mental health MC Flashcards

1
Q

what is the role of benzodiazapines and Z drugs for treatment of insomnia?

A
  • First try sleep therapy and have a better bedtime routine, try and use non-pharmacological first (sleep hygiene). Then if this doesn’t work and they have chronic insomnia then move to benzodiazepine.
  • Benzodiazepine = short acting are more at risk of dependence and tolerance and these are used if you have trouble going to sleep.
  • Longer acting agents are used if you have trouble staying asleep. You have to be careful driving and using machinery as you could get sleepy.
  • Extreme caution in elderly with risk of dependency issues.
  • Need to make sure they are only used for a few days
  • These may increase amount of sleep but won’t be quality as you reduce the time in REM
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2
Q

what is the role of benzodiazepines and Z drugs in the treatment of anxiety?

A
  • Z drugs not used and licensed in anxiety but usually used for insomnia
  • Benzodiazepine are licensed for anxiety for short term in a chronic state – but they are used if the symptoms severe enough
  • They are not always the most effective as they can make the anxiety worse
  • Only used in rare cases for panic anxiety disorders
  • Benzo being sedative depends on the dose as they may be analgesics unless at a much higher dose.
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3
Q

what is the risk of tolerance and dependence with the use of benzos and Z drugs and how do we minimise these?

A

• Tolerance develops after long term use especially for long term doses, the more you use the higher the dose you need for the same effect – usually short-term use
• Help minimise the risk by considering other treatment options such as non-pharmacological
• Patient needs to know risk and benefits of being on this long term
• Diazepam is long acting so it’s less potent and longer half-life to less likely to cause tolerance so you might choose to swap a patient to this.
• Stage dispensinggive the patient less of the medications so they can be reviewed more regularly to limit the supply
• Treat the underlying cause that may be causing the insomnia
o Depression
o Mental health

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4
Q
  1. Describe any high risk patient groups who may be more likely to experience adverse effects associated with benzodiazepines and z drugs
A
  • Elderly patients, as they make you drowsy so increased risk of falls
  • Previous dependency as these can be cause dependency issues and this is a risk
  • Addictive personality as this is an issue as these drugs can be very addictive
  • Patients which have drugs which will interact with these levels
  • People with liver and kidney issues as they need to be cleared
  • People who are have issues with alcohol as this makes membranes more fluid and this makes it easier for alcohol to cross  chloride ions are more likely to flow. Makes the benzos more lethal and this can lead to an overdose
  • They are cautioned in people with respiratory disorders, if severe issues we need to try and avoid these drugs
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5
Q

Describe how a patient who has been taken regular lorazepam 1mg BD for more than more than 1 year how can you do this safely?

A

• Need to make sure the patient wants to do this and knows the risks
• It’s a long process can take 4 months to a year
• Need to swap the patient to diazepam as lorazepam is more potent and only comes in 2 doses forms (1mg or 0.5mg) and this means that the change would be too significant but benzos have multiple doses so being able to switch to this makes it easier to titrate down
o usually withdrawn 10% every 2 weeks
o 1mg of lorazepam is 10mg of diazepam – shows how potent lorazepam is

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6
Q

what happens if withdrawl symptoms start to shwo?

A
  • If withdrawal symptoms show you need to slow or halt the process and sometimes you may even need to increase the dose to get rid of this
  • Withdrawal symptoms include anxiety, insomnia, headache, irritability
  • May need to refer to specialist if there are serious issues such as alcohol dependency or any previous mental health
  • Diazepam has a longer half-life and is less potent so it is likely to cause dependency and this is why it might be better
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7
Q

how do dopamine D2 agonists work?

A

locks the dopamine receptor which prevents dopamine neurotransmitter being able to bind. Blocks the effect of the dopamine. If you have too much dopamine this is when you would chose to use it.
b) Positive = treats these and if you stopped taking these you would present with symptoms

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8
Q

how to COMT inhibitors work?

A

a) Stop the breakdown of dopamine within the brain, you would want to inhibit this for if you don’t have enough dopamine. Stays along longer in the synapse
b) You don’t want this increase for psychosis so it would worsen positive symptoms, but it would help for cognitive deficits (memory and learning).

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9
Q

how does L-dopa work?

A

A. This would be used if you don’t have enough dopamine as it increases dopamine everywhere you lose the specificity and it would increase in all pathways. This might not be beneficial but could be useful for treating Parkinson’s. if you have too much tyrosine you won’t be able to produce anymore L-Dopa

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10
Q

how do dopamine transport blockers work?

A

a. You are blocking the reuptake you would only do this if you didn’t think you had enough, and they are blocking transporter. There are allow of transporters in the reward pathway as they increase dopamine, not as many in the mesocortical and this might drive the strategy that you use.

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11
Q

how do dopamine 1 agonists work?

A

a. You would use this when you don’t have enough dopamine and this is could, but this doesn’t increase dopamine levels it just mimics what the dopamine would do. This may not have an effect on psychosis. May be good for cognition

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12
Q

how would you treat the positive symptoms of schizophrenia?

A
  • Control dopamine and activate D2 receptors and this is normal function
  • In psychosis you have over activation of the D2 receptors and this is what you are trying to treat as you have excessive production of dopamine
  • This means you want to treat with D2 receptor antagonists to try and treat the positive symptoms. You still have the increased dopamine but you just are blocking the receptors so the dopamine can no longer activate them.
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13
Q

how would you treat EPS symptoms of schizophrenia?

A
  • Dopamine regulation of movement there are 2 pathways (D1 direct) and (D2 indirect)
  • In schizophrenia dopamine levels in motor pathways are normal (they do not have movement issues like Parkinson’s).
  • If you were to give these drugs you would block D2 receptors and this would mean they would think they had not enough dopamine and you would have reduced movement – Parkinsonal like symptoms
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14
Q

how would you control hyperprolactinemia?

A
  • Take a dopamine antagonist you would block the D2 receptors and this would increase the production of prolactin and this is a side effect.
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15
Q

how doesEscitalopram work?

A
  • SSRI, prevents reuptake of serotonin in the synaptic cleft
  • If you increase serotonin levels this should help to increase mood
  • If this doesn’t work swap to another SSRI
  • Take in morning, as it can cause insomnia
  • SSRI is 1st line
  • Need to follow up and monitor her and make sure she isn’t getting side effects
  • May want to offer to reduce weight as a high BMI
  • Interaction with warfarin = severe increased risk of bleeding. Doesn’t mean you cannot use it. Increase monitoring at INR let warfarin clinic know. If they have excessive bruising they need to go to a and e.
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16
Q

how does mirtazapine work?

A
  • Noradrenergic and specific serotonin antidepressants
  • Increases conc of serotonin and noradrenaline in synaptic cleft within normal range
  • Auto receptors in pre synaptic neurone so feedback loops – if you block an auto receptor you will get more neurotransmitter – KEY!
  • Binds to both a2 adreno receptors as an antagonist
  • Well tolerated but interaction with warfarin – BLEEDING
  • Monitor INR closely to minimise the risk
  • Weight gain is a common side effect  BMI is already high so this could be an issue, she also wants to lose weight so this might be an issue
  • Sedation could affect her job as she is a nurse but maybe try and give this to night
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17
Q

what are examples of SSRIs?

A

Sertraline, Citalopram, Fluoxetine, Escitalopram, Paroxetine, Fluvoxamine

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18
Q

how do SSRIs work?

A

It is a selective serotonin reuptake inhibitor.
SSRIs function by increasing the extracellular level of the neurotransmitter serotonin by limiting its reabsorption (reuptake) into the presynaptic cell, increasing the level of serotonin in the synaptic cleft available to bind to the postsynaptic receptor.

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19
Q

when would you use SSRIs?

A

These are used as a first line choice for depression. If it doesn’t work NICE suggests swapping to another type of SSRI.

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20
Q

what are the side effects of SSRIs?

A

• Well tolerated generally work well
• Initial agitation, anxiety
– need to warn a patient of this so they aren’t surprised if this does happen
• GI side effects, hyponatraemia (low sodium, especially in the elderly)
• Bleeding risk
– avoid using with NSAIDS/anticoagulants  GI bleeds, may need omeprazole if wanting to give SSRI and aspirin
– Effect of platelets
• QT prolongation
• Fewer concerns about sedation, overdose risk, cardiac problems
– Advise to take in morning or it may disrupt your sleep
• Sexual dysfunction

21
Q

what are examples of SSNRIs?

A

Venlafaxine, Duloxetine

22
Q

how do SSNRIs work?

A

Selective serotonin and noradrenaline reuptake inhibitors.
SNRIs work by blocking the reabsorption (or reuptake) of serotonin and norepinephrine back into the nerve cells that released them, which increases the levels of active neurotransmitters in the brain.

23
Q

when would you use SSNRis/

A

Usually used when SSRIs have not be successful.

24
Q

what are the side effects of SSNRIs?

A

• Venlafaxine seen more frequently, but can have problems with tolerability – not first line.
• Venlafaxine has a harsher side effect profile
• Nausea
• Dry mouth
• Dizziness
• Headache
• Excessive sweating
• Other possible side effects may include:
• Tiredness
• Constipation
• Insomnia
• Changes in sexual function, such as reduced sexual desire, difficulty reaching orgasm or the inability to maintain an erection (erectile dysfunction)
• Loss of appetite
Venlafaxine is not to be used in hypertension

25
Q

what are examples of NaSSA?

A

Mirtazapine, Trazodone, Nefazodone, Mianserin

26
Q

howdo NaSSAs work?

A

NaSSAs block negative feedback effects on norepinephrine and serotonin secretion by the presynaptic cell. This action increases the concentrations of these neurotransmitters in the synaptic cleft. They also block some serotonin receptors on the postsynaptic cell, which enhances serotonin neurotransmission

27
Q

when would you use NaSSAs?

A

Considered to be a well-tolerated antidepressant (newer

28
Q

what are the side effects od NaSSAs?

A
  • Sedation – this might help if the patient is not sleeping very well – but can be an issue if it affects there day to day.
  • Weight gain – might help if patient is easting very well but can also be an issue if they have weight issues
  • Blood disorders – very rarely see it
  • They can make you have very suicidal thoughts when you first start – this needs to be monitored
29
Q

what is an example of NARI?

A

Reboxetine

30
Q

how do NARIs work?

A

Selective Nor-Adrenaline Reuptake inhibitors work specifically to increase nor-adrenaline (norepinephrine)

31
Q

when would you use NARIs?

A

These are not frequently used and should NOT be used in elderly

32
Q

what are the side effects of NARIs?

A
  • Accommodation disorder; anxiety
  • appetite decreased;
  • hyperhidrosis
  • insomnia;
  • sexual dysfunction
  • skin reaction
  • tachycardia
  • Altered taste
33
Q

what are examples of MAOIs?>

A

Phenelzine, Tranylcypromine, Isocarboxazid

34
Q

how do MAOIs work?

A

Monoamine Oxidase inhibitors. An enzyme called monoamine oxidase is involved in removing the neurotransmitters norepinephrine, serotonin and dopamine from the brain. So if you inhibit this you will keep them in the brain for longer

35
Q

when would you use MAOIs?

A

Not widely used as Monoamine oxidase is needed to break down tyramine, when you inhibit this it means you build them up to toxic levels and this may cause bleeds on brain.
This means you need to caution with certain foods (cheese)

If switching antidepressants you need to have a 2 week break to reduce the risk of interactions

36
Q

what are the side effects of MAOIs?

A
  • Dry mouth.
  • Nausea, diarrhea or constipation.
  • Headache.
  • Drowsiness.
  • Insomnia.
  • Dizziness or lightheadedness.
  • Skin reaction at the patch site.
37
Q

what are examples of TCAS?

A

Amitriptyline, Clomipramine, Nortriptyline, Lofepramine, Dosulepin

38
Q

how do you use TCAs?

A

Tricyclic antidepressants increase levels of norepinephrine and serotonin by inhibiting re uptake of both serotonin and nor-adrenaline two neurotransmitters, and block the action of acetylcholine, another neurotransmitter.
This balance is meant to reduce the risk of depression

39
Q

when would you use TCAs?

A

Not first line as they are not well tolerated .

Risk in overdose– if patient has suicide risk do NOT give and if you had to would only give 7 days. Dangerous in overdose, due to cardiotoxicity

40
Q

what are the side effects of TCAs?

A

• Antimuscarinic side effects
o Constipation, urine retention, blood pressure, hypotension, sedation, falls, blurred vision (elderly AVOID)
• Has risk of cardiotoxicity so AVOID most MI

41
Q

what are examples of typicals?

A

Haloperidol, Chlorpromazine

42
Q

how do typicals work?

A

High affinity for dopamine D2 receptors so block the binding of dopamine

43
Q

when would you use typicals?

A

These are used if you have positive symptoms but arent effective for the negative symptoms.
Typicals usually used over atypicals

44
Q

what are the side effects of typicals?

A

cause motor control impairments, due to their increased blockade of Dopamine D2 receptors Parkinsonal like symptoms. Also don’t treat the negative symptoms

45
Q

what are examples of atypicals?

A

Clozapine, Olanzapine, Resperidone

46
Q

how do atypicals work?

A

They have a higher affinity for serotonin (5-HT2) than dopamine D2 receptors

47
Q

when would you use atypicals?

A

Work for the positive symptoms but less evidence they work for the negative symptoms

48
Q

what are the side effects of atypicals?

A
dirty drug’ bad side effects
Less effect on motor impairment but more significant side effects
•	Weight gain
•	Metabolic syndrome
•	Agranulocytosis