Depression

Question 1

What are the 2 main types of Depression?

Answer 1

Unipolar and Bipolar

Question 2

Why is it different to schz?

Answer 2

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).

Question 3

What type of response is Unipolar depression?

Answer 3

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

Question 4

Features of Depression

Answer 4

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

Question 5

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.

Answer 5

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

Question 6

Type of depression

Minor depression

Answer 6

has a limited negative effect on your daily life.

Question 7

type of depression

Major Depression

Answer 7

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.

Question 8

type of depression

SAD

Answer 8

“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.

Question 9

type of depression

Post-natal depression

Answer 9

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.

Question 10

Comparison of ICD-11 and DSM-5 - Differences

Answer 10

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

Question 11

Comparison of ICD-11 and DSM-5 - Similarities

Answer 11

• 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)

Question 12

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

Answer 12

A Coward Super Power

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

Question 13

Affective symptoms (emotional)

Answer 13

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

Question 14

Cognitive symptoms

Answer 14

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.

Question 15

Social symptoms

Answer 15

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

Question 16

Physical symptoms (behavioural)

Answer 16

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).

Question 17

McGuffin et al. (1996)

Answer 17

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.

Question 18

The Monoamine Hypothesis - Hirschfeld (2000)

What are monoamines?

Answer 18

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

Question 19

The Monoamine Hypothesis - Hirschfeld (2000)

Why is serotonin important?

Answer 19

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

Question 20

The Monoamine Hypothesis - Hirschfeld (2000)

When serotonin levels are low?

Answer 20

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

Question 21

The Monoamine Hypothesis - Hirschfeld (2000)

When serotonin levels are low?

Answer 21

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

Question 22

What does low levels of serotonin cause?

Answer 22

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

Question 23

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

Answer 23

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

Question 24

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

Answer 24

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

Question 25

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

Answer 25

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.

Question 26

Monoamine hypothesis

What are depressed mood states caused by?

Answer 26

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

Question 27

monoamine

What is the 5-HTT gene linked to?

Answer 27

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.

Question 28

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

Answer 28

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.

Question 29

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

Answer 29

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.

Question 30

Monoamine hypthesis evidence

Hall (1998)

Answer 30

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.

Question 31

Monoamine hypthesis evidence

Mann (2003)

Answer 31

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).

Question 32

Strengths of Monoamine Hypothesis

Drevets et al. (1999)

Answer 32

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

Question 33

strength of Monoamine hypothesis

Sargent et al. (2000)

Answer 33

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.

Question 34

Limitations of Monoamine hypothesis

Thase et al. (2002)

Answer 34

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

Question 35

Limitations of Monoamine hypothesis

Answer 35

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

Question 36

Drug therapy - Evaluation

Answer 36

• 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).

Question 37

Drug therapy timeline

Answer 37

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

Question 38

drug therapy

Applying biological treatments for depression

Answer 38

• 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.

Question 39

drug therapy

The course of treatment - antidepressants

Answer 39

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

Question 40

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

Answer 40

• antidepressants
• anti-anxiety drugs

Question 41

drug therapy

What do SSRIs (antidepressants) increase the level of?

Answer 41

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

Question 42

drug therapy

What are Benzodiazepines (BZs) a range of?

Answer 42

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

Question 43

How do Benzodiazepines (BZs) work by?

Answer 43

• 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.

Question 44

When prescribed antidepressants, consider:

Answer 44

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.

Question 45

Other medicines used with the antidepressants

Answer 45

• 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.

Question 46

Limitations of Drug Therapy

Answer 46

• 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.

Question 47

Strengths of drug therapy

Answer 47

• 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.

Question 48

drug therapy

Benefits of combined treatment

Answer 48

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).**

Question 49

Cognitive Explanation of Unipolar Depression

What does the cognitive approach believe?

Answer 49

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).

Question 50

Cognitive explanation of Unipolar Depression

What did Aaron Beck believe?

Answer 50

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.

Question 51

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

Answer 51

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

Question 52

beck

1. The Cognitive Triad

Answer 52

• 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

Question 53

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

Answer 53

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

Question 54

beck

2.Negative Self-Schemas

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

Answer 54

• 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.

Question 55

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

Answer 55

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

Question 56

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.

Answer 56

• 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.

Question 57

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

Answer 57

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.

Question 58

Evidence - beck
cognitive exp
Lewinsohn et al (2001)

Answer 58

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.

Question 59

Limitations - Beck

Answer 59

-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.

Question 60

What is Cognitive Behavioural Therapy (CBT)?

Answer 60

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

Question 61

What is CBT based on?

Answer 61

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

Question 62

What is CBT aim

Answer 62

• 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.

Question 63

CBT

What does the cognitive therapist teach clients?

Answer 63

• 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.

Question 64

CBT

Activity Scheduling

Answer 64

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)

Question 65

CBT

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

Answer 65

• 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.

Question 66

CBT

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

Answer 66

• 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.

Question 67

CBT

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

Answer 67

A new interpretation based on evidence that conforms to reality.

Question 68

CBT- Strengths/Evidence

Answer 68

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

Question 69

CBT- limitations

Answer 69

• 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.