NUPY 5_Cerebrovascular disease Flashcards

Covers the pathology of cerebrovascular disorsders (58 cards)

1
Q

**Stroke or TIA?
* acute onset neurologic signs and symptoms with a vascular basis
* persist beyond 24 hours
* imaging studies demonstrate infarction

A

Stroke

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2
Q

**Stroke or TIA?
* acute onset
* neurologic signs and symtoms with a vascular basis
* symptoms resolve within 4 hours
* evidence of brain infarction seen on imaging

A

Stroke

Presence of infarction implies a stroke diagnosis

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3
Q

**Stroke or TIA?
* acute onset
* neurologic signs and symtoms with a vascular basis
* symptoms resolve within 4 hours
* no evidence of brain infarction seen on imaging

A

TIA

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4
Q

ischemic but reversibly dysfunctional tissue surrounding a core area of infarction

A

Penumbra

target of revascularization therapy

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5
Q

2 causes for increase in intracellular calcium during cerebral ischemia

A
  1. Decreased ATP–>membrane ion pumps stop functioning–>neurons depolarize–>intracellular calcium rises
  2. Neuronal depolarization –>glutamate release from synaptic terminals–>activates NMDA receptors–>calcium influx
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6
Q

4
mechanisms of ischemic-reperfusion injury

A

Oxidative stress
Intracellular calcium overload
Inflammation
Activation of the complement system

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7
Q

Causes of global cerebral ischemia

aka diffuse hypoxic ischemic encephalopathy

A
  1. Generalized reduction in cerebral perfusion: Cardiac arrest, MI, shock
  2. Decreased oxygen carrying capacity of blood: CO or cyanide poisoning
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8
Q

List the CNS cell types that are most sensitive to hypoxia

A
  1. Pyramidal neurons in the hippocampus
  2. Cerebellar Purkinje cells
  3. Pyramidal neurons in the cerebral cortex (esp. III and V)
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9
Q

**What’s the level of the lesion? **
Posture - Flexion of the elbows and wrists and supination of the arm , lower limbs extended

A

above the red nucleus/ bilateral damage rostral to the midbrain

decorticate posturing

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10
Q

**What’s the level of the lesion? **
Posture - Extenmsion of the elbows and wrists with pronation , lower limbs extended

A

Below the red nucleus/ damage to motor tracts caudal to the midbrain

decerebrate rigidity

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11
Q

**Vegetative state/ brain-death? **
* awake but non-responsive
* Persistent yawning, cough, swallow, limb and head movement functions
* Few to no responses to external/ internal environment
* Absent response to visual stimuli
* Decerebrate/ decorticate posturing

A

Vegetative state

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12
Q

What confounding factors should be ruled out before diagnosing brain death?

A
  1. Hypothermia
  2. Drug intoxication
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13
Q

2 elements required for diagnosis of brain death after ruling out confounding factors

A
  1. Widespread cortical destruction
  2. Brainstem damage
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14
Q

List signs of brainstem damage

A
  • Pupils dilated and non reactive bilaterally
  • Corneal reflex absent
  • Loss of oculocephalic and oculovestibular reflexes
  • complete and irreversible apnea
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15
Q

Signs of widespread cortical destruction

A

Deep coma, unresponsive to all forms of stimulation

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16
Q

Clinical consequences of a watershed infarct in the MCA-ACA borderzone

A

proximal arm and shoulder weakness with preserved strength distally in the lower limbs (person in a barrel syndrome)

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17
Q

Gross morphology of a borderzone infarct

A

bilateral,wedge-shaped, strips that are parallel and a few centimeters lateral to the interhemispheric fissure

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18
Q

Microscopic morphology of a borderzone (watershed) infarct

A

diffuse laminar necrosis

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19
Q

Pattern of necrosis in a cerebral infarct

A

Liquefactive
(release of hydrolytic enzymes)

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20
Q

Causes of cerebral vessel occlusion by emboli

A
  • Cardiac mural thrombi – atrial fibrillation, myocardial infarction, valvular heart disease
  • Originating from arteries- atheromatous plaques within the carotids
  • paradoxical thromboemboli – patent foramen ovale/atrial septal defect.
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21
Q

Causes for an ischemic stroke due to cerebral vasospasm

A
  1. Subarachnoid hemorrhage
  2. Drugs- cocaine, marijuana, amphetamines, pseudoephedrine
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22
Q

Identify the vessel most likely to have been occluded:
right face and arm weakness
right face and arm sensory loss
Expressive aphasia

A

left MCA

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23
Q

Identify the vessel most likely to have been occluded:
Left face and arm weakness
Left face and arm sensory loss
Left hemineglect

A

Right MCA

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24
Q

Identify the vessel most likely to have been occluded
* right pure upper motor hemiparesis

A

Lenticulostriate branches of the left MCA (damage to basal ganglia and genu of internal capsule on the left side)

25
**Identify the vessel most likely to have been occluded** * left pure upper motor hemiparesis
Lenticulostriate branches of the right MCA (damage to basal ganglia and genu of internal capsule on the right side)
26
**Identify the vessel most likely to have been occluded:** * Right leg weakness - damage to motor cortex * right leg sensory loss -damage to sensory cortex. * Grasp reflex, frontal lobe behavioral abnormalities * transcortical aphasia - seen if the prefrontal cortex and supplemental motor areas are involved.
Left ACA
27
**Identify the vessel most likely to have been occluded:** * Left leg weakness - damage to motor cortex * Left leg sensory loss -damage to sensory cortex. * Grasp reflex, frontal lobe behavioral abnormalities * Left hemineglect - seen if the prefrontal cortex and non-dominant association areas are involved.
Right ACA
28
**Identify the vessel most likely to have been occluded:** * contralateral homonymous hemianopia with macular sparing * Contralateral hemisensory loss
PCA
29
**See the attached image and identify whether it is an ischemic or a hemorrhagic stroke:** 78 year old with focal neurologic deficits 1 day ago
Ischemic stroke (Low attenuation on CT) | At about 24 hours, the lesion becomes relatively well circumscribed
30
Most cerebral infarcts develop as pale infarcts. Why do some undergo secondary hemorrhagic transformation?
Ischemic reperfusion injury
31
Timeline at which this morphologic finding is most likely to be visible:
6-12 hours | red neurons
32
****Timeline at which this morphologic finding is most likely to be visible: Foamy macrophages first become visible
48-72 hours
33
Fomay macrophages that appear after a cerebral infarct to perform phagocytosis originate from which cells?
Activated microglia
34
****Timeline at which this morphologic finding is most likely to be visible: reactive astrocytes and newly formed vessels begin to be seen at the periphery
By 1 week
35
****Timeline at which this morphologic finding is most likely to be visible: dense meshwork of glial fibers admixed with new capillaries and perivascular connective tissue
After several months
36
Most common risk factors for a lacunar stroke
**chronic hypertension,** hyperlipidemia, diabetes
37
Commonly affected regions in a lacunar stroke
putamen, caudate nuclei, internal capsule,thalamus
38
2 morphologic lesions associated with lacunar strokes
1. Lipohyalinosis 2. Microatheromas
39
**Diagnosis? ** 82 year old male with chronic hypertension, presents with acute onset focal neurologic deficits and then passes away. Gross morphology is shown in the attached image.
Lacunar infarct
40
41
Predominant and earliest mechanism of cerebral edema in an ischemic stroke
Cytotoxic edema- to failure of the Na+/K+-ATPase pump followed by vasogenic edema due to damage to the blood brain barrier.
42
most common cause of a hemorrhagic stroke involving the basal ganglia and thalamus
hypertension
43
most common cause of a hemorrhagic stroke in the lobes of cerebral hemispheres in the elderly
cerebral amyloid angiopathy
44
most common location of hemorrhagic strokes due to hypertension
putamen (50-60%)
45
minute aneurysms in the brain that occur in small penetrating blood vessels and cause hemorrhagic styrokes when they rupture and bleed
Charcot Bouchard microaneurysms
46
How does hypertension cause a hemorrhagic stroke?
accelerated atherosclerosis in larger arteries, hyaline arteriolosclerosis in smaller arteries-->more vulnerable to rupture than normal vessels--> hemorrhagic stroke
47
Is this an ischemic or a hemorrhagic stroke?
Hemorrhagic stroke ( increased density on nonenhanced CT scans of the brain immediately after the event)
48
clinical signs of a putamen bleed
contralateral hemiplegia, slurred speech, eyes deviate away from lesion; upper brainstem compression (coma), decerebrate rigidity, bilateral Babinski signs, fixed, dilated pupils, irregular/ intermittent respiration
49
most common cause of a non traumatic subarachnoid hemorrhage
Saccular (berry) aneurysm
50
Most common sites of a berry aneurysm in descending order of frequency
(1) the proximal portions of the anterior communicating artery (2) at the origin of the posterior communicating artery from the stem of the internal carotid (3) at the first major bifurcation of the MCA, and (4) at the bifurcation of the internal carotid into middle and anterior cerebral arteries
51
CSF finding in subarachnoid hemorrhage
Xanthochromia
52
Radiologic findings in subarachnoid hemorrhage
Blood in the basal cisterns and sylvian fissures
53
Complications of subarachnoid hemorrhage
1. Rebleeding 2. Seizures 3. Communicating hydrocephalus 4. Vasospasm 5. Hyponatremia
54
most common mechanism of hydrocephalus in subarachnoid hemorrhage
blood-induced impairment of absorption of cerebrospinal fluid by the arachnoid granulations.
55
Most likely cause of a hemorrhagic stroke in an individual with the following radiologic finding
arteriovenous malformation | tangled networks of wormlike vascular channels
56
* tufts of capillary sinusoids that form within the deep hemispheric white matter and brainstem * no normal intervening neural structures * Risk of intracranial hemorrhage
cavernous hemangioma
57
accumulation of cognitive deficits from serial strokes in a stepwise manner Etiology: Multifocal vascular disease due to cerebral atherosclerosis
vascular dementia
58
subtype of vascular dementia that mainly involves the subcortical white matter
Binswanger disease