Stroke Flashcards

1
Q

what is neurodegeneration?

A

Progressive damage or death of neurons leading to a gradual deterioration of the bodily functions controlled by the affected part of the nervous system.

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2
Q

what are some causes of brain damage?

A
  • genetics
  • trauma
  • tumour
  • alterations in blood flow
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3
Q

what is a cerebral stroke?

A
  • Blockage/interruption of cerebral artery
  • Death of cells
  • symptoms: depend on location
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4
Q

what is the prevalence of stroke?

A

in the Uk
- 250-400 strokes per 100 000 people
- 3rd cause of death
- 1st cause of disability (in adults)

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5
Q

what are Ischemic stroke?

A

80% of strokes
- brain deprived of blood
- due to blood clots (thrombus) blocks flow of blood in brain or fatty plaque or blood clot (embolism) breaks away and flows to brain where it blocks the artery

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6
Q

what is haemorrhagic stroke?

A
  • 20 % of strokes
  • bleeding in brain
  • breaks blood vessel (aneurysm) in brain
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7
Q

what are the risk factors of a stroke?

A
  • all stages of life (over 400 childhood strokes per year in UK, 1 in 4 strokes in working adult age)
    Medical conditions
  • High blood pressure, diabetes, atrial fibrillation, high cholesterol
    Lifestyle
  • Smoking, drinking, diet, exercise
    Family history and ethnicity
  • Likely related to incidence of other risk factors e.g. high cholesterol, diabetes
    Specific for women
  • Pregnancy, contraceptive pill
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7
Q

clinical symptoms of a stroke

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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8
Q

cognitive impairments from a stroke

A
  • Amnesia
  • Inattention
  • Confusion
  • Depression
  • Mood and behaviour changes
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9
Q

depression after a stroke

A
  • Common after stroke
  • Not simply a consequence of physical effects
  • Patients with post-stroke depression (PSD) often differ from those with primary depression in that they have more cognitive impairment (memory and concentration problems), irritability, more psychomotor slowing, and more mood liability.
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10
Q

Transient Ischemic Attack (TIA)

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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11
Q

Ischemic stroke – core and penumbra

A
  • The core area is where blood flow is below critical, leading to cell death
  • Penumbra is the reversibly injured brain tissue around the ischemic core
  • over time after a stroke has occurred then the area of irreversibility injured brain tissue increases
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12
Q

what is cerebral stoke - patholgy

A

massive cell death
- primary cause of cell death is excessive amounts of glutamate
ischemic lesion = excitotoxic lesion
- causes a cascade of further complex events
- inflammation, cell death, reperfusion

inflamation
- 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

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13
Q

cell death in a cerebral stoke

A

neurocrosis → low oxygen → depleted ATP → cellular swelling and membrane break down

apoptosis → triggers programme death → intraceelular signalling (capases) → cells fragment into vesicles → phagocytosis by neighbouring cells

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14
Q

Cerebral stroke – reperfusion injury

A

Hyperfusion
- a major increase in cerebralblood flow (CBF), well above metabolic demands of CNS tissue

Intracranial haemorrhage/edema
- Mortality 36-63%
80% patients significant morbidity

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15
Q

How does Excitotoxicity lead to cell death?

A
  • decrease in blood flow → mitochondria mysfunction → disruption of Ion homeostatis → NMDAR → cell death
    OR
    decrease in blood flow → mitochondria mysfunction → less ATP → cell death
16
Q

what happens in the core and Penumbra during a cerebral stroke?

A

Core
- Rapid necrotic cell death
- Mainly due to excessive NMDA receptor stimulation
- further glutamate release
Penumbra
- Slower (days) apoptotic cell death
- More moderate NMDA receptor hyperactivity

16
Q

Amino acid neurotransmitters

A
  • Excitatory = glutamate and aspartate
  • Inhibitory = GABA and glycine
  • Glutamate and GABA – closely related
17
Q

glutamate receptors

A

Iontropic
- NMDA
- AMPA
- Kainate

Metbotropic
- Many subtypes

18
Q

what do excess amino acids do?

A

Excess amino acids results in prolonged depolarization of receptive neurones which leads to their eventual damage or death

19
Q

what are some cerebral stroke treatments?

A
  • Pharmacological
  • Thrombolysis
  • Aspirin
  • Modifiable risk factors
  • Physiotherapy
20
Q

How do drugs treat strokes?

A

they alter synaptic function by increasing/decreasing neurotransmitters

21
Q

drugs and receptors

A

Drugs affect neurotransmitter functioning
- Agonist = increases NT function
- Antagonist = decreases NT function

Sites of actions of drugs
- Direct = attaches to NT binding site (post-synaptic)
- Indirect = drug binds to alternative binding site (pre-synaptic)
- Non-competitive binding = does not compete with NT

Drugs
- Direct agonist/antagonist
- Indirect agonist/antagonist

22
Q

what is Neuroprotection?

A
  • Aims to protect neurones from injury
  • Limited by: Therapeutic time window, Effectiveness/outcome
23
Q

what has it been proven to be the best pharmacological method to treat a stroke, but failing clinical trials?

A
  • NMDA receptor antagonists
  • Proved to be the most successful compounds ever generated to protect against cell death in vitro and in vivo (models)
  • Various compounds developed
  • BUT is failing clinical trials due to: Lack of efficacy, Toxic side effects
24
Q

what is Thrombolysis?

A

trying to break down the blood clot

25
Q

drug treatment for thrombolysis

A

Tissue Plasminogen Activator (t-PA)
- Thrombolytic
- only drug licensed in US for stroke
- most affective if administed within 3 hours
- CT scan used to determine which type as doesn’t work on haemorrhagic stroke

26
Q

surgical treatment for Thrombolysis

A

Carotid endarterectomy
- To remove build-up of fatty deposits within arteries
- Intra-arterial thrombolysis

27
Q

how can asprin be used in strokes?

A
  • Antiplatelet agents (and anticoagulant)
  • Prevention of recurring strokes
  • Reduction of severity of stroke
  • Inhibit production of thromboxane
  • makes platelets less sticky
28
Q

what are cerebral stroke risk factors?

A
  • High blood pressure*
  • Smoking
  • Physical inactivity
  • Obesity
29
Q

How can physiotherapy be used to help stroke symptoms?

A
  • Weakness/paralysis
  • Improve motility/avoid injury
  • Everyday activities
  • Independent living
  • Exercise, manipulation, massage, skills training, electrical treatment
30
Q
A