202 - Stroke Flashcards

0
Q

What are the two types of stoke and how common is each?

A

Ischaemic (85%) - embolic (lodging of a blood clot fat or gas in blood stream) and ‘in situ thrombotic (forming of a blood clot in place)

Haemorrhagic (15%) - burst blood vessel

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1
Q

Define a stroke

A

A neurological deficit related to a non traumatic vascular event

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2
Q

Define a Transient Ischaemic Attack

A

A neurovascular event with symptoms lasting less than 24 hours

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3
Q

what are the cardinal features of strokes?

A
  • Focal - particular location
  • Negative clinical phenomena - no added signs like twitching
  • Relate to arterial anatomy (i.e. not veins)
  • Sudden onset
  • Px has identifiable vascular risk factors - poor diet, smoking, no exercise
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4
Q

What are the risk factors for embolic strokes?

A
  • Atheromatous disease - smoking, family Hx, diabetes, hypertension
  • Cardiac causes - AF, endocarditis, shunts, cardiomyopathy
  • Low cardiac output states
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5
Q

What are the risk factors for ‘In Situ’ thrombotic strokes?

A
  • Atheromatous Disease
  • Hyperviscosity -excess RBCs
  • Vasculitis
  • Thrombophilic states - F5 leiden (blood clotting disorder), pregnancy, oral contraceptive pill
  • Incr. alcohol intake
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6
Q

What are the risk factors for Haemorrhagic strokes?

A
  • Hypertension
  • on anti coagulation drugs
  • on thrombolysis drugs
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7
Q

What are the risk factors for venous strokes?

A
  • Dehydration
  • Infection
  • Heart Failure
  • Thrombophilic states - CA, pregnancy, OCP
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8
Q

Describe a Primary Intracranial haemorrhage (PICH)

A
  • Hyper acute and sometimes LOC & headache due to incr. in Intracranial pressure (cushing’s reflex)
  • A ruptured vessel in R hemisphere would cause L hemiparesis
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9
Q

Describe a Sub Arachnoid Haemorrhage (SAH)

A
  • Hyper acute & meningism (neck stiffness) & LOC
  • Extra-cerebral anuerysm
  • Thunderclap headache
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10
Q

Describe Cerebral Venous Sinus Thrombosis (CVST)

A
  • DVT of the brain
  • Sub acute / evolving - back pressure in the veins
  • Secondary bleeding, incr. in ICP
  • Don’t respect arterial territories
  • Affects young people, women on OCP
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11
Q

Describe Brainstem and spinal strokes

A
  • Ataxia, diplopia (double vision), dysarthria, lower CNS hemiparesis
  • Ipsilateral on face and contralateral on arms and legs
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12
Q

What does optic disc selling indicate?

A

Incr. BP caused over a long time - therefore not a stroke

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13
Q

Describe the autoregulation of cerebral blood flow.

A

CBF is maintained at the same rate over a range of blood pressures (50-170 mmHg) by variation in arteriolar control

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14
Q

How does chronic hypertension affect affect autoregulation of CBF?

A

The range is reset to a higher level. If BP too low arteriolar system no longer compensates and Px blacks out (CBF inadequate for metabollic demands, impaired cellular metabolism & decr. neuronal activity). If BP too high leads to cerebral oedema, hypertensive encephalopathy and hyperaemia.

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15
Q

What can cause the failure of autoregulation?

A
  • Incr. age
  • Head Trauma
  • SAH or Ischaemic stroke
  • Cerebral Hypoxia
  • High pCO2
16
Q

At what percentage fall from the normal range of CBF will tissue be at a risk of ischaemic damage?

A

50%

17
Q

Describe what glial cells are and how they metabolise

A

They are non-neuronal support cells that maintain homeostasis, form myelin and supply lactate to adjacent neurons. They metabolise aerobically and anaerobically.

18
Q

Describe what neurons metabolise and how they metabolise

A

They can metabolise glucose but mostly metabolise lactate from the glia. They are obligate aerobes and are very sensitive to ischaemia, suffering irreversible damage after 5-7 mins of hypoxia.

19
Q

What is the difference between ischaemia and hypoxia?

A

Ischaemia is a restriction in blood supply that leads to dysfunction +/- damage.
Hypoxia is oxygen deprivation due to low 02 in inspired air, airway obstruction, lung disease, reduced O2 carrying capacity of blood, ischaemia & inhibition of aerobic respiration

20
Q

What are the effects of ischaemia/hypoxia dependent on?

A

The degree and duration of ischaemia/hypoxia, temp (low temp prevents damage) and blood glucose (incr. glucose causes incr. damage due to build up of lactic acid that cannot be metabolised.

21
Q

What is global ischaemia?

A

Interruption of circulation and general reduction in cerebral profusion due to:

  • Cardiac arrest
  • Severe hypotension
  • Shock
22
Q

What does global ischaemic lead to?

A
  • Selective neuronal necrosis
  • Cortical Laminar Necrosis
  • Watershed infarcts - at areas between different arterial supplies due to poor blood supply from distal end arteries
23
Q

What does global ischaemia cause clinically?

A
  • Transient confusion
  • Focal deficits
  • Non perfused brain and brain death (ICP>arterial BP)
24
Q

How is the risk of a stroke affected if a Px has a TIA?

A

7-10% risk

25
Q

Where do intracerebral haemorrhages most commonly found?

A

Thalamus/basal ganglia

26
Q

What most commonly causes sub arachnoid haemorrhages?

A

Rupture of saccular Aneurysms.

Aneurysm most commonly occur in anterior circle of willis

27
Q

What is a Lacunar Infarction?

A

Ischaemic stroke cause by occlusion of lenticulostriate arteries (arise off MCS). Associated with chronic hypertension and affect the basal ganglia, thalamus, internal capsule and pons leading to formation of a small lacuna (holes)

28
Q

what causes a stroke secondary to cerebral vasculitis and how is it treated?

A

inflammation of blood vessel walls in brain often due to rheumatoid arthritis, SLE or drug abuse. Treated by immunosupression (glucocorticoids)

29
Q

What is Binswager’s disease?

A

Multi-infarct dementia caused by a combiation of artherosclerosis, embolism, chronic HTN

30
Q

What imaging technique works best for venous strokes?

A

CT venography

31
Q

How are venous strokes treated?

A

Anticoagulation even if small haemorrhages present as you must remove the thrombus to remove the back pressure first. Thrombolysis if anticoagulation not working.