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SL22044 Neuroscience > Stroke and excitotoxicity > Flashcards

Stroke and excitotoxicity Flashcards

1
Q

What does stroke cause?

A

Neuronal cell death

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2
Q

What is the root cause of a stroke?

A

Transient or permanent interruption in cerebral blood supply

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3
Q

What is ischaemia?

A

A lack of blood supply to a part of the body

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4
Q

Two main causes of stroke?

A

Ischaemic and haemorrhagic

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5
Q

What causes an ischaemic stroke?

A

Blocked blood vessels

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6
Q

What causes a hemorrhagic stroke?

A

Ruptured blood vessels

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7
Q

What are the two types of ischaemic stroke?

A

Thrombotic or embolic

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8
Q

What is a thrombotic blockage?

A

A blockage caused by the blood clotting

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9
Q

What is an embolic blockage?

A

Things like air or fat blocking the blood vessels

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10
Q

Which type of stroke is more fatal?

A

Haemorrhagic

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11
Q

What are the two types of haemorrhagic stroke?

A

Intracerebral or subarachnoid

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12
Q

Intracerebral hemorrhagic stroke?

A

Ruptured blood vessel is inside the brain/provides blood to the centre of the brain

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13
Q

Subarachnoid hemorrhagic stroke?

A

Ruptured blood vessels are around the outside of the brain

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14
Q

Symptoms of stroke?

A

Face falling on one side, difficulty raising arms, slurred speech

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15
Q

Time issue with stroke?

A

Must be treated within 3 hrs

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16
Q

What is necrosis?

A

cell/tissue death

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17
Q

Two regions of damage post-stroke?

A

Core and penumbra

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18
Q

What is the core of a stroke?

A

Where the ischaemia first happened

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19
Q

What is the penumbra in a stroke?

A

The region around the core

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20
Q

What happens to the core and penumbra regions of a stroke if treatment isnt applied?

A

The core will grow into the penumbra, damaging more regions of the brain

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21
Q

What is the primary cause of cell death in stroke?

A

Excitotoxicity

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22
Q

What causes excitotixicity?

A

Excessive release of glutamate

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23
Q

What happens as a result of excessive glutamate release?

A

A Ca2+ overload

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24
Q

What allows neurons to have a resting membrane potential of -70mV

A

The sodium potassium pump

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25
Q

Concentration difference of Na+ in neuronal cells?

A

Higher outside than inside

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26
Q

Conc grad of K+ in neuronal cells?

A

Higher inside than outside

27
Q

What is required for the Na K pump to work?

A

ATP

28
Q

Why does ischaemia cause neuronal cell death?

A

A lack of oxygen/glucose to the neurons

29
Q

Why does a lack of oxygen/glucose to neurons cause excitotoxicity?

A

Cant generate ATP to fund NaK pump

30
Q

What happens if the NaK pump stops working?

A

The resting potential goes from -70 to +40, all affected neurons will depolarise

31
Q

What happens if the presunaptic neuron depolarises?

A

Ca2+ flows in and causes the release of glutamate

32
Q

What happens if the postsynaptic neuron depolarises?

A

Positive ions flow in

33
Q

Consequences of an excessive release of glutamate?

A

Activate AMPA and KAINATE receptors (both lead to Na+ going into the postsynaptic neuron (more depolarisation))

34
Q

What happens to NMDA receptors at higher than -40mV?

A

The magnesium block is removed meaning Na+ can flow through

35
Q

What does the sodium calcium exchanger do?

A

Protects the neurons from having too much sodium in them by swapping intracellular Na+ for extracellular Ca2+

36
Q

Why does having excessive Ca2+ in a neuron cause issues?

A

It is a signalling molecule that can cause free radicals to form which damage the membrane and cytoskeleton

37
Q

Which enzymes does Ca2+ activate?

A

Proteases, lipases, caspaces

38
Q

What happens as a result of caspase activation?

A

Cell death

39
Q

What happens if Ca2+ activates too much of its enzymes?

A

The lipid bilayer is digested (lipases), as well as anything made of proteins (proteases)

40
Q

What happens to the neurons in the core of a stroke?

A

They never repoalrise

41
Q

What happens to the neurons in the penumbra of a stroke?

A

They can repolarise

42
Q

What is difficult about repolarising a penumbra neuron?

A

The ATPase NaK pump has to work very hard to restore the concentrations of the ions to the correct level for a -70mV membrane potential, and this uses a lot of energy

43
Q

Which treatment is only for thrombotic ischaemic strokes?

A

Tissue plasminogen activator (tPA)

44
Q

What does tPA do?

A

Breaks down blood clots

45
Q

Treatment for hemorrhagic stroke?

A

Surgery to fix the ruptured blood vessel

46
Q

What are targets for neuroprotective agents for stroke treatment?

A

AMPA/NMDA receptor blockers, Na+/Ca2+ blockers, enzyme inhibitors

47
Q

How could neuronal cells be recovered after a stroke?

A

Stem cells

48
Q

What are some things that prevent people from having a stroke again?

A

Antihypertensives

49
Q

Why are antihypertensives used to prevent stroke?

A

Reduce high blood pressure

50
Q

What lifestyle choices can increase risk of stroke?

A

Obesity, lack of exercise, smoking, alcohol

51
Q

For which type of stroke are blood thinners prescribed?

A

Ischaemic

52
Q

What is a transient ischaemic attack?

A

Short lived neurological signs similar to those from a stroke

53
Q

What do the long term stroke symptoms depend on?

A

The brain region affected

54
Q

Symptoms if motor cortex is affected?

A

Skeletal muscle movement affected

55
Q

Symptoms if wernicke’s area of brain is affected?

A

Difficulty understanding language/listening

56
Q

Symptoms if Brocas area of brain is affected?

A

speech and writing

57
Q

Symptoms if right motor cortex is comprimised?

A

Left half of body is affected

58
Q

What can cause exitoxicity?

A

Domoic acid

59
Q

Why can domoic acid cause excitotoxicity?

A

It is a glutamate receptor agonist

60
Q

Where is domoic acid found?

A

Amnesic shellfish

61
Q

What produces domoic acid?

A

Algae

62
Q

Which glutamate agonists can cause excitotoxicity?

A

Domoic acid, oxalydiaminopropionic acid, beta-Methylamino-L-alanine

63
Q

Which foods can cause excitotoxicity?

A

Shellfish, grass pea, cycad seeds

SL22044 Neuroscience (9 decks)

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