Cerebral Vascular Diseases Flashcards

1
Q

In stroke symptoms are usually on both sides of the body. True/false?

A

False. In stroke, symptoms are usually on one side of the body eg arm weakness, face drop is dichotomized due to crossing in the brain

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2
Q

Motor symptoms in stroke are experienced due to a crossing in which tract?

A

Pyramidal tract

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3
Q

Name 6 symptoms of stroke

A

Hemiparesis(motor deficit)
Dysarthia- abnormality in speech articulation
Dysphagia- difficulty in swallowing
Aphasia- inability to understand a word. Sing but not talk
Sensory deficit
Ataxia
Visual disturbance- problem in right occipital cortex-left hemianopia, CRAO-stroke of the eye
Headache
Impaired consciousness

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4
Q
Match  the artery to the symptom
Anterior cerebral artery
Middle cerebral artery
Posterior cerebral artery
Posterior circulation
A

Anterior cerebral artery- hemiparesis (lower extremity), apraxia
Middle cerebral artery - hemiparesis (upper extremity)
Posterior cerebral artery-visual, thalamic, memory
Posterior circulation-brain stem syndromes eg oculomotor

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5
Q

What is a transient ischemic attack ie TIA?

A

Brief, majority less than 15 minutes, max 24 hr episodes of focal loss of brain function due to ischemia

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6
Q

What are the symptoms of a TIA?

A

No persistent deficit
abrupt onset of hemideficit(paresis, numbness), slurred speech, difficulty to understand, loss of consciousness
50% demonstrate DWI abnormalities
CT/MRI may reveal abnormalities
Every third stroke heralded by a TIA
Annual risk of stroke during first 5 years at 5%

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7
Q

In the case of a TIA would you administer TPA?

A

no, because tissue plasminogen activator is administered to reopen a blocked vessel

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8
Q

What are examples of cererbral vascular diseases?

A

Ischemic stroke 85%- atherothrombotic, cardioembolic, microangiopathic
Subarrachnoid hemorrhage 10%
Primary intracerebral hemorrhage 5%

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9
Q

Which treatments of acute ischemic stroke have proven efficacy?

A
1. Thrombolysis 
Stroke Unit
Thrombolysis with rtPA (recombinant tissue plasminogen activator) i.v within 4.5 hours of symptom onset and exclusion of hemorrhage
Endovascular treatment within 6 hours
2. Thrombectomy
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10
Q

Thrombolysis is the only clinically proven treatment for ischemic stroke. True or false

A

True

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11
Q

Define thrombectomy

A

When a stent is inserted into a blood vessel to remove a clot. Clot is caught in stent and removed

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12
Q

What is a stroke unit?

A

A specialized facility for thrombolysis, checking body temperature, blood pressure, glucose, oxygenation levels to monitor and treat complications

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13
Q

more men than women can expect to suffer from stroke. True/false

A

True. 25% men Vs 20% of women by age 85

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14
Q

Ischemic stroke is a syndrome and not a single disease state. True/false

A

True

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15
Q

List some common unavoidable risk factors of stroke

A

age, gender, race, other genetic factors

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16
Q

List some common modifiable risk factors of stroke

A

Hypertension, smoking, diabetes

17
Q

What are some secondary prevention methods of stroke?

A
300 mg asprin, clopidrogrel/ dipyridamol + ASS
cardiac embolism: anticoagulation
treat hypertension
quit smoking
statins with CHD/hypercholesterinemia
Carotid-TEA if stenosis is more than 70%
18
Q

Define a Penumbra

A

Pene (near), umbra (shadow). Regioin of silence in electrical activity but with preserved metabolism (electrophysiological/morphological)

19
Q

Name two features of a penumbra

A

decreased blood flow, increased oxygen extraction (misery perfusion PET)
tissue at risk
reduced prerfusion, normal diffusion MRT

20
Q

What is the main principle of diffusion weighted imaging?

A

Diffusion of protons between Intracellular volume (low ADC) and extracellular volume (high ADC). ADC is the apparent diffusion coefficient and decreases by about 30-50% in the case of ischemia due to cells swelling hence lower proton conc in extracellular

21
Q

How does ischemia lead to cell death

A

As a result of ischemia, cells are deprived of substrate , which causes an energy deficit due to decreased ATP in the cells, therefore leading to cell death

22
Q

What is the difference between a functional and structural lesion?

A

For an ischemic penumbra to occur, at the core, there is a structural lesion in which cells will die. A functional lesion is the penumbra where neurons are no dead but cells are arrested

23
Q

What does MR measure?

A

MR measures the spinning of proton molecules

24
Q

What happens to neurons that are low in energy?

A

Neurons low in energy will depolarize, release glu into ECM, receptors in ECM sense glu that is massively released, calcium entry, sodium entry, radicals, water enters cells, cells swell, potassium released leading to spread in depol, ECM shrinks….apoptosis

25
Q

Name two depolarizing agents in the case of low energy neurons durign excitotoxicity.

A

Potassium and glutamate. Potassium is released causing spread in depolarization. Glu and K diffuse into the penumbra and into neighbouring cells.

26
Q

In the pathobiology of stroke, name events that take place within minutes

A

Damage: Energy failiure,
Protection: Endogenous neuroprotection

27
Q

In the pathobiology of stroke, name events that take place after hours into days/ weeks

A

Damage: secondary damage eg inflammation and apoptosis
Protection: Repair regeneration

28
Q

During excitotoxicity, what substrate is blocked?

A

Glucose entry, oedema

29
Q

How does spreading depolarization occur

A

A series of depolarizations preceed spreading. When neurons are low in energy, release glu ie depolarize easily. Enry of sodium and water, cells swell.Depolarizing agents such as K and glu are released after cells swell causing peri-infract depolarizations/ spread in depolarization as the ions diffuse into the penumbra and into neighbouring cells

30
Q

What molecules are involved in excitotoxicity and which ones would be used for anti-excitotoxicity that takes place within minutes

A

Excitotoxicity: glutamate, calcium, OFR

Anti-excitotoxicity:GABA, adenosine, Katp activation

31
Q

Which molecules are involved in inflammation/apoptosis and anti-inflammation/apoptosis (hours)?

A

Inflammation/apoptosis: IL-1,COX-2, MMPs, caspases

Anti: IL-10, EPO (erythropoietin)

32
Q

What occurs during repair and regeneration during protection?

A

scar formation, vasculogenesis, neurogenesis, BM-derived cells, sprouting

33
Q

How does stroke injury induce immunosupression?

A

After CNS injury, there is release of immune modulators from blood vessels, nerves, adrenal glands. eg NE, glucocorticoids, acetylcholine. Leads to apoptosis of neutrophils, killing of t helper cell type 1, and upregulate t helper cell type 2.
Overall effect: immunodepression

34
Q

How does stroke induce changes in the metabolic system?

A

Paresis/stress/CNS local damage leads to impaired signalling/neuroendocrine activation/local inflammation that leads to increased catabolic signals and decreased anabolic signals