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B and Neuro > Stroke > Flashcards

Stroke Flashcards

1
Q

Acute neurodegenerative disorder

A

Stroke

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2
Q

Chronic Neurodegenerative disorder

A

Alzheimer’s, Parkinson’s

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3
Q

Cerebral stroke

A
  • Blockage/interruption of cerebral artery
    ► Death of cells
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4
Q

Prevalence in the UK

A
  • 250-400 strokes per 100 000 people
    • 3rd cause of death
    • 1st cause of disability (in adults)
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5
Q

Types of stroke

A

Ischemic
Haemorrhagic

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6
Q

Ischemic stroke

A

Occurs when blockage within blood vessel stops/reduces flow
Blood clot formed within the vessel

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7
Q

Haemorrhagic stroke

A

Area of bleeding as blood vessel bursts
High blood pressure
cerebral arteries under pressure
May experience aneurism

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8
Q

Risk of stroke

A

At all stages of lifespan
1 in 4 strokes occur in working age adults

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9
Q

Risk factors

A

Age
Medical conditions (High blood pressure, diabetes, atrial fibrilation, high cholesterol)
Lifestyle (smoking, drinking, diet)
Family history and ethnicity
Specific for women (pregnancy, contraceptive pill)

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10
Q

Consequences of stroke : clinical symptoms

A

Sudden or gradual onset
One-sided limb weakness/paralysis
Confusion, loss of speech/vision
Headache
Loss of consciousness

= results in dysfunctional cognitive and motor behaviour determined by size and location of cell loss

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11
Q

cognitive impairment of stroke

A

Amnesia
Inattention
Confusion
Depression
Mood and behaviour changes

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12
Q

Depression due to stroke

A

Common after a stroke
Not simply a consequence of physical effects
Patients with post-stroke depression (PSD) differ from those with primary depression in that they have more cognitive impairment, irritability, more psychomotor slowing and more mood liability

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13
Q

pathology of stroke

A
  • Transient episode of neurological dysfunction without acute tissue death
  • Disruption of CBF
  • Mini-strokes
  • Risk factor for subsequent stroke
    • 10% strokes within 90 days of TIA
  • Silent strokes
    • No visible symptoms
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14
Q

Cerebral stroke - pathology

A

Massive cell death
Ischemic lesion
Cascade of further complex events
Inflammation

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15
Q

Massive cell death

A

Primary cause of cell death is excessive amounts of glutamate

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16
Q

Cascade of further complex events

A

inflammation, cell death, reperfusion

trying to reestablish blood flow

17
Q

Inflammation

A
  • Sodium ions – water, swell, inflammation
    • Microglia – become phagocytic
    • Phagocytosis = ‘cell-eating’
    • Blood-brain barrier breakdown – influx of blood-borne immune cells (neutrophils, macrophages)
    • Oedema formation, adhesion molecules, cytokines
18
Q

2 mechanisms of cell death

A

Necrosis and Apoptosis

19
Q

Necrosis

A

Lower in oxygen
Depleted ATP
Cellular swelling and membrane break down

20
Q

Apoptosis

A

= triggering of death programme
intracellular signalling
cells fragment into vesicles
phagocytosis by neighbouring cells

21
Q

Cerebral stroke- reperfusion injury

A
  • Hyperperfusion
    • A major increase in cerebral blood flow (CBF), well above metabolic demands of CNS tissue
  • Complication of surgical intervention
    • E.g. intracranial stenting
  • Intracranial haemorrhage/edema
    • Mortality 36-63%
    • 80% patients significant morbidity
  • Damage to the blood-brain barrier
22
Q

Excitotoxicity

A
  • 1957 Lucas & Newhouse reported that s.c. glutamate caused retinal damage
  • 1969 Olney reported that glutamate produced brain damage in neonatal mice
  • Ultrastructural studies
    • amino acid treatment = postsynaptic (but not presynaptic) alterations
    • Excitotoxic hypothesis
    • Excess amino acids results in prolonged depolarization of receptive neurones which in some way* leads to their eventual damage or death
23
Q

GABA system

A
  • GABA system – functions in opposite to glutamate
  • During ischemia
    • GABA accumulates in extracellular space
24
Q

Cerebral stroke treatments

A
  • Pharmacological
    • Thrombolysis - breaks down clots
    • Aspirin
    • Modifiable risk factors
    • Physiotherapy
25
Q

Drugs and receptors

A
  • Drugs have effects and sites of action
  • In the CNS, they alter synaptic function

Increase or decrease action of neurotransmitter

26
Q

Pharmacological treatments

A

Neuroprotection
- aims to protect neurons from injury
- limited by therapeutic time window and effectiveness

NMDA receptor antagonists
- proved to be most successful in protecting against cell death

ALL clinical trials failed

27
Q

Thrombolysis

A

Tissue Plasminogen Activator (t-PA)
- 3 hours
- CT scan

Surgical intervention

Intra arterial thrombolysis

TO BREAK UP BLOOD CLOTS

28
Q

Aspirin

A
  • Antiplatelet agents (and anticoagulant)
  • Prevention of recurring strokes
  • Reduction of severity of stroke
  • Inhibit production of thromboxane (decrease natural levels of blood clotting)
29
Q

An ischemic stroke occurs as direct consequence of

A

A blockage in a blood vessel

30
Q

Within the penumbral area of a ischemic stroke…

A

Blood flow is sub-optimal and tissue is salvagable

31
Q

What is a common cellular process which results in apoptosis during ischemic stroke

A

Caspase activation

B and Neuro (17 decks)

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