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Year 1 SBA revision > 123 - Depression > Flashcards

123 - Depression Flashcards

1
Q

Key aspects of history taking in suspected depression

A

History of depression
Mood elevation
Previous treatments
Nature of social network

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2
Q

Core symptoms of depression

A 
Depressed mood
Anhedonia
Reduced energy
Tiredness after minimal effort
Lasted at least 2 weeks
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3
Q

How does depressed mood change in depression

A

Varies little from day to day
Diurnal variation (worse AM)
Unresponsive to circumstances

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4
Q

Other symptoms of depression

A 
Impaired concentration
Reduced self esteem
Ideas of guilt and unworthiness
Pessimistic about future
Ideas/acts of self harm/suicide
Disturbed sleep
Diminished appetite
Irritability
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5
Q

Physical symptoms of depression

A 
Anhedonia
Early morning wakening
Lifelessness or agitation
Weight loss
Loss of libido
Loss of emotional reactivity
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6
Q

What is mild depression

A

2 core symptoms + 2 others

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7
Q

What is moderate depression

A

2 core symptoms + 3-4 others

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8
Q

What is severe depression

A

2 core symptoms + >4 others. Can include psychotic symptoms

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9
Q

Psychotic symptoms associated with depression

A

Delusions of sin, guilt, poverty, imminent disaster,
Hypochondira
Auditory hallucinations - defamatory or accusatory
Olfactory hallucinations of faeces or rotting flesh
Severe retardation or stupor

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10
Q

What do 70% of patients with depression present with

A

Physical symptoms only

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11
Q

Symptoms of anxiety

A 
Foreboding
Physical symptoms
Dry mouth
Palpitations
Dizziness
Sweating
Butterflies
SOB
Choking
May develop into panic attacks
Feeling life isn't real
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12
Q

If depression present - also need to consider what?

A

Anxiety. Closely linked and rarely present separately.

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13
Q

When prescribing anti-depressants need to take into consideration

A

Overdose toxicity.

May need to increase level of support to patient

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14
Q

Epidemiology of depression
How common
High risk groups

A

4th leading cause of disability and disease worldwide. In UK - 1/10 men and 1/4 women will need treatment for depression at some point. Mean age of onset 27 but elderly, adolescents and those with chronic diseases at more risk

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15
Q

Hopelessness depression model

A

Stressor (bad event)
Attributes blame, infers consequences and inferences about self - feels cannot do anything to change it.
Hopelessness

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16
Q

Theory of stress vulnerability

A

The more vulnerable you are, the less stresses are needed to trigger depression. If remove some stresses or increase resilience then can improve threshold for depression.

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17
Q

Remission from depression classes as

A

Absence of depressive symptoms for 2 months.

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18
Q

How long does depression generally last?

A

6-8 months. If relapse - more likely to be more severe in future.

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19
Q

What is Beck’s triad

A

How you think about:
World
Future
Self

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20
Q

How efficient is CBT at treating depression

A

Can be more effective than antidepressants over long-term

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21
Q

How does CBT work

A

Underlying model - events trigger thoughts
Thoughts influence feelings, responses and actions.
CBT acts to teach the patient how to intervene to think things through and change their thoughts

22
Q

When is ECT used

A

To treat severe depressive illness where suicide is a high risk. Usually course of 8-10 treatments with response after 2-3

23
Q

What non-drug therapies can be useful for depression?

A 
CBT - increasing levels - individual guided self help, computerised CBT, structured group therapy.
Interpersonal therapy
Behavioural therapy
Relationship therapy
ECT
24
Q

Commonly prescribed antidepressants.

A

SSRIs as less side effects and equally effective as others. Antidepressants are non-addictive.

25
Q

Side effects of antipsychotics

A

Weight gain, reduced glucose tolerance, affect lipid levels.

26
Q

When giving lithium to augment antidepressants need to

A

Monitor renal and thyroid function. Consider ECG monitoring as affects blood viscosity.

27
Q

Treatment for mild depression

A

On presentation:
Assess risk
Lifestyle interventions
Watchful waiting - review in 2 weeks. Drugs have poor risk:benefit on presentation

28
Q

SSRIs - Examples, when to give and side effects

A

Citalopram, Sertraline, Fluoxetine.

Give for 6 months after resolution of depression for first treatment or 2 years if recurrence.

Mainly GI issues but also hyponatraemia

29
Q

What is hyponatraemia

A

Drowsiness, confusion, convulsions

30
Q

Tricyclic antidepressants.

Examples

A

Amitryptilline, Butryptilline

31
Q

Tricyclic antidepressants.

How do they work

A

Inhibit serotonin and noradrenaline reuptake

32
Q

Tricyclic antidepressants.

Side Effects

A

Cardiotoxic (especially in overdose).

Dry mouth, blurred vision, sedation, poor concentration

33
Q

Tricyclic antidepressants.

Contraindications

A

Epilepsy and heart disease

34
Q

Use of monoamine-oxidase inhibitors

A

e.g. Phenylzine
Inhibit breakdown of MAO neurotransmitters (e.g. serotonin)
Use only in severe depression

35
Q

How does synaptic transmission work

A

Action potential - Na+ floods into neutron.
Ca2+ gates open so Ca2+ floods in and binds to vesicle.
Vesicles mature and release neurotransmitters into synapse.
NTs diffuse across synapse and bind post synaptic receptors.
Na+ gates opens - floods in - starts new action potential

36
Q

Key drug targets for neurotransmitters

A 
Neurotransmitter synthesis/release
Post synaptic reception
Presynaptic reception
Reuptake
Degredation
37
Q

What are ionotrophic receptors

A

Ion channels. Ligand binding either opens or prevents opening of channel

38
Q

What are metabotropic receptors

A

Receptors where ligand binding affects intracellular signalling pathways

39
Q

Glutamate

A

Excitatory neurotransmitter. Main excitatory NT of CNS

Hyper stimulation can cause seizures, inhibition can cause sedation.

40
Q

Glycine

A

Inhibitory NT. Inhibited by strychnine

41
Q

GABA

A

General inhibitory neurotransmitter. Hyperstimulation causes sedation while inhibition causes hyper excitability and seizures

42
Q

Serotonin

A

Located in gut and brainstem (Raphae nuclei). Involved in depression, appetite, nausea and sleep.

43
Q

Where is dopamine found?

A

Located in midbrain.
Found in substance nigra - involved in movement (destroyed in Parkinsons) and Ventral segmental area - involved in motivation, reward and novelty.

44
Q

Disorders of dopamine

A

Schizophrenia
Parkinsons
Tourettes

45
Q

Noradrenaline

A

Found in brainstem, acts on sympathetic system.
Involved in attention and arousal.
Targeted by adrenaline, ritalin, TCAs.

46
Q

Opioids

A

Located in hypothalamus. Involved in analgesia and reward.

Neuromodulators - affect release and effect of other neurotransmitters.

47
Q

Acetylcholine

A

NT located in basal forebrain (involved in memory and cognition) and the brainstem (involved in arousal and sleep). Binds to nicotinic (ionotropic, excitatory) and muscarinic (metabotropic) receptors.

48
Q

Loss of acetylcholine is involved in

A

Alzheimers disease

49
Q

What is dysthmia

A

Has up to 1 core symptoms of depression and 3 total symptoms of depression

50
Q

What is the first line treatment for depression after MIs

A

Setraline.

51
Q

Treatment for depression and anxiety

A

Amitriptyline is best choice.

52
Q

Side effects of TCAs

A

Can’t see
Can’t pee
Can’t shit
Can’t spit

Year 1 SBA revision (37 decks)

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