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csi (phase 1b) > case 14 - low mood > Flashcards

case 14 - low mood Flashcards

1
Q

what is depression?

A

persistent feelings of unhappiness and hopelessness, losing interest in the things you used to enjoy and feeling very tearful

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2
Q

what do people with depression commonly present with?

A

anxiety

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3
Q

what are the symptoms of depression?

A

constant feeling of tiredness

poor sleep

lack of appetite

low libido

aches and pains

persistent low mood

feelingsof hopelessness and low slef-esteem

lack of energy

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4
Q

what is the spectrum of depression?

A

mild to very severe

mild = persistently low in spirits

very severe = suicidal thoughts

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5
Q

what are the causes of depression?

A

sometimes, there is a trigger (i.e. bereavement, losing your job, giving birth etc)

family history of depression

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6
Q

how is depression treated?

A

lifestyle changes (Exercise, self-help groups)

talking therapies (e.g. CBT)

medication (e.g. antidepressants)

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7
Q

how is the form of treatment determined?

A

the level of depression diagnosed (mild, moderate, severe)

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8
Q

what is ‘watchful waiting’?

A

waiting to see if mild depression improves on its own

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9
Q

what is the action plan for mild depression?

A

watchful waiting = waiting to see if mild depression improves on its own

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10
Q

what is the action plan for moderate depression?

A

often talking therapies (e.g. CBT)

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11
Q

what is the action plan for severe depression?

A

referred to a specialist mental health term for intensive specialist talking treatments

prescribed medicine

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12
Q

what are the common lifestyle changes that are made by people with depression?

A

increased exercise

cutting down on alcohol

smoking cessation

balanced diet

(reading a self-help book, joining a support group)

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13
Q

what is the biopsychosocial model?

A

suggests that biological, psychological and social factors are all interlinked and important with regard to promoting health or causing disease

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14
Q

according to the biopsychosocial model, what is the relationship between the mind and body?

A

connected and interdependent things

what affects the body will often affect the mind; and vice versa, what affects the mind will also often end up affecting the body

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15
Q

what do wellness and illness refer to?

A

not just physical state, but also psychological and social status too

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16
Q

how is the biopsychosocial model used?

A

to explain phenomena such as depression by examining all relevant biological, psychological, and social factors that might be contributing to the development or maintenance of the disorder

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17
Q

what is the biological dysfunction that occurs in depression?

A

significantly disturbed with regard to endocrine (hormone), immune, and neurotransmitter system functioning

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18
Q

what is the relationship between physical disorders and depression?

A

depression can make a person more vulnerable to developing a range of physical disorders

a person who has a physical disorder is often more likely to develop depression

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19
Q

why is a family history of depression important?

A

genes can influence transmission of depression from generation to generation

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20
Q

what are the psychological factors that affect depression?

A

characteristic negative patterns of thinking, deficits in coping skills, judgment problems, and impaired emotional intelligence

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21
Q

what are some social factors that can cause depression?

A

experiencing traumatic situations, early separation, lack of social support, or harassment (bullying)

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22
Q

how can a social stressor trigger a physical cause of depression?

A

stressful social events are capable of serving as triggers for turning genes on and off, causing changes in brain functioning

= leading to depression

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23
Q

what is the DSM-V?

A

descriptive manual for assessment and diagnosis of mental disorders (i.e. listing disorders and their presentations)

used in the NICE guidelines

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24
Q

what is the ICD?

A

catergorise diseases, health-related conditions, and external causes of disease and injury in order to be able to compile useful statistics in mortality and morbidity

include physical health disorders as well as mental ones

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25
Q

which is used in the UK to diagnose depression: DSM or ICD?

A

the NICE guidelines indicate that DSM-5 is used to diagnose depression

(in preference to ICD-10/11)

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26
Q

differentiate between DSM and ICD

A

DSM-5 = descriptive manual for assessment and diagnosis of mental disorders only

ICD-10 = global categorization system for physical and mental illnesses

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27
Q

what does DSM stand for?

A

diagnostic and statistical manual of mental health disorders

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28
Q

what does ICD stand for?

A

international criteria for diseases

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29
Q

what is depression formally known as?

A

major depressive disorder

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30
Q

what is the severity scale for depression?

A

mild, moderate, severe

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31
Q

what is the criteria for major depressive disorder?

A

≥1 key symptom
AND
≥5 total symptoms

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32
Q

what are the key symptoms of major depressive disorder?

A

1) persistent sadness or low mood
2) marked loss of interests or pleasure (anhedonia)

= for most days, for most of the time for at least two weeks

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33
Q

what are the associated symptoms of major depressive disorder?

A
  • disturbed sleep (decreased/increased compared to usual)
  • decreased/increased appetite/weight
  • fatigue or loss of energy
  • agitation or slowing of movements
  • poor concentration or indecisiveness
  • feelings of worthlessness or excessive or inappropriate guilt
  • suicidal thoughts or acts
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34
Q

what must be assessed in any patient with a mental health disorder?

A

risk of self-harm

risk of suicide

risk of harm to others

= whether they have had thoughts about it OR have acted on it

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35
Q

in which demographic is self-harm most common?

A

in females aged 17-19

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36
Q

in which demographic is suicide most common?

A

in males aged 40-59

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37
Q

why is it important to ask about self-harm and suicide?

A

asking about self-harm and suicide does not increase the risk of them happening

must explore this sensitively if anything in the history flags that the patient might be at risk = have a duty to assess the risk of harm to self in order to establish how best to support and manage our patients

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38
Q

when is it important to assess the risk to others?

A

especially in patients with psychosis

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39
Q

true or false?

self-harm is most common in elderly males

A

false

most common in young females (aged 17-19)

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40
Q

true or false?

only healthcare professionals that know the patient well should explore their risk of harm and suicide

A

false

if patient expresses behaviors indicative of self-harm = MUST ASSESS !!! = any health care professional must assess risk and talk to the patients

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41
Q

true or false?

asking about self-harm and suicidal thoughts increases the risk of the patient going away doing these things

A

false

doesn’t seed idea into their head – imperative that you document what you have asked (!!!)

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42
Q

true or false?

self-harm is usually a way of coping with or expressing difficult feelings

A

true

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43
Q

true or false?

suicide is a fatal act of self-harm initiated with the intention of ending one’s own life

A

true

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44
Q

true or false?

an overdose of medication should always be considered a suicide attempt rather than an episode of self-harm

A

false

not always

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45
Q

true or false?

may take other forms such as punching a wall, banging one’s head against a hard object, and even getting into fights

A

true

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46
Q

true or false?

self-harm can involve cutting, scratching, burning, hair-pulling etc

A

true

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47
Q

true or false?

history of self-harm is associated with an increased risk of suicide

A

true

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48
Q

what is parasuicide?

A

any nonfatal, self-injurious behaviour with a clear intent to cause bodily harm or death

= thus includes both lethal suicide attempts and more habitual or low-lethality behaviours such as cutting

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49
Q

categorise the following biological factors into blue circle

diet/lifestyle
drug intake
sleep
physical health
metabolic disorders
immune/stress response, neurochemistry
genetic vulnerability
cognitive factors/IQ
emotions

A
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50
Q

categorise the following psychological factors into pink circle

coping skills/self-esteem
attitudes/beliefs
interpersonal relationships
personality
emotions
traumatic life events
cognitive factors/IQ
sleep

A
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51
Q

categorise the following social factors into purple circle

culture
diet/lifestyle
traumatic life events
financial security
work/school
interpersonal relationships
drug effects
family circumstance
social support

A
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52
Q

explain how genetic vulnerability is a risk factor for depression

A

family history of depression, epigenetic changes in utero

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53
Q

explain how sleep is a risk factor for depression

A

poor sleep because of underlying biology or psychological elements

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54
Q

explain how diet/lifestyle is a risk factor for depression

A

poor diet and sedentary lifestyle

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55
Q

what are ACEs?

A

potentially traumatic events that can have negative, lasting effects on health and well-being

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56
Q

how is ACE exposure determined in patients?

A

a BRFSS ACE questionnaire

that asks a patient, specific questions regarding their life prior to the age of 18

(then assess ACE exposure and link to any current physical/mental health problems)

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57
Q

which of the following behaviours have a significant association with ACE scores?

A
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58
Q

when is bias introduced in research?

A

when systematic error is introduced into sampling or testing by selecting or encouraging one outcome or answer over others

= can occur at any phase of research, including study design or data collection or in the process of data analysis and publication

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59
Q

what is statistical significance?

A

statistical significance implies that the difference seen in the sample also exists in the population

= less than 5% chance that these things happen by fluke

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60
Q

what is clinical significance?

A

clinical significance implies that the difference between treatments in effectiveness is clinically important

= can lead to changes in clinical practice

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61
Q

differentiate between statistical and clinical significance

A

statistical significance = the difference seen in the sample also exists in the population

clinical significance = implies that the difference seen is clinically significant

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62
Q

what is the drug type labelled 1?

A

selective serotonin reuptake inhibitor

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63
Q

what is the drug type labelled 2?

A

post-synaptic serotonin receptor agonist

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64
Q

what is the drug type labelled 3?

A

tryptophan hydroxylase inhibitor

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65
Q

what is the drug type labelled 4?

A

monoamine oxidase inhibitor

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66
Q

what is the drug type labelled 5?

A

serotonin auto-receptor antagonist

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67
Q

how and why does a selective serotonin reuptake inhibitor have an anti-depressive effect?

A

inhibits the reuptake of serotonin back into the pre-synaptic neurone so more serotonin is present in the synapse

= increased wakefulness + better mood

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68
Q

how and why does a post-synaptic serotonin receptor agonist have an anti-depressive effect?

A

acts as another version of serotonin

= agonist binds to post-synaptic serotonin receptors and enhances/activates them the same way as serotonin would to have the same effect

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69
Q

how and why does a tryptophan hydroxylase inhibitor have an anti-depressive effect?

A

it does not have an anti-depressant effect

= as it blocks the enzyme responsible for serotonin production in the pre-synaptic neurone

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70
Q

how and why does a tryptophan hydroxylase inhibitor have an anti-depressive effect?

A

it does not have an anti-depressant effect (!!!!)

= as it blocks the enzyme responsible for serotonin production in the pre-synaptic neurone

71
Q

how and why does a monoamine oxidase inhibitor have an anti-depressive effect?

A

inhibiting the activity of monoamine oxidase, thus preventing the breakdown of serotonin

= pre-synaptic serotonin concentration increases, decreasing the concentration gradient
= increasing synaptic serotonin availability

72
Q

how and why does a serotonin autoreceptor antagonist have an anti-depressive effect?

A

negative feedback receptor

= agonist stops the autoregulation and negative feedback (i.e. decrease) of serotonin production
= so more serotonin released continuously

73
Q

what information must patients be given before starting antidepressants?

A
  • drugs will take several weeks to work
  • symptoms may worsen initially
  • need to continue for approx 6 months after remission of symptoms
  • need to wean off the drugs gradually (stopping suddenly can lead to side effects)
  • antidepressants interact w many commonly prescribed drugs so it’s important to tell doctors you’re taking them
74
Q

how quickly do patients taking antidepressants see results?

A

drugs take several weeks to work - so unlikely to see immediate improvements

75
Q

how long do antidepressants need to be taken for?

A

approx until 6 months after remission of symptoms

76
Q

how do symptoms progress with antidepressant administration and why is this important?

A

symptoms will worsen initially before getting better

77
Q

when the time is right, how are antidepressants stopped?

A

need to wean the drugs gradually

as suddenly stopping can lead to side effects

78
Q

when are antidepressants most effective?

A

when prescribed for severe depression

79
Q

besides drug administration, what other measures must be taken to manage a patient with depression?

A

must look at the other social support and lifestyle that needs to be changed to help the patient

(i.e. consider social prescribing)

80
Q

what is social prescribing?

A

a means of enabling healthcare professionals to refer people to a range of local, non-clinical services

81
Q

why is social prescribing important?

A

recognises that health is determined by a range of social, economic and environmental factors and seeks to address needs in a holistic way

82
Q

what is the main aim of social prescribing?

A

aims to support individuals to take greater control of their own health

83
Q

what do social prescribing scheme usually involve?

A

variety of activities which are typically provided by voluntary and community sector organisations

84
Q

how is social prescribing usually delivered?

A

local and non-clinical services

supported through the involvement of a link worker/navigator who works with people to access local sources of support

85
Q

give examples of social prescribing

A
  • creative outlets
  • food and diet
  • social support and engaging with people
  • gardening
  • volunteering
  • online educational programmes
86
Q

name the monoamine neurotransmitters

A

serotonin
epinephrine
norepinephrine
dopamine

87
Q

what is the function of monoamine oxidase?

A

metabolise and break down the neurotransmitters norepinephrine, serotonin, and dopamine when they are in excess and not packaged in vesicles

88
Q

explain the mechanism of action of monoamine oxidase inhibitors

A

inhibitor the action of monoamine oxidase

increasing the amount of serotonin that can be released into the synapse

= increased binding of serotonin to the post-synaptic receptor

= more action potential are generated

89
Q

what are TCAs?

A

tricyclic antidepressants

= three-ring structure

90
Q

what do TCA target?

A

increase norepinephrine and serotonin concentration in the synapse

91
Q

explain the mechanism of action of tricyclic antidepressants

A

block the reuptake of serotonin and norepinephrine in presynaptic terminals, which leads to increased concentration of these neurotransmitters in the synaptic cleft

92
Q

how are tricyclic antidepressants different to SSRIs?

A

while TCAs usually have more of an effect on norepinephrine levels than on serotonin levels, SSRIs cause mores synaptic serotonin availability, by selectively inhibiting serotonin transporters only

93
Q

what class of antidepressants do MAOIs and TCAs belong to?

A

first generation

= oldest antidepressants around

94
Q

what class of antidepressants do SSRIs belong to?

A

second generation

= newer antidepressant drugs

95
Q

why are first-generation antidepressants such as MAOIs and TCAs associated with many side effects?

A

affect multiple different monoamine NTs (not just serotonin, but also adrenaline, noradrenaline and dopamine)

= increase available neurotransmitter in entire body, not just brain

96
Q

why is it important to consider other regular medication being taken when prescribing MAOIs?

A

all MAOIs interfere with liver processes that metabolise drugs

= so with MAOIs, the metabolism of some medication is impaired so dangerously high levels of the another drug being taken can build up in the body

97
Q

how must diet vary with MAOIs?

A

diet becomes hugely restricted when taking MAOIs

(most fruits, dairy, caffeinated drinks, meats are restricted)

98
Q

how common are MAOIs currently and why?

A

many side effects

hugely restrict diet

(still used at times when other treatments do not work as well)

99
Q

how do the side effects compare in MAOIs, TCAs and SSRIs?

A

MAOIs = target all the monoamine NTs all over the body so huge scope for side effects

TCAs = target serotonin and norepinephrine transported only so fewer side effects

SSRIs = selectively target specific serotonin transpoters so even fewer (if not the fewest) side effects

100
Q

why can TCAs cause fatigue and sluggishness?

A

when TCAs interfere with histamine

= can lead to fatigue and sluggishness

101
Q

what is the toxicity of TCAs like?

A

extremely toxic at high levels

= overdose can cause cardiac arrest

102
Q

what must you ensure in patients who take TCAs?

A

as TCAs are toxic at extremely high levels, an overdose (accidental or deliberate) can lead to cardiac arrest

= need to be carefully monitored by doctors, especially if there is an increased risk of suicide

103
Q

what can occur as a result of TCA overdose?

A

cardiac arrest

104
Q

which condition are TCAs commonly used to treat and alongside which other drug?

A

they are the first-line treatment for bipolar disorder

= TCAs are prescribed alongside lithium to treat bipolar disorder

105
Q

when are SSRIs not the first line preferred treatment for depression?

A

when depression occurs in the form of bipolar disorder

106
Q

why are SSRIs not used to treat bipolar disorder?

A

can cause manic episodes

107
Q

why are SSRIs most commonly the first-line treatment for depression?

A

have the fewest side effects as they are the most selective

= target selective serotonin receptors

108
Q

what are the common side effects of SSRIs and why do they occur?

A

sleep problems, weight gain, sexual dysfunction

= not only do SSRIs act in the brain, but they act all over the body (resulting in the above side effects)

109
Q

what is serotonin syndrome and why is it risked in patients on SSRIs?

A

when multiple medications are taken and they collectively build up serotonin levels in the blood

(as SSRIs already increase synaptic serotonin, any other serotonin-enhancing medications can risk serotonin syndrome)

110
Q

what are some potential new drugs being trialled as antidepressants?

A

SSRIs + SNRIs = selective serotonin/noradrenaline reuptake inhibitors

NDRIs = noradrenaline and dopamine reuptake inhibitors

NDRAs = noradrenaline and dopamine-releasing agents

111
Q

what are SSRIs + SNRIs and how do they work?

A

selective serotonin/noradrenaline reuptake inhibitors

= work to block some specific serotonin and noradrenaline receptors (enhanced TCAs)

(TCAs will block all but SSRI/SNRIs are more specific)

112
Q

what are NDRIs and how do they work?

A

noradrenaline and dopamine reuptake inhibitors

= increase synaptic noradrenaline and dopamine concentration by preventing reuptake

113
Q

what are NDRAs and how do they work?

A

noradrenaline and dopamine-releasing agents

= stimulate increased release of noradrenaline and dopamine into the synapse

114
Q

differentiate between NDRIs and NDRAs

A

both increase synaptic noradrenaline and dopamine concentrations however NDRIs do so by blocking reuptake whereas NDRAs increase release

115
Q

what is CBT?

A

cognitive behaviour therapy

a type of talking therapy - common treatment for a range of mental health problems

116
Q

how does CBT work?

A

teaches you coping skills for dealing with different problems

focuses on how
your thoughts, beliefs, and attitudes affect your feelings and actions

117
Q

explain the theory behind CBT

A

based on the idea that how we think about situations can affect the way we feel
and behave

e.g. if you interpret a situation negatively, you might experience
negative emotions = those bad feelings might lead you to behave in a certain way

118
Q

which two therapies does CBT combine?

A
  • cognitive therapy = examining the things you think
  • behaviour therapy = examining the things you do
119
Q

which conditions does CBT treat?

A

anxiety and panic attacks

bipolar disorder

depression

addiction

OCD

phobias

PTSD

schizophrenia

self-harm

120
Q

what is TF-CBT?

A

trauma-focused cognitive behavioural therapy (adaptation of CBT)

= usually offered to treat PTSD

121
Q

what is stepped care in terms of CBT?

A

try CBT as first-line treatment and if it does not work, can try other talking therapies

122
Q

what are CBT sessions like?

A

you work with a therapist to identify and challenge negative thought patterns
and behaviour

(might focus on what is going on in your life right now or how past experiences have affected you)

123
Q

how long does CBT last?

A

short-term treatment with a set number of sessions

124
Q

what does a typical CBT session include?

A
  • working through exercises with your therapist to explore your thoughts, feelings and behaviour
  • agreeing on some activities to work on in your own time
  • going over what you did in previous sessions and discussing what progress you’ve made
125
Q

what are patients expected to do outside of their CBT session?

A

can be something like filling worksheets or keeping a diary

(may need to/find it useful to continue with work after treatment has ended)

126
Q

can CBT be done individually by a patient themselves?

A

yes - through a computer or workbook

(can be useful if waiting for treatment)

  • computerised CBT should not be used to treat phobias individually (!!) = NICE guidelines
127
Q

what is social prescribing also known as?

A

community referral

128
Q

where do social prescribing referrals often come from?

A

often from professionals working in primary care settings

(e.g. GPs and practice nurses)

129
Q

what is the main idea that pins the concepts of social prescribing?

A

people’s health and wellbeing are determined mostly by a range of social, economic and environmental factors

= social prescribing therefore aims to address people’s needs in a holistic way + encourages people to take greater control of their health

130
Q

who provides the activities as part of social prescribing?

A

voluntary and community sector organisations

131
Q

what kind of activities can be classified as social prescribing?

A

volunteering, arts activities, group learning, gardening, befriending, cookery, healthy eating advice and a range of sports

132
Q

who is most likely to benefit from social prescribing schemes?

A

people with mild or long-term mental health problems

people with complex needs

people who are socially isolated

people with multiple long-term conditions who frequently attend either primary or secondary health care

133
Q

what is key in the delivery of social prescribing schemes?

A

best delivered through a link worker

= who works with people to access local sources of support

134
Q

does social prescribing work?

A

growing body of evidence that social prescribing can lead to a range of positive health and wellbeing outcomes

135
Q

which aspects of life is social prescribing said to improve?

A

quality of life and emotional wellbeing, mental and general wellbeing, and levels of depression and anxiety

136
Q

what impact does social prescribing have on the NHS?

A
  • may also lead to reduction in use of NHS services like A&E attendance, outpatient appointments, and inpatient admissions
  • reduction in GP consultation rates for most people who received social prescribing
137
Q

what are the drawbacks to social prescribing success studies?

A

studies are small scale

do not have a control group

focus on progress rather than outcomes

relate to individual interventions rather than the social prescribing model

evidence relies on self-reported outcomes and is mostly qualitative

138
Q

how does social care fit in with wider health and care policy?

A

the NHS 5-year-forward plan placed an emphasis on social prescribing schemes and their positive impact

the GP forward view noted the role of voluntary and community organisations to provide community support

the NHS long term plan incorporates SP into its model of personalised care

funding to increase the number of link workers rather than funding for the social interventions

set up the National Academy of Social Prescribing

139
Q

what does the monoamine hypothesis propose?

A

proposes that patients with depression have depleted concentrations
of serotonin, norepinephrine, and dopamine

140
Q

what are the two lines of evidence that led to the development of the monoamine hypothesis?

A

1) the effects of reserpine on serotonin and catecholamines
2) the pharmacological mechanisms of action of antidepressant drugs

141
Q

what is reserpine and what was it used for?

A

a drug used to treat hypertensive vascular disease that was found to have depressive effects

142
Q

explain the mechanism of action of reserpine in terms of depression

A

inhibit vesicular monoamine transporter, and as a
result, depletes brain monoamines (i.e. serotonin and catecholamines)

(inhibition of the ATP/Mg2+ pump responsible for the sequestering of neurotransmitters into storage vesicles located in the presynaptic neurone)

143
Q

how did the action of reserpine contribute to the monoamine hypothesis?

A

the depletion of monoamine neurotransmitter release caused by reserpine results in evidence of the rolw of serotonin, noradrenaline and dopamine in depression

144
Q

how did the mechanisms of action of antidepressant drugs contribute to the monoamine hypothesis?

A

antidepressant drugs
primarily target the monoamine neurotransmitters

= to increase their presence in the synaptic space
to activate postsynaptic receptors

145
Q

which recent evidence has led to the monoamine hypothesis being altered and how?

A

evidence = monoamine depletion in healthy subjects does not produce
depressive symptoms

= so, not as simple as depleted concentrations of serotonin, norepinephrine, and dopamine leading to MDD

146
Q

what is the altered monoamine hypothesis?

A

monoamine depletion influences other neurobiological systems
(e.g. intracellular signalling or other neurotransmitter and neuropeptide systems) or must be present
in the context of stressors

147
Q

what is isoniazid?

A

a successful anti-tubercular drug that was trialled on patients with depression and discovered to have antidepressant effects

= first successful pharmacological depression treatment
= first MAO inhibitor

148
Q

what is the function of MAO and how many types are there?

A

causes the breakdown of biogenic amines (e.g. serotonin, dopamine, epinephrine,
and norepinephrine)

two isoenzymes: MAOa and MAOb

149
Q

what are biogenic amines?

A

serotonin, dopamine, epinephrine,
and norepinephrine

150
Q

which MAO isoenzyme is responsible the breakdown of the monoamine neurotransmitters (serotonin, dopamin, noradrenaline) and where is it located?

A

MAOa

= MAOs responsible for the breakdown of biogenic amines are located in
the presynaptic terminal

151
Q

what is the impact of inhibiting MAOs in the pre-synaptic nerve terminal?

A

monoamine neurotransmitter
concentrations increase in the presynaptic terminal and are readily available for release when action potentials reach the nerve terminal

152
Q

why was isoniazid removed from the market eventually?

A

non-selective irreversible MAO inhibitor,
which led to safety concerns (e.g. hypertensive crises),

153
Q

what is moclobemide?

A

reversible
and selective MAOa inhibitors produced after isoniazid was removed from the market (as it was non-selective and irreversible)

154
Q

how is moclobemide as a drug?

A

moclobemide is generally well tolerated with the most common side effect being nausea and insomnia

155
Q

why are TCAs classified so?

A

classification of TCAs based on three benzene ring molecular core since mechanism of action was unknown at time

156
Q

what are the drug targets and pharamcological actions of TCAs?

A

reuptake transporters

  • inhibiting presynaptic noradrenaline reuptake transporters
  • inhibiting presynaptic serotonin reuptake transporters

receptor proteins

  • blocking postsynaptic adrenergic alpha 1 and 2 receptors
  • blocking postsynaptic muscarinic receptors
  • blocking postsynaptic histamine H receptors
157
Q

which reuptake transporters are commonly targeted by TCAs?

A
  • inhibiting presynaptic noradrenaline reuptake transporters
  • inhibiting presynaptic serotonin reuptake transporters
158
Q

which receptor proteins are commonly targeted by TCAs?

A
  • blocking postsynaptic adrenergic alpha 1 and 2 receptors
  • blocking postsynaptic muscarinic receptors
  • blocking postsynaptic histamine H receptors
159
Q

what is the impact of TCAs inhibiting reuptake proteins?

A

responsible for the therapeutic effects of TCAs and result in increased concentrations of
norepinephrine and serotonin in the synaptic clef

160
Q

what is the impact of TCAs antagonising the adrenergic, muscarinic and histaminergic receptor proteins?

A

contribute primarily to the side effects of
dizziness, memory impairments, and drowsiness, respectively

161
Q

what is fluoxetine?

A

the first SSRI approved for use (Prozac)

162
Q

how selective are SSRIs?

A

approx 20-1500 fold more selective for inhibiting serotonin over norepinephrine at their
respective transporter proteins

+ have minimal binding affinity for other postsynaptic receptors
such as adrenergic α1, α2, and β, histamine H1, muscarinic, and dopamine D2 receptors

163
Q

what causes the increased post-synaptic activity following the administration of SSRIs?

A

result of increased concentrations of serotonin in the synaptic cleft via reuptake inhibition rather than direct binding at the postsynaptic receptor

(do not stimulate pre-synaptic NT release AND do not stimulate post-synaptic receptors directly either)

164
Q

what are the most common side effects of SSRIs?

A

nausea, insomnia, and sexual dysfunction

165
Q

what is venlafaxine?

A

a serotonin-norepinephrine reuptake inhibitor

= specifically targets and inhibits serotonin and norepinephrine transporters

166
Q

how are SNRIs similar to TCAs?

A

both inhibit the reuptake of serotonin and norepinephrine at the serotonin and
norepinephrine transporters

167
Q

how are SNRIs different to TCAs?

A

unlike TCAs, SNRIs have minimal or no pharmacological action at adrenergic (α1, α2, and β), histamine (H1), muscarinic, dopamine, or
postsynaptic serotonin receptors (while TCAs do)

( = so fewer side effects)

168
Q

what is comparable between SNRIs and other antidepressants?

A

clinical tolerability and prevalence of sexual dysfunction

169
Q

which development supports the monoamine hypothesis?

A

the introduction of SSRIs

= by showing that increasing serotonin has clinical benefits for patients with depression

170
Q

how many of the aspects listed below do most models of social prescribing share in common?

  • link worker or navigator
  • local activities
  • support groups
  • lifestyle advice
  • online educational programmes
A

all of the above are key aspects of social prescribing in many areas and are important at making the activities accessible to lots of individual

171
Q

when are mirtaxapine an dvenlafaxine used?

A

to treat major depression

(not ever given as first line treatment - usually a less severe drug tired first)

172
Q

what does the altered monoamine hypothesis state?

A

not everyone with low levels of monoamine neurotransmitters develops depression, meaning there are other external factors which play a role

173
Q

explain how statistical and clinical significance can be applied to this scenario

A

the drug is significantly better statistically BUT in terms of clinical significant, an increase in survival by only 10 more days seems insufficient to risk taking two drugs

csi (phase 1b) (8 decks)

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