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Introduction to Metabolism and Pharmacology > Drugs acting on the central nervous system > Flashcards

Drugs acting on the central nervous system Flashcards

1
Q

Local anaesthetic (such as lidocaine) act by ?

A

Blocking conduction along never fibres

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2
Q

What does blocked voltage-gated Na+ ion channels prevent ?

A

Action potentials

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3
Q

Generally, small fibres (e.g. Aδ and C fibres) are?

A

Blocked more easily than larger ones

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4
Q

So, pain conduction is blocked before ?

A

Other sensory pathways - e.g. touch (Aβ fibres) or motor (Aα fibres)

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5
Q

What is anxiety ?

A

Normal response to threatening situations such as:

  • Defensive behaviours
  • Arousal and alertness
  • Negative emotions
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6
Q

Anxiety disorders occur when ?

A

These reactions are produced without a specific stimulus

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7
Q

What are Anxiolytics ?

A

Drugs used to treat anxiety (worry and fear)

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8
Q

What are Hypnotics ?

A

Drugs used to treat insomnia (being unable to sleep)

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9
Q

Many drugs have ?

A

Both effects

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10
Q

Many anxiolytic drugs were first developed to treat other conditions such as ?

A
  • Depression
  • Epilepsy
  • Schizophrenia
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11
Q

What drugs are used to treat anxiety ?

A
  1. Benzodiazepines - most commonly used
    - For short-term (2-4 weeks) relief of anxiety and insomnia that is severe, disabling or causing the patient extreme distress
  2. Antidepressants
    - SSRIs, SNRIs, tricyclic antidepressants (TCAs), MAO inhibitors
  3. Buspirone
  4. Anti-epileptic drugs
  5. Antipsychotic drugs (used to treat schizophrenia)
  6. β-adrenoreceptor antagonists (e.g. propanolol)
    - Treat the symptoms associated with anxiety, e.g. tremor, sweating, palpitation, etc.
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12
Q

What is the mechanism of action of benzodiazepines?

A
  1. Binds to GABAa receptor anf increase their affinity for GABA
  2. Effects:
    - Reduction of anxiety
    - Sleep
    - Anticonvulsant
    - Amnesia
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13
Q

Where does Benzodiazepines bind at ?

A

An allosteric site at interface between α and γ subunits

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14
Q

What is Flumazenil ?

A

It is a competitive antagonist of BDZ

- Used to treat overdose

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15
Q

What is β- carboline ?

A

This is an inverse agonist

  • Causes increased anxiety
  • Stabilises inactive form of GABA receptor and decreases affinity for GABA
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16
Q

What happens when Benzodiazepines is used as hypnotics ?

A

Short acting benzodiazepines (midazolam, lorazepam) - less ‘hangover’ effects (do not feel sleepy/drowsy the next morning)

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17
Q

Why should it not be used for long periods ?

A

(2 to 4 weeks only for severe anxiety and insomnia) due to tolerance and dependence

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18
Q

What are some other hypnotics ?

A
  1. Zaleplon, zolpidem, zopiclone
    - Known as the ‘z’- drugs
    - Bind to GABAa receptor similar to benzodiazepines (but not benzodiazepines structurally)
    - Specific for α1 subunit - no anxiolytic activity
  2. Chlormethiazole
    - Binds to GABAa receptor at a different site to benzodiazepines
  3. Melatonin receptor agonists, e.g. melatonin
    - Involved in setting diurnal (day/night) rhythm
  4. Antihistamines (1st generation), e.g. promethazine
    - Develop for hay fever, but can cause drowsiness
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19
Q

According to the monoamine theory of depression, drugs that ?

A

Drugs that increase serotonin or noradrenaline transmission enhanced mood

20
Q

Explain the serotonin (5HT) signalling in neurones ?

A
  • 5-HT synthesised with nerve terminal and released into the synaptic cleft upon depolarisation
  • 5-HT is recovered into presynaptic nerve terminal by 5-HT reuptake transporter for degradation
  • Selective Serotonin Reuptake Inhibitors (SSRIs) thus increases synaptic levels of serotonin
  • MAO also degrades 5-HT
  • Presynaptic 5-HT1D receptor acts as an autoreceptor to provide negative feedback on 5-HT release
21
Q

Where is Noradrenaline synthesised ?

A

In the nerve termini and released into synaptic cleft upon depolarisation

22
Q

What is on the presynaptic nerve termini and what does it do ?

A

There is NA reuptake transporter on the presynaptic nerve termini transporting NA back to the presynaptic neurons for degradation by enzymes such as monoamine oxidase (MAO)

23
Q

What does presynaptic α2-adrenoceptors act as and what does it provide?

A

Presynaptic α2-adrenoceptors act as autoreceptors to provide negative feedback on NA release

24
Q

What is the basis of action of the antihypertensives clonidine and methyldpopa?

A

α2-agonists that cause sympathetic inhibition - lowers blood pressure

25
Q

What are drugs acting indirectly on noradrenergic pathways ?

A

Sympathomimetics

26
Q

What are sympathomimetic amines structurally similar to ?

A

Noradrenaline

27
Q

What does Amphetamine produce ?

A

Strong stimulation (also release 5-HT and dopamine in brain)

28
Q

What is Ephedrine used as?

A

Decongestant (in colds)

29
Q

What do Monoamine oxidase inhibitors ?

A

Inhibit monoamine oxidases and therefore increase levels of neurotransmitters (e.g. NA, 5-HT) in neurons

30
Q

What are the two forms of MAOs ? and what do they break down ?

A

Type A and Type B

  • Type A preferably breaks down NA and 5-HT
  • Both Type A and B breaks down Dopamine and Tyramine
31
Q

Give example of MAO irreversible inhibitors ?

A
  • Isocarboxazid, phenelzine, tranylcypromine
  • Bind to the enzyme covalently
  • Non-selective for type A and B MAO
32
Q

Give example of MAO reversible, selective inhibitors ?

A
  • Moclobemide
  • Selective for MAO- A (NA and 5-HT specific)
  • (MAO-B inhibitors, e.g. Selegilline are used as an adjunct in the treatment of Parkinson’s disease)
33
Q

What are the side effects of MAOIs ?

A
  1. Hypotension
  2. Increased appetite and weight gain
  3. Insomnia
  4. ‘Cheese reaction’
    - Cheese and other fermented food rich in tyramine
    - Normally metabolised by MAOs in gut and liver
    - With MAOIs, tyramine enters the bloodstream
    - Displaces NA in nerve terminals causing sympathomimetic effect
    - Causes acute hypertension
34
Q

Why are Selective Serotonin Reuptake Inhibitors (SSRIs) currently the most commonly prescribed (first-line drig treatment) ?

A
  • Fewer side-effects than MAOIs or TCAs
  • Safer in overdose (some risk of cardiac arrhythmia)

However, relatively more expensive

35
Q

What does Fluoxetine and paroxetine inhibit ?

A

CYP2D6 - should not be used with TCAs

36
Q

What are some other examples of SSRIs ?

A

Citalopram, escitalopram, sertraline, fluvoxamine

37
Q

What is Parkinson’s disease ?

A
  1. Progressive neurodegenerative disease characterised by:
    4 main symptoms:
    - Tremor
    - Muscle rigidity
    - Bradykinesia (reduction in voluntary movement)
    - Postural instability
38
Q

What do some other symptoms include ?

A
  • Sleep, sensory and autonomic disturbances

- Cognitive impairment

39
Q

What are the possible causes of Parkinson’s disease ?

A
  1. Genetic and environmental factors
    - Mutation in a gene coding for a synaptic protein called α-Synuclein has been implicated
    - Toxin MPTP and chronic systemic exposure to pesticides can cause Parkinson-like symptoms
  2. Drug-induced (known as ‘Parkinsonism’
    - Affects 10-15% of patients using dopamine receptor antagonists (e.g. antipsychotics)
    - Drugs implicated in induing Parkinson-like symptoms include:
    - Antiemetics
    - Antipsychotics
    - SSRIs, lithium, cinnarizine, valproate
40
Q

What is the Pathogenesis of PD ?

A
  • Loss of dopaminergic neurons in basal ganglia, especially substantia nigra and nigrostriatal pathway
  • PD becomes clinically significant when ~80% of the dopaminergic neurons in substantia nigra is lost (there is a ~5% year latency period)
41
Q

What is the pharmacological treatment of PD ?

A
  1. Disease progression can be rapid particularly in early onset (young patients) PD
  2. All agents used only to treat symptoms, do not reverse or stop the progression of the disease
    - Dopamine Precursor; Levodopa
    - Dopamine receptor antagonists
    - Monoamine oxidase B (MAO-B) inhibitors
    - Catechol-O-methyltransferase (COMT) inhibitors
    - Anticholinergics (antimuscarinics)
42
Q

Explain Levodopa (L-dopa)?

A
  • Most effective treatment
  • Dopamine (DA) cannot cross BBB, so ineffective given orally or IV
  • Levodopa (L-dopa) is the precursor of DA, absorbed well from GI tract and actively transported across the BBB (the brain’s natural source of DA)
  • However, 99% of L-dopa is metabolised peripherally to DA by dopa decarboxylase, contributing to side effects (e.g. nausea & vomiting, postural hypotension)
43
Q

Explain DOPA decarboxylase inhibitors ?

A
  1. L-dopa given with inhibitors of dopa dearboxylase, cabidopa or benserazide
    - Prevent L-dopa decarboxylation in periphery
    - Cannot cross BBB, so L-dopa can be converted to DA only within the brain
    - Reduces levodopa dose needed by 10 fold, and reduces side-effects
44
Q

L-dopa + carbidopa =

A

Co-careldopa (Sinemet)

45
Q

L-dopa + benserazide =

A

Co-beneldopa (Madopar)

46
Q

Explain the relationship between CBD and Parkinson’s ?

A

A significant increase in well-being & quality of life was observed in Parkinson’s patients with the use of CBD

Introduction to Metabolism and Pharmacology (16 decks)

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