L6- CVAs Flashcards
list the types of strokes
1) Ischemia: thrombotic or embolic
2) Hemorrhagic: vascular rupture; intracerebral or subarachnoid
both –> (3) Hypoxic: global or focal
all –> infarction
how is imaging used in the diagnosis of stroke
CT (preferred- quicker) or MRI
1) Ischemic Stroke: lesion seen w/in hrs on MRI, appears negative w/in 24hrs on CT
2) Hemorrhagic Stroke: lesion appears immediately after onset
So in ED w/ stroke sxs –> imaging (CT) –> neg will r/o hemorrhagic
list some general causes of functional hypoxia in the brain
- low partial pressure: high altitude
- toxins: cyanide
- dec O2 carrying capacity: anemia
ischemia in the brain occurs in (transient/permanent) fashion due to (2) or (3)
(hypoperfusion)
1- either
2- low BP
3- vascular obstruction
Global Cerebral Ischemia:
- (1) cause
- (2) factors affected outcome
- (3) are the outcomes
1- severe systemic hypotension (MI, shock)
2- severity, duration (rapid, slow), cell type involved
3- widespread neuron death –> severe neurological impairment OR death
describe the susceptibility of different brain cells to ischemia
neurons more than glial cells
-pyramidal cells, Purkinjee cells
______ are the most susceptible brain cells to ischemia (include location)
Pyramidal cells: hippocampus, neocortex
Purkinjee cells: cerebellum
(only mild ischemia is sufficient to cause severe damage)
In (1) ischemia, only the affected area supplied by the vessel is damaged, and (2) is very important in limiting this damage
1- focal cerebral ischemia
2- collateral blood supply
______ area has the greatest risk of a watershed infarction
border zone between ACA and MCA
Watershed infarctions occur more in (global/focal) cerebral ischemia, commonly after (2) events occur. The damage produces a (3) appearance, commonly in (4) location.
1- global
2- hypotensive episodes
3- sickle-shaped band necrosis over cerebral convexity
4- few cms lateral to interhemispheric fissure (for ACA/MCA zone)
what are the types of CVAs due to ischemia, indicate which is more common
- Embolic (more common)
- Thrombolytic
embolic ischemic CVA:
- (1) source
- (2) risk factors (pre-disposing conditions)
1- cardiac mural thrombus, carotid atheromatous plaque
2- AFib, valvular disease, myocardial dysfunction
define paradoxical emboli
venous emboli crosses over to arterial side (bypassing lungs to cause PE) via R –> L shunt (ASD, VSD, patent foramen ovale) leading to ischemia (legs or stroke)
thrombotic occlusion ischemic CVA:
- (1) definition
- (2) list the possible progressions
1- thrombus superimposed on atherosclerotic plaque
2:
- can have anterograde extension
- can fragment / embolize
- can lead to Small Lacunar infarcts
define small lacunar infarcts
- via thrombotic occlusion ischemic CVA
- -> occlusion of penetrating arteries via HTN
describe the gross morphology of ischemia of the brain
- swollen brain: wide gyri, narrowed sulci
- poor demarcation between white/gray matter
- liquefied tissue => fluid filled cavity
Histological changes of brain ischemia: 12-24hrs
- cytoplasmic eosinophilia
- nuclear death
- neutrophil infiltration (begins at lesion edges, where vascular supply is intact)
Histological changes of brain ischemia: 1day-2wks
- tissue necrosis (liquefactive)
- macrophage influx (surrounds gliosis)
- vascular proliferation
- reactive gliosis (hypertrophied cells)
Histological changes of brain ischemia: >2wks
- removal of necrotic tissue
- residual gliosis (hypertrophied cells)
list the classifications of intracranial hemorrhages leading to stroke
- Intraparenchymal hemorrhages (w/in brain): hypertensive (most cases) or non-hypertensive
- subarachnoid hemorrhage
Primary Intraparenchymal hemorrhage = (1):
- (2) mechanism of hemorrhage
- (3) clinical features
1- hypertensive hemorrhage
2- HTN –> small intraparenchymal vessel rupture
3- based on size and location: small = silent, large = apparent, if extended to ventricles = death
Hypertensive Intraparenchymal hemorrhage usually occurs in the following locations….
basal ganglia*, thalamus, pons, cerebellum
HTN can cause (1) morphological change in the brain of (2) vessels, mostly in (3) parts of the brain. (2) are then weakened, causing (4- two names) to occur, leaving (2) at risk for (5).
1- hyaline arteriolar sclerosis
2- deep penetrating arteries / arterioles
3- basal ganglia*, brainstem, hemospheric white matter
4- small microaneurysm / Charcot-Bouchard aneursym
5- rupture
define Charcot-Bouchard aneurysm
small microaneurysm resulting from weakened vessels walls of penetrating cerebral arteries and arterioles due to hyaline arteriolar sclerosis
describe the possible pathological outcomes of hypertensive cerebral arteries besides rupture –> hemorrhagic stroke
1) slit hemorrhages: rupture of small caliber penetrating vessels
2) lacunar infarcts: cavitary infarcts secondary to thrombosis of vessel w/ arteriolosclerosis changes of single penetrating branch
3) acute hypertensive encephalopathy: sustained inc in diastolic BP (>130) –> global cerebral dysfunction (varied Sxs)
Non-hypertensive cerebral hemorrhages:
- (1) describes location
- (2) causes, hint- 5
1- lobar, limited to affected lobe
2:
- coagulopathy
- vascular malformation
- amyloid angiopathy
- cortical vein OR dural sinus thrombosis
- tumor hemorrhage
Of all the non-hypertensive cerebral hemorrhages, (1) has the greatest potential for hemorrhage because of (2) changes in blood distribution. (2) also leads to possibility of causing (3) overall in the body. Treatment includes (4).
1- vascular / arteriovenous malformation
2- high flow channels w/o arterial structure –> shunts blood away
3- high output CHF
4- excision, endovascular occlusion
_____ is a non-hypertensive cerebral hemorrhage with a similar mechanism as hypertensive hemorrhages
Amyloid angiopathy: amyloid deposition –> weakens vessel wall –> risk of rupture and hemorrhage
Subarachnoid hemorrhage:
- (1) cause (include location)
- (2) and (3) are conditions with high risk of (1)
1- rupture of saccular / berry aneurysms at branch points in the Circle of Willis
2- AD PCK
3- Ehler-Danlos syndrome
describe the progression and location distribution of berry aneurysms
-not present at birth –> develop over time due to defect in tunica media
- 90% in anterior circulation
- 40% at ACA, 34% at MCA, 20% at int. carotid, 4% at basilar art.
Berry Aneurysm:
- (1) appearance
- they are lined by (2) with (3) importantly missing
- (4) is most common site of rupture on aneurysm
- blood from rupture will enter (5)
1- saccular aneurysm, thin walled outpouching of artery
2- thickened hyalinized intima (maybe some continuous tunica adventitia)
3- muscular wall (muscularis), IEL
4- apex
5- subarachnoid space
Berry aneurysms will rupture in response to….
acute inc in ICP: straining at stool, organism
list the clinical features of Subarachnoid hemorrhage
- worst HA of life, ‘thunderclap HA’
- Meningismus (features of meningitis due to irritation of meninges): neck stiffness, photophobia, etc
Subarachnoid hemorrhage:
- (1) prognosis
- (2) investigations w/ results
1- poor, high mortality and worsens with successive bleeds
2- CT scan /// lumbar puncture: RBCs present, xanthochromia (yellowing of CSF due to bilirubin)
list the complications of subarachnoid hemorrhages
Rebleed- common, inc risk of mortality
Vasospasm- early period of hemorrhage
Hydrocephalus: via healing and meningeal fibrosis –> obstructs CSF flow OR absorption
list the vascular malformations of the brain
arteriovenous malformation
cavernous malformation
capillary telangiectasias
venous angiomas
(1) is the most common vascular malformation in the brain, affecting (fe-/males) more in the (3) age range.
1- AV malformation (arteriovenous)
2- males 2x
3- 10-30 y/o
gross appearance of AV malformation
appears like tangled network of wormlike vascular channel
microscopic appearance of AV malformation
enlarged BV
separated by gliotic tissue
often evidence of previous hemorrhage
describe the clinical features / complications of AV malformations
seizure, intracerebral hemorrhage, OR subarachnoid hemorrhage
Newborn: possibly high output CHF (blood shunting from arteries to veins)
