Mental Health Lectures Flashcards

1
Q

What is the bucket model of stress-vulnerability?

A

The bucket already contains a baseline amount of vulnerability including genetic and developmental factors.

Stressors that may be added to the bucket:
Social
Financial
Environmental

Eventually the bucket may overflow i.e an acute mental crisis occurs.

There are also ways to manage these stressors and reduce levels of stress in the bucket. Brabben and Turkington 2002.

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2
Q

When do mental health symptoms become pathological?

A

When the symptoms cause clinically significant distress or problems functioning in daily life.

Clinically significant relies on perspective of the treatment provider.

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3
Q

What is diagnosis based on?

A

Internationally recognised sources:
ICD-10 (WHO)
DSM-V (American, commercialised)

Usually a key role of the psychiatrist.

People can become very attached to their diagnosis.

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4
Q

Individuals can be sectioned and detained against their will as per what act?

A

Mental Health Act.

Treatment can be given without consent using proportionate force if necessary.

Such a dramatic suspension of human rights needs safeguards - Pharmacists play an important role in this.

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5
Q

What is Schizophrenia not?

A

Split personality.
Comes from Greek words meaning ‘split’ and ‘mind’.
It was intended to indicate that processes of thought; feeling and intention no longer interact to form a coherent whole.

Does not usually make people dangerous.

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6
Q

What is Schizophrenia?

A

Illness where parts of the brain responsible for emotion and sensation stop working properly.

Psychotic episodes form a part of schizophrenia.

Symptoms divided into two groups:
Positive - Experience which are in addition to reality - adding something which is not usually present.

Negative - loss of normal responses or experiences

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7
Q

What are 5 characteristic diagnostics of Schizophrenia?

A
  1. Delusions
  2. Hallucinations
  3. Disorganised speech
  4. Grossly disorganised behaviour
  5. Negative symptoms.

Significatn duration: continuous signs of the disturbance persist for at least six months.

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8
Q

What is the dopamine hypothesis wrt to Schizophrenia?

A

Drugs which increase dopamine in the CNS (Amphetamine) produce psychotic like symptoms occasionaly.

Current pharmacological treatments block dopamine receptors and dopamine blockade seems to be linked to acute antipsychotic effect.

Does not offer a complete explanation - some people seem to have underactivity of dopamine.

Glutamate and serotonin also play a role - it may be that these biochemical signals indicate more complex upstream abnormalities.

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9
Q

What are examples of the positive symptoms of schizophrenia?

A

Hallucinations: hearing voices, may also include smell, taste and touch.

Delusions: paranoid, grandiose behaviour.

Thought disorders,
Passivity phenomena.

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10
Q

How do the negative symptoms differ?

A

Less dramatic presentation
More persistent throughout disorder though.

Slowed down thought and movement.

Indifferent to social contact and a lack of interest in previously pleasurable things.

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11
Q

What is the prognosis of Schizophrenia?

A

1 in 5 will get better within five years of first episode.

2 in 5 will get better, but will have bad times.

1 in 5 will continue to have problems.

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12
Q

Long term treatment goals for Schizophrenia

A
  1. Symptom control
  2. Prevention of relapse and re-admission.
  3. Improved QoL
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13
Q

What are 3 key symptoms of depression?

A

Lowered mood.
Anergia - lethargy or lack of physical activity.
Anhedonia - inability to experience pleasure from activities usually found fun.

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14
Q

What was the bereavement exclusion?

A

It has been removed from the DSM-V and therefore a diagnosis can be given to bereaved persons experiencing significant and pervasive symptoms of clinical depression after death of a loved one.

Over-medicalisation??

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15
Q

What are some possible causes of depression?

A
Psychological adverse life events. 
Genetic factors. 
Biochemical 
Drugs
Concurrent chronic illness is a very strong risk factor for depressive illness.
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16
Q

What is the Monoamine hypothesis?

A

Suggests a biological basis for depression
A depletion in the levels of serotonin, noradrenaline and/or dopamine in the CNS
Proposed in 1965
Based on the drug action of reserpine observed to cause depression

This forms the most current pharmacological approaches.

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17
Q

PHQ-9

A

A widely used screening tool, the patient health questionnaire based on the DSM-IV (previous version, not current version) for depression.

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18
Q

Treatment options for depression

A
ECT - electric shock therapy. 
Psychological treatments: CBT, Problem solving, Guided self-help, Interpersonal therapy. 
Exercise. 
Sleep and anxiety management
Social interventions
Mindfulness
Watchful waiting.
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19
Q

What does the choice of antidepressant depend on?

A

Safety: previous antidepressant therapy.
Effectiveness: previous antidepressant therapy.
Tolerability: previous antidepressant history.
Cost.

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20
Q

Classic antidepressants increase both/either of

A

NA

Serotonin

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21
Q

Classic antidepressants work by increaseing levels of NA and/or serotonin by

A

Preventing breakdwon

Preventing reuptake

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22
Q

What class of mediations is the first line treatment of depression?

A

SSRIs

All have similar side effect profile - GI, sexual dysfunction, may increase anxiety initially.

Different duration of actions.

Safer in overdose than TCA.

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23
Q

What is the main benefit of using SSRIs over TCAs?

A

SSRIs are safer in overdose than TCA.

Also TCAs generally have more side effects than SSRIs: postural hypotension, sedation, anticholinergic effects.

TCA more toxic in overdose: causing cardiac toxicity and seizures.

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24
Q

What are the side effects of TCAs?

A

Postural hypotension
Sedation
Anticholinergic effects
Cardiac toxicity and seizures in overdose.

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25
Q

What is mirtazapine?

A

is an atypical antidepressant with noradrenergic and specific serotonergic activity. It blocks the α2 adrenergic auto- and heteroreceptors (enhancing norepinephrine release), and selectively antagonizes the 5-HT2 serotonin receptors in the central and peripheral nervous system.

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26
Q

What are the side effects of Mirtazapine?

A
Weight gain (can be beneficial)
Sedation.
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27
Q

Why is Mirtazapine often used in combination with other SSRI or SNRIs?

A

It has a slightly different mode of action.

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28
Q

What are venlafaxine and duloxetine?

A

SNRIs - serotonin AND NA reuptake inhibitors.

Not sure if have any benefits over SSRIs.

Venlafaxine above 75mg daily has the NA inhibitor efficacy but below those doses does not happen.

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29
Q

What is reboxetine?

A

NA reuptake inhibitor, fallen out of favour, one of our few drugs that does not cause serotin side effects.

30
Q

What are the major restrictions with MAOis?

A

Dietary, cheese, and co-prescription restrictions.

31
Q

What is Agomelatine?

A

It works via melatonin receptors - useful to be used in combination perhaps?

32
Q

What is vortioxetine?

A

It is an atypical antidepressant (a serotonin modulator and stimulator)

33
Q

What are the main things patients need to know about antidepressant medication treatment?

A
  1. Antidepressants are one tool to combat depression, they cannot fix all problems.
  2. Treatment should be continued for at least 6 months after recovery.
  3. Depression often reoccurs
  4. The chances of staying well are improved by antidepressants
  5. Some people need treatment for several years
  6. Antidepressants are not addictive
  7. Antidepressants should not usually be stopped or changed suddenly – discontinuation effects may occur
34
Q

What are the maudsley prescribing guidelines useful for?

A

Stopping and swapping antidepressants.

35
Q

What key monitoring is required with venlafaxine?

A

Blood pressure - especially at higher doses.

36
Q

When initiating antidepressants in eldery patients what needs to be considered? [4]

A
  1. Due to PK changes they usually require lower doses.
  2. They are more sensitive to adverse effects - increased risk of falls.
  3. It may take longer to respond to treatment.
  4. Older patients take more meds, more change for interactions.
37
Q

How can we treat treatment resistant depression?

A
  1. MAO: Phenelzine.
  2. Augmentation of existing antidepressant treatment with lithium, or an atypical antipsychotic or a different antidepressant with a different mode of action: mirtazapine.
38
Q

Why should care be taken with normal use of paroxetine?

How about when stopping it?

A

More interactions than other SSRIs.

Withdrawal symptoms more likely due to its short half life.

39
Q

Which antidepressant is the preferred in patients who have suffered a myocardial infarction or who have unstable angina?

A

Sertraline.

40
Q

What is the child dose of fluoxetine?

A

10mg daily, use the 20mg/5ml syrup.

41
Q

Which antidepressants are classed as first-line in pregnancy?

A

TCAs (amitriptyline and imipramine) are often considered the choise when starting an antidepressant in pregnancy - based on trial data demonstrating no evidence of increased birth defects.

42
Q

Fluoxetine and paroxetine use in pregnancy is linked to

A

Small increase in risk of cardio congenital defects

43
Q

All ADs used in pregnancy carry the risk of

A

neonatal withdrawal/toxicity - needs to be monitored.

44
Q

ADs of choice for breastfeeding mothers

A

Sertraline or TCAs

NOT citalopram or fluoxetine as levels in breast milk found to be high.

45
Q

What are the signs of hyponatremia?

A

Drowsiness, confusion or convulsions.

46
Q

Why should use of SSRIs in patients with an increased risk of GI bleeds be queried?

A

SSRIs block the uptake of serotonin into platelets which leads to reduced platelet aggregation and a prolonged bleeding time.

If a patient does require SSRIs and NSAIDS then a PPI should be prescribed.

Patients prescribed heparin or warfarin should not be started on an SSRI.

47
Q

Almost all antidepressants are known to decrease what?

A

The seizure threshold to varying degrees - problem for epileptics who can often have depression.

SSRIs are the best - least pro-convulsive.

48
Q

What is mirtazapine?

A

A presynaptic alpha2-antagonist

Side effects of benefit in those with depression: weight gain and increased appetitie (anorexic patients etc).

49
Q

What is the SSRI side effect profile?

A

GI
Sexual dysfunction
Increased initial anxiety.

50
Q

What is the TCA side effect profile?

A

Postural hypotension
Sedation
Anicholinergic

Generally people have more side effects from the TCAs than from SSRIs

51
Q

Issues with MAOIs

A

Dietary restrictions (interactions with tyramine - cheese and red wine D:)

Can lead to a hypertensive crisis.

52
Q

How does NICE recommend the choice of agent in schizophrenia be made?

A

By service user and HCP together, taking into account the views of the patient and carer.

Inform on likely benefits/possible side effects of each drug.

Treatment with antipsychotic medication should be considered an explicitly individual therapeutic trial.

53
Q

According to DSM-5, subthreshold depression is

A

<5 symptoms.

54
Q

DSM-5 severe depression

A

Most symptoms present and markedly interfere with everyday life.

55
Q

What monitoring should occur in patients with a severe mental illness such as schizophrenia?

A

There should be monitoring at baseline when first diagnosed and then at least every 12 months, maybe more often depending on medication.

U and Es
LFTS
FBC
Thyroid function 
Lipid profile 
Prolactin
Weight
Height
BP
HR
56
Q

If SSRIs are contraindicated in depression what should be used first line

A

Mirtazapine
Presynaptic alpha -2-antagonist
Weight gain/increased appetite

57
Q

Liver disease patients are treated with what 1st line antidepressant?

A

Paroxetine (then citalopram)

?short half life.

58
Q

Renal impairment first line antidepressant

A

Citalopram or sertraline

59
Q

The maximum citalopram dose for depression is 40mg, apart from in what circumstances?

A

When the patient:
>55
Liver disease
Low body weight.

60
Q

How can we switch from one antidepressant to another? (SSRI)

A

Cross tapering not needed.
Usually can start the new one the next day.
Unless it is FLUOXETINE due to its long-half life. We need a couple of days wash out period.

61
Q

How should we switch from a TCA to an SSRI?

A

Gradual withdrawal then switch OR cross taper.

Cross taper = increased risk of side effects

62
Q

What are the negative symptoms associated with schizophrenia and how might these be affected by treatment with 1st generation/typical antipychotics?

A

Negative symptoms are those that lead to a decrease or loss of normal function, including lack of emotion, apathy, or non-existent social functioning, lack of motivation, reduced speech.

The first generation antipsychotics are very beneficial for the positive symptoms of schizophrenia but have no effect on the negative symptoms.

63
Q

What are first generation antipsychotics? Include examples

A

D2 antagonists, chlopromazine, loxapine, haloperiodol

64
Q

What are the second antipsychotics (atypical)? Give examples

A

5HT2A/D2 antagonists - more blockade of 5HT2A than D2.

Clozapine, risperidone, olazapine

65
Q

What is the only 3rd generation antipsychotic that exisits? how does it work?

A

Aripiprazole - partial dopamine antagonist

66
Q

What are the side effects typically associated with typical antipsychotics?

A

EPS e.g. tardive dykineasia, other side effects include sexual dysfunction, increased prolactin.

67
Q

Whatare the side effects typically associated with atypical antipsychotics?

A

Metabolic side effects - hyperglycemia, weight gain and hyperlipdiemia.

68
Q

What possible differential diagnoses should be considered before diagnosing depression?

A

Oral contraceptive pill
Anemia - check Hb, B12 and folate levels
Hypothryoidism - check TSH and T4 levels. Have they gained weight?

69
Q

What is trifluperazine?

A

First generation typical antipyschotic

70
Q

How can we manage EPS side effects caused by typical antipyschotics?

A

Reduce dose or stop medication - although sometimes can be irreversible