CSI 11- Depression Flashcards

1
Q

What is the DSM criteria for diagnosing depression

A

5 or more symptoms with at leasy one of the symptoms being a key symptom

Must be persistent on most days for 2 weeks.

Symptoms are:

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2
Q

what is framework for assesing pt with mental health conditions (like depression) on whether they are at most risk.

A

always ask about THOUGHTS and ACTIONS

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3
Q

what is parasuicide

A

Taking your own life WITHOUT THE INTENTION OF IT.

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4
Q

Explain the biopsychosocial model for the aetiology of depression.

draw the diagram wiht examples

A

The mind and the body are not independent and separate things but rather are connected and interdependent things

What affects the body will often affect the mind; and vice versa

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5
Q

in how many pts with depression is serotonin present in

A

onlky 50% in which there’s a low amount.

there are clinical history to fall back on

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6
Q

Using the adverse childhood experience model, which condtions/living states are they STATISTICALLY more likely to develop?

A
  • Binge drinking
  • Heavy drinking
  • Current smoking status
  • High risk HIV incidence
  • Depression
  • Disability caused by poor mental health
  • Use of special equipment due to disability
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7
Q

in research what kind of bias must we look for and why?

A

Bias camn occur anywhere from study design to colleciton, analysis and publicaiton of data.

E.g are:

  • confirmation
  • recall
  • selection bias
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8
Q

Below is a serotonin neuron, give the number and what they do

A
  1. SSRI- most common
  2. Post synaptic serotonin receptor agonist
  3. Tryptophan hydroxylase inhbitor- DOES NOT HELP WITH DEPRESSION
  4. Monoamine oxidase inhibitor
  5. Serotonin auto-receptor antagonist- decrease serotonin release normally due to negative feedback.

Anti-depressant drugs try to increase serotonin receptors in synaptic cleft

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9
Q

What does a TCA do?

A

it inhibits reuptake of serotonin AND Noradrenaline and hence has worse side effects than SSRI.

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10
Q

Give examples of mechanistic antidpressant drugs

A
  • Monoamine oxidase inhibitors (MOAIs)
  • TCAs
  • SSRI
  • NDRI
  • Noradrenaline and dopamine releasing agents
  • SNRI
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11
Q

What do studies say is the relationship between glutamate and depression.

How about the hippocampus ?

A

Low glutamate associated with depression

hippocampus- it reduces with depression, serotonin increases it but it takes time. Hence pt won’t feel better for sometime after taking the drugs.

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12
Q

What crucial information must pts know who are going on antidepressant drugs

A
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13
Q

what do you give pts who are resistant to normal antidepressants drugs

A

ACT (assessment and commitment therapy)

KETAMINE (faster timing of effects and it’s an anti-depressant): glutamate NMDA receptor blocker

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14
Q

Why are the 6-8 weeks after starting antidepressants crucial;

A

The drugs are starting to work at this time and as they are coming out of this mental state, this is the time period where they could start having suicidal tendencies.

It is important to monitor and ASK questions

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15
Q

Explain the concept of social prescribing

A
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16
Q

What could you get from the video of Am?

A
  • fiddling with hoodies
  • stay away from friends
  • self harm thoughts
  • eats too much when low
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17
Q

what is CBT?

A

Cognitive behavioural therapy (CBT) is a type of talking treatment which focuses on how your thoughts, beliefs and attitudes affect your feelings and behaviour, and teaches you coping skills for dealing with different problems.

Combines:

cognitive therapy, examining the things you think

behaviour therapy, examining the things you do.

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18
Q

What other mental health issues can CBT be used to treat?

A

anxiety, depression, bipolar, OCD or schizophrenia.

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19
Q

what theory is CBT based on?

A

if you have negative thioughts then it’d affect your behaviour. it can elad to a vicious cycle.

20
Q

How does CBT work?

A

In CBT you work with a therapist to identify and challenge any negative thinking patterns and behaviour (now or in the past) which may be causing you difficulties. In turn this can change the way you feel about situations, and enable you to change your behaviour in future.

21
Q

what can cause depression

A

It could be a life changing event.

Maybe family history or maybe no obvious reason.

Biopsychosocial model.

22
Q

What are the different therapeutic methods to help with depression

A

For MILD: do “watchful waiting” to see if it goes. You could go to self help[ groups and exercise.

For MILD that isn’t improving: CBT and antidepressants.

Moderate to severe- combiantion of CBT and antidepressants

Severe: specialist mental heatlh team.

23
Q

What lifestyle changes can you make to help wiht depression

A
  • getting more exercise
  • cutting down on alcohol,
  • giving up smoking and
  • eating healthily
  • Reading self help book
  • Join support group
24
Q

What are SOME of the PHYSICAL symptoms of depression?

A
  • feeling constantly tired
  • sleeping badly
  • having no appetite or sex drive
  • various aches and pains.
25
Q

what are some of the reasons for the monoamine hypothesis?

Why isn’t this prevalent anymore

A
  • Effects of reserpine (vascular disease drug) on seretoin and catecholamines- find to onhibit MAOs and cause depression
  • Pharamacological mechanisms of antidepressant drugs- antidepressant drugs target MA NTs

Not exciting anymore as monoamine depletion didn’t precipitate depression in healthy patients.

Hence Monoamine could play modualtory roles that affects other biological systems (intracellurlar signals ), or must be in context of stressors.

26
Q

where does TCA act on?

A
  • inhibiting presynaptic norepinephrine reuptake transporters
  • inhibiting presynaptic serotonin reuptake transporters
  • blocking postsynaptic adrenergic α1 and α2 receptors -SIDE EFFECTS
  • blocking postsynaptic muscarinic receptors- side effects
  • blocking postsynaptic histamine H1 receptors- side effects
27
Q

what are the some of the side effects of TCA

A

dizziness (adrenergic a1 and a2 receptors)

memory impairments (muscarinic receptors)

drowsiness (histamine H1 receptor)

28
Q

Explain the pharmacology of SSRI and give side effects.

A

SSRIs are 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.

MOST COMMON Side effects are:

  • nausea,
  • insomnia,
  • sexual dysfunction.
29
Q

Explain the pharmacology of SNRI.

A

affects BOTH serotonin and noradrenaline reuptake proteins.

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

30
Q

what questions are asked to get a sense of Adverse childhood experience?

A
31
Q

Why was MOA inhibitors reduced in prescriptions for pts with depression and not firstline?

A

Restricitve diet - so much that pts hate it and go off it.

Also too many side effects.

Can still be use if pts is very resistant to other treatments

32
Q

Whats Amy pt persona

A
  • likes art
  • likes fried chicken
  • takes 40mg citalopram a day and sumotriptan for migraines
  • locket- from dead grand-mum
  • exercise
33
Q

How does a monoamine oxidae work?

A

Enzyme that produces oxidative disamination (or break down) of:

  • biogenic amines (e.g. serotonin, dopamine, epinephrine, and norepinephrine)
  • sympathomimetic amines (e.g. tyramine, benzylamine, etc)
34
Q

What are the 2 MAO isoenzymes?

A

MAOa -responsible for serotonin, melatonin, noradrenaline, dopamine and adrenaline

MAOb- mainly dopamine

35
Q

Name a well tolerated MAOI?

A

moclobemide

reversible and selective MAOA inhibitor

Coomon side effects: nausea and insomnia

36
Q

What might happen in a trypical CBT session?

A

working through exercises with your therapist to explore your thoughts, feelings and behaviour

agreeing some activities to work on in your own time

going over what you did in previous sessions and discussing what progress you’ve made.

37
Q

How can you get CBT?

A

You might be able to access CBT through the NHS, charities, your place of work or education, or the private sector.

38
Q

Who does social prescribing help?

A

Social prescribing is designed to support people with a wide range of social, emotional or practical needs, and many schemes are focused on improving mental health and physical wellbeing.

39
Q

How has social prescribing been adopted by healthcare?

A

Been recommended in:

The NHS five year forward view (2014)

General practice forward view (2016)

NHS long-term plan (2019) - combined social prescribing with model of personalised care

40
Q

Who recieved funding for social prescribing?

A

Rather than seeking to directly fund the groups that deliver social interventions, the Long-Term Plan commits funding to the link workers who connect people to the range of support and engagement opportunities

41
Q

What are characteristic psychological factors infulencing depression?

A

characteristic negative patterns of thinking

deficits in coping skills

judgment problems

impaired emotional intelligence (the ability to perceive, understand, and express emotions)

42
Q

What are social factors that can influence depression?

A

experiencing traumatic situations

early separation

lack of social support

harassment (bullying)

43
Q

Can you do CBT alone?

A

You may be able to do it alone through a computer or workbook. For example, the NHS apps library.

Doctors might:

  • give you caess to online CBT sevices
  • recommend books
  • suggest worksheets
44
Q

What was the first MAOI dicovered? What was the problem with it?

A

Isoniazid

Was origionally used in the treatment of TB

Patients taking it were found to have euphoria, psychostimulation, increased appetite, and improved sleep

It was found to help treat depression after this

Iproniazid is a non-selective irreversible MAO inhibitor, which led to safety concerns (e.g. hypertensive crises), and ultimately led to the removal of iproniazid from the US market

45
Q

Why are TCA’s preferred over SSRIs for bipolar desorder?

A

SSRIs can trigger manic episodes due to increase in seretonin so TCAs are safer