Anxiety and Depression Flashcards

1
Q

What is the NHS definition of anxiety? When is a diagnosis made?

A
  • “A feeling of unease; worry or fear, that can be mild or severe (chronic or acute”
  • Diagnosis of anxiety made if:
    > Anxiety occurs all the time.
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2
Q

What are the different types of anxiety?

A
  • Panic disorder
  • Obsessive compulsive disorder (OCD)
  • Post-traumatic stress disorder (PTSD)
  • Phobias; specific or social
  • Generalised Anxiety Disorder (GAD)
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3
Q

What is Panic disorder? What symptoms is is characterised as?

A
  • Intense and abrupt feeling of fear or discomfort

Symptoms:

1) Sudden temperature change
2) Chest pain/interruption to normal blood circulation; palpitations/tingling sensation
3) Nausea + dizziness
4) Overwhelming feelings

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4
Q

What is OCD? What are the characteristics of each part?

A
  • A combination of obsessive thoughts and compulsive activity

Obsession:
- Unwanted/unpleasant thoughts that cause anxiety e.g. being burgled

Compulsive:
- Repetitive behaviour a person undertakes to relieve the unpleasant feeling

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5
Q

What is PTSD? What are its symptoms? Onset?

A
  • Post-traumatic stress disorder; after experiencing a trauma e.g. serious accident, natural disaster, criminal assault, returning from war etc.
  • Can develop immediately or years later

Symptoms:

  • Insomnia
  • Nightmares
  • Flashbacks
  • Isolation
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6
Q

What is Specific phobia?

A

Intense fear of something that in reality is of little or no actual danger.

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7
Q

What is Social phobia?

A
  • Fear of social/performance situations, resulting from thoughts of negative judgement, embarrassment or humiliation
  • Person ‘tolerates’ with dread, or avoids the situation
  • Common with performers/actors etc
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8
Q

What is GAD?

A
> Generalised anxiety disorder
Excessive, uncontrollable worry about everyday things such as:
- Job
- Finances
- Health
- Family
- Chores
- Car repairs
- Late for appointments
  • Intensity, duration and frequency of worry is disproportionate to the issue
  • May occur w/other anxiety disorders, depressive disorders or substance abuse
  • May also present w/physical symptoms e.g. difficulty sleeping, palpitations & tingling in hands
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9
Q

What are some potential causes of anxiety?

A
  • Genetics? (no gene isolated, but familial history can predispose risk)
  • Neurochemical/neurohormonal
  • Environmental factors
  • Substance abuse
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10
Q

What symptoms that can present as anxiety could be due to organic disease? Give examples.

A

SOB:
- Asthma

Palpitations, tachycardia:
- Heart disease

Palpitations, sweating, tremor:

  • Hyperthyroidism
  • Phaeochromocytoma (adrenal tumour)

Dizziness:

  • Vestibular dysfunction (inner ear problem)
  • Hypoglycaemia

Sweating:
- Menopause

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11
Q

What are the considerations that need to be made during assessment for anxiety?

A
  • Mental health history
  • Environmental stressors
  • Medical and drug history
  • Degree of distress and functional impairment (e.g. insomnia)
  • Risk of suicide; doctor should outright ASK > refer
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12
Q

What is the aim of anxiety (e.g. GAD) management/treatment?

A
  • Relieve symptoms
  • Improve QoL
  • Prevent relapse
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13
Q

What non-pharmacological treatments are there for anxiety (GAD)?

A
  • CBT (NICE recommendation, evidence-based, whilst following are not:)
  • Mediation and relaxation (complements pharmacological therapy)
  • Mindfulness “stop and smell the roses”; appreciating what’s around you
  • Exercise (complements pharmacological therapy)
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14
Q

How are autonomic symptoms (palpitations/tingling) managed in anxiety (GAD)?

A

β-adrenoceptor antagonists (propranolol)

  • Reduces autonomic effect
  • Used on PRN basis
  • DO NOT withdraw abruptly; prevent rebound effects
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15
Q

What are the pharmacological options of treating anxiety (GAD)?

A

Selective serotonin reuptake inhibitor (SSRI):

  • Serotonin (off-label treatment in GAD)
  • Licensed; escitalopram and paroxetine
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16
Q

What are the options if there is no improvement of Patient A’s anxiety after 2 months treatment w/SSRI?

A

1) Increase dose if max. dose not yet achieved
2) Swap to another SSRI
3) Consider a serotonin-NA reuptake inhibitor (venlafaxine, duloxetine)
4) Consider anticonvulsant agent, pregabalin (last line due to large S/E profile; blocks Glu transmission)

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17
Q

What are the therapeutic properties of Benzodiazepines (BDZ)?

A
  • Anxiolytic (appropriate for GAD)
  • Sedative ‘minor tranquilisers’
  • Muscle relaxant; central effects (e.g. used when intricate surgery required)
  • Hypnotic (induces sleep)
  • Anticonvulsant
  • Amnesic
  • Reduce aggression
  • Treats alcohol withdrawal
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18
Q

What are the pharmacokinetic properties of BDZ?

A
  • No enzyme induction; can monitor pharmacokinetic profile
  • Metabolism through oxidation and conjugation (after getting to brain, like lorazepam)
  • Oxidation reduced by agel effects may be prolonged in older patients (risk of toxicity if drug not metabolised; give lorazepam; metabolism through conjugation)
  • Active metabolites
  • Relatively safe in overdose
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19
Q

What are the disadvantages with BDZ use?

A
  • Some tolerance (higher dose may be required)

- Dependence and withdrawal symptoms (2-3 weeks; use short-term)

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20
Q

What BDZs are suitable for GAD treatment? Are they first line?

A
Drugs with a short (1-10 hours) half-life:
Hypnotics:
- Temazepam
- Nitrazepam
- Zolpidem
Drugs with longer half-life (1-4 days):
Anti-anxiety:
- Diazepam
- Chlordiazepoxide (alcohol withdrawal)
- Lorazepam

> > > SSRIs first line; BDZs best avoided, but use restricted to 2-4 weeks.

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21
Q

What is the GABAa receptor complex? Why is it complex?

A
  • Receptor complex for the inhibitory NT, GABA
  • Pentameric structure w/Cl- pore in middle
  • 5-sub-unts, each with a different binding site:
    > Barbiturate (+ alcohol?)
    > Picrotoxin (antagonist of GABA action)
    > GABA site
    > Steroid
    > Benzodiazepines (and anaesthetics)
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22
Q

How do BDZs work?

A
  • Occupy site on GABAa complex
  • Increases affinity for GABA (conformational change of GABAa receptor complex)
  • Thus greater flow of Cl- ions into neurone
  • HYPERPOLARIZATION occurs; hence inhibitory action (and anxiolytic nature)
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23
Q

What are the risk factors for suicide?

A
  • Own history of depression, suicide attempt
  • Illness e.g. chronic pain syndrome (most common cause)
  • Schizophrenia and dementia etc.
  • Family history of depression
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24
Q

What is DSM-5, and what are the markers of depression?

A
  • Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition

Core symptoms of depression (1+2):

1) Depressed mood; “Does not feel able to get back on track”
2) Loss of interest or pleasure “not attending rambling or yoga”

3) Fatigue; “Weary and lacking in energy during the day”
4) Feelings of worthlessness, guilt or inappropriate grief “husband’s death”
5) Recurrent thoughts of death or suicide/actual suicide attempts
6) Reduced ability to think or concentrate
7 Psychomotor agitation or retardation
8) Altered sleep “problems dropping off to sleep, early morning waking”
9) Significant weight change; “lost a lot of weight”

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25
Q

What are the categories of depression?

A
  • Subthreshold
  • Mild
  • Moderate
  • Severe
26
Q

What is classified as subthreshold depression?

A
  • At least 2 but less than 5 symptoms (as laid out by DSM-5)

- One ‘core’ symptom

27
Q

What is classified as mild depression?

A
  • Few but in excess of 5 symptoms

- Minor functional impairment

28
Q

What is classified as moderate depression?

A
  • Some marke symptoms

- Presence of functional impairment

29
Q

What is classified as severe depression?

A
  • Multiple symptoms

- Markedly interfere w/functioning (e.g. not sleeping/doing anything)

30
Q

How much do genes or the environment contribute to severe and mild depression respectively?

A
  • Severe; more influence from genes (familial component), minor environmental influence
  • Mild; more influence from environment (e.g. death of a partner) than genes
31
Q

What is bipolar disorder, when does it first present and what populations are more prone?

A
  • Cycle between depressed mood and mania
  • First episode observed before age 30, with a peak incidence between 15-19 years of age (early-onset)
  • Increased incidence in ethnic minorities (in the UK)
32
Q

Describe what the ‘depressed mood’ phase of bipolar disorder entails.

A

Period of at least two weeks with core symptoms accompanied by at least 4 other symptoms (DSM-5)

33
Q

Describe what the ‘mania’ phase of bipolar disorder entails.

A
  • Elevated mood
  • Increased energy
  • Incomprehensible speech
  • Racing thoughts
  • Poor concentration
    “Hyperexcitability”
34
Q

What is the process involved in diagnosing bipolar disorder?

A
  • Eliminate misdiagnosis; differential diagnosis

- Confirmed by a specialist mental health professional (as bipolar treatment is complicated)

35
Q

How is the acute phase (mania) of bipolar disorder treated?

A

Antipsychotics:

  • Haloperidol
  • Olanzapine
  • Quetiapine
  • Risperidone

> If ineffective, swap to another antipsychotic from above

> > If ineffective, add lithium (not favoured due to narrow therapeutic window, but used prophylactically for 60+ years) or sodium valproate (anti-convulsant)

36
Q

What is involved in maintenance therapy of bipolar mania?

A
  • Continue treatment as per acute phase
  • Long term treatment; use lithium or sodium valproate
  • Consider psychological intervention (CBT)
37
Q

What are the NICE recommendations for treating the depression phase in bipolar disorder?

A

Different treatment tree in bipolar:
> Quetiapine alone (anti-psychotic w/efficacy in bipolar)
» SSRI (Fluoxetine) combined w/olanzapine
»> Olanzapine alone
»» Lamotrigine alone (anti-epileptic)

38
Q

Which part of the brain is markedly affected in depression? How so?

A
  • The Limbic system ‘emotional brain’
  • Reduction in size of the limbic system in patients suffering from severe depression (imaging studies)

The Limbic system consists of:
> Thalamus
> Hippocampus
> Amygdala

39
Q

What are the different NTs involved in depression?

A
  • 5-HT
  • NA
  • DA
40
Q

What is 5-HT responsible for, and how is it affected in depression?

A
  • Anxiety, obsessions, compulsions

- Depression due to decreased levels of 5-HT/serotonin

41
Q

What is NA responsible for, and how is this affected in depression?

A
  • Alertness, anxiety, interest in life

- Role in rewards and stress (thus decreased levels of NA = depression)

42
Q

What is DA responsible for, and how is it affected in depression?

A
  • Attention, motivation, reward

- Decreased levels of tyrosine (precursor to DA) results in decreased DA = depression

43
Q

What are some animal models used for depression, and what do they entail?

A

Forced swimming test:
- Animal is submerged in narrow cylinder, rat tries to stay afloat (mobile), eventually ‘gives-up’ (non-mobile)
»> If given antidepressant, rat tries to become mobile again

Tail suspension test:
- Similar to above (mobile vs. immobile)

  • Learned helplessness
  • Stress models (e.g. food deprivation)
  • Olfactory bulbectomy; results in loss of interest, but drug restores interest.
44
Q

What are the aims of managing/treating severe depression? (NICE)

A
  • Manage suicide risk
  • Improve QoL
  • Prevent relapse
45
Q

What non-pharmacological options are there for treating severe depression? (NICE)

A
  • High intensity CBT

- Good sleep hygiene

46
Q

What is considered when deciding on pharmacological therapy for severe depression? (NICE)

A
  • Choice of drug based on Mrs D’s preference
  • Adverse effect profile
  • Toxicity in overdose
  • Interaction w/other treatments
47
Q

What is first-line pharmacological therapy for treating severe depression? Why are they preferred? Give examples.

A

Generic SSRIs:

  • Citalopram, Fluoxetine, Sertraline, Paroxetine
  • Favourable S/E profile; less sedating, fever cardiotoxic effects
  • Less toxic in overdose
  • Complements CBT
48
Q

How should a patient be counselled re. medication for severe depression?

A
  • Symptoms worsen before improving (compliance; “bear with them”)
  • Takes 2-4 weeks for symptoms to improve
  • Vigilant on suicidal ideas, especially when commencing or changing medication
    »> Review every 1-2 weeks initially, then every 4
  • Take medication for a minimum of 6 months after recover, then titrate down(prevent relapse and minimise side effects)
49
Q

What are the side effects associated w/SSRIs?

A
  • Nausea & vomiting (common)
  • Diarrhoea (and other GI disturbances)
  • Dizziness
50
Q

How is depression treated in U18s?

A
  • Antidepressants avoided; but Fluoxetine is recommended if needed
  • Lifestyle advice, including positive coping strategies
    »> Evidence is limited
51
Q

How do SSRIs work?

A
  • Drug binds to 5-HT reuptake transporter on presynaptic membrane
  • Thus 5-HT not taken back up from cleft; good level in cleft, 5-HT readily binds to receptors on postsynaptic membrane
    = Cellular response
52
Q

Why do SSRIs take 2-4 weeks to work?

A
  • As some 5-HT binds to 5-HT1 autoreceptor in the pre-synaptic membrane after SSRI binding (to 5-HT reuptake transporter)
  • Results in no new 5-HT release from pre-synaptic membrane; there is no exocytosis whilst bound to 5-HT1 autoreceptor
  • Meanwhile, MAO and COMT continue metabolising 5-HT to metabolites; 5-HT levels are acutely depleted in clef (hence symptoms worsen before improving)
    »> BUT, 2-4 weeks later, 5-HT1 autoreceptor is DOWNREGULATED (desensitised), thus new 5-HT1 can be exocytosed.
53
Q

What other pharmacological therapies are availible for depression other than first-line SSRIs?

A
  • SNRA; Serotonin-noradrenaline reuptake inhibitor
  • TCA; Tricyclic antidepressants
  • MAOI; Monoamine oxidase inhibitor
  • NaSSA; Noradrenergic and Specific Serotonergic Antidepressant
  • NARI; Noradrenaline Reuptake Inhibitor

> > > Antidepressants all similarly effective; patient-dependent decision.

54
Q

What are SNRIs? Give examples.

A

Serotonin-noradrenaline reuptake inhibitor (SNRI)
> E.g. Venlafaxine, duloxetine
> Similar to SSRIs

55
Q

What are TCAs, and where is their place in antidepressant therapy? Give examples.

A

Tricyclic Antidepressants (TCAs)
E.g. Amitriptyline, imipramine (old school)
- Inhibit 5-HT and NA reuptake
- Sedative properties; H1 receptor antagonism (useful for insomnia)
- Anticholinergic side effects; dry mouth, blurred vision etc. (antimuscarinic)
- Cardiovascular and epileptogenic effects; fatal in overdose
- Lofepramine associated w/lowest risk in overdose
»> S/E profile not as favourable.

56
Q

What are MAOIs? What is the ‘cheese reaction’? Give examples.

A

Monoamine oxidase inhibitors (MAOIs)
E.g. phenelzine, tranylcypromine (not used any more)
- Cheese reaction; tyramine (found in cheese, marmite, soya) competes w/NA for reuptake, leading to hypertensive crisis
»> Loads of NA left in cleft; binds to random alpha-adrenoceptors = massive hypertension

57
Q

What are NaSSAs, and where is their place in treating depression?

A

Noradrenergic and Specific Serotonergic Antidepressant
E.g. mirtazapine
- α2 auto-heteroreceptor antagonism (normally inhibits NA release); thus permitting 5-HT1 and NA release.
»> Second line after SSRIs, of clinical benefit.

58
Q

What are NARIs? Give an example.

A

Noradrenaline Reuptake Inhibitor

E.g. Reboxetine (more NA in cleft)

59
Q

What is St. John’s Wort, and why should it be avoided?

A
  • Herbal derived from Hypericum perforatum
  • Insufficient evidence on its benefit in promoting remission; only slightly more efficacious than placebo
  • AVOID in depression; lack of understanding WRT dose, drug interaction and potency
    »> Some SSRI-esque activity, increasing 5-HT levels; overdose w/drug therapy at same time?
60
Q

What is the approach to treating insomnia (w/depression)?

A

Don’ts:

  • Daytime naps
  • Caffeine
  • Heavy meal at night
  • Gadgets before sleep (avoid for hour prior to sleep)
  • Alcohol

Do:

  • Sleep mask
  • Exercise
61
Q

What approaches can complement sleep hygiene?

A
  • CBT
  • Sleeping tablets (e.g. Nytol)
  • Benzodiazepines:
    > Hypnotics (temazepam, nitrazepam; short half-life) - restrict use to 2-4 weeks. In some cases, taken 2/3 nights per week, rather than daily.
  • Z-meds; zolpidem, zopiclone, zaleplon (same as BDZs)
  • TCAs; H1-receptors, have sedative element
  • Melatonin (Circadin); licensed for short-term use in adults > 55 years