Week 5-Depression Flashcards

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1
Q

When does depression become clinically relevant?

A

-We all have periods of ‘depression’ or more specifically of sadness and low mood across our lives. These experiences are often understandable reactions to difficult circumstances

-These experiences become clinically relevant when depression becomes pervasive and long-lasting

-Suicide and injury with unknown intent are the leading causes of death in people aged 20-34 (Office for National Statistics, 2020)

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2
Q

What is Positivism?

A

-Positivism assumes depression is a ‘natural kind’ reflecting the natural world rather than human interest

-Sadness has been documented for as long as human records have existed (Cromby et al., 2013). Ancient Greeks and religious scriptures reference low mood and sadness

-The presence of sadness throughout human history does not mean that the experience has been unchanging. The word ‘depression’ has evolved to capture a cluster of phenomena around sadness (However, it ignores social and contextual influences)

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3
Q

What are the historical understandings of depression?

A

-Solanus, 1st Century AD: Melancholy, thought to be caused by an excess of black bile, centred on distress, silence, animosity, suspicion, crying and ‘occasional joviality’ (mood swings) (Melechi, 2003). More common in middle aged men (Cromby et al., 2013)

-“Depression refers to a wide range of mental health problems characterised by the absence of a positive affect (a loss of interest and enjoyment in ordinary things and experiences), low mood and a range of associated emotional, cognitive, physical and behavioural symptoms” NICE (2022) (This is a more modern definition of depression)

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4
Q

How does culture influence the classification of depression?

A

-Cultural variations exist around how much physical symptoms are deemed as part of depression (Cromby et al., 2013)

-The Western view of depression leads to assumptions that all Westerners experience the same pattern of symptoms. This gets compared to assumptions about Eastern differences rather than thinking about individual cultures (Kirmayer, 2001)

-West tends to separate mind and body (Jenkins et al., 1991) (We tend to heavily separate the mind and body in our model of mental health (which other cultures do account for))

Relates to individualistic culture (Cromby et al., 2013)

-Even within western cultures there are individual differences e.g., UK and France

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5
Q

How good is validity and reliability in depression diagnoses?

A

-Depression diagnoses are not distinct from one another. Co-occurrence is higher than chance levels (Andrews et al., 2008; Cromby et al., 2013)

-E.g., if someone has major depressive disorder, you wouldn’t expect them to also have a prevalence of pre-menstrual dysphoric disorder like the rest of the public BUT the prevalence of this happening is higher than it reliably should be.

-NICE (2007) - Depression is too heterogeneous and is limited in predictive validity for treatment plans

-Cromby et al (2013) - single symptom research might be better than research using psychiatric categories

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6
Q

What are some Physiological causes of depression?

A

-Vitamin D, B6 and B12 as well as folate have all been linked to depression (would the disorder be deficiency or depression?)

-Is depression a real reliability of a category? Or a cluster of symptoms?

-If depression is a symptom of deficiency, which is the natural kind? what if there’s a social cause of the symptoms? They tend to ask if you feel healthy, if the answer is yes they tend to just refer for treatment rather than doing blood tests for example

-Some research takes this to mean that supplements would prevent depression (Sangle et al., 2020)

-Not a single cause for depression so to say B12 causes all forms of depression e.g., it would be very inappropriate especially if their depression has a social cause

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7
Q

How are Neurotransmitters involved in depression?

A

-Monoamine hypothesis: Norepinephrine, dopamine and serotonin. All 3 are involved in sleep, appetite and emotion.

-Antidepressants work by increasing levels of one or more monoamines in the brain. Discovery worked backwards: found antidepressants impact NT function and influenced mood

-By discovery working backwards, they assumed that chemicals play a role in depression (but doesn’t mean drugs are good for them even if it influences mood)

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8
Q

What are Tricyclic antidepressants (TCAs)?

A

-Prevents serotonin reabsorption

-Impacts norepinephrine and to a lesser extent dopamine

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9
Q

What are Monoamine oxidase inhibitors (MAOIs)? (antidepressants)

A

-They break down the enzyme that breaks down serotonin, norepinephrine and dopamine

-Can impact blood pressure and risk of stroke

-MAOIs are used left often nowadays as risks may not be worth it most times

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10
Q

What are Selective-serotonin reuptake inhibitors (SSRIs)?

A

-Most popular option in the West

-Associated with fewer risks and side effects than TCAs and MAOIs

-Some risks exist, including a small but significant risk of suicidal feelings. SSRIs can affect heart rhythm and fatigue

-All these antidepressants can all counter feelings of low mood and sadness and are associated with feeling content

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11
Q

What’s the Serotonin Hypothesis?

A

-SSRIs (e.g., Prozac) slow down serotonin reuptake, gradually increasing serotonin levels

-No strong evidence for the serotonin or monoamine hypothesis. No evidence for what a typical balance should look like or why some people have an imbalance (Cromby et al., 2013)

-If we could support this hypothesis, should we diagnose depression or a serotonin deficiency/imbalance of some kind?

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12
Q

What’s Seasonal Affective Disorder?

A

ICD-11: Recurrent depression unspecified. DSM-5: Major depressive disorder with a seasonal pattern

-Linked to sunlight exposure: (1) reduced melatonin (which affects our sleep schedule), (2) lower levels of serotonin (3) circadian rhythm

-NHS acknowledge potential for a reverse pattern of depression over summer

-Treated with SAD light therapy: Efficacy uncertain (NICE, 2022). Review=46% still developed SAD, low quality evidence and there was a lack of studies comparing to alternative treatments (Dong et al., 2022; Nussbaumer et al., 2015)

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13
Q

Premenstrual Dysphoric Disorder

A

ICD-11: Mood, somatic or cognitive symptoms during the majority of menstrual cycles that are severe enough to cause significant distress or impairment in functioning

-Cause is unknown but is believed to be a sensitivity to normal hormonal changes associated with PMS. Causes of sensitivity point to (1) genetics, (2) smoking and (3) trauma and stress (Mind, 2023)

-Treatments include: SSRIs, combined oral contraception, painkillers, Gonadotropin releasing hormone (GnRH) analogue injections, therapy or surgery (Carlini et al., 2022)

-PMD hints to a significant impact on a person’s wellbeing e.g., suddenly feeling suicidal

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14
Q

What are some less common Biomedical Treatments used for depression?

A

-Benzodiazepines (e.g., Valium) - Increase GABA and inhibit neurotransmitter activity leading to calming effects. Linked to dependency and withdrawal.

Electro-convulsive therapy (ECT):
-Electrical currents passed through brain, now seen as a ‘last resort’
-started in 1930s - thought that schizophrenia and epilepsy were mutually exclusive. Began with drug injection, switched to electrocution after witnessing a pig in a slaughterhouse experience a seizure after electrocution

-On anaesthetics during ECT. NICE guidelines suggest ECT should be a last resort unless the patient REALLY wants to

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15
Q

What are the Modern ECT Guidelines for Depression?

A

NICE (2022) guidelines: Consider ECT if:
-Patient preference
-‘Rapid response needed. For example, if the depression is life-threatening because the person is not eating or drinking.’
-Other treatments unsuccessful

-Must be fully informed of risks -1 in 200 died as a result

-Still a listed option which is bizarre despite origins, issues and the key fact that schizophrenia tends to not be associated with epilepsy

-Risks include headaches and retrograde amnesia which can lead to longer term or permanent memory loss. Blood pressure changes and heart irregularities can result (Bregg, 1997). Reviews indicate a marked risk of death (Read, 2004)

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16
Q

What are 4 criticisms of Biological approaches and treatments in depression?

A
  1. Our biology is bound up in other aspects of our lives, such as psychological processes. Evidence suggests biology enables low mood rather than causing it (Cromby et al., 2013)
  2. Biological treatments aren’t without risks, patients should be aware of risks and have a choice over treatment (NICE, 2022)
  3. It overlooks depression as a cluster of smaller phenomena that can be clustered together in different ways. Depression is a common symptom of many conditions, why have a BMM of depression but not pain?
  4. NT hypotheses under-supported and so mechanisms underlying medication effects are not well understood
17
Q

What is the cognitive approach for depression?

A

-Situations don’t determine what people feel, rather it is about the meaning we apply to them (Beck, 1964) e.g., a friend walking past without acknowledging you

-Assumes our most central core beliefs are enduring and so deep that we don’t articulate them even to ourselves. Our beliefs become treated as absolute truths (Beck, 1964)

-Vulnerability from the negative triad (Beck, 1967): (1) self, (2) world, (3) other

18
Q

What is the Cognitive Model?

A
  1. Early life experiences
  2. Core beliefs (e.g., feeling like you’re a failure)
  3. Conditional assumptions
  4. Activating event
  5. Negative automatic thoughts
  6. Symptoms of Depression (emotional, physical, behavioural)
19
Q

What is Beck’s Model of Depression?

A

Negative triad: Schemas or beliefs that a person holds
-Schemas can be problematic as it can lead to stereotyping AND can get in the way of wellbeing

The self
- “I’m incompetent”
- “I’m worthless”

Other people
- “No nobody loves/cares for me”
- “Others always let you down in the end”

The world
- “The world is a cruel place, there is no point trying”
- “The world is full of pain, life is about suffering”

20
Q

What is CBT in relation to depression?

A

-Preferred treatment for ‘less severe depression’ (NICE, 2022)

-Draws upon Beck’s model of depression and focuses on identifying unhelpful thought patterns or biases. Often uses thought diaries and records to help people identify unhelpful and challenge problematic thinking patterns.

-Associated with long term efficacy and reducing relapse compared to medication alone not not enough long-term research. Sometimes combined with mindfulness (MBCT) to address relapse risk (Cromby et al., 2013). MBCT focuses on changing relationship to negative feelings

-You might not realise the impact of your thoughts which CBT brings to light

-CBT is low cost

-Single episode depression doesn’t mean it won’t reappear in the future especially due to negative life events

21
Q

What are some cognitive biases?

A

-Over generalisations (because it happens in this occurrence it will always happen)

-All or nothing

-Jumping to conclusions

-Labelling

-Emotional reasoning

-Magnifying & minimising (Often risks victim blaming)

-Mental filter disqualifying the positives

22
Q

What are 3 criticisms of the Cognitive approach?

A
  1. Cognitive biases can still risk pathologising difference and risk implying blame on the person with depression
  2. CBT often follows a prescriptive approach and applies logic to emotion
  3. When used alone, doesn’t take account of biological influence and can be seen as downplaying social influences
23
Q

What are some Uni of Liverpool apps made for mental health?

A
  1. Catch it - you identify a thought you’ve had and essentially it asks you what you would say if someone else said that to reduce negative feelings (Not been approved as not yet tested)
  2. Pin it - you pin good times and bin the bad times to forget about it to create more positive experiences cognitively
24
Q

How cab social inequality play a role in depression?

A

-2 possible links to distress (Cromby et al., 2013). (1) Inequality is distressing (2) depression impacts relationships and employment leading to downward social mobility

-Study that explored 3 generations with major depression history between 70s-90s found evidence inequality led to depression but not the other way around (Ritsher et al., 2001)

-Stack (2021): Review suggests political focus on social welfare and low income assistance is associated with lower rates of suicide

25
Q

How can gender influence depression?

A

-Women more likely to receive clinical intervention (Cromby et al., 2013). Over 3 times the amount of deaths by suicide in men (Office for National Statistics, 2020)

-Traditionalo male breadwinner role explains M:F ration (pressure to financially provide)

-Women still at a relative economic disadvantage (Cromby et al., 2013) with unemployment and low socio-economic status linked to depression and suicidality (Stack, 2021)

-Shows social differences affect genders in different ways regarding depression which cannot be nuanced by biological factors

26
Q

How can gender influence depression? Part 2

A

-Post-natal depression draws upon biological explanations. It overlooks the profound change of having a child (Cromby et al., 2013) together with women being more likely to be the primary carer (Himmelweit, 1998)

-In heterosexual relationships women often do more nurturing, and are less likely to have their own needs met (Perrons, 2000)

-Gender minorities at risk of depression (symptom rate 52% Cisek & Rogowska, 2023) and suicidality due to stigma

-This shows this occurs in the household AND the workplace

27
Q

What does Adverse childhood experiences include?

A

-It includes violence, abuse, neglect, family members with mental health and/or addiction struggles or loss of a parent. Around 61% of adults have had at least one ACE (CDC, 2023)

-Depression is associated with 5 of 10 leading causes of death (CDC, 2019)

28
Q

What are the impacts and risk of Adverse Childhood Experiences?

A

Meta-analysis and review (Hughes et al., 2017) 4 or more ACEs:
-Moderate risk of smoking, cancer, heart and respiratory disease
-Strong risk of sexual risk taking, mental ill health and problematic alcohol use
-Strongest for drug use, interpersonal violence and self-directed violence

-Briggs et al. (2021): 4+ has become a way to define ‘high risk’ but not all ACEs are equal. Sexual abuse had a greater association with negative outcomes. Sexual abuse linked to diagnoses of depression and PTSD and with suicidality (Paolucci et al., 2001)

29
Q

What are 4 Behavioural theories of Depression?

A
  1. Inadequate of insufficient reinforcement (Lazarus, 1968) - sees depression as coming from reduced reinforcement. Unclear if it’s a quality or quantity reduction being proposed.
  2. Reduced frequency of social reinforcement (Lewisohn, 1975) - people drop positive socially reinforcing activities due to extinction by a low rate of response contingent positive reinforcement (they can’t make good things happen).
  3. Loss of reinforceable behaviour (Ferster, 1973) - don’t receive reinforcement due to not having the response that would elicit it.
  4. Loss of reinforcer effectiveness (Costello, 1972) - same behaviours and consequences but they lose potency.
30
Q

What are 3 criticisms of the behavioural and social models of depression?

A
  1. Behaviourism can over-simplify complex human experiences and subsequent responses to behaviour.
  2. While social models account well for biological interactions, and behaviourism allows room for biological mechanisms to be considered, both risk overlooking psychological responses.
  3. Need to exist within a bio-psycho-social model to effectively consider how we can reduce the impacts of social issues e.g., ACEs
31
Q

NHS Approach: What treatments are provided?

A

-In the UK, NHS GPs can offer medication or IAPT (Improving Access to Psychological Therapies) service referral without diagnoses or referral to psychiatric services

-IAPT is suggested for ‘mild’ experiences of depression and medication is offered together with therapy for experiences of depression deemed to be moderate to severe

32
Q

NHS Approach: How is Depression severity characterised by?

A

Symptoms, Duration and Impact on personal and social functioning (Severity= interaction of all 3 elements 1=less severe 2=more severe)

-Takes into account history, duration and course without relying on symptom count

NICE guidelines for depression (2022)

33
Q

NHS Approach: What are risks and recommendations used?

A

-People at immediate risk to themself or others should be referred urgently for mental health services.

-If there is a risk of suicide, should account for toxicity in overdose if antidepressants are prescribed. Clinicians should consider whether they need to limit the amount of available medicine.

-Recommends not starting patients on TCAs as routine practise due to TCAs creating a greater risk of overdose. TCAs and MAOIs are used in secondary care.

34
Q
A
35
Q

What factors make someone with depression more likely to relapse?

A

-History of recurrent depression especially in the past 2 years

-History of incomplete treatment

-Unhelpful coping styles (e.g., avoidance or rumination)

-Other chronic physical or mental health problems

-Personal, social or environmental factors that contributed and are ongoing

36
Q

What are the treatment guidelines in the event of depression reoccuring?

A

-Review what was learnt previously and what was helpful

-Make plans to maintain progress

-Identify circumstances or signs that can worsen depression and make contingency plans

-Plan for any challenging events over the coming 12 months

37
Q

What are the 3 criticisms against NHS Approaches and NICE guidelines?

A
  1. Still need a research and policy approach to address adverse effects of medication and this should be measured against effectiveness. Important for recommendation guidelines and for informed consent.
  2. Although conceptualisation has improved, it can still be argued to centre around pathologised understandings of human experience.
  3. Lack of homogeneity across depression subtypes is overlooked, depression is still treated as a valid category without acknowledgement of subjective knowledge creation.