make sure diastole is NOT TOO LOW)
volume tx for the management of HTN
: Diuretics/ACEI
tx that target the tone for the treatment of HTN
CCB
modifiable risk factors for the prevention of CVA
o HTN, atherosclerosis, dyslipidemia
AND
o Smoking, DM, sickle cell, carotid stenosis, atrial fibrillation: irregular heartbeat (arrhythmia) that can lead to blood clots, stroke, heart failure, or other heart-related complications
MCC of stroke
Elderly - thrombotic & embolic strokes 2˚ atherosclerosis MC
how do we manage HTN in post CVA pts
lower BP w/ 2 classes of agents
(↓ volume: ACE inhibitors & diuretics. ↓ Vascular tone: CCB)
how to we manage lipids in post CVA pts
o Lipids - treat dyslipidemia (LDL = ~ 130-159)
how do we promote anticoagulation
o Platelets - prevent blood clots w/ anticoagulants (ASA, ASA + ERDP, clopidogrel)
why do we use 81mg of ASA
Risk reduction equivalent at low & high doses = 50-100mg/day sufficient–> lower dose preferred, try to minimize the risk of GIB
daily ASA tx reduces
” ↓ CVA risk 22% (improves cardiac risk too)
how does ASA inhibit coagulation
Also Inhibits prostaglandin synthesis
Inhibits cyclooxygenase, prevents thromboxane A2 formation, platelet activation & aggregation
