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Y3 Patient Sem 2 > Drugs in CNS > Flashcards

Drugs in CNS Flashcards

1
Q

where to most drugs that have an affect on CNS take action?

A

Neurones

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2
Q

what can deficits in neurotransmitters cause?

A

linked to disease states such as Parkinsons

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3
Q

what are dendrites?

A

these are the part that recieve the information, they have a lot of receptors.

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4
Q

is a neurotransmitter activates a receptor what might happen?

A

they might change the membrane potential and this will then get converted into an electrical signal which is how signals travel down a neuron

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5
Q

what is an axon/

A

an axon is what an action potential needs to travel down

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6
Q

which type of axons tend to be longer/

A

motor neurones tend to be much longer

brain are usually short

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7
Q

what is an axon terminal?

A

where the message is passed between neurones. this is where the synaptic activity takes place as electrical signals cannot pass through without the help of a neurotransmitter

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8
Q

what is on the outer brain (grey matter)?

A

this is where there is a collection of cell bodies, these can group together and form a nuclei

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9
Q

what is the white matter of the brain?

A

this is where teh axons are and it is covered in myelin sheath

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10
Q

what is an action potential?

A
  • occurs when a neuron sends information down an axon

- neurons can alter their resting membrane potential

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11
Q

what is the resting membrnae?

A

around -70mV

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12
Q

what happens during depolarisation?

A

this is caused due to actiation of chanels, so they open and this allows sodium to pass in and makes the neurone more positive

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13
Q

what happens when an electrical signal arrives at a pre synaptic membrane?

A

causes an opening of voltage gated calcium channels. Calcium will come into the cell and this is essential for neurotransmitter release as it causes binding of the pre synaptic vesicles to the membrane then exocytosis occurs and neurotransmitters diffuses across the synaptic cleft where it activates receptors on the post synaptic terminal

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14
Q

what is GABA?

A

the main inhibitory neurotransmitter within the body

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15
Q

where is acetylcholine stored?

A

synaptic vesicles in the axon terminal

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16
Q

when is acetylcholine released?

A

released into the cleft upon the arrival of an action potential which causes and influx of calcium ions

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17
Q

what does acetylcholine bind to/

A

binds to postsynaptic receptors
M1-5 muscarinic receptors
each has a differnt subtype so you can get more specific binding

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18
Q

what are the 5 subtypes of nicotinic receptors?

A 
	Alpha (1-10) 
	Beta (β2- β5)
	Delta
	Epsilon & 
	Gamma
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19
Q

what are the two division of nicotinic receptors?

A

muscle and neuronal

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20
Q

where do you find muscle ?

A

neuromuscular junctions

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21
Q

what is the structure of a muscle receptor?

A

aaBeG

ligand gated ion channel

22
Q

where do you find neuronal receptors?

A

autonomica ganglia CNS

23
Q

what is the structure of a neuornal receptor?

A

various aB receptors

ligand gated ion channel - receptor binds and causes the opening of the channel

24
Q

what is an autoreceptor?

A
  • Synthesis inhibiting
  • Release inhibiting
  • Different types
  • Receptor where the transmitters can stop excessive release
25
Q

how much choline is taking up at the presynaptic terminal?

A

40-50%

26
Q

how is choline taken upat presynpatic terminal?

A

active, high affinity transporters specific to cholinergic cells

27
Q

what is a neuronal pathways/

A

cell body with an axon projecting through it, and it controls the function within a circuit.

28
Q

what are the two major components on neurotransmitter within theCNS?

A

gABA and glutamate

29
Q

what is the release of acetylcholine iniated by?

A

arrival of anaction potential along the axon of the motor neurone.
depolarisation leads to opening of the calcium ion channels
depolarisation of post synaptic neurone means that sodium ions can move into the muscle cells
therefore, an action potential is generated

30
Q

what is myasthenia gravis?

A

autoimmune condition that affects the nerves and muscles causes them to waste away.

31
Q

what causes myasthenia gravis?

A

immune system prodcues antibodies that block or damage the muscle acetylcholine receptors which prevents the muscle contracting.
This prevents the messagesbeing passes from nerve endings so they become weak.

32
Q

what is the rate limiting step of dopamine synthesis?

A

tyrosine hydroxylase

33
Q

where is dopamine stored?

A

synaptic vesicles. in the axonal terminal

34
Q

where is dopamine released?

A

released in the synpatic cleft upon arrival of an action potential anf influx of calcium ions from voltage gated channels

35
Q

where is dopamine metabolised?

A
  • Catechol-O-methyltransferase (COMT)
  • Monoamine oxidase (MAO)
  • Breakdown dopamine so it is no longer in the synapse
36
Q

where is dopamine reuptaken?

A
  • Catecholamines have highly specific active transport mechanisms to remove transmitter from synapse into presynaptic terminal
  • Takes dopamine out of the synaptic cleft through the presynaptic membrane
  • Dopamine Transporter - DAT
37
Q

what are the fourmajor dopamine pathways?

A
  1. Nigrostrital pathway
  2. Mesolimbic pathway
  3. Mesocortical pathway
  4. Turberoinfundibular pathway
38
Q

what is the nigrostrital pathway?

A

usually needed for the motor and involuntary control

  • associated with Parkinson’s disease
  • associative striatum - learning, memory, sleep, attetnion and mood
39
Q

what happens in Parkinson’s diease?

A

you have aloss of dopamine in the motor stratum

40
Q

how could you combat Parkinson’s disease?

A

L–dopa would be useful in this pathway to increase the rate of producing dopamine. It will increase dopamine in all the pathways – you don’t want to increase in all circuits. you just want to increase synthesis in the motor neurones. If you increase it in the associated stratum you will lead to side effects of psychosis – schizophrenia. As you can see the other pathways and their function you can see what sort of side effects you may encounter.
• You need to balance the increase of dopamine that will be beneficial but not cause side effects.
• Another way to prevent the decrease in dopamine you can activate the receptors that dopamine usually activate. Dopamine agonist. You could make these very specific for certain dopamine receptors, so you reduce the side effects.

41
Q

what is schizophrenia?

A

increasein dopamine activating receptors

42
Q

how could you possibly treat schizophrenia?

A
  • If you add in an antagonist it will block the receptors and trick the brain you have the right amount od dopamine. D2 receptor antagonists.
  • Side effects of this could be that you get an overproduction of prolactin (hyperprolactinaemia). Side effects dependent on the drug you use (specificity, level of blockage).
  • It may also cause brain not thinking there is enough dopamine so you ger Parkinson like side effects
43
Q

what is an agonist?

A

 Substances which stimulate the receptors and mimic the natural ligand (e.g. neurotransmitter, hormone)
 Half life for that drug you might need to take it twice a day

44
Q

what is an antagonist?

A

Substances that block the receptor and prevents/stop the effect of the natural ligands. Chemical compound which competes for the receptor so you need a certain dose that you know you will get blockage – but may lead to blocking receptors in other areas – patient to patient variability and this will lead to side effects

45
Q

what is a partial agonist?

A

A partial agonist is an agonist which is unable to induce maximal activation of a receptor population, regardless of the amount of drug applied. Not quite as strong just partially stimulates

46
Q

what could you possibly give in partial agonist?

A

• In schizophrenia you have too much dopamine, you could give a partial agonist as it will compete with dopamine to get to the receptor but will only partially bind and therefore dampening down the signal. In the motor circuit you would only get partial so less Parkinson like side effects.

47
Q

what is an ionotropic receptor?

A

fast acting, fast movement of ions
 Receptor is part of ligand-gated ion channel protein and activation results in ion conductance changes
 These receptors are opened by the transmitter to allow the passage of Na+ (excitatory) or K+/Cl– ions (inhibitory) and are involved in fast transmission (msecs)
 Examples include some receptors for Acetylcholine, Glutamate & GABA

48
Q

what is a metabotropic receptor?

A

slightly slower acting, causes a small change insecond messenger system

 Receptor protein in membrane is coupled to effector mechanism via G-proteins
 In this signalling mechanism, agonist molecule combines with receptor proteins in the membrane
 The resulting conformational change causes activation of a membrane-associated enzymes via G-protein
 The cellular effect is usually much slower than that associated with ionotropic receptors. E.g. Dopamine receptors

49
Q

what are kinase-linked receptors?

A

slower responses

endogenous agonists include hormones and growth facotrs

50
Q

what is an intracellular receptor?

A

very slow response

reponses are long lasting and remain long acting binding

Y3 Patient Sem 2 (26 decks)

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