Brainscape's Knowledge GenomeTM

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


See full index

LCRS Pharm > Anti-depressants > Flashcards

Anti-depressants Flashcards

1
Q

How are psychoses classified and subclassified?

A 
Schizophrenia
Affective disorders (mania and depression)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the two classifications of depression?

A

Unipolar

Bipolar

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

How is unipolar depression further subdivided? Give some facts about these.

A 
Endogenous 
- familial pattern 
- unrelated to external stresses
Reactive 
- Non familial 
- reactive to stressful life events
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the biological symptoms of depression

A 
Slowing of thought 
Slowing of action 
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

List the psychological symptoms of depression

A 
Misery
Apathy
Pessimism
Low self-esteem
Loss of motivation
Anhedonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Compare the onset of unipolar vs bipolar depression

A

Unipolar - late onset

Bipolar - early adult onset

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

Describe the monoamine theory of depression

A

Schildkraut’s theory
Depression = functional deficit of central monoamine transmission (NA + 5HT)
Mania = functional excess

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

State two bits of evidence which disagree with the theory

A

Lower levels of MAO metabolites in urine, however no correlation with severity

Clinical effects are delayed, suggesting body may be ADAPTING to the drug by downregulating a2, beta or 5HT receptors instead of this being pathological

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

Give three examples of pharmacological interventions which increase mood and support the theory

A

Increased mood seen after:
TCAs which block MA reuptake
MAOi which increase MA stores
ECT which increases response to NA&5HT

note: MA = NA+ 5HT

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

Give three examples of pharmacological interventions which decrease mood and therefore support the theory

A

Decreased mood seen after:
Reserpine - inhibits NA + 5HT storage
Alpha methyl tyrosine - inhibits NA synthesis + calms manic patients
Methyldopa - inhibits NA synthesis

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

What are the emerging theories of depression?

A

Increase in CRH/HPA activity

Hippocampal neurodegeneration

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

How do TCAs work?

A

Inhibit reuptake of monoamines

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

Describe the efficacy of action of TCAs on NA, 5HT and dopamine

A

Equal effects on NA + 5HT
Less effect on dopamine

NA=5HT>DA

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

Describe the chemical structure of TCAs

A

3 rings (tri-cyclic!)

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

Give an example of a TCA

A

Amitriptyline

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

Where else do TCAs work? List some examples

A

On other receptors:

  • α2 antagonism
  • mAChRs antagonism
  • histamine
  • 5-HT

MASH

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

TCAs result in delayed downregulation of what?

A

Beta adrenoceptors

5HT2 receptors

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

Describe the plasma protein binding of TCAs

A

Heavily PPB

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

Describe the metabolism and excretion of TCAs

A

Active metabolites produced by liver

Glucoronide conjugation, excreted via kidneys

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

What is the half life of TCAs?

A

10-20hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the side effects of TCAs at therapeutic doses? Link these to TCAs’ actions on other receptors

A

mAchR antagonism - atropine like anti-PNS effects
H1 antagonism - sedation/drowsiness
Postural hypotension - direct effects via vasomotor centre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the side effects of TCAs at toxic doses?

A

Attempted suicide
CNS - excitement, delirium, seizures, coma, respiratory depression
CVS - VF, dysrhythmias, sudden death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

List some drugs which should not be given with TCAs/monitored closely?

A

Aspirin
Warfarin
Phenytoin
Neuroleptics e.g. antipsychotics

Oral contraceptives
Antihypertensives (monitor closely)
SSRIs

Alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why should oral contraceptives, antipsychotics and SSRIs be avoided when giving TCAs?

A

These drugs will compete with TCAs for hepatic microsomal enzymes and therefore increase plasma TCA

25
Why should aspirin, warfarin and phenytoin not be given with TCAs?
They can displace TCAs from the plasma proteins and therefore increase TCA bioavailability
26
Describe the interaction between hypertensives and TCAs
Increase or decrease TCA bioavailability, therefore monitor closely
27
Describe the mechanism of action of monoamine oxidase inhibitors, and give an example
Phenelzine (MOAi) | IRREVERSIBLY inhibits MOA non-selectively, thereby rapidly increasing cytoplasmic serotonin and dopamine levels
28
Give the two subclasses of MAO and their preferences for binding
MAO-A - Noradrenaline + serotonin | MAO-B - Dopamine
29
Describe the chemical structure of monoamine oxidase inhibitors, and given an example of a subgroup
Single ring structures Carbon side chains and functional groups Example: hydrazine
30
Where else do MAOi act?
Inhibit other enzymes Downregulate beta receptors Downregulate 5HT2 receptors
31
Describe the half life and duration of action of MAOi
Short plasma half life BUT: | Long duration of action (irreversible inhibition)
32
Give the side effects of MAOi at therapeutic doses
SIMILAR TO TCAs: Atropine like anti-PNS effects Postural hypotension Sedation Other SE: Weight gain
33
Give the side effects of MAOi at toxic doses
Hepatotoxicity | Seizures
34
In relation to diet, what should you advise patients who take MAO inhibitors?
AVOID FOODS WITH TYRAMINE e.g. cheese Cheese reaction - tyramine increases NA levels. Monoamine oxidases normally break down the tyramine to decrease the noradrenaline levels. Inhibiting the enzyme = increased tyramine = hypertensive crisis
35
What would be the consequences of the cheese reaction?
Hypertensive crisis Throbbing headache Intracranial haemorrhage
36
State and explain the consequence of giving MAOi with TCAs
Hypertensive episodes (noradrenaline overload)
37
Which other drug should be avoided with MAOi?
Pethidine (opiod for child birth)
38
What are the consequences of giving Pethidine with MAOi?
Hyperpyrexia Restlessness Hypotension Coma
39
Give the name and site of action of a newer drug which is selective for an MAO.
Moclobemide - reversible MAO-A inhibitor
40
What class of drugs does moclobemide come under?
RIMA - reversible inhibitors of monoamine oxidase A
41
Give an advantage of using RIMAs instead of conventional MAOi
RIMA interact less with other drugs
42
Give two disadvantages of using RIMAs instead of conventional MAOi
``` Shorter duration of action (due to being reversible) Less efficacy (as it only works on MAO-A) ```
43
Describe the structure of SSRIs and give an example
Ring structures Aliphatic side chain Example: Fluoxetine
44
Why are SSRIs the most commonly prescribed antidepressant?
Less troublesome side effects | Safer in overdose
45
What is the disadvantage of using SSRIs?
Less effective against severe depression
46
What is the plasma half life of SSRIs?
18-24hrs
47
When do SSRIs start working?
After 2-4 weeks
48
What are the side effects of SSRIs?
Nausea Diarrhoea Insomnia Loss of libido
49
Out of all three classes of anti-depressants, which has the least side effects?
SSRIs
50
Which two classes of drugs cause downregulation of beta and 5HT2 receptors?
TCAs and MAOi
51
Which drugs should be avoided when taking SSRIs and why?
TCAs - competition for hepatic enzymes
52
Why should you advise patients to avoid alcohol when taking TCAs?
To avoid CNS depression
53
What is the second line treatment for severe depression and how does this work?
Venlafaxine - SNRI: serotonin and noradrenaline reuptake inhibition
54
Describe the dose-dependent inhibition of Venlafaxine
At low doses - inhibits reuptake of serotonin At high doses - inhibits reuptake of noadrenaline 5HT>NA>DA
55
What drug is given to patients who are intolerant to SSRIs? How does this work?
Mirtazapine - alpha 2 receptor antagonist (therefore increases noradrenaline and serotonin levels)
56
What other actions does mirtazapine have?
Other receptor actions including on histamine receptor: | Sedative effects
57
Name a drug which decreases mood by inhibiting stores of noradrenaline and serotonin
Reserpine
58
Name two drugs which inhibit NA synthesis and lowers mood/causes calming effects in manic patients
Alpha methyl tyrosine (calms manic patients) | Methyldopa

LCRS Pharm (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions