Brainscape's Knowledge GenomeTM

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


See full index

notes to flashcards year 2 - LCRS1 > antidepressant drugs > Flashcards

antidepressant drugs Flashcards

1
Q

What can psychoses be split up into?

A
  • schizophrenia (disorder of thoughts processes)
  • affective disorders (disorders of mood)
  • affective disorders can be split into depression and mania
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the emotional/ psychological symtpoms of depression?

A
  • misery
  • apathy
  • pessimism
  • low self esteem
  • loss of motivation
  • anhedonia (loss of enjoyment from activities)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the biological/ somatic symptoms of depression?

A
  • slowing of action/ thoughts
  • loss of libido
  • loss of appetite
  • sleep disturbance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the types of depression?

A
  • unipolar depression (depressive disorder)

- bipolar depression (manic depression)

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

describe unipolar depression

A
  • mood swings only in ONE direction
  • relatively late onset
  • all types respond in same way to drug treatments
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the 2 types of unipolar depression?

A
  • reactive depression: stressful life event, non-familial inheritance
  • endogenous depression: unrelated to external events, familial pattern
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

describe bipolar depression

A
  • oscillating b/ depression and mania
  • less common
  • have early adult onset
  • strong hereditary tendency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what treatment can be used for bipolar depression?

A
  • lithium
  • can stabilise swings between mania and depression
  • but has narrow therapeutic window
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the monoamine theory of depression?

A
  • depression is a functional deficit of central MA transmission
  • mania is a functional excess of MA transmission
  • MA = NA and 5-HT
  • related to NA and 5-HT deficits/excesses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the pharmacological evidence to support this theory?

A
  • TCAs: block NA and 5-HT (inc. mood)
  • MAOIs: inc. stores of NA and 5-HT (inc. mood)
  • Reserpine: inhibits NA and 5-HT storage (dec mood)
  • alpha-methyltyrosine: inhibits NA synthesis (dec. mood, calming of manic pt)
  • methyldopa: inhibits NA synthesis (dec. mood)
  • ECT: inc. CNS responses to NA and 5-HT (inc. mood)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the biological evidence like?

A
  • reduction in NA metabolites not concurrent with worse depression
  • delayed onset of clinical effect of drugs
  • this maybe due to adaptive changes and not MA theory
  • there is downregulation of alpha 2, beta and 5-HT receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the MoA of TCAs? give an example

A

monoamine re-uptake inhibitor

e.g. amitriptyline

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

what receptors do TCAs also act on?

A
  • alpha 2: block pre-synaptic inhibition of NA release
  • mAChR
  • H2 (histamine) receptors
  • 5-HT receptors
  • TCAs down regulate beta-adrenoreceptors and 5-HT2 receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the pharmacokinetics of TCAs?

A
  • oral admin
  • highly PPB (90%)
  • hepatic metabolism to active metabolites –> excreted in urine
  • plasma half life = 10-20 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the unwanted effects of therapeutic doses of TCAs?

A
  • atropine like effects (TCAs interfere with muscarininc receptors) –> anti-PNS effects (dry mouth, constipation)
  • postural hypotension –> effects on vasomotor centre
  • sedation: due to effects on H1 antagonism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the unwanted effects of acute toxicity of TCAs?

A
  • CNS: excitement, delirium, seizures (= coma, resp depression)
  • CVS: cardiac dysrhythmias (= VF and sudden death)
17
Q

what are drug interactions of TCAs?

A
  • very PPB, so can be a massive inc. in bioavaliability if co-administered with something that displaces it from plasma proteins e.g. aspirin
  • hepatic enzymes (drugs that compete w/ metabolizing hepatic enzymes)
  • potentiation: drugs that potentiate effects of CNS depression e.g. alcohol
  • antihypertensives
18
Q

what is the MoA of MAOIs?

A
  • INHIBITORS
  • MAO-A: breaks down NA and 5-HT
  • MAO-B: breaks down DA e.g. Selegiline
  • most non-selective
19
Q

what are the rapid effects of MAOIs?

A
  • inc. cytoplasmic NA, 5-HT
20
Q

what are the delayed effects of MAOIs?

A
  • delayed clinical respone due to down regulation of beta-adrenoreceptors and 5-HT2 receptors
21
Q

what are the pharmacokinetics of MAOI?

A
  • oral absorption
  • short plasma half life but longer DoA
  • metabolised in liver, excreted in urine
22
Q

what are the unwanted effects of MAOIs?

A
  • atropine-like effects (less than TCAs)
  • postural hypotension
  • sedation (seizures in OD)
  • weight gain (excessive)
  • hepatotoxicity
23
Q

what are the drug interactions of MAOIs?

A
  • cheese reaction
  • MAOIs + TCAs = HT episodes
  • MAOIs + pethidine = hyperpyrexia, restlessness, coma, HT
24
Q

describe the cheese reaction

A
  • tyramine found in foods
  • tyramine is indirectly acting sympathomimetic (inc. SNS activity)
  • goes up into NA neurones, pushes NA out in synapses
  • normally tyramine in food broken down by MAO
  • pt w/ inhibition not protected against tyramine
  • leads to HT crisis, inc. BP
25
Q

what is meclobemide?

A
  • reversible
  • selective MAO-A inhibitor
  • reduced drug interactions
  • reduced DoA
26
Q

what is the MoA of SSRIs? give an example

A
  • 5-HT re-uptake inhibitor
  • has less bad side effects
  • less effective against severe depression
27
Q

what are the pharmacokinetics against SSRIs?

A
  • oral admin
  • plasma half life = 18-24 hours
  • delayed onset of action (2-4 weeks)
  • fluoxetine competes w/ TCAs for hepatic enzymes –> avoid co admin
28
Q

what are the unwanted effects of SSRIs?

A
  • nausea
  • diarrhoea
  • insomia
  • loss of libido
  • fewer side effects so most prescribed
29
Q

what is a drug interaction of SSRIs?

A
  • interacts w/ MAOIs so avoid co-admin
30
Q

what are 2 other anti-depressants?

A
  • venlafaxine

- mertazapine

31
Q

when is mertazapine useful?

A

SSRI tolerant patients

32
Q

What is the MoA of venlafaxine?

A

dose-dependent re-uptake inhibitor

33
Q

what is the MoA of mertazapine?

A
  • 2 receptor antagonist

- inhibits negative inhibition of NA release, inc. NA and 5-HT release

notes to flashcards year 2 - LCRS1 (58 decks)

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