V A S C U L A R Flashcards

1
Q

What kind of sx do you expect in a patient with a stroke affecting the basilar artery?

A

Coma, “locked in” syndrome, cranial nerve palsies, apnea, visual sx, drop attacks, dysphagia, dysarthria, vertigo, “crossed” weakness and sensory loss affecting ipsilateral face and contralateral body

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2
Q

Immediate labs to get when pt presents with stroke

A

CBC with platelets, cardiac enzymes and troponin, electrolytes, BUN, creatinine, serum glucose, PTT, PT, INR, lipid profile, and O2 sat

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3
Q

Most sensitive modality for diagnosing acute ischemic infarct

A

Diffusion weighted MRI

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4
Q

If you suspect an embolic stroke, what tests should you order next

A

ECG, echo

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5
Q

Contraindications to tPA tx

A
SAMPLE STAGES
Stroke or head trauma within last 3 most
Anticoag with INR >1.7 or prolonged PTT
MI (recent)
Prior intracranial hemorrhage
Low platelet count (185 OR diastolic>110
Surgery in the past 14 days
TIA
Age 400 mg/dL) or decreased (<50) blood glucose
Seizures at onset of stroke
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6
Q

If anticoag is contraindicated in pt who just had a stroke, what meds can you give them instead?

A

ASA + clopidogrel.

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7
Q

Target INR for pts with prosthetic valve

A

3-4. OR you can add anti-platelet agent.

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8
Q

Thrombotic stroke is due to rupture of…?

A

Atherosclerotic plaque, which usually develops at branch points e.g. bifurcation of internal carotid and MCA in circle of Willis. It results in a PALE infarct at the periphery of the cortex.

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9
Q

Embolic stroke is due to …?

A

Thromboemboli, usually 2/2 afib. Usually involves MCA. Results in HEMORRHAGIC infarct at periphery of cortex.

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10
Q

Ischemic stroke – describe the pathology

A

Results in liquefactive necrosis*. Eosinophilic change in the cytoplasm of neurons (red neurons) is an early finding, 12 hours after. Necrosis occurs in 24, infiltration by neutrophils days 1-3, and microglial cells (days 4-7), and gloss (weeks 2-3) then ensue. This results in a formation of a fluid filled cystic space surrounded by gliosis.

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11
Q

Which cranial nerve is associated with berry aneurysms?

A

CN III palsy with pupillary involvement

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12
Q

What should you do if you suspect SAH but get a negative CT?

A

Immediate LP to look for RBCs, xanthochromia, increased protein (2/2 RBCs) and increased ICP. LP results can be falsely negative in first 6-12 hours bc xanthochromia not yet developed and after first 24-28 hours because its resolved.

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13
Q

7 conditions associated with berry aneurysms (aka SAH)

A
MAKE SAH.
Marfans
Aortic coarctation
Kidney dz (ADPKD)
Ehlers danlos
Sickle cell anemia
Atherosclerosis
History (familial)

Additionally, being black has a higher risk.

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14
Q

Intracerebral hemorrhage is classically due to rupture of?

A

Charcot Bouchard micro aneurysms of lenticulostriate vessels. Usually in BASAL GANGLIA.

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15
Q

What feature of berry aneurysms make them more prone to rupture?

A

Lack of a media layer

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16
Q

Pt presents with intractable vomiting, FEVER, occipital headache, blepharospasm, severe dizziness and inability to walk. Muscle strength is preserved and no sensory abnormalities noted. What is the most likely etiology?

A

Cerebellar hemorrhage. Fever is common in any intracranial hemorrhage.

17
Q

What kind of sx expected in MCA stroke

A

Aphasia if dominant (usually left) hemisphere or neglect if non dominant (right) hemisphere
CL paresis and sensory loss in face and arm
Gaze preference* toward side of lesion
Homonymous hemianopsia

18
Q

What kind of sx expected in ACA stroke

A

C/L paresis and sensory loss in log
Cognitive or personality changes –abulia, emotional disturbance, etc.
Dyspraxia
Urinary incontinence

19
Q

What kind of sx expected in PCA stroke

A
Homonymous hemianopsia
Memory deficits
Dyslexia/alexia
Dysphagia
Dysarthria
20
Q

What kind of sx expected in posterior limb of internal capsule stroke

A

Unilateral motor impairment with no sensory or cortical deficits
No visual field abnormalities

21
Q

Describe how homocysteinuria can cause CVA and what tx is.

A

CVA 2/2 pathologic changes in vessel walls and increased adhesiveness of the platelets usually involving cerebral vessels. Give Vit B6, folate, and B12 as well as anti-platelets or anti-coagulation. Don’t confuse with Marfans (same body habitus!)

22
Q

4 causes of craniocervical dissection

A

Trauma
FMD
Inflammatory/infectious diseases
Marfans

23
Q

Presentation of cingulate “subfalcine” herniation

A

Displacement of cingulate gyrus under fall cerebra; occurs 2/2 mass lesions of frontal lobes. Could compress ACA leading to infarction

24
Q

Presentation of transtentorial herniation

A
Pushes midbrain inferiorly
Presents with rapid change in mental status
B/L small and reactive pupils
Cheyne-Stokes respirations
Flexor or extensor posturing
25
Q

Presentation of uncal herniation

A

CN III becomes intrepid – leading to fixed and dilated IPSILATERAL pupil followed by eye that is deviated down and out.
Ipsilateral hemiparesis from compression of cerebral peduncle against tectorial edge
Compression of PCA
Rupture of paramedic artery leads to Duret (brainstem) hemorrhage

26
Q

Cerebellar tonsillar herniation into foramen magnum - signs and sx

A

Tonsillar herniation – > medullary compression –> respiratory arrest. Usually rapidly fatal.

27
Q

Which tracts affected in ASA stroke? Sx?

A

Infarct of paramedian branches of ASA and vertebral arteries (medial medullary syndrome): lateral corticospinal tract, medial lemniscus, caudal medulla –hypoglossal nerve.
Sx: contralateral hemiparesis of lower limbs, decreased contralateral proprioception, ipsilateral hypoglossal dysfunction (tongue deviates ipsilaterally).

28
Q

Which tracts affected in PICA stroke? Sx?

A

Lateral medullary (Wallenbergs) syndrome: lateral medulla affecting vestibular nuclei (vertigo, nystagmus, vomiting); lateral spinothalamic tract (decreased pain and temp sensation to limbs); spinal trigeminal nucleus (decreased pain and temp sensation to face); nucleus ambiguus (dysphagia, hoarseness, decreased gag reflex); sympathetic fibers (ipsilateral Horners); inferior cerebellar peduncle (ataxia, dysmetria).

29
Q

Which tracts affected n AICA syndrome? Sx?

A

Lateral pons–cranial nerve nuclei; vestibular nuclei (vomiting, vertigo, nystagmus); facial nucleus (paralysis of face, decreased lacrimation, salivation, decreased taste from anterior 2/3 of tongue, decreased corneal reflex); spinal trigeminal nucleus (Decreased pain and temp sensation); cochlear nuclei (ipsilateral decreased hearing); sympathetic fibers (ipsilateral Horners syndrome)

30
Q

Besides the lateral pons, what else does AICA supply?

A

Inferior and middle cerebellar peduncles.

31
Q

If a pt has a berry aneurysm with a CN III palsy, where is the lesion?

A

Posterior communicating artery

32
Q

Which kind of hematoma crosses suture lines?

A

Subdural hematoma

33
Q

Which kind of hematoma can cross falx, tentorium?

A

Epidural hematoma

34
Q

When does irreversible damage begin to the brain in hypoxia?

A

5 minutes

35
Q

4 most vulnerable areas of the brain to hypoxia

A

Hippocampus
Neocortex
Cerebellum
Watershed areas