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Pharmacology - Year 2 AC > Week 10 - Antidepressants > Flashcards

Week 10 - Antidepressants Flashcards

1
Q

Where are neurotransmitters stored?

A

In vesicles within the terminal of the pre-synaptic neurone

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2
Q

Where is monoamine oxidase found and what does it do?

A

-found on the membrane of mitochondria

  • breaks down monoamines
  • involved in removing the neurotransmitters norepinephrine, serotonin and dopamine from the brain (MAOIs prevent this from happening making these chemicals more available)
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3
Q

Where is most serotonin in the body found?

A

-mast cells and platelets in the blood

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4
Q

What are the serotonin neurones and pathways which lie in or near the midline of the brain stem?

A

Raphé nuclei

-nine main clusters of cells

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5
Q

What is the chemical name for serotonin?

A

5-hydoxytryptamine (5-HT)

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6
Q

Name the monoamine transmitters mad why they are called that

A
  • serotonin
  • noradrenaline
  • dopamine

(Derived from amino acids)

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7
Q

What enzyme can inactivate serotonin (5-HT)?

A

Monoamine oxidase

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8
Q

How are serotonin, dopamine and noradrenaline taken out of the synaptic cleft?

A

-specific reuptake transporters

  • takes neurotransmitter out of the synaptic cleft and back in to the presynaptic terminal to end its ‘transmission’
  • can be repackaged in vesicles and used again

-some drugs act by inhibiting reuptake transporters which means the transmitter stays in the synaptic cleft and have a prolonged action

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9
Q

Name the categories of SERT inhibitors

A
  • tricyclic antidepressants (also affect NA reuptake)
  • selective serotonin-reuptake inhibitors
  • SERT inhibitors/5-HT releasers
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10
Q

Name some tricyclic antidepressants

A
  • desipramine

- imipramine

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11
Q

Name some selective serotonin-reuptake inhibitors

A

-sertraline
-citalopram
Fluoxetine (Prozac)

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12
Q

Name some SERT inhibitors/5-HT releasers

A
  • fenfluramine

- MDMA (methylenedioxymethamphetamine)

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13
Q

How do the classic tricyclic antidepressants work?

A
  • inhibit both serotonin and noradrenaline reuptake in to mere terminals
  • later antidepressants - more selective inhibitors of serotonin reuptake
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14
Q

What do the action of SERT inhibitor drugs have an effect on?

A

-maintain higher levels of monoamines in the synaptic cleft

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15
Q

What is the mechanism of SERT inhibitors/5-HT releasers?

A
  • maintain higher levels of monoamines in the synaptic cleft
  • transporters can sometimes function in the opposite direction to release transmitters from the terminal
  • fenfluramine and MDMA act on the serotonin transporter and not only inhibit the transport of serotonin in to the cell but also facilitate its outward transport
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16
Q

What does serotonin bind to?

A
  • 14 known serotonin receptors, fall in to 7 families
  • 7 trans-membrane spanning G-protein-coupled receptors
  • have an external amino terminal which contains the ligand binding site, and an internal carboxy terminal linked to GTP-binding proteins
  • when receptor is activated by serotonin, the G-proteins bind GTP which causes dissociation of the a-subunit (then can activate messenger systems)
17
Q

What is the 5-HT3 receptor?

A

A ligand-gated ion channel

  • includes the NMDA glutamate receptors and GABAa receptors
  • ionotropic NOT metabotropic
  • 5-HT3 receptor forms a channel which is non-selective for positively charged ions (e.g. Na+, K+ and Ca2+)
18
Q

What are dopamine and noradrenaline?

A

Catecholamines

19
Q

What is Parkinson’s disease caused by!

A

Loss of dopamine and noradrenaline from neurones in the substantia nigra of the midbrain

20
Q

What does the substantia nigra do?

A

Projects to parts of the brain, the basal ganglia and dorsal striatum, involved in voluntary movement

-another group of dopaminergic neurones in the ventral tegmental area that give rise to the mesocorticolimbic system - these are the dopaminergic neurones involved in mood

21
Q

Explain the synthesis of catecholamines

A

Tyrosine –> L-DOPA –> Dopamine –> Noradrenaline

22
Q

What enzymes break down dopamine?

A
  • monoamine oxidase (MAO)

- catechol-O-methyl transferase (COMT)

23
Q

What are adrenergic receptors?

A

-bind to both adrenaline and noradrenaline

  • a-receptors have a higher affinity for noradrenaline
  • a1-adrenergic receptors are linked to phospolipase C and a2-adrenergic receptors block adenylate cyclase
  • B-receptors are linked positively to adenylate cyclase
24
Q

What do people with depression often have high levels of?

A

Cortisol

25
Q

What are monoamine oxidase inhibitors (MAOIs)?

A
  • non-selective blockers of the metabolism of all monoamines
  • still used commonly for severe depression in patients who have failed to respond to other treatments - but last line for pharmacological intervention
  • phenelzine (Nardil) - treats depression and bi-polar
  • tranylcypromine (parnate) - severe depression
26
Q

What are the side effects of monoamine oxidase inhibitors?

A
  • hypertensive crisis -especially due to interactions with other drugs
  • foods high in tyramine (cheese effect)
  • inhibition of cytochrome P450 (degrades other drugs)
  • tryptophan supplements or other psychoactive drugs should be avoided or there is risk of ‘serotonin syndrome’
  • weight gain
  • oedema
  • sexual dysfunction
  • sedation
27
Q

What are the contraindications of MAOIs?

A
  • impaired renal or hepatic function
  • hypertension
  • pregnant or lactating women
28
Q

How do tricyclic antidepressants work?

A

-non-selectively blocking the reuptake of noradrenaline and serotonin, leading to an increase in the availability of these transmitters at their respective receptors

29
Q

Name some tricyclic antidepressants and what they treat

A

-tricyclic antidepressants are most useful for treating major depressive episodes (can be prescribed for panic disorder and for OCD)

  • imipramine - depression
  • amitriptyline - depression
  • doxepin - depression and anxiety
30
Q

What are the side effects of tricyclic antidepressants?

A
  • weight gain
  • sexual dysfunction
  • inhibition of cytochrome P450
  • adrenergic effects - contraindicated for patients with CV problems
  • antihistaminergic effects - sedation (avoid other CNS depressants or anti-histamines e.g. cimetidine)
  • anticholinergic effects - dry mouth, blurred vision, dizziness, headache and constipation
31
Q

What system in the brain controls our moods and emotions?

A

The limbic system

32
Q

Name some SSRIs and what they treat

A

Most widely prescribed class of antidepressants

Fluoxetine (Prozac) - depression and OCD

Paroxetine (Paxil) - depression and panic disorders

Sertraline - depression and panic disorders

Citalopram - depression

33
Q

What is the delay to therapeutic effects for SSRIs?

A
  • 2-4 weeks

- but effect on serotonin levels is almost immediate

34
Q

What are the side effects of selective serotonin-reuptake inhibitors (SSRIs)?

A
  • sexual dysfunction
  • dependence and withdrawal
  • weight loss
  • MAOIs (serotonin syndrome -concurrent use between SSRIs and MAOIs can cause serotonin syndrome - characterised by severe agitation, disorientation, ataxia, muscle spasms and exaggerated autonomic function)
  • cimetidine (decreases SSRI breakdown), warfarin

Contraindications - patients with a history of mania and/or anxiety - exacerbate mania/anxiety

35
Q

Name some miscellaneous next generation antidepressants

A

Bupropion - (aminoketone - inhibits the reuptake of serotonin, noradrenaline and dopamine) - depression

Venlafaxine - (strong inhibitor of serotonin and noradrenaline reuptake, but a weak blocker of dopamine reuptake) - depression

36
Q

Name some mood stabilisers and what they treat

A

Lithium carbonate - prophylaxis and treatment of acute mania

Lithium citrate - prophylaxis and treatment of acute mania

Carbamazepine (anticonvulsant) - mania, epilepsy

Valproate (anticonvulsant) - mania, epilepsy

37
Q

What are the side effects of mood stabilisers?

A

-contraindicated for patients with renal dysfunction, leukaemia, dehydration or sodium depletion

  • sodium bicarbonate
  • other antipsychotic drugs, diuretics and NSAIDS
  • dizziness, headache, confusion, hair loss, oedema, cardiac dysrhythmias, nephrotoxicity
  • toxicity and withdrawal
  • anticonvulsants - birth deformities

Pharmacology - Year 2 AC (14 decks)

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