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Spring 2 > Depression, Anxiety + ADHD > Flashcards

Depression, Anxiety + ADHD Flashcards

1
Q

Define Depression

A

Definition of clinical depression relies upon an understanding of what a normal response to a given situation should (culturally and sociologically) be
Depression and mania are affective disorders

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2
Q

What is affective disorder?

A

an objective description of a person’s emotional behaviour

Thus, affective disorders include illnesses with abnormally high or low mood , i.e. mania and depression.

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3
Q

How do we classify depression? (5)

A

Severity
Presence or absence of physical (somatic/biological) features.
Presence or absence of psychotic features.
Course (duration and recurrence).
Presence or absence of intervening manic phases.

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4
Q

What % of people suffer from depression? % of those who will develop chronic depression?

A

20-30% of people will experience a depressive episode at some point in their life.
Of these, ~20% will develop chronic depressive illness

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5
Q

What % of population have major depression?

A

~5% of the population

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6
Q

Which gender is more likely to suffer from depression?

A

Female

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7
Q

What are the aetiological factors of depression? (3)

A
  1. Biochemical:
    Reserpine (anti-hypertensive) is a non-specific central amine depleter that causes depression
  2. Psychiatric:
    Thought to arise from unconscious mental conflicts

But, no objective evidence to support this

  1. Genes and environment:
    Family history is common in depression

Unclear whether this has a genetic and/or environmental components

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8
Q

What is the biogenic amine theory/monoamine hypothesis?

A

Low level of monoamine function in brain = depressive symptoms

e.g serotonin, dopamine, noradrenaline

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9
Q

What symptoms are generally expressed in MILD/MODERATE depression?

A 
Labile mood
Initial insomnia
Ideas or acts of self-harm
Reduced drive
Withdrawal
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10
Q

What symptoms are generally expressed in SEVERE depression?

A

Agitation
Fixed Mood variation
Weight loss
Early waking

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11
Q

What symptoms are generally expressed in VERY SEVERE depression?

A 
Guilty feelings
Delusions of inadequacy 
Severe retardation
Suicidal ideas
Hallucinations
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12
Q

How is a diagnosis of depression made? (4)

A 
Patient must exhibit low mood and at least four of the following:
pessimism
negative thoughts;
weight change;
sleep disorder;
psychomotor agitation or retardation;
fatigue;
feelings of inadequacy or guilt;
difficulty in concentrating;
suicidal thoughts or actions

For at least 2 weeks

Not consistent with previous behaviour/personality

Not secondary to other treatment

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13
Q

Which scales are used to formalise the diagnosis of depression?

A

Hamilton Depression Rating Scale

Beck Depression Inventory

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14
Q

What are the 5 treatment aims of depression? In order of priority

A
  1. Prevent suicide
    consider custody and compulsory treatment if suicide is a risk
    Individual can be detained under the Mental Health Act, 1983 for up to 28 days
  2. Identify possible primary causes, such as chronic or iatrogenic illness.
  3. Provide symptomatic therapy to relieve the patient’s misery.
  4. Investigate any adverse social, domestic or financial circumstances and provide support where possible.
  5. Initiate long-term therapy to prevent relapse or recurrence.
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15
Q

Name the 3 principal treatment types of depression?

A
  1. Physical (ECT, pharmacological etc.)
  2. Social
  3. Psychological
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16
Q

What criteria is used for determining the most appropriate treatment for depression?

A 
Urgency
Efficacy
Prior history
Presence of psychosis
Contraindications/ADRs
Cost
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17
Q

Describe the psychological treatments for depression?

A

Used for MILD DEPRESSION

Therapy types:
Group
Marital
Family
Cognitive behavioural therapy (CBT) can be very successful
Unhelpful or negative ways of thinking can be countered by encouraging the patient to think constructively about his or her illness and plan strategies to overcome specific symptoms.
Psychoanalysis can be useful in neurotic depression.
Psychosocial treatment involves improving a patient’s social situation.

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18
Q

What is ECT? What does NICE say about it?

A 
Electroconvulsive Therapy (ECT)
NICE guidance on ECT: “to be used short term in severe depression where other treatments have failed, especially where suicide is a serious risk”.
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19
Q

What are the 4 categories of pharmacological treatment for depression?

A
  1. Tricyclic antidepressants (TCAs)
  2. Second generation cyclics (can be considered with TCAs)
  3. Selective serotonin reuptake inhibitors (SSRIs)
  4. Monoamine oxidase inhibitors (MAOIs)
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20
Q

What distinguishing features are there between the drugs used for depression?

A
  1. Antimuscarinic, anti-adrenergic and antihistaminic activity (conferring adverse effects).
  2. Sedative action (not linked to any single transmitter).
  3. Cardiotoxic and/or convulsant action in overdose.
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21
Q

Why are MAOIs not used as frequently anymore? What is used instead?

A

poor side-effect profile and risk of life threatening side-effects with some foods

SSRIs and TCAs most commonly used

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22
Q

What are the concerns with the use of St Johns Wort?

A

OTC but unlicensed. Unknown mechanism

Induces drug metabolising enzymes, affecting levels of ciclosporin, warfarin, digoxin, oral contraceptives etc

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23
Q

What is the treatment strategy for depression?

A 
1. Select suitable drug 
2 weeks - escalation of dose (Dose escalation phase not necessary with SSRIs)
4-6 weeks - onset of action
1-3 months - Remission
4-6 months - Continuation 
2-3 years Prophylaxis
4 weeks - Withdrawal
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24
Q

How would you treat resistant depression?

A

Switch to agent with different action

Combination therapy:

  1. Steroid augmentation
  2. SSRI+ Tricyclic / SSRI +Pinadolol / SSRI + Buspirone
  3. Cyclic + MAOI / High dose cyclic
  4. Lithium + Cyclic / Lithium + SSRI / Lithium + Cyclic + Tryptophan
  5. Levothyroxine augmentation
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25
What is the mechanism of action of Selective serotonin inhibitors?
Molecular target is the transporter 5HTT (SERT). When serotonin is released from a nerve terminal its concentration rises in the synaptic cleft, then rapidly falls as it is removed by being drawn back into nerve terminal. SSRIs produce a rapid block of this uptake.
26
Name 5 SSRIs
``` Citalopram Escitalopram Fluoxetine Paroxetine Sertraline ```
27
Is there any difference in the SSRIs?
No, all have similar efficacy and long halve lives. Fluoxetine has been favoured in children as showing efficacy but like many other SSRIs may have potential to increase self-harm and suicidal thoughts in young people, so used with caution.
28
What are some side effects of SSRIs?
Dystonia or Parkinsonism (could be treated using antichlolinergics) Nausea / Diarrhoea Insomnia - usually at the beginning Constipation, dry mouth, urinary retention Sexual dysfunction
29
Why should SSRIs and MAOI not be taken together?
Risk of fatal Central Serotonin Syndrome. Considering the long half lives of both drugs, necessary to have a long drug-free period when switching between these two classes.
30
Give examples of TCAs? Tricyclic antidepressants
``` Amitryptyline Clomipramine Dosulepin Lofepramine Imipramine ```
31
What is the mechanism of action of TCAs?
Non-specific biogenic amine uptake inhibitors. They inhibit the uptake of noradrenaline and serotonin by binding to the transporter proteis in the pre-synaptic and glial sites.
32
What are the side effects of TCAs?
Anticholinergic effects: blurred vision, dry mouth, constipation, tachycardia Wear off after a few weeks. Important to titrate dose up. Toxicity on overdose associated with cardiac conduction abnormalities
33
Are there any differences between TCAs?
Sedating effects More sedating = clomipramine being beneficial for agitated patients Less sedating = Lofepramine for those more withdrawn patients
34
Define Mania and Bipolar disorder
Severe recurrent psychotic affective disorder that is the: Abnormally elevated mood, unwarranted optimism, exuberance, over-confidence, inflated self-esteem, hyperactivity, excessive libido and little sleep. Increased drive and extrovert behaviour but often socially tactless. Patients enjoy their episodes of mania which makes compliance with problematic. Attack usually lasts no more than a few days
35
How is Mania classified ?
Type I M-D disorder = more severe mania | Type II M-D disorder = more depressed phases, mania less severe
36
What are the aims of treatment of bipolar disorder?
1. Control manic and depressive attacks | 2. Minimise recurrence and stabilise mood.
37
What drugs are used to control maniac attacks?
Use of sedative anti-psychotics | Olanzapine, Risperidone and Quetiapine
38
What is lithium used for?
Prophylactic treatment of choice in bipolar disorder Needs to be taken for life No clear mechanism of action
39
Why does Lithium have to be used with caution? What should be monitored?
Very narrow therapeutic window Blood monitoring – aim for 0.5-1 mM, toxic above 1.5 mM Also monitor renal and thyroid function Takes 1-3 weeks to have effect Many side effects – reduced by lowering dose Drug interactions may affect blood levels (NSAID, diuretics)
40
What are the alternatives to Lithium?
``` In patients unresponsive to lithium: Antiepileptic drugs Carbamazepine Valproate topiramate ``` Typically Na+ or Ca2+ channel blockers that decrease AP firing
41
What is anxiety?
Minor affective disorder that manifests as a reaction to stress and adjustment “a prolonged or exaggerated response to a real or imagined threat, which interferes with normal life and cannot be attributed to any known neurological or organic dysfunction.”
42
When does anxiety require medical attention?
A threat is real but the individual’s response is disproportionate (compared to most other people) The threat is imagined
43
What are the two views of causes of anxiety?
Psychiatrists: conflict between primitive urges and socialised/civilised behaviours Biologists: biochemical dysfunction (e.g. monoamine neurotransmitters)
44
What are the two groups of symptoms/clinical features exhibited by neurotic syndromes and give examples?
Psychological – awareness of threat, unpleasant anticipation, mental tension Somatic – cardiovascular, muscle tension, GI, Respiratory breathing, sweating
45
What are the two diagnostic manuals used internationally for anxiety?
WHO International Classification of Diseases (ICD-10) US Diagnostic and Statistical Manual of Mental Disorders 4th Edition (DSM-IV)
46
What are the treatment aims of anxiety? (5)
1. Discover cause and address/remove it Cause may not always be self-evident! 2. Assess the severity of the anxiety response 3. Relieve distress ASAP 4. Institute long-term measures to avoid same/related recurrence 5. Institute long-term measures in cases of chronic anxiety
47
What are the psychological treatments available for anxiety?
Commonly used and effective approaches include: Counselling Cognitive behavioural therapy Exposure therapy Relies on habituation and cognitive dissonance Relaxation training Bibliotherapy
48
Drug treatment of anxiety?
Use of benzodiazepines e.g diazepam, lorazepam very useful for short term
49
What are some side effects of benzodiazepines?
Sedative and hypnotic Reduce muscle tone and coordination Anterograde amnesia (loss of the ability to create new memories after the event that caused the amnesia)
50
What is the mechanism of action of benzodiazepines?
Positive allosteric modulators of GABA binding to GABAA receptor = reducing neuronal excitability
51
What are the advantages of bezodiazepines?
1. Rapid onset 2. Powerful anti-anxiety action 3. Low toxicity and side effect profile
52
What are the disadvantages of bezodiazepines?
1. Drowsiness when reduction of anxiety is required | 2. development of tolerance and dependence of a number of weeks
53
When can anti-depressants be used for anxiety?
Use of SSRIs and TCAs in chronic anxiety
54
What is the treatment strategy for anxiety?
Psychotherapy (+/- benzodiazepine/hypnotic) then long term antidepressant use.
55
Define Attention deficit hyperactivity disorder
persistent pattern of inattention or hyperactivity—impulsivity that is more frequently displayed and more severe than is typically observed in individuals at a comparable level of development”
56
ADHD facts?
Starts in early childhood (<7 years old) Prevalence: 2-10% of children Higher incidence in boys than girls No objective diagnostic process
57
Symptoms of ADHD?
``` Hyperactivity Inattention Impulsiveness Accidents Learning difficulties owing to poor attention Anti-social behaviour ```
58
What are the factors that affect ADHD?
Neurodevelopmental impairment: Typical developmental lag of 3-5 years MRI suggests that brain areas used in problem solving, planning, empathy and impulse control are affected Genetic factors Like hyperactivity, 75% of cases have a genetic factor Genetic dysfunction in ADHD: dopamine transporter, D4 receptor, dopamine beta-hydroxylase, MAOA, catecholamine-methyl transferase, SLC6A4, 5-HT2A, 5HT1B, DAT1 gene, DRD4 gene. Environmental/Social factors E.g. Lead exposure, smoking/alcohol in pregnancy
59
What treatments are there for ADHD?
Behavioural treatments Psychoeducational input, cognitive behavioral therapy (CBT), interpersonal psychotherapy (IPT), family therapy, school-based interventions, social skills training and parent management training ``` Stimulant drugs ADHD children require more stimulation to maintain attention. Methyphenidate (Ritalin) Dexamfetamine (Dexedrine) Atomoxetine (Strattera) ```
60
What are the controversies around ADHD?
Is it a legitimate disorder or a manifestation of the way in which children are brought up is/has changed? Dietary interventions (additives etc.); mostly disregarded now 8% of professional baseball players in the US have ADHD It is requires a clinical diagnosis for which there are no objective tests Diagnostic criteria frequently change There is no curative treatment Therapy often includes stimulant drugs with abuse potential Rates of diagnosis and of treatment substantially differ across countries

Spring 2 (23 decks)

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