Brainscape's Knowledge GenomeTM

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


See full index

BRS Year 2 > Pharm - pharmacology of depression > Flashcards

Pharm - pharmacology of depression Flashcards

1
Q

the seven step process

A
  1. identify the patient’s problem
  2. Specify the therapeutic objective
  3. Select a drug on the basis of:
    - comparative efficacy
    - safety
    - cost
    - suitability
  4. Discuss choice of meds with patient and carer and make a shared decision about treatment
  5. Write a prescription
  6. Counsel patient on appropriate use of medicine
  7. Make appropriate arrangements for follow up
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how does angiotensin 2 receptor agonist raise bp?

A

Angiotensin II acts on the adrenal cortex, causing it to release aldosterone, a hormone that causes the kidneys to retain sodium and lose potassium.
-> Elevated plasma angiotensin II levels are responsible for the elevated aldosterone levels present during the luteal phase of the menstrual cycle.

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

What questionnaire can be used to diagnose depression?

A

PHQ-9

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

Why are SSRIs first line treatment for depression?

A
  • typically have less side effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Mechanism of action of SSRIs?

A
  • they stop reuptake of serotonin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Most common SSRIs?

A
  • sertraline
  • citalopram
  • fluoxetine
  • fluvoxamine
  • escitalopram
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what effect do erythromycin and citalopram do on an ECG?

A

prolong QT interval

  • > this is a severe interaction- can lead to torsades de pointes
  • > don’t give to someone on antihypertensives
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what’s a problem with SSRIs?

A
  • Side effects can present before benefits

- slow acting so takes 4-6 weeks for an effect

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

Problem with SSRIs?

A
  • the increase in positive effects is relatively small
  • increase in side effects can be exponential
  • got to get the dose right
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why do you taper off drugs when you stop taking them?

Give an example of drugs we have to do this for?

A
  • to avoid withdrawal

- Sertraline and citalopram and venlafaxine

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

venlafaxine targets:

A 
serotonin transporter (mood, personality, wakefulness)
noradrenaline transporter (emotions, cognition) SNRI (serotonin noradrenergic reuptake inhibitors)

Venlafaxine works by increasing serotonin levels, norepinephrine, and dopamine in the brain by blocking transport proteins and stopping its reuptake at the presynaptic terminal.

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

mirtazipine (receptor antagonist) targets:

A
  1. alpha 2 receptors (Antidepressant effect)
    - It blocks alpha 2 autoreceptors in noradrenergic neurons and alpha 2 heteroreceptors in serotonergic neurons.
    - This means that when mirtazapine blocks alpha 2 receptors it blocks the inhibitory signal, which increases norepinephrine release to the synaptic cleft.
  2. histamine H1 receptor (less vasodilation and sedation-> sleepiness)
  3. 5HT2A receptor (blocks serotonin binding- anti-depression effect)*
  4. 5HT3A receptor (blocks serotonin binding- antiemetic effect))*

*This means more serotonin binds to 5HT1A (related to depression)

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

what does noradrenaline do the the heart?

A

increase HR by beta 1
beta-1 receptor in the heart increases sinoatrial (SA) nodal, atrioventricular (AV) nodal, and ventricular muscular firing, thus increasing heart rate and contractility.

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

what does noradrenaline do to blood vessels?

A

constricts via alpha 1

“Blood vessels with α1-adrenergic receptors are present in the skin, the sphincters of gastrointestinal system, kidney (renal artery) and brain”

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

do antagonists have efficacy?

A

no - its an antagonist

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

what offsets anti-histamine activity of mirtazipine?

A

noradrenergic effect (at higher doses)

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

What are the two classes of MAOIs and what are the difference?

A

Non-selective monoamine oxidase inhibitors - targets MAO A and MAO B- increases dopamine, noradrenaline and serotonin
Selective monoamine oxidase inhibitor - targets MAO B only- increases dopamine only (often used to treat parkinson’s)

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

What’s the problem with non-selective MAOIs?

A

Have many side effects

Bind irreversibly to the enzymes

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

When would MAOIs be used?

A

Used to treat atypical depression

20
Q

What are atypical antidepressants and what are examples?

A

Treat depression through many mechanisms- target other receptors e.g. a2 receptor, histamine receptor, serotonin receptor

E.g.
Mirtazipine
Bupropion

21
Q

What are side effects of SSRI’s?

A

GI effects (nausea, diarrhea), sexual dysfunction, anxiety, insomnia

22
Q

What extra effects can sertraline have?

A

Mild inhibition of dopamine transporter

Partial inhibition of CYP2D6 at high doses (150mg)

23
Q

What extra effects can citalopram have?

A

Mild antagonism of muscarinic and histamine receptors

24
Q

What is citalopram metabolised by?

A

CYP2C19

25
Q

What are extra effects of fluoxetine?

A

Mild agonism of 5HT2A AND 5HT2C receptors

Complete inhibition of CYP2D6 and significant inhibition of CYP2C19 (caution with warfarin)

26
Q

What are side effects of venlafaxine?

A

GI effects (nausea, diarrhea), sexual dysfunction, anxiety, insomnia , hypertension (at higher doses)

27
Q

What are side effects of mirtazapine?

A

Weight gain
Sedation
May get REM sleep behavior disorder

28
Q

How do scores on the PHQ-9 questionnaire correlate to severity of depression?

A 
0-4 none
5-9 mild
10-14 moderate
15-19 moderately severe
20-27 severe
29
Q

What does mirtazapine have the highest affinity for and the lowest affinity for?

A 
Highest to lowest:
Histamine H1 receptor
A2 receptor
5HT2 receptor
5HT3 receptor
30
Q

What is the mechanism of mirtazapine?

A

Antagonises central presynaptic alpha-2-adrenergic receptors, which causes an increased release of serotonin and norepinephrine.

Antagonises central 5HT2 receptors, which leaves 5HT1 receptors unopposed causing anti-depressant effects.

31
Q

What is the target of mirtazapine?

A

Alpha-2 receptor



5-HT2 receptor

32
Q

What is the mechanism or sertraline?

A

Inhibition of serotonin reuptake results in an accumulation of serotonin. Serotonin in the central nervous system plays a role in the regulation of mood, personality, and wakefulness.

33
Q

What is the target of sertraline?

A

Serotonin transporter

34
Q

What are the main side effects of sertraline?

A

GI effects (nausea, diarrhoea), sexual dysfunction, anxiety, insomnia

35
Q

What is the mechanism of citalopram?

A

Inhibition of serotonin reuptake results in an accumulation of serotonin. Serotonin in the central nervous system plays a role in the regulation of mood, personality, and wakefulness.

36
Q

What is the target of citalopram?

A

Serotonin transporter

37
Q

What are side effects of citalopram?

A

GI effects (nausea, diarrhoea), sexual dysfunction, anxiety, insomnia

38
Q

What is the mechanism of fluoxetine?

A

Inhibition of serotonin reuptake results in an accumulation of serotonin. Serotonin in the central nervous system plays a role in the regulation of mood, personality, and wakefulness.

39
Q

What is the target of fluoxetine?

A

Serotonin transporter

40
Q

What are side effects of fluoxetine?

A

GI effects (nausea, diarrhoea), sexual dysfunction, anxiety, insomnia

41
Q

What is fluoxetine an antagonist off?

A

Mild antagonism of 5HT2A and 5HT2C receptors



42
Q

What does fluoxetine inhibit?

A

Complete inhibition of CYP2D6 and significant inhibition of CYP2C19 (caution with warfarin).

43
Q

What is the mechanism of venlafaxine?

A

Venlafaxine is a more potent inhibitor of serotonin reuptake than norepinephrine reuptake.

Noradrenaline in the central nervous system is implicated in the regulation of emotions and cognition.

44
Q

What is the target of venlafaxine?

A

serotonin transporter

Noradrenaline transporter

45
Q

What are side effects of venlafaxine?

A

GI effects (nausea, diarrhoea), sexual dysfunction, anxiety, insomnia, hypertension (at higher doses)

BRS Year 2 (110 decks)

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