Depression Flashcards

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1
Q

What are the 2 main types of Depression?

A

Unipolar and Bipolar

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2
Q

Why is it different to schz?

A

its non-psychotic(the depressed person understands the difference between imagination and reality and recognises that their own depressed mood may be irrational or inappropriate, but can’t help feeling the way they do).

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3
Q

What type of response is Unipolar depression?

A
  • can be reactive, a response to adverse life events or arise for no observable reason (endogenous depression as it has no apparent environment trigger).
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4
Q

Features of Depression

A

Unipolar depression is the most common mental health disorder. It affects 3.5 million people
in the UK. According to the British Psychological Society (BPS):

-Depression is more prevalent among women (30%) than men (15%)

-People in lower-income households are more likely to report depression compared to
wealthier households

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5
Q

What are the types of depression?

TIP: If the Examiner asks for “features” of depression,
describe its types, statistics, and the people it affects.

Do NOT describe symptoms.

A

My Mother Sends Post
- Mild Depression
- Major Depression
- Seasonal Affective Disorder (SAD)
- Post-natal Depression

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6
Q

Type of depression

Minor depression

A

has a limited negative effect on your daily life.

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7
Q

type of depression

Major Depression

A

interferes with daily life - with eating, sleeping and other everyday activities.

Some people may experience only one episode of major depression, but others experience several episodes in a lifetime.

It can lead to hospital admission, if the person is at risk of harm to themselves.

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8
Q

type of depression

SAD

A

“Affect” is the psychological term for
moods/emotions, so an AFFECTIVE disorder is a mood disorder— SAD can last all winter
until longer days bring more daylight.

SAD can interfere with moods and with sleeping and eating patterns.

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9
Q

type of depression

Post-natal depression

A

is different from the ‘baby blues’. Post-
natal depression can leave new mothers feeling completely overwhelmed, with panic attacks or negative feelings towards their child.

It affects one in ten mothers and usually
begins two to three weeks after the birth.

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10
Q

Comparison of ICD-11 and DSM-5 - Differences

A

ICD11
- split into mild(4), moderate(5-6), severe (7+) for symptoms
- hopelessness about the future -> not mentioned in DSM

DSM divides to major(5+)/minor(2-4) depressive episodes

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11
Q

Comparison of ICD-11 and DSM-5 - Similarities

A
  • Depressed mood (ICD) most of the day, nearly every day (DSM- all the sentance)
  • Sig weight loss when not dieting or weigght gain, or decrease or increase in appetite nearly every day. (DSM) / sig changes in apetite or weight (ICD)
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12
Q

Symptoms of depression fall into four categories:
what are they?

A

A Coward Super Power

  • Affective symptoms (emotional)
  • Cognitive symptoms
  • Social symptoms
  • Physical symptoms (behavioural)
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13
Q

Affective symptoms (emotional)

A

depressed mood, feelings of worthlessness and guilt, pessimism about the future and a lack of interest in things that used to be enjoyable are all reported by people with depression. This is called negative affect.

Some sufferers experience anger, which can be directed at themselves, or others. Anger
can also lead to self-harming behaviours

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14
Q

Cognitive symptoms

A

other symptoms include fatigue, difficulty concentrating and indecisiveness (these are mental symptoms but they’re not to do with emotion). Some cases experience recurrent thoughts of self-harm, death or suicide.

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15
Q

Social symptoms

A

people with depression often abandon hobbies and pastimes, work and
study; they withdraw from relationships with friends and family.

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16
Q

Physical symptoms (behavioural)

A

people with depression often experience loss of appetite (or sometimes increased appetite) along with unexplained aches and pains; they
move and speak slowly and there are changes in their sleep patterns (some sleep all the
time, some can’t sleep at all).

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17
Q

McGuffin et al. (1996)

A

researched 177 twins suffering from depression. The concordance rate of major depressive disorder for MZ twins was 46% and for non- identical (DZ) twins was 20%. This shows that there is a heritability factor for major depression. There is a strong genetic component to major depressive disorder, and no evidence for it being caused by a shared family environment.

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18
Q

The Monoamine Hypothesis - Hirschfeld (2000)

What are monoamines?

A

are a group of neurotransmitters that regulate mood; they include serotonin, norepinephrine (noradrenaline), and dopamine.

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19
Q

The Monoamine Hypothesis - Hirschfeld (2000)

Why is serotonin important?

A

it regulates the other neurotransmitters.
Without serotonin regulation,** brain functioning becomes erratic**.

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20
Q

The Monoamine Hypothesis - Hirschfeld (2000)

When serotonin levels are low?

A

levels of noradrenaline drop (noradrenaline provides attention and reward).
Low levels of noradrenaline are linked to a lack of pleasure.

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21
Q

The Monoamine Hypothesis - Hirschfeld (2000)

When serotonin levels are low?

A

levels of noradrenaline drop (noradrenaline provides attention and reward).
Low levels of noradrenaline are linked to a lack of pleasure.

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22
Q

What does low levels of serotonin cause?

A

causes dopamine levels to drop (related to alertness and energy). Low levels of dopamine are also linked to anxiety.

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23
Q

The monoamine hypothesis of mood disorders.
(b) In depression

A

fewer monoamine molecules are available for binding to receptors, leading to a mood disorder;

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24
Q

The monoamine hypothesis of mood disorders.
(a) In normal brain,

A

monoamine molecules are released and bind to receptors on the neighbouring neuron;

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25
Q

The monoamine hypothesis of mood disorders.
(c) Treatment with a reuptake inhibitor (the red shape blocking the reuptake transporter channel; here the SSRI Prozac’)

A

increases the number of monoamine molecules in the synaptic gap, so more are available to bind to receptors on the neighbouring neuron. This corrects the mood disorder.

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26
Q

Monoamine hypothesis

What are depressed mood states caused by?

A

low levels of noradrenaline or dopamine, but the key transmitter is serotonin, which controls the other two.

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27
Q

monoamine

What is the 5-HTT gene linked to?

A

regulating serotonin levels (5-HTT is the 5-HT transporter).

People with variations of the 5-HTT gene that are under-active seem more likely to suffer depression after stressful life events.

However, there may be a problem with the receptors that pick up the neurotransmitters when they cross the synapse from one neuron to another. If there aren’t enough receptors - or if the receptors are malfunctioning - this will have the same effect as a lack of the neurotransmitter.

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28
Q

What does the chemical monoamine oxidase A (MAO-A) do?

A

removes monoamines from the synapse. This is an important brain function called “re-uptake” that recycles neurotransmitters when they don’t appear to be needed.

If there is too much MAO-A in the synapse, it will remove monoamines that are needed, starving the brain of serotonin, noradrenaline and dopamine, leading to symptoms of depression.

This is the basis for a lot of antidepressant drugs, which inhibit (reduce) the activity of MAO-A.
This leads to more monoamine activity, increases levels of monoamines, and reduce the
symptoms of depression.

29
Q

Levels of noradrenaline and serotonin increase within hours of taking antidepressants.
However, symptoms do not improve for up to six weeks. Why?

A

Low levels of noradrenaline and serotonin change the neuro-circuitry of the brain, causing an up-regulation in the receptor sites (when there is too little stimulation of postsynaptic
receptors, more receptors are made).

When levels of neurotransmitters are increased through medication, there is a down-regulation where receptors are desensitised (decrease in number of receptors).

This process can account for the delay in the effect of the drug and alleviation of the symptoms.

30
Q

Monoamine hypthesis evidence

Hall (1998)

A

Levels of 5-HT seem to be correlated with depression. For example, patients who have low levels of a 5-HT metabolite were found to be more likely to have committed suicide.

31
Q

Monoamine hypthesis evidence

Mann (2003)

A

Post-mortem studies of patients who committed suicide show reduced levels of serotonin and an increased number of serotonin receptor sites (i.e., the brain was starved of serotonin and adapted by increasing its serotonin receptors to process as much
of it as possible).

32
Q

Strengths of Monoamine Hypothesis

Drevets et al. (1999)

A

demonstrated that the 5-HT-receptor-binding potential (BP) was reduced in the mesiotemporal cortex in unmedicated depressives relative to controls using PET.

33
Q

strength of Monoamine hypothesis

Sargent et al. (2000)

A

found decreased 5-HT-receptor-binding potential (BP) in unmedicated depressed patients relative to healthy controls in the mesiotemporal cortex, pre-frontal cortex and orbital cortex using brain imaging.

34
Q

Limitations of Monoamine hypothesis

Thase et al. (2002)

A

found that depressed patients had increased levels of noradrenaline.
This is the opposite of what the Monoamine Hypothesis predicts.

35
Q

Limitations of Monoamine hypothesis

A

These drugs only mask the symptoms of depression and have unpleasant side-effects. The research into the 5-HTT gene offers hope that in the future therapies could “turn up” the level of serotonin in individuals who show early symptoms of depression, which would prevent depression from developing in the first place.

Antidepressant drugs do not work for all patients. These drugs increase the levels of the monoamines immediately but can take weeks before the depressive symptoms fade, which challenges a direct link between neurotransmitters and depression. Other studies show abnormal serotonin function continuing after recovery from depression. This also suggests that there is not a clear-cut link between serotonin and depression.

  • too reductionist- only focuses on biolgical ignores psycholgical and environ factors.
  • deterministic
36
Q

Drug therapy - Evaluation

A
  • In the 1950s antidepressants were more effective and more ethical than the shock therapy that had been in use before.
  • New research goes on to improve antidepressants, so that they have fewer side-effects than the old MAOls and tricyclics.
  • There is a growing concern that antidepressants are being over-prescribed. The study by Kirsch et al. (2008) caused a stir by showing that** SSRIs weren’t any better than placebos when it came to mild depression.** This would mean doctors were prescribing pills that carried side-effects but weren’t doing mildly depressed patients any good (and perhaps weren’t doing severely depressed patients enough good to justify the side- effects).
37
Q

Drug therapy timeline

A

1950s- hydrazines worked by blocking MAO. when inhibited levels of MAO increased - caused improvement in mood. if inhibited too much showed aggressive/psychotic symptoms -> lead to 1st antidepressent drug MAOI (monoamine oxidase inhibitors) - often used last if others don’t work as can cause irriversible high blood pressure

1960- 2nd gen antidepressent drug -> tricyclic antidepresseants - they boost serotonin and noroadrenaline activity. Have bad side effects, possible to overdose leading to psychosis and coma.
provided releif to 60-80% patients - serious side effects caused withdrawal symptoms caused occasional death on overdose

1980s- 3rd gen drugs work by preventing reuptake of serotonin, boosting the amount of serotonin active in synapses but leaving dopamine unaffected -> known as SSRI (Selective serotonin reuptake inhibitor) - famous brand Prozac
SSRI - have fewer side effects than earier meds but have adverse reactions like weight gain, headaches etc
SSNI drugs followed - prevent reuptake of noradrenalin and leave other neurotransmitters unaffected. Affective for people with anxiety or OCD. similar side effects to SSRI

38
Q

drug therapy

Applying biological treatments for depression

A
  • MAOIs and tricyclics react badly together and shouldn’t be taken within 2 weeks of each other.
  • About 30% of patients fail to respond to any particular drug or show only faint benefits. However, clients who do not respond to one drug, often respond to a different one, therefore “trial-and-error” is needed.
39
Q

drug therapy

The course of treatment - antidepressants

A

It may take 3 weeks, before antidepressants take effect. often take them for 6-12 months even if symptoms gone if stopped too soon, symp return

least 30% people diagnosed don’t take their drugs as recommended- forget to take them, don’t like taking drugs everyday etc

stop taking due to side effects - some report they remove negative feelings leaving them not caring about anything - prefer to come off to feel again

40
Q

Two types of drug are used for the treatment of OCD:

A
  • antidepressants
  • anti-anxiety drugs
41
Q

drug therapy

What do SSRIs (antidepressants) increase the level of?

A

serotonin in the synapse and result in more serotonin being received by the receiving cell, thus reducing the symptoms.

42
Q

drug therapy

What are Benzodiazepines (BZs) a range of?

A

anti-anxiety drugs, which include trade names like Valium and Diazepam.

43
Q

How do Benzodiazepines (BZs) work by?

A
  • enhancing the action of the neurotransmitter GABA.
  • GABA tells neurons in the brain to ‘slow down’ and ‘stop firing’ which means that BZs have a general quietening influence on the brain and consequently** reduce anxiety experienced** as a result of the obsessive thoughts.
44
Q

When prescribed antidepressants, consider:

A

Some antidepressants work better for certain individuals than others. It’s not uncommon to try different depression medicines during treatment.

Some people need more than one medicine for depression treatment.

Antidepressants carry a boxed warning about increased risk for suicidal thinking and behaviour in children, adolescents, and young adults 18-24 years old.

45
Q

Other medicines used with the antidepressants

A
  • other meds prescribed particularly in treatment resistant depression. EG of meds that add-on to antidepressant treatment
  • Antipsychotic medications have been shown to enhance the effects of an antidepressant when an initial response is poor. These include aripiprazole (Abilify).
  • Lithium carbonate, usually thought of for its mood stabilizing effects in bipolar disorder, has also long been considered a useful add-on treatment to antidepressants for people with major depressive disorder.
46
Q

Limitations of Drug Therapy

A
  • Relatively slow onset of action. Antidepressants can take up to eight weeks before they take full effect.
  • Possible withdrawal symptoms.
  • Side effects.
  • Problems of compliance — patients taking the medication.
  • Stigma - fear of judgement by others
  • Fear of addiction or personality change.
47
Q

Strengths of drug therapy

A
  • motivation to enact lifestyle changes - such as excersise, hobbies, balanced diet etc normally beneficial in dealing with mental illness. Depressed person cannot always be motivated enoguh to make adjustments. Antidepressants can provide a start of healthier way of living
  • Antidepressants are relatively safe - There are studies demonstrating that antidepressants can even be safe for pregnant women (Batkowiec et al., 2017), and organ transplant recipients (Mullish et al., 2014)

-** Antidepressants are effective** - tested against a placebo. Antidepressants are proven to be more effective than a placebo with respect to relieving depressive symptoms and shortening the length of a depressive episode.

48
Q

drug therapy

Benefits of combined treatment

A

Patients with severe depression show more robust and clinically significant responses to combined treatment (Thase et al., 1997).

Combined treatment produces not only faster and greater short-term benefits, but greater long-term benefits as well. Patients receiving combined treatment with CBT have a lower relapse rate than do patients receiving medications alone
** (Teasdale et al., 2000).**

49
Q

Cognitive Explanation of Unipolar Depression

What does the cognitive approach believe?

A

believes that mental illness stems from faulty cognitions about others,
our world and us.

This faulty thinking may be through cognitive deficiencies (lack of planning)
or cognitive distortions (processing information inaccurately). These cognitions cause distortions in the way we see things; Ellis (1962) suggested it is through irrational thinking, while Beck (1967) proposed the cognitive triad (negative thoughts about the self, the world, and the future).

50
Q

Cognitive explanation of Unipolar Depression

What did Aaron Beck believe?

A

that a person’s reaction to specific upsetting thoughts may contribute
to abnormality.

As we confront the many situations that arise in life, both comforting and upsetting thoughts come into our heads. Beck calls theseunbidden cognition’s automatic thoughts.

51
Q

Beck (1967) identified 3 mechanisms that he thought were responsible for depression.
What are they?

A
  1. The Cognitive Triad
  2. Negative Self-Schemas
  3. Cognitive Distortions
52
Q

beck

  1. The Cognitive Triad
A
  • are 3 forms of negative thinking that typical of ind with depression: - negative thoughts about self, the world and the future.
  • thoughts tend to be automatic in depressed peiole as they occured spontaneously

Eg: depressed ind tend to view themselves as helpless and worthless. events in world as unrealistically negative- obstacles can’t be handled. see future as totally hopless

53
Q

In the cognitive triad when the 3 components interact what do they interfere with?

A

normal cognitive processing, leading to impairments in perception, memory and problem solving with the person becoming obsessed with negative thoughts.

54
Q

beck

2.Negative Self-Schemas

Beck believed that depression prone individuals develop a negative self-schema.

A
  • possess a set of beliefs and expectations about themselves that are essentially negative and pessimistic
  • beck claimed that negative schemas may be acquired in childhood due to traumatic event.
55
Q

What do people with negative self-schemas become prone to?

A

making logical errors in their thinking and they tend to focus selectively on certian aspects of a situation while ignoring equally relevant info

56
Q

beck

3.Cognitive Distortions

Beck (1967) identifies a number of illogical thinking processes
(distortions of thought processes). These illogical thought patterns are self-defeating and can cause great anxiety or depression for the individual.

A
  • Arbitrary interference: Drawing conclusions on the basis of sufficient or irrelevant evidence: for example, thinking you are worthless because an open air concert you were going to see has been rained off.
  • Selective abstraction: Focusing on a single aspect of a situation and ignoring others: E.g., you feel responsible for your team losing a football match even though you are just one of the players on the field.
  • Magnification: exaggerating the importance of undesirable events. E.g., if you scrape a bit of paint work on your car and, therefore, see yourself as a totally awful driver.
  • Minimisation: underplaying the significance of an event. E.g., you get praised by your teachers for an excellent term’s work, but you see this as trivial.
  • Overgeneralization: drawing broad negative conclusions on the basis of a single insignificant event. E.g., you get a D for an exam when you normally get straight As and you, therefore, think you are stupid.
  • Personalisation: Attributing the negative feelings of others to yourself. E.g., your teacher looks really cross when he comes into the room, so he must be cross with you.
57
Q

Evidence - beck
cognitive exp
Boury et al. (2001)

A

found that patients with depression were more likely to misinterpret information negatively (cognitive bias) and feel hopeless about their future (negative triad), which supports different components of Beck’s theory and the idea that cognitions are involved in depression.

58
Q

Evidence - beck
cognitive exp
Lewinsohn et al (2001)

A

assessed teenagers with no existing history of depression and measured their level of negative thinking. A year later those scoring highest for negative thinking were the ones most likely to be diagnosed with major depression. This would seem to be clear evidence for the negative thinking arising before the depression.

59
Q

Limitations - Beck

A

-does not explain all aspects of depression. Patients often exp mult emotions, theory doesn’t account extreme emotions. Freud’s psychodynamic theory of repressed anger seems best. Some forms of depression such as bipolar also involve some loss of contact with reality such as hallucinations and delusions which again Beck’s model is unable to explain.

  • Mcintosh and Fischer (2000) believe Beck’s theory to be unnecessarily complex. Rather than the triad of self, world and future, they suggest that only self is necessary. All other negative thoughts then arise from this.
  • be seen to be an over-simplification (reductionist). Biology, particularly genes and brain chemistry are involved in depression. Beck’s model doesn’t consider these.
60
Q

What is Cognitive Behavioural Therapy (CBT)?

A
  • is a form of talking therapy which can be used to treat people with a wide range of mental health prob.
61
Q

What is CBT based on?

A

based on the idea that how we think, how we feel and how we act all interact together.
Specifically, out thoughts deltermine our feelings and our behaviour

62
Q

What is CBT aim

A
  • to change the way a client thinks, by challenging irrational and maladaptive thought processes which will lead to a change in behaviour as a response to new thinking patterns.
63
Q

CBT

What does the cognitive therapist teach clients?

A
  • how to identify distorted cognitions and errors in logic that cause them to be depressed through a process of evaluation.
  • client learns to discriminate between their own thoughts and reality.
  • learn the influence that cognitions has on their feelings, and taught to recognize observe and monitor their own thoughts.
64
Q

CBT

Activity Scheduling

A

depressed ind withdraw from activities, so increasing opportunities to interact with others should help to improve their mood.
- can be schedueld for routine activities(shower), necessary activities (going to work) and pleasurable activities (meeting friends for coffee)

65
Q

CBT

Encouraging awareness of automatic cognitions
How did Beck belief cognitions are generated?

A
  • cognitions are generated automatically in response to environmental event in accordance with cognitive biases and negative schemas.
  • By recognising and acknowledging that these cognitions are automatic rather than based on evidence, patients can see that cognitions are changeable.
66
Q

CBT

Encouraging awareness of automatic cognitions
What are patients encouraged to recognise?

A
  • how their cognitions can alter how they feel, how their body reacts and their behaviour

Thoughts, emotions, physiological response and behaviour are all linked.
Looking at these factors together as well as individually is important.

67
Q

CBT

Using interpretations based on reality
What are patients encouraged to form?

A

A new interpretation based on evidence that conforms to reality.

68
Q

CBT- Strengths/Evidence

A

Hollon and Beck (1994) — Cognitive therapy has been very effective for treating depression.

Goaguen et al. (1980) — meta-analysis showed that cognitive therapy was found to be better than a placebo, suggesting that it is an effective form of treatment.

Wampold et al. (2002)— found that cognitive therapy was equal to other psychological treatments for depression.

  • has practical application - basis of CBT is Becks theory. The components of the negative triad can be easily identified and challenged. This is a positive as it shows it can be translated into a form of treatment.
  • reduces ethical issues - client is actively involved and in control.
  • tend to be short - 3 to 6 months
  • CBT in general proved most effective in teating disorders inc depression and anxiety. widely addpoted supports validiity
69
Q

CBT- limitations

A
  • requires motivation. patients with severe depression may not be able to engage with CBT or attend sessions so treatment ineffective in treating patients - antidepressants more effective
  • reductionist - critisied for its overemphasis on role of cognition - suggests irrational thinking is cause of depression - ignores circumstances that constribute to depression (domestic abuse). Biology, particularly genes and brain chemistry are involved in depression and Beck’s model doesn’t consider these.
  • Lewinsohn (1981) studied a group of participants before any of them became depressed and found that those who later became depressed were no more likely to have negative
    thoughts than those who did not develop depression. This suggests that hopeless and negative thinking may be the result of depression, rather than the cause of it.
  • The precise role of cognitive processes is yet to be determined. It is not clear whether faulty cognitions are a cause of the psychopathology or a consequence of it.