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Clin Med - NEURO > Cerebrovascular disease and stroke > Flashcards

Cerebrovascular disease and stroke Flashcards

1
Q

what is the definition of a stroke

A

a neurologic deficit attributed to an acute FOCAL injury of the CNS by a VASCULAR CAUSE, including cerebral infarction, intracerebral hemorrhage (ICH), and subarachoid hemorrhage (SAH)

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2
Q

what is a ischemic stroke

A

blood clot stops the flow of blood to an area of the brain

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3
Q

what is a hemorrhagic stroke

A

weakened/diseased blood vessel rupture - blood leaks into brain tissue

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4
Q

What are common stroke symptoms

A

sudden neurological deficit:
Vision, Speech,Sensory, Motor, Impaired coordination/balance
non-specific - AMS, confusion, dizziness, vertigo, headache, lightheadedness, memory impairment

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5
Q

what are vision changes in a stroke

A

diplopia, visual field cut

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6
Q

What are speech changes in a stoke

A

asphasia, dysarthria, dysphagia

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7
Q

what are sensory changes in a stroke

A

one-sided numbness/altered sensation

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8
Q

what are motor changes in a stroke

A

one-sided weakness

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9
Q

what are non-sepecific symptoms associated with stroke

A

AMS, Confusion, dizziness, vertigo, headache, lightheadedness, memory impairment

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10
Q

what are stroke risk factors

A

smoking, sedentary lifestyle and an unhealthy diet, air pollution, HTN, obesity, hyperglycemia, hyperlipidemia

sleep apnea, DVT/PFO, Atrial septal defect, Arterial dissection, hyper-coagulability, sicks cell, autoimmune disorders, contraceptives, pregnancy, PCOS, binge drinking, poor nutrition, cocaine and amphetamine use

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11
Q

what is the first branch of the internal carotid artery

A

Opathalmic artery

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12
Q

how do you differentiate between the internal and external carotid arteries

A

The external carotid has many branches and branches early and the internal carotid has less branches and delayed branching

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13
Q

what is the definition of ischemic stroke

A

an episode of neurological dysfunction caused by focal cerebral, spinal or retinal infraction.
Time based definition: >24 hours of neurological deficit
Radiographic definition: MRI needed

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14
Q

what are special cases of ischemic strokes

A

MRI-negative strokes: infarcts can be missed on MRI. stroke is ultimately a clinical diagnosis

Silent Strokes: imaging/pathological evidence of infarction without history of acute neurological dysfunction attributable to the lesion

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15
Q

What is the TOAST classification

A

classification of stroke by mechanism or cause:

Large-artery atherosclerosis (embolus/thrombosis)
Cardioembolism
small-vessel occlusion
Stroke of other determined etiology
stroke of undetermined etiology

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16
Q

what is cardioembolic

A

when a clot forms in heart and then travels to the brain (common in afib, cardiomyopathy and MRI)

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17
Q

what is a lacunar infarction

A

a small vessel stroke

infarction following atherothrombotic or lipohyalinotic occlusions

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18
Q

what is hypoperfusion

A

also known as borderzone stroke
decreased global blood flow (hypotension, heart failure, hypovolemia) can stress the most distal reaches in a vascular territory

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19
Q

what is a paradoxical embolism

A

a patent foramen ovale (PFO) acts as an open window to allow venous clots to bypass the lungs and enter the arterial pathway to the brain.

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20
Q

what needs to be identified in regards to paradoxical embolism

A

need to identify source of embolus, eg DVT to implicate it in stroke

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21
Q

what is stroke syndrome

A

pattern of deficits you will (may) see when a specific arterial territory in the brain is affected

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22
Q

what is aphagia

A

inability to effectively communicate

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23
Q

What are the classic lacunar syndromes

A

Pure motor hemiparesis
pure sensory stroke
sensorimotor
ataxic hemiparesis
dysarthria clumsy hand

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24
Q

how many neurons die per minute during a stroke

A

2 million per minute until reperfusion is achieved

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25
Q

what is the ischemic core

A

brain tissue destined to die

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26
Q

what is penumbra

A

salvageable brain area (the shadow)

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27
Q

what is early thrombolytic/thrombectomy aimed at

A

rescuing tissue in the penumbra

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28
Q

what is key to establish during a stroke alert

A

Last Known Well Time (which is NOT the same as first seen abnormal)

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29
Q

what strokes are typically not eligible for thrombolytics or thrombectomy

A

“wake-up” strokes

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30
Q

what makes patients contraindicated for TPA treatment

A

hemorrhagic strokes

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31
Q

what is the initial stroke used to determine

A

hemorrhage vs not- hemorrhage to determine treatment (tPA or not)

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32
Q

what does the MRI assess for

A

necrotic brain tissue

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33
Q

what is the hyperacute phase of ischemic stroke treatment

A

tPA if within < 4.5 hours of symptom onset

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34
Q

what does tPA do

A

breaks down thrombus

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35
Q

what is the benefits of tPA

A

therapeutic benefit of tPA is greatest when given very early and declines throughout the first 4.5 hours after onset

reduced mortality
reduced symptomatic intracranial bleeding
higher rates of independent ambulation at discharge
higher rates of discharge to home

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36
Q

how many patients see improvement with tPA

A

1 out of every 3 patients

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37
Q

what is the risk of tPA

A

hemorrhage

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38
Q

what are the current inclusion criteria for tPA

A

diagnosis of ischemic stroke causing measurable neurologic deficit
onset of symptoms < 3 hours before beginning treatment
Aged greater than or equal to 18 years

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39
Q

what are the exclusion criteria for tPA treatment

A

history of head trauma/prior stroke in pervious 3 months
aterial puncture at noncompressible
intracranial tumor/mass
elevated BP
active internal bleeding
blood glucose

40
Q

what test is required prior to tPA treatment

A

CT and blood glucose stick

41
Q

what are relative exclusion criteria for tPA treatment

A

minor/rapidly improving stroke symptoms
pregnancy
seizure at onset
major surgery/trauma within past 14 days
over the age of 80
severe strokes

42
Q

what does LVO stand for

A

Large vessel occlusion

43
Q

What has the greatest benefit of treatment for LVO

A

tPA and thrombectomy

44
Q

what are key questions during stroke work up

A

where is the lesion?
What is the mechanism (etiology)?

45
Q

what are the key parts of stroke initial evaluation

A

History and physical exam
quick, focused stroke scale
CT (rule out bleed/structural abnormality)
Labs
MRI
vessel imaging
echocardiogram
EKG
special labs
rhythm monitoring

46
Q

what is the mainstay long-term treatment of stroke

A

antiplatelets (aspirin, clopidogrel, etc), high intensity statin

47
Q

When is DAPT used

A

short term after severe intracranial stenosis or after high-risk TIA or minor stroke

not helpful long term or if initiation is delayed >2wks

48
Q

what is DAPT

A

dual-antiplatelet therapy

49
Q

what is the efficacy of aspirin

A

best when given early, may reduce Severity of early recurrent stroke
~17% risk reduction over 3 years

50
Q

what is the efficacy of Anticoagulation in Afib

A

warfarin ~66% effective in reducing stroke, possibly superior

51
Q

what is the efficacy in high intensity statins

A

~20% risk reduction

52
Q

what is the most important factor in treating a stroke

A

Risk factor management
over 80% risk reduction

53
Q

what are common post stroke complications

A

stroke deficits (vision, speech, sensorimotor, balance/gait)
seizures, aspiration pneumonia, pressure ulcers, urinary retention/incontinence
pain syndromes, cognitive impairment/dementia, falls/fractures, emotional/psychological impact, relationship/family stress
anxiety/dression

54
Q

what are the 10 warning signs of stroke

A
  1. confusion
  2. difficulty understanding
  3. dizziness
  4. loss of balance
  5. numbness
  6. severe headache
  7. trouble speaking
  8. trouble walking
  9. vision changes
  10. weakness
55
Q

what does BEFAST stand for

A

Balance
Eyes
Face
Arm
Speech
Time

56
Q

how many strokes are recurrent

A

1 in 4 strokes are recurrent

57
Q

how do you modify risk factors

A

control BP
control cholesterol
control your blood sugar
discontinue smoking
reduce/stop drinking alcohol
exercise at least 30 minutes daily
eat a heart-healthy diet

58
Q

What is a TIA

A

transient ischemic attack - episode of temporary and focal neurological dysfunction of vascular origin, which are variable in duration, commonly lasting from 2-15 minutes.

They leave no persistent neurological deficits

59
Q

how do you differentiate between TIA and stroke

A

TIA has no evidence of infarct on brain imaging

60
Q

what is the minimum treatment for TIA

A

anti-platelet agent plus statin
plus control of blood pressure, blood sugar and other risk factors

61
Q

what is the ABCD2 score used for

A

risk stratification for TIA
Age
Blood pressure
Clinical features
Duration of symptoms
Diabetes

62
Q

what is a hemmorrhagic stroke

A

caused by intraparenchymal hemorrhage: rapidly developing clinical signs of neurological dysfunction attributable to a focal collection of blood within the brain parenchyma or ventricular system that is NOT CASUED BY TRAUMA

63
Q

what is the definition of silent cerebral hemorrhage

A

a focal collection of chronic blood products within the brain parenchyma, subarachnoid space, or ventricular system on neuroimaging or neuopathological examination that is not caused by trauma and without a history of acute neurological dysfunction attributable to the lesion

64
Q

how is ICH categorized

A

medical emergency

65
Q

what is the management of ICH

A

treat the cause

rapid head CT (or MRI) to distinguish ischemic stroke from ICH, aneurysmal SAH
give platelets if thrombocytopenic
if on coumadin with elevated INR, reverse with vitamin K/K-centra
acute BP lowering

ICU monitoring

66
Q

what is an asymptomatic aneurysm

A

unruptured - usually asymptomatic, unless they are large and causing symptoms from mass effect and compression on adjacent structures

67
Q

what is the prognosis of a ruptured aneursym

A

fatality up to 60%

68
Q

what is the pathophysiology of aneurysms

A

congenital/FH
atherosclerosis
HTN
genetic abnormalities
vasculopathies/inflammation
arteriovenous malformations
CT disorders
infections
sickle cell disease
trauma
neoplasms
cigarette smoking
illicit drug use
alcohol

69
Q

what are the primary cerebral aneurysms

A

Saccular, fusiform, mycotic and giant aneurysm

70
Q

what is a saccular aneurysm

A

also known as berry aneurysm - bulges from one side of an artery, A neck leads to it.

71
Q

what is a fusiform aneurysm

A

bulges from all sides of an artery - it rarely has a neck

72
Q

what is a giant aneursym

A

can involve more than one artery. it is over 2.5 cm wide

73
Q

what is a mycotic aneursym

A

caused by infected artery wall. this type is fairly rare.

74
Q

what is the main cause of mycotic aneurysms

A

endocarditis

75
Q

what are the most common locations of aneurysms

A

ACA, PCOM, branches of the MCA and top of the Basilar artery

76
Q

what are the common signs and symptoms of aneurysms

A

incidental finding/asymptomatic
minor aneurysmal hemorrhage with mild symptoms (fever, N/V, sweating, chills)
catastrophic - aneurysmal subarachnoid hemorrhage (SAH) - “worst headache of my life”, AMS, seizure, focal deficit due to mass effect or secondary ischemia

77
Q

SAH is caused by what

A

rupture of the aneurysm
- filled with blood causing sudden, intense headaches - sometimes described as “worst headache of one’s life”

78
Q

what is required if CT does not r/o SAH and there is a strong suspicion

A

do a lumbar puncture - xanthochromia (blood in the CSF) develops after 6 hours

79
Q

What does the modified Fisher Scale have benefit for

A

determining vasospasm risk

80
Q

what are complications of aneurysmal SAH

A

recurrent bleeding
hyponatremia
paroxysmal sympathetic hyperactivity
seizure
hydrocephalus
vasospasm

81
Q

what is the clinically applicable aneurysmal SAH scale

A

Hunt and Hess Scale - for prognosis

82
Q

what are the surgical treatments for aneurysms

A

clipping and coiling

coiling is used more frequently than clipping or ligation

83
Q

what are medication treatments for aneurysmal SAH

A

Nimodipine (calcium channel blocker to reduce vasospasm)
+/- antihypertensive
osmotic agents if welling present
antiepileptics
pain/fever control
stool softeners

84
Q

Where is a subdural hemmorrhage

A

collection of blood in the subdural spaece - usually the result of head trauma

85
Q

what is the presentation of subdural hemorrhage

A

shear damage to the bridging cortical veins as they cross the dura mild or indolent symptoms

86
Q

how do you distingush a subarachnoid hemorrhage

A

cortical shaped
arterial blood

87
Q

how do you distinguish a subdural hemorrhage

A

crescent shaped, venous blood - located in the potential space between the dura and arachnoid matter

88
Q

what is the presentation of extradual hemorrhage

A

blood collection between the skull and the dura - associated with head trauma/skull fracture

89
Q

how do you distinguish a extradural hemorrhage

A

lens shaped (higher pressure)
arterial blood does not cross sutures

90
Q

what is GCA

A

giant cell arteritis
inflammatory vasculitis

91
Q

what is the serious complication of GCA

A

irreversible vision loss

92
Q

what is GCA linked to

A

polymyalgia rheumatica

93
Q

what is the SSX of GCA

A

sudden or insidious onset
+/- prodrome anorexia, weight loss, fever, night sweats
headache
PMR pattern (shoulders, neck, hips/thighs)
fatigue/malaise
jaw claudication
fever
vision changes
eye motion abnormalities

94
Q

what are differential diagnosis for GCA

A

acute angle closure glaucoma
herpes zoster
iritis/uveitis
tia/stroke
migraine

95
Q

how is GCA diagnosed/worked up

A

labs (CBC, ESR, CRP, LFTs)
standard of care: emergent temporal artery biopsy
non-invasive imaging (ultrasound, MRI/MRA)

96
Q

what is the treatment of GCA

A

high dose steroids (at least prednisone 60mg)
best within 24 hours
duration of steroids can be up to 2 years

can also use low-dose aspirin, proton pump inhibitor, bisphosphonates, calcium and vitamin D for bone protection)

Clin Med - NEURO (13 decks)

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