Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y2 LCRS Pharmacology and Therapeutics > anxiety/sedation/depression > Flashcards

anxiety/sedation/depression Flashcards

anti-depressants: explain the mechanism of action of clinically useful anti-depressant drugs and how this contributes to efficacy and side effects; Identify proposed mechanisms underlying the delayed therapeutic effects of antidepressant drugs.

1
Q

2 groups of psychoses

A

schizophrenia, affective disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

2 groups of affective disorders (disorders of mood)

A

mania, depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

emotional (psychological) symptoms of depression

A

misery, apathy, pessimism, low self-esteem, loss of motivation, anhedonia (joyment of activities is lost)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

biological (somatic) symptoms of depression

A

slowing of thought and action (psychomotor retardation), loss of libido, loss of appetite, sleep disturbance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

2 types of depression

A

depressive disorder (unipolar depression), manic depression (bipolar depression)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

depressive disorder: main feature and onset

A

mood swings in same direction, relatively late onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

depressive disorder: 2 types of depressive disorder

A

reactive, endogenous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

depressive disorder: what causes reactive depression

A

stressful life events, non-familial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

depressive disorder: what causes endogenous depression

A

unrelated to external stresses, familial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

depressive disorder: treatment type

A

drug treatment (similar groups for both reactive and endogenous)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

manic depression: main feature and onset

A

oscillating depression/mania, less common with early adult onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

manic depression: cause

A

strong hereditary tendency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

manic depression: treatment type

A

drug treatment (including oral lithium which stabilises mood, reducing cAMP and IP3, but has narrow therapeutic window)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

example of tricyclic antidepressant (TCA)

A

amitriptyline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

method of action of TCA

A

neuronal monoamine re-uptake inhibitors (NA and 5-HT equally)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

4 other possible receptor actions of TCA

A

a2 (antagonise NA release inhibition), mAChRs, histamine, 5-HT (antagonise 5-HT release inhibition)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what 2 receptors do TCAs cause delayed down-regulation

A

B-adrenoceptors, 5-HT2 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

number of chemical structures of TCAs

A

2 main classes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

pharmacokinetics of TCAs: absorption, plasma protein binding, metabolism, excretion, plasma half life

A

rapid oral absorption, highly plasma protein binding, undergo hepatic metabolism into active metabolites, renal excretion as glucuronide conjugates, plasma half life of 10-20 hours (relatively long so give once a day)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

3 unwanted effects of TCAs at therapeutic dose

A

atropine-like effects (mACh antagonist e.g. dry mouth, constipation, blurred vision), postural hypotension (vasomoter centre - possibly a2), sedation (H1 antagonism - used to treat insomnia in depressed patients as well)

21
Q

4 unwanted effects of TCAs at acute toxicity (overdose) in CNS

A

excitement, delirium, seizures -> coma, respiratory depression

22
Q

unwanted effect of TCAs at acute toxicity (overdose) in CVS

A

cardiac dysrhythmias -> ventricular fibrillation and sudden death (NA and mACh)

23
Q

due to CNS and CVS effects of TCAs, what can patients take an overdose for in care

A

attempted suicide

24
Q

2 drug interactions of TCAs which increase TCA effects, with drug examples

A

plasma protein binding (aspirin, phenytoin, warfarin), hepatic microsomal enzymes (neuroleptics (anti-psychotics), oral contraceptives)

25
Q

2 other effects of TCA drug interactions

A

potentiate CNS depressants (e.g. alcohol), potentiate antihypertensive drugs (must monitor closely)

26
Q

example of monoamine oxidase inhibitor (MAOI)

A

phenelzine

27
Q

what do MAO-A preferentially break down

A

NA and 5-HT

28
Q

what do MAO-B preferentially break down

A

DA (relevant to Parkinson’s)

29
Q

selectivity and duration of action of MAOIs

A

most are non-selective, and have irreversible inhibition so long duration of action

30
Q

rapid effects of MAOIs

A

increased cytoplasmic NA and 5-HT

31
Q

what receptor down-regulation cause a delayed clinical response with MAOIs

A

B-adrenoceptors and 5-HT2 receptors

32
Q

what else can MAOIs inhibit

A

other enzymes e.g.

33
Q

how many main chemical structures of MAOIs

A

3, with single cyclical section (phenalzine is a hydrazine, with hydrazine group being very active)

34
Q

pharmacokinetics of MAOIs: absorption, plasma half life, metabolism, excretion

A

rapid oral absorption, short plasma half life (few hours) but longer duration of action, metabolised in liver, excreted in urine

35
Q

6 unwanted effects of MAOIs

A

atropine-like effects (some mAChR antagonism but less than TCAs), postural hypotension (common - vasomotor centre), sedation (seizures in overdose), weight gain (increase in appetite; possibly excessive), hepatotoxicity (especially hydrazines, but rare)

36
Q

drug interaction of MAOIs: “cheese reaction”

A

tyramine-containing foods (indirectly acting sympathomimetic drug) and MAOI -> high levels of tyramine compete with NA for MAO that’s left, so NA remains high and causes hypertensive crisis (throbbing headache, increased BP, intracranial haemorrhage)

37
Q

drug interaction of MAOIs: with TCAs

A

hypertensive episodes so avoid

38
Q

drug interaction of MAOIs: with pethidine (opioid analgesic)

A

hyperpyrexia, restlessness, coma, hypotension

39
Q

what is a reversible MAO-A inhibitor (RIMA), and effect on drug interactions and duration of action (give instead of MAOI)

A

moclobemide, which decreases MAO-A inhibitor drug interactions (e.g. cheese reaction due to MAO-B being available to break down NA) and duration of action

40
Q

example of selective serotonin reuptake inhibitors (SSRIs)

A

fluoxetine (most prescribed anti-depressant drug)

41
Q

mechanism of action of SSRIs

A

selective 5-HT reuptake inhibition

42
Q

relative effectiveness and side effects of SSRIs vs other anti-depressants

A

less troublesome side effects so safer in overdose, but less effective against severe depression

43
Q

pharmacokinetics of SSRIs: administation, plasma half life, onset of action, drug interaction with TCAs

A

oral administration, plasma half life of 18-24 hours (long acting so can take daily), delayed onset of action (2-4 weeks); fluoxetine competes with TCAs for hepatic enzymes, so avoid co-administration

44
Q

unwanted effects of SSRIs

A

less than TCAs or MAOIs, but cause nausea, diarrhoea, insomnia, loss of libido, and interact with MAOIs and TCAs (avoid co-administration)

45
Q

2 other antidepessant drugs

A

venlafaxine, mirtazapine

46
Q

mechanism of action of venlafaxine (SNRI - serotonin and noradrenaline reuptake inhibitors)

A

dose-dependent reuptake inhibitor: 5-HT>Na»DA; 2nd line treatment for severe depression

47
Q

mechanism of action of mirtazapine

A

a2 receptor antagonist, increasing NA and 5-HT release; has sedative effect also

48
Q

when is electroconvulsive therapy (ECT) used (along with suxemethonium as NM blocker)

A

severe black depression

Y2 LCRS Pharmacology and Therapeutics (68 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions