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brain and behaviour > neuropharmacology > Flashcards

neuropharmacology Flashcards

1
Q

what are primary issues that determine the success of treatment? give examples

A

• Primary issues – related directly to the disease and its pathology

o Understanding of the pathophysiology of the disease
o Choice of the correct treatment target

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2
Q

what are secondary issues that determine the success of treatment? give examples

A

• Secondary issues – related directly to the therapeutic regime
o Ensure that drugs reach the target
o Minimise the adverse effects
o Manage any potential drug-resistance

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3
Q

why is it difficult for a disease to be clearly associated with a specific CNS region?

A

neurological diseases have a much higher level of complexity and involved interconnected circuits.

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4
Q

what is the target of therapeutics?

A

well-defined entity

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5
Q

what questions are important to ask when looking at CNS diseases?

A
  • Is it possible to identify the CNS structure?
  • What is the best target for a disease?
  • Can we make drugs to affect the target?
  • Will the drugs reach the target?
  • Do patients always respond to treatment?
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6
Q

what are the symptoms of parkinson’s?

A

• Tremor, slow movement, rigidity, slurred speech, affected gait

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7
Q

is parkinson’s reversible?

A

no

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8
Q

what causes parkinson’s?

A

• Loss of a specific group of cells (known as substantia nigra –> midbrain, role in reward and movement) in the brain which produce dopamine

deficit in dopamine at the level of receptor

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9
Q

what is the substantia nigra?

A

group of cells in the midbrain which have a role in reward and movement

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10
Q

what is parkinsonism?

A

any condition that causes a combination of the movement abnormalities seen in Parkinson’s disease (an umbrella term for any symptoms related to Parkinson’s).

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11
Q

how is dopamine synthesised?

A

tyrosine –> L-Dopa –> Dopamine

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12
Q

what catalyses the formation of L-Dopa –> Dopamine?

A

L-aromatic amino acid

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13
Q

what type of chemical is dopamine?

A

monoamine neurotransmitter

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14
Q

why does supplementing dopamine not work as a treatment for parkinsons?

A

dopamine doesnt reach the brain after peripheral administration

Systemic oral administration of L-Dopa leads to conversion into dopamine outside the brain

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15
Q

what does conversion of L-Dopa outside the brain lead to?

A

can trigger intense vomiting, triggered by peripheral formation of dopamine

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16
Q

how is parkinsons treated and how does this work?

A

L-Dopa combined with an inhibitor of the enzyme L-aromatic amino acid decarboxylase (which doesn’t have access to the brain)  L-Dopa is converted into dopamine only in the brain, protected in the periphery.

Another solution is to stimulate dopamine receptors directly with dopamine receptor agonists

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17
Q

what is an agonist?

A

a compound that stimulates receptors directly

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18
Q

what is schizophrenia?

A

a significant cognitive disruption

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19
Q

what are symptoms of schizophrenia?

A

hallucinations, delusions, paranoid behaviour, disruption of social contact, withdrawal from friends and family

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20
Q

what causes schizophrenia?

A

result of hyperactivity in the ventral striatum which leads to an increased release of dopamine and increased stimulation of receptors

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21
Q

what is the ventral striatum?

A

major portion of the basal ganglia: functions as reward system

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22
Q

what are the treatment options for schizophrenia?

A

• Dopamine receptor antagonists (known as antipsychotic or neuroleptic drugs) - these drugs block dopamine receptors

23
Q

what is another name for dopamine receptor antagonists?

A

antipsychotics or neuroleptics

24
Q

why can antipsychotics cause adverse effects?

A

they block other receptors due to lack of specificity

25
Q

what adverse effects can antipsychotics have?

A 
o	Extrapyramidal effects (parkinsonism)
o	Rise in prolactin (breast enlargement, amenorrhoea  absence of menstruation)
o	Weight gain 
o	Allergic and toxic reactions
o	Anticholinergic effects
o	Postural hypotension.
26
Q

what do individuals with depression experience?

A

• low mood, lack of energy, disrupted sleep, loss of interest, tiredness, dysfunction in the activity of monoamine systems (dopamine, noradrenaline, serotonin release) in the brain.

27
Q

what is the mechanism of depression?

A

insufficient level of serotonin and noradrenaline (at the level of receptors)

28
Q

what are the treatment options for depression?

A

antidepressants

29
Q

how do antidepressants work?

A

increase monoaminergic transmission/neurotransmitters. The following medications (reuptake inhibits) stop neurotransmitters being taken up back by the presynaptic element, so enhances the number of neurotransmitters left in the synaptic cleft and taken up by the post synaptic element

30
Q

what is a type of antidepressant?

A

tricyclic antidepressant

31
Q

how do tricyclic antidepressants work?

A

o Inhibit reuptake of monoamines such as serotonin/noradrenaline

32
Q

why can tricyclic antidepressants have adverse effects?

A

also have affinity for H2 receptors, muscarinic cholinergic receptors etc…

33
Q

what adverse effects can tricyclic antidepressants have?

A

dry mouth, constipation, blurred vision, fatigue, weight gain, dizziness

34
Q

how can you balance efficacy and the adverse consequences?

A

reduce the dose or switch to a different drug

35
Q

when can resistance to treatment be seen?

A

apparent immediately after the onset of the treatment or it can develop after a period of treatment

36
Q

what can cause resistance to treatment?

A

genetic variations in drug transporters

37
Q

what does addiction involve?

A

abuse of a substance (cocaine, ecstasy, heroin, ketamine, alcohol, nicotine).

38
Q

what is the effect of ectasy?

A

increases release of monoamines from presynaptic cleft

39
Q

what is the effect of cocaine?

A

inhibits uptake of monoamines back into presynaptic cleft

40
Q

what is the effect of heroin?

A

Opioid receptor agonist on post synaptic receptors

41
Q

what is the effect of ketamine?

A

glutamate receptor antagonist on post synaptic receptors

42
Q

what is the effect of nicotine?

A

nicotinic cholinergic receptor agonist

43
Q

what are treatments for addiction?

A

drug substitute
vaccine
decrease toxicity associated with condition
aversion therapy

44
Q

how is heroin addiction treated?

A

provide a drug substitute (methadone for heroin substitute)

45
Q

how is cocaine addiction treated?

A

provide a vaccine

antibodies against cocaine

46
Q

how is nicotine addiction treated?

A

nicotine replacement patches

47
Q

how is alcohol addiction treated?

A

aversion therapy (induce sickness upon alcohol consumption e.g. block metabolism of alcohol with disulfiram

48
Q

what are the main treatment challenges in cns diseases?

A
  • Define the most relevant treatment target
  • Increase the specificity of action of drugs, so that adverse effects are avoided
  • Improve the prediction of response to treatment
  • Develop drugs which can reach the CNS
49
Q

what does reaching targets in the brain involve?

A

involves successful passage of drugs across the BBB

50
Q

why may drug targets in the CNS never be reached?

A

bc of intrinsic or acquired overexpression of multidrug transporters (such as ABC family) at the BBB restricts brain uptake of drugs

51
Q

what are antiepileptic drugs?

A

substrates of ABC transporters which work on the central nervous system.

52
Q

what is P-glycoprotein?

A

a drug transporter implicated in drug resistance and drug efflux back from the endothelium into the blood

53
Q

what are examples of inhibitors of ABC transporters?

A

verapamil, cyclosporine A

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