Depression Flashcards

1
Q

What is the Beck’s cognitive triad in depression?

A

Negative views about the world
Negative views about the future
Negative views about the oneself

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2
Q

What are the criteria for depression diagnosis?

A

Diagnosis of depression requires symptoms to occur for a minimum of 2 weeks and cause a loss of functioning/signficant distress, in absence for secondary effects such as drugs, bereavement and medical disorder.

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2
Q

What is the epidemiology of suicide in the UK?

A

Most common in men aged 45 to 59 and the method via hanging or strangulation.

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3
Q

What is the aetiology of depression?

A

Multiple gene variants
Drugs which are steroids, contraceptive pills, beta blockers and digoxin.
Adverse childhood events
Recent life events such as childbirth
Low sunlight
Neurotic personality, due to hyperarousal to emotional stimuli and negative bias for attention and processing of emotional material
Social environment
Physical illness
Pre-existing mental illness such as psychosis, dementia, anxiety and addiction

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3
Q

What are the risk factors for suicide?

A

->Completed suicide is more common in men and suicide attempt is greater in women
->Middle aged
-> Previous self harm
->Single, widowed or divorced
->Insecure employment/unemployment or retired
->Occupation such as vets, farmers, pharmacists and doctors
->Lower socioeconomic status
->Recent life events such as sexual assault or war
->Poor social support such as elderly, prisoners, immigrants
->Physical or mental illness history

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4
Q

How is mild depression classified?

A

The patient fulfils 4 of the main core symptoms for depression in the ICD-10 category for over 2 weeks, where they are distressed but still able to function. This is more common in those with anxiety, premorbid personality traits or stressful life events.

This is subdivided into somatic syndrome or non-somatic syndrome.

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4
Q

What is the management plan for a patient with a suicide risk?

A

1) Carry out a mental state assessment, with particular focus to mood and excluding psychosis
2) Is the patient returning to the same situation and are there any protective factors
3) Ask about suicidal ideation

Dependant on the risk assessment and the patient’s social support network. The discharge may be managed by a crisis team to provide additional support and supervision and referral to GP or community mental health team for follow up or care co-ordination.

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5
Q

How is moderate depression classified?

A

They must fulfil 5-6 depressive symptoms of the ICD-10 where they have great difficulty continuing with daily life, subdivided into somatic and non-somatic symptoms.

This is more common in those with anxiety, premorbid personality traits or stressful life events.

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5
Q

What is parasuicide?

A

Any act which resembles suicide but does not result in death and may have been a means of expressing despair or attention rather than the sole purpose of death. Parasuicide is a form of deliberate self-harm.

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6
Q

How is severe depression classified?

A

They must fulfil at least 7 to 10 of core symptoms, where they are completely unable to work and function. This is further subdivided into psychotic and non-psychotic symptoms.
These can present with psychotic depression and somatic symptoms such as anhedonia, amenorrhoea and constipation.

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7
Q

What is the process of CBT for severe depression?

A

CBT involves three main areas:
It targets negative automatic thoughts which affect mood, behaviour and physiology.
Behavioural activation through tracking activities, goal setting and activity scheduling
It includes therapy for empathy and CBT specific skills

Negative automatic thoughts arise from early experiences that create core beliefs based on dysfunctional assumptions. There is typically a critical incident which reinforces these underlying beliefs and maintained by distorted thinking, triggering depression.

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7
Q

What are the symptoms of core depression?

A

D: depressed mood, present most of the day

E: energy loss

P: Pleasure loss (anhedonia)

R: Retardation/Agitation

E: Eating changes such as weight loss, in absence of dieting

S: Sleep changes, where early morning waking 2-3 hours than usual is common and difficulty falling asleep. Atypical depression features hypersomnia.

S: Suicidal thoughts

I: I’m a failure, ideas of guilt and unworthiness
O: Only me to blame

N: NO/Reduced concentration and self-esteem
Bleak and pessimistic views of the future

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8
Q

What are the levels of CBT?

A

Self-help materials such as books or website
Assisted self-help presented by health workers
CBT approaches for specific issues such as anxiety management, which is not adapted to the patient
Formulation driven CBT, where the patient is engaged in a therapeutic alliance to adapt a CBT technique

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8
Q

What are the somatic symptoms of depression?

A

Loss of emotional reactivity
Diurnal mood variation, where mood is worst upon first waking and improves over the course of the day
Anhedonia
Psychomotor agitation
Loss of appetite
Loss of libido

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9
Q

What are the key characterisitcs of formulation based CBT?

A

Frequent weekly sessions based on an agenda created between the patient and the therapist based on the present. Homework and rating scales are frequently used.

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9
Q

What is the epidemiology of depression?

A

More common in women
Physical illness, especially chronic pain and neurological disorders
Childhood adverse experiences
Co-morbidity with psychiatric disorders such as addiction, anxiety and personality disorder

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10
Q

Which behavioural techniques are used in CBT?

A

Activity monitoring and scheduling to encourage planning
Systematic desensitisation
Anxiety management through breathing control and imagery

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11
Q

What is the evidence base for CBT?

A

CBT is highly effective in the management of anxiety and depression equivalent to medication. There is evidence of its effectivity in schizophrenia, however this evidence is less valid.

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11
Q

How does brain pathology contribute to aetiology of depression?

A

Sevre depression is associated with ventricular enlargement and subclass prominence. There is reduced GABA function on post-morgen findings and expression of serotonin transporter in the dorsal rather nuclei.
Depression is featured by initial insomnia, frequent waking and unsatisfactory sleep, where early morning waking is common due to a reduced REM latency and total slow wave sleep.

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12
Q

What is the differential diagnosis for depression?

A

Psychosis
Seasonal affective disorder
Dementia
Anxiety
Adjustment disorder
Grief
Alcohol dependence

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12
Q

What are the categories of depression?

A

Depression with somatic symptoms
Depression without somatic symptoms
Depression with psychotic symptoms

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13
Q

What are the risk factors for depression?

A

Recent bereavement
Physical illlness
Social problem
Past history of depression
Chronic disease

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13
Q

What is the presentation of depression with somatic symptoms?

A

Patients will have psychomotor disturbances such as motor retardation, periodic agitation and impairment of cognitive function that can objectively be measured by a clinician.

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14
Q

What are the red flags for depression?

A

Feeling of hopelessness
Suicidal thoughts/ideation
Chronic pain
Disabling symptoms
Severe and prolonged symptoms

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14
Q

What is the common presentation of depression in absence of somatic symptoms?

A

Hostile depression which is more common in younger people with anxiety that have a history of hostile behaviours in response to stress like yelling, physical damage to objects and impulsivity. They have a poor response to antidepressants.

AND

Anxious depression: typically an early onset depression, where they are shy and withdrawn. There is a higher likelihood of substance dependency and self-harm and suicide, but a better response to antidepressants

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15
Q

What are the common presenting symptoms of depression in GP’s?

A

Tiredness
Low mood
Headache
Backache
Indigestion
Chest pain
Sleep disturbances
Stress
Dizziness

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15
Q

What is the common presentation of depression with psychosis?

A

Psychotic depression is a severe depressive episode accompanied by psychotic symptoms such as
Delusions, typically nihilistic in nature such as guilt, responsibility for world events and deserving of punishment

Hallucinations that may be auditory like accusatory voices, olfactory sense of rotting or visual images of torment like demons or torture.

This typically occurs within the context of schizophrenia or bipolar disorder, and presents with typical symptoms of depression. Psychotic depression typically features psychomotor changes and suicide ideation.

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16
Q

What is the screening tool used for depression?

A

PHQ-2 tool used in primary care and general hospital where patients are screened, based on the first two questions from the PHQ-9 that detects a majority of cases of depression:
“Do you struggle with feelings of depression and hopelessness?”
“Do you struggle with a loss of interest of hopelessness or loss of interest?”

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17
Q

What is abnormal grief reaction?

A

Cluster of depressive symtpoms with preoccupation with the deceased where it:
->Intense enough to be diagnosed by clinical depression
->Delayed to avoid grief
->Last longer than 6 months

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18
Q

What is the normal grief reaction?

A

Grief is the emotional response to a loss where a person may experience shock, numbness, sadness, helplessness and depression.

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19
Q

What are the aspects of the mental state examination:?

A

Appearance
Behaviour
Speech
Thoughts
Perception
Mood
Cognition
Insight

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19
Q

What are the positive prognostic factors for depresssion?

A

Acute onset, earlier age of onset, endogenous depression

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20
Q

What is the framework for approaching patient aetiology for depression?

A

3 P’s
Predisposing factors: features of patient history which puts them at risk based on the aetiology of depression

Precipitating factors: Important recent events that occurred in the patient’s life

Perpetuating factors: Which aspects of the patient’s social or biomedical history is making the depression worse

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20
Q

What are the prognostic factors for a poor outcome of depression?

A

Insidious/slow onset
Elderly
Neuroticism
Co-morbidity
Lack of social support
Neuroticism
Low self confidence

21
Q

What is the framework for approaching patient aetiology for depression?

A

3 P’s
Predisposing factors: features of patient history which puts them at risk based on the aetiology of depression
Precipitating factors: Important recent events that occurred in the patient’s life
Perpetuating factors: Which aspects of the patient’s social or biomedical history is making the depression worse

OR
Physical
Psychological factors such as stress
Social factors such as job or relationship

21
Q

When should antidepressants be considered?

A

History of moderate or severe depression
Sub threshold depressive symptoms that have not warranted treatment but have been. Present for at least 2 years

Antidepressant choice is based on tolerability, safety and history of prior treatments. There will be initially frequent follow up 1-4 weeks to monitor treatment response and any unwanted side effects

22
Q

What is the theory for the physiological cause of depression?

A

Depression occurs due to the monoamine theory, where there is a depletion of serotonin and noradrenaline, therefore treatment using MAO inhibitors act to increase its availability. Depression is an independent risk factor for osteoporosis and coronary heart disease, and many patients report medically unexplained physical symptoms.

22
Q

What is the first-line treatment for non-psychotic depression?

A

For mild to moderate: Psychotherapies such as CBT and counselling
Antidepressant drugs exclusively for severe cases, which are shown to be effective for majority of patients.

Ideally, a combination of pharmacological and psychological approaches.

23
Q

What are the features of depression with psychosis?

A

Guilt and nihilism, with delusions of worthlessness and self-harm.

23
Q

Which medication should be avoided for suicide risk?

A

Tricyclic antidepressants due to correcting previous psychomotor retardation with greater noradrenaline and serotonin.

24
Q

What are the recommendations for patients with depression?

A

Avoid alcohol and illicit drugs
CBT has evidence of high effectivity
Treatments include anti-psychotics, anti-depressants, lithium and electro convulsive therapy.

24
Q

What is the second line treatment for depression?

A

Failure of antidepressants is
Alternative antidepressant from a different class or side effect profile

Addition of lithium

Electroconvulsive therapy for severe biological features like significant weight loss and psychomotor retardation

25
Q

What is the NICE recommendations for the management for mild to moderate depression?

A

Low intensity psychosocial interventions for guided self-help CBT, and avoid drug treatment when possible. Techniques such as watchful waiting, sleep hygiene and managing anxiety.

25
Q

What is the maintenance therapy for depression?

A

Compliance for effective treatment for 6 months to 1 year after remission, and discontinuation should be gradual

Patients with severe or frequent episodes should continue treatment for at least 5 years

-> There is a high risk of relapse with 70-90% when stopping medication within 5 years

26
Q

What is the NICE reccomendations for moderate to severe depression?

A

Antidepressant drugs, but always offer high intensity CBT sessions with 16-20 sessions over 3-4 months.

26
Q

What is the treatment for depression with psychotic symptoms?

A

Antipsychotics are the first line treatment and highly effective and should be commenced for at least a few days before beginning secondary treatment such as antidepressants. Antidepressants and antipsychotics are more effective as a combination therapy than independently, however they may worsen side effects.

As a second line treatment, Electroconvulsive therapy is highly effective for psychotic depression, and can be used in combination with antipsychotics

27
Q

What are the NICE reccomendations for severe/complex depression?

A

Inpatient admission
Home treatment team and Crisis treatment team
Electroconvulsive therapy

27
Q

What is atypical depression?

A

Subtype of depressive disorder with clinical features of:
Depressed mood
Hypersomnia for at least 3 days a week for 3 months
Hyperplasia with weight gain
Leaden paralysis
Oversensitivity to perceived rejection
Reversed diurnal mood: Better mood in morning, worse throughout day

28
Q

What is the NICE recommendation for recurrent depression?

A

Individual CBT and mindfulness-based CBT

28
Q
A
29
Q

What is the escalation of drugs for use in depression use?

A

1) SSRIs
2) Tricyclic antidepressant, MAO inhibitor, venlafaxine
3) Antipsychotic drug
4) Electroconvulsive therapy

30
Q

What do psychotherapies involve?

A

Therapeutic conversation
Therapeutic alliance between t he patient and therapist
A therapist rationale
A therapeutic base for regular meeting

31
Q

What is the NICE guidelines for Electroconvulsive therapy?

A

Only use for rapid short term improvement in severe or life-threatening depression when all other treatments have failed, such as:
Psychosis including schizophrenia and mania
Catatonia
Severe depressive illness

It involves the use of general anaesthetic and neuromuscular blocker to sedate the patient during the procedure. An electrical current is passed through the brain to induce a brief grand mal seizure, following this, patients will typically experience mild to moderate amnesia.

The benefits of ECT reduce after a few weeks, so a maintenance plan should be in place and ECT should not be the maintenance treatment.

32
Q

What are the physiological effects of ECT?

A

Increases metabolic requirements
Cerebral blood flow
Greater vagal tone causing bradycardia and atrial fibrillation
Adrenaline release during seizure peas and causes tachycardia and hypertension
Increases cortisol and may worsen insulin resistance

33
Q

Which groups should have closer monitoring for ECT treatment?

A

Cerebral aneurysm
Recent MI or cardiac arrhythmia
Phaemochromocytoma

34
Q

What are the side effects of ECT?

A

The therapeutic dose window is important to achieve high effectivity. Side effects are more likely to occur in women or the elderly and immediate side effects include:
Aches and Headaches commonly induced by suxamethonium
Stiffness and tension in the jaw
Confusion and nausea
Damage to teeth

Longer term side effects will include memory loss of gaps of time.

35
Q

What is the hypothesis for the mechanism of action of ECT?

A

A machine is used to deliver electrical currents on the electrodes placed on the patient’s head on the right temple unilaterally or bitemporally, with one electrode superior to the left eye.

->Anti-convulsant hypothesis
->Neurogenesis hypothesis

36
Q

What is the anti-convulsant hypothesis for ECT?

A

The post-ictal phase of the grand mal seizure is mediated by the pre-frontal cortex, which enhances the actions of GABA, and also increases the threshold of seizures following this therapy. ECT causes an increase in seizure threshold, delta activity and levels of other inhibitory neurotransmitters like opioids.

37
Q

What is the neurogenesis hypothesis for ECT?

A

ECT stimulates the proliferation of brain derived growth factor cells that is important for neuroplasticity which also occurs in humans with pathological epileptic seizures, however there is no clear link to drop in depression symptoms.

38
Q

Why is a unilateral ECT preferred method?

A

Minimise memory issues or cognitive impairment and there was a previous good response.

39
Q

What is the dichotomous cognitive style?

A

‘All or nothing’ thinking, where they evaluate situations as black or white.

40
Q

What is catastrophisation cognitive thinking?

A

Where the patient’s reality and their perception of a situation is disproportionate.

41
Q

What is selective abstraction cognitive thinking?

A

Patient tends to focus on the small negative that overshadows their experience rather than the whole picture.

42
Q

What is personalisation cognitive thinking?

A

Individuals will attribute the entire blame of a situation on themselves, including external factors.

43
Q

What is emotional reasoning cognitive style?

A

The individual’s personal feelings about a situation will determine the conclusions they come to rather than reason, eg “I feel anxious so it is not going to go well.”

44
Q

What is the minimisation cognitive style?

A

Disqualifying positive attributes you have or experiences and magnifying others.

45
Q

What is the over-generalisation cognitive style?

A

Making broad conclusions based on a few instances from the past.

46
Q

When is a repeat ECT considered?

A

There has been a review of the previous use of ECT
Alternative options have been considered
Risks and benefits have been discussed with patient and/or carer

47
Q

What is the NICE guidance for obtaining consent for ECT?

A

Valid and informed consent should be made with no coercison jointly with the patient, taking into account the Mental Health act especially for at risk groups such as pregnant women, elderly and children/young people.

The patient should be reminded that they have the right to withdraw consent at any point, and providers should have strict adherence to guidelines about consent. Where informed consent is not possible, ECT should only be given if it does not interfere with advance directives and a patient’s carer has been consulted.

48
Q

What impacts the efficacy of ECT treatment?

A

Electrode placement, where bilaterally has greater effectivity but a higher risk for cognitive impairment compared to unilateral ECT.

49
Q

What is the NICE guidance for monitoring of ECG?

A

Clinical outcome and cognitive function following ECT should be measured before and after at least 3-4 treatments of ECG based on:
—> Orientation and time to reorientate
—> **Measuring new learning, retrograde amnesia and subjective memory impairment at least 24 hours after treatment. **

50
Q

What are the advantages of ECT treatment?

A

Proven effectivity with severe mental illness, where other treatments don’t work.

51
Q

What are the disadvantages of ECT treatment?

A

Requires the use of multiple brief anaesthetics
Induces an acute confusional state following administration of the anaesthetic
Causes both anterograde and retrograde memory impairment

52
Q

What is seizure threshold?

A

Minimum amount of electrical energy required to induce cerebral paroxysmal neuronal discharge. There is a greater seizure threshold in older people, women and those receiving bilateral ECT treatment

53
Q

How does taking anti-depressants affect ECT?

A

Patients with severe/treatment resistant depression such as catatonia must first establish that ECT is effective, prior to beginning a course of anti-depressants. ECT as a stand alone treatment has a high risk of relapse following treatment, therefore it is important that supplemental treatment is also used, such as CBT.

54
Q

How does taking anti-psychotics improve ECT?

A

Anti-psychotics are effective when used alongside ECT as they improve the acute positive manic symptoms of psychosis, however it is not useful for the residual symptoms or negative schizophrenia

55
Q

Which medications are contraindicated with ECT?

A

Unless the medications are part of a patient’s long term history, these should be avoided:

Anticonvulsant will raise the seizure threshold
Lithium will raise the seizure threshold, prolong seizures and increase post-ictal confusion
Benzodiazepines unless they are are a repeat medication, because they reduce the antidepressant efficacy of ECT

56
Q

What are the short term adverse effects of ECT?

A

Headache and muscle ache
Confusion
Short term memory loss
Damage to teeth, tongue and lips from administration of the general anaesthetic

57
Q

What are the long term adverse effects of ECT?

A

Long term Memory impairment and cognitive function on tasks

58
Q

How does ECT affect noradrenaline transmission?

A

ACUTE: Increases the levels of plasma catecholamines, especially noradrenaline. It increases cerebral nnoradrenaline and plasma tyrosine hydroxylase activity for the formation of dopamine.

CHRONIC: Decreases density of beta-adrenoreceptors

59
Q

How does ECT affect serotonin transmission?

A

ACUTE: Increases cerebral serotonin

CHRONIC: Increases post-synaptic 5-HT2 receptors

60
Q

How does ECT affect dopamine transmission?

A

ACUTE: Increases cerebral concentration of dopamine and dopamine metabolites and responsiveness to dopamine agonists

CHRONIC: Increases D1 receptor density and potential ion of secondary messengers of D1

61
Q

How does ECT affect GABA transmission?

A

ACUTE: Increases the release of GABA and GABA-b binding, and may contribute to the hypo metabolic state following ECT administration

78
Q
A