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PA20023 > Stroke and excitotoxicity > Flashcards

Stroke and excitotoxicity Flashcards

1
Q

What is a stroke?

A

A transient or permanent interruption in cerebral blood supply.

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2
Q

What is ischaemia?

A

A restriction of blood supply to tissues, resulting in a lack of oxygen and/or glucose.

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3
Q

What are risk factors for having a stroke?

A

Hypertension, obesity, smoking and alcohol.

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4
Q

What is the difference between an ischaemic stroke and a haemorrhagic stroke?

A

An ischaemic stroke is a blockage of vessels in the brain, whereas a haemorrhagic stroke is a rupturing of vessels in the brain.

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5
Q

What is the incidence and mortality of ischaemic strokes?

A

80% incidence and 40% mortality.

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6
Q

What is the incidence and mortality of haemorrhagic strokes?

A

20% incidence and 50% mortality.

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7
Q

What is the difference between a thrombotic ischaemic stroke and an embolic ischaemic stroke?

A

Thrombotic strokes are caused by a clot (thombus) to the brain, whereas an embolic stroke is caused by a clot elsewhere in the body that travels to the brain.

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8
Q

What is a transient ischaemic attack?

A

It is a thombotic clot that is caused by a temporary disruption in the blood supply to the brain. They are called “mini strokes” and some people may not even realise they have had one.

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9
Q

What is the duration of a transient ischaemic attack?

A

Around 24 hours - there is no permanent damage.

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10
Q

How many of people who have transient ischaemic attacks will go onto have a full stroke?

A

40% - 5% progress within 2 days and 10-15% within 3 months.

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11
Q

What are some symptoms of a stroke?

A

Difficulty talking or understanding words, severe headache, loss of feeling or strange feelings on one side, sudden blurred vision, weakness of the face/arm/leg on one side, unexplained dizziness.

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12
Q

What do PET scans measure?

A

Neuronal metaboliosm - how active neurons are.

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13
Q

What is seen in PET scans of people who have had strokes?

A

A lot of dead neurons - large non-functional areas.

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14
Q

What happens within minutes of having a stroke?

A

Neurons in the area will be dying - structural damage but also functional damage around the direct area.

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15
Q

What happens as time progresses after a stroke has occurred?

A

The area of structural damage increases. The area of reduced function is starting to recover. Eventually, all affected neurons have structural damage and none have reduced function anymore.

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16
Q

What is the primary cause of cell death in stroke?

A

Excitotoxicity.

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17
Q

What is excitotoxicity?

A

It is an excessive release of glutamate - the neurons are excited to death due to a Ca2+ overload.

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18
Q

What is excitotoxicity also thought to be involved in?

A

Alzheimer’s, Parkinson’s, Huntingdon’s and amyotrophic lateral sclerosis.

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19
Q

What can cause excitotoxicity?

A

Dietary intake of amino acid agonists.

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20
Q

What happens in the first stage of excitotoxicity?

A

Ischaemia - oxygen and glucose supply are cut off. This makes the sodium/potassium pump to lose function. This means the sodium and potassium gradient will run down to zero. This results in lots of glutamate release due to calcium being let into the cell.

21
Q

What are some of the receptors present on the synaptic terminal on the post-synaptic neuron?

A

Na-Ca exchanger, AMPAr, NMDAr, VGCC calcium, VGSC sodium.

22
Q

What happens if there is lots of glutamate present at the post-synaptic terminal to the AMPAr during excitotoxicity?

A

The AMPA receptors open and let sodium into the cell which depolarizes the membrane.

23
Q

What happens to the VGSC if there is lots of glutamate present at the postsynaptic terminal in excitotoxicity?

A

The sodium channel will open due to the depolarisation occurring due to the AMPAr receptor opening. This depolarizes the cell even further.

24
Q

What happens to the NMDA receptors when there is lots of glutamate present at the posynaptic neuron in excitotoxicity?

A

Due to the large depolarisation, the magnesium that blocks the channel is displaced and they become active. Lots of calcium is allowed into the cell.

25
Q

What happens to the VGCC when there is lots of glutamate present at the postsynaptic cell in excitotoxicity?

A

Due to the depolarisation due to the AMPA receptor, the VGCC open and lots of calcium is let into the cell.

26
Q

What happens to the sodium that is inside the cell during excitotoxicity (postsynaptic)?

A

The Na-Ca exchanger removes sodium from the cell, but this lets more calcium into the cell.

27
Q

What is the overall effect of excess glutamate on the postsynaptic cell in excitotoxicity?

A

There is overall a very large increase in calcium.

28
Q

What is the effect on increased calcium in excitotoxicity?

A

Lots of enzymes become active such as proteases and lipases as they are calcium dependent.

29
Q

What is also another effect of increased calcium in excitotoxicity?

A

There is free radical production such as peroxide and nitrile ion - these are damaging and will damage the membrane structure.

30
Q

What is the overall effect of excitotoxicity?

A

The cell membrane is damaged - calcium can leak in and further excel the problem.

31
Q

What happens to neurons in the core after a stroke has occurred?

A

They never repolarise and there is death by necrosis.

32
Q

What is the penumbra?

A

The surrounding area of the core of the stroke.

33
Q

What happens to neurons in the penumbra after a stroke?

A

They repolarise and recover.

34
Q

What happens when the penumbra repolarise?

A

This uses energy (ATP) and the cells are rundown, resulting in depolarisation - cycles occur.

35
Q

How long to cycles of depolarisation and repolarisation last in a stroke?

A

6-8 hours.

36
Q

What happens after the cycle in the stroke?

A

There is more excitotoxic death.

37
Q

What are other factors involved in strokes?

A

The increased sodium levels increase the water levels due to osmosis, resulting in swelling of cells.

38
Q

What is the result of swelling of cells in a stroke?

A

The resulting blood supply is reduced to the oedema in the penumbra. There is increased ischaemia.

39
Q

What happens to repolarised neurones in a stroke?

A

They become hyperactive when the blood/O2 is restored.

40
Q

Are there many treatments for strokes?

A

No - currently only one. This is called tissue plasminogen activator (tPA).

41
Q

How does stroke treatment work?

A

It restores the blood flow and dispurses the thrombus. It only works for ischaemic strokes and has to be given within 3 hours.

42
Q

What are some neuroprotective agents?

A

AMPA/NMDA receptor blockers, glutamate release blockers, Na+/Ca2+ blockers, free radical scavengers, NO synthase blockers, protease inhibitors and acid-sensitive sodium channel inhibitors.

43
Q

What are the problems with neuroprotective agents?

A

They have positive effects in animals but not in clinical use.

44
Q

How can stroke risk be reduced?

A

ACE inhibitors to reduce blood pressure and statins to reduce cholesterol levels.

45
Q

What could you eat to reduce the risk of stroke?

A

Tumeric - contains an antioxidant (curcumin) that is a free radical scavenger.

46
Q

What are some other examples of excitotoxicity?

A

Blue mussel poisoning - neurological symptoms and seizures of blue mussels. This is due to high concentrations of domoic acid in the plasma and brain, there was damage to the hippocampus, amygdala and entorhinal cortex.

47
Q

What is neurolathyrism?

A

Poisoning by the grass pea as it is an AMPAr agonist that targets the spinal cord. It causes muscle rigidity, paralysis of lower limbs and damage to the thoracic and lumber motor neurons.

48
Q

What is guam disease?

A

Due to seeds of the sago palm that are AMPA and NMDAr agonists. It causes symptoms of amyotrophic scelrosis, Alzheimer’s and PArkinson’s. It causes muscle weakness, paralysis and dementia.

PA20023 (17 decks)

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