Lecture 16 and 17 -- CVD Flashcards
what are two types of stroke
what is the only way to differentiate the two?
Hemorrhagic and Ischemic
Imaging
what are the two types of hemorrhagic stoke?
what imaging type is best for to see a hemorrhagic stroke
SAH
ICH
CT scan – quick and good for fluid
underlying causes of SAH
Berry Anuerysm – ballooning of an artery, weakening of the wall; typically in the branch points of Ant. Comm artery
Arterio-Venous Malformation – abnormally direct communication between arteries —> Veins without intervening capillary bed. Venous system exposed to high arterial pressures.
underyling causes of ICH?
HTN – long standing atheroscloerosis
Cerebral Amyloid Angiopathy – degenerative deposition of Amyloid in aterial walls of cortical vessels
Aneurysm, AVM
Treatment of hemorrhagic stroke?
Medical emergency; ICU; Neurosurgery consult
do not give TPA
Clinical defition of an ischemic stroke?
what imaging is used to view acute ischemic stroke?
Clinical manifestation of a CNS Infarcton
Sudden onset, focal deficits lasting > 24 hours
evidence of infarctioin on imaging
diffuse weighted MRI (this will not show up on CT)
brain’s compesnation mechanisms for reduced blood flow…
Vasodilation – increased transit time
Anaerobic metabolism – but when all energy resoruces depleted….
electrical failure — TIA, stroke
what is a TIA
how should it be managed clinically
TIA – transiet ischemia attach
transiet focal neurological deficits
No actual infarction
Technically TIA if symptoms last less than 24 hours (but in reality if symptoms last more than 2 hours, they are going to last more than 24 hours)
Warning sign for acute ischemic stroke; should not be ignored
ischemic penumbra vs ischemic core
penumbra: reversbile infarction
Core: irreversible
core grows with time
time = brain
rank the following in regards to sensitivity to ischemia from least to most:
oligodendrocytes, neurons, endothelium, astrocytes
Least: Endothelial cells
astro
Oligo
Neurons (hippo, purkinje cells, pyramidals of cortex, neostriatum)
what are 4 ways in which patients can deteroirate in the setting of ischemic stroke
Cytotoxic Edema –
Hemorrhagic Conversion
Herniations
Recurrent ischemic stroke –
Cytotoxic edema
pathophysiology –
how does this kill you?
how can this be alleviated?
Increased permeability of neuronal and glial cell membranes results in intracellular swelling
Kills you - – mass effect–> herniation
Alleviated – Hemicraniectomy
Review of imaging for storkes:
hemorrhagic?
acute ischemic?
cytotoxic edema?
CT
Diffusion weighted MRI
CT
Hemorrhagic COnversion -- what is it? difference between large and small strokes? how does it kill you? alleviate this?
Friable endothelium; blood leaks out into parenchyma upon reperfusion
Large stroke – parenchyma is dead and therefore will not be symptomatic
Small stroke - parenchyma is viable; reperfusion will lead to further damage == symptoms
Kills you — herniation
alleviate this – hemicraniectomy
hemicraniectomy differences between and outcomes for lesions above the tentorium and below the tentorium
above the tentorium – slower deterioration; hemicraniectomy will save your life but you have had a massive stroke; therefore quality of life outcomes poor as patients have significant neuro deficits
below the tentorium (cerebellum) – can deteriorate very quickly without intervention; but following hemicraniectomy, outcomes are good becuase of redundant wiring of the cerebellum
Treatment for ishcemic stroke
TPA (alteplase)
Mechanical Clot Extraction Devices
Know anterior vs posterior vascular lesions and manifestations; esp regarding vision
Example:
Isolated Homonymous hemianopia = ?
Unilateral monocular blindness = ?
Isolated Homonymous hemianopia = PCA
Unilateral monocular blindness = Ophthalamic artery
Etiologies and subtypes of ischemic stroke ***
atherothrombotic cerebrovascular disease
Penetrating artery Disease – Small artery Disease – Lacunar Stroke
Cardiogenic Embolism
Other unusual Stroke
Idiopathic – 20 to 40%
atherothrombotic cerebrovascular disease
what vessels?
how can this be visualzed?
pathogenesis
Arterial Stenosis in the Head or Neck (Large intra cranial arteries; Extra cranial – carotid arteries)
Artery to artery Emboli
Stenosis –> slowed blood –> thrombus –> Embolism
treatment of atherothrombotic cerebrovascular disease -
l Carotid Endarterectomy –
Angioplasty Stenting –
Penetrating artery Disease – Small artery Disease – Lacunar Stroke
what vessels?
pathology of these vessels –
Base of brain, lenticulostriates, cerebellum
Lipohyalnaosis – thickening of the vessel wall, but its weak
Antherosclerosis
Manifestations of Penetrating artery Disease – Small artery Disease – Lacunar Stroke
Deep penetrating arteries — therefore don’t have cortical deficits
Lacunar clinical Syndromes — No Cortical Dysfunction:
Pure Motor Hemiparesis — no sensory findings, visual findings
Pure hemi-sensory loss — just sensation
Cardiogenic Embolism
most commonly?
imaging?
AFIB
Mechanical heart valves, Acute MI, Abn heart valves, Endocarditis
acute infarcts on MRI that are on both hemipshers, anterior and posterior
treatment and previton of Cardiogenic Embolism
Treatment – TPA
Prevention – Full does Anticoagulation
Wafarin (VKOR1)
Dabigitran (direct thrombin)
Rivorxaban/Apixaban (direct 10a)
antiplatelet therapies
ASA
Plavix
Aggrenox – ASA/Extended release dipyridamole
Non modfiable risk factors
Age — exponential increase; although any age can get a stroke
Gender – post menopausal women (lower estrogen)
Race – African Americans
Prior stroke –
TIA
Modifiable risk factors
most easily modifiable?
Afib – Warfarin;
Stenosis of Internal carotid Artery – HTN – 30-40% reduction in stroke when HTN is controlled Tobacco Use – Framhingham HLD –atherothrombotic stroke; vascular disease elsewhere
DM
Most easily modifiable – HTN and Tobacco
