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Clinical Pharmacology & Applied Therapeutics > Depression + Anxiety > Flashcards

Depression + Anxiety Flashcards

1
Q

What is the DSM 5 diagnostic criteria for major depressive episode?

A

A) more than 5 symptoms on most days for 2 weeks (that present change from precious functioning)
- depressed mood or loss of interest must e present
- weight gain/loss, insomnia/hypersomnia, psychomotor agitation/retardation, fatigue, feelings of worthlessness/guilt, decreased concentration, suicidal ideation

B) symptoms must cause significant clinical impairment in functioning

C) episode not attributable to direct physiological effects of substance or medication

D) not better explained by presence of schizophrenia, delusional disorder or any other psychotic disorder

E) no history of manic or hypomanic episode

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2
Q

Explain the mechanism of action of antidepressants.

A

Increase NT in synaptic cleft by:

  1. Blocking degradation of NT - MAOI
  2. Blocking NT reuptake - SSRI, TCA, SNRI
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3
Q

Name three examples of drugs that are in the TCA dug class.

A

Amitriptyline
Nortriptyline
Imipramine

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4
Q

Name three examples of drugs that are in the SSRI drug class.

A

Fluoxetine
Citalopram
Sertraline
Paroxetine
Escitalopram

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5
Q

Name two examples of drugs that are in the SNRI drug class.

A

Venlafaxine
Duloxetine

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6
Q

Name two examples of drugs that are in the MAOi drug class.

A

Selegiline
Phenelzine

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7
Q

Patients who are on MAO inhibitors should be warned about consuming aged foods in large quantities, why is this the case?

A

Aged foods like cheese and wine contain tyramine, which is broken down by MAO. If patient is on a MAO inhibitor, the tyramine will accumulate in the synapse, thereby increasing it effect.
Causes release of norepinephrine, resulting in a hypertension crisis.

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8
Q

What is the primary mechanism of action of TCAs?

A

Inhibition of reuptake of monoamines.
- TCAs block the reuptake of serotonin and norepinephrine into presynaptic nerve terminals by inhibiting their respective transports (SERT and NET).
- leads to an increase in the synaptic concentration, enhancing their signalling and improving mood.

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9
Q

Describe the secondary effects of TCAs on other receptors.

A
  1. Histamine H1 receptor blockade (drowsiness and weight gain)
  2. Muscarinic receptor blockade (anticholinergic sides effects - dry mouth, constipation, blurred vision, urinary retention, cognitive impairment)
  3. Alpha 1 receptor blockade (orthostatic hypotension)
  4. Sodium channel blockade (cardiotoxicity in overdose - arrhythmias)
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10
Q

List the adverse effects of TCA use.

A

Tachycardia
Arrhythmias
Urinary retention
Blurred vision
Nausea
Drowsiness
Weight gain
Dry mouth
Constipation

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11
Q

List the adverse effects of SSRI use.

A

Insomnia
Anxiety
Sexual dysfunction
Drug interaction
Nausea

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12
Q

Describe the mechanism of action of SSRIs.

A

They bind to and inhibit the SERT on the presynaptic neuron. This prevents the reuptake of serotonin from the synaptic cleft and as a result, serotonin levels in the synaptic cleft increase, allowing for prolonged activation of post synaptic serotonin receptors.

Does not interfere with other NTs. Selectivity reduced the likelihood of side effects compared to TCAs.

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13
Q

What is the risk of taking “strong” pain tablets like tramadol when on SSRIs?

A

Pain medication inhibits the reuptake of serotonin, therefore serious side effect when combined with SSRIs. Increases serotonin activity - serotonin syndrome.

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14
Q

What are the symptoms present in serotonin syndrome?

A

Mydriasis
Agitation
Diaphoresis
Tachycardia
Autonomic instability - often hypertensive
Increased bowel sounds - possibly diarrhoea
Clonus (esp in lower extremities)
Tremor (esp in lower extremities)
Hyperflexia (esp in lower extremities)

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15
Q

What is treatment of choice in major depressive disorder in pregnancy and breastfeeding women?

A

1st line - Cognitive behavioural therapy
2nd line (safe) - citalopram, escitalopram, sertraline

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16
Q

Outline the approach to poor response to 1st line antidepressants.

A

Full clinical response may take 6-8 weeks or longer.
If no response after 8 weeks at optimal dose:
- re-evaluate symptoms
- review adverse side effects
- review adherence
- switch to another class

17
Q

What are the symptoms of a manic episode?

A

Elevated/expansive mood and irritable mood

AND 3 or more of these:
- inflated self esteem/gradiosity
- increased goal directed activity/agitation
- risk taking
- decreased need for sleep
- distractible/poor concentration
- more talkative pressure speech
- flight of ideas/racing thoughts

18
Q

Outline the approach to the management of acute mania in Bipolar Mood Disorder.

A

1st line:
- lithium or valproate

Other:
- choice of antipsychotics: olanzepine, quetiapine, risperidone, haloperidol, ariprazole

19
Q

Outline the approach to the management of acute depression in Bipolar Mood Disorder.

A

Monotherapy:
- quetiapine, olanzopine, lamotrigine, lithium, valproate

2nd line options (combinations):
- olanzaoine + fluoxetine
- lithium + valproate/lamotrigine
- lithium/valproate + antidepressant

20
Q

Outline the approach to the maintenance therapies in Bipolar Mood Disorder.

A

Same medication that was a success in acute phase is typically selected for maintenance.

Mood stabilisers:
- lithium
- lamotrigine, valproate

Antipsychotics with mood stabilising effects:
- quetiapine
- olanzepine

21
Q

What measures need to be put in place when treating a patient with lithium?

A

Lithium has a narrow therapeutic index:
- requires TDM
- annual serum creatinine and TSH (nephrotoxic and thyrotoxic)

22
Q

What are the symptoms of lithium toxicity?

A

Neurotoxic - convulsions, ataxia, dysarthria, coma
Renal dysfunction with electrolyte imbalance

23
Q

What are the adverse effects of lithium use?

A

Neutrophilia, weight gain
Polydipsia + polyuria
Hypothyroidism
Renal toxicity

24
Q

Which medications have significant interactions with Lithium?

A

Thiazide diuretics
ACE inhibitors (ACEi)
NSAIDs

25
Q

What are the possible options for a patient with moderate depression, on beta blockers for stable angina, also complaining of erectile dysfunction?

A

Bupropion (atypical antidepressant)

26
Q

What are the common anxiety signs and symptoms?

A

Feeling nervous
Having a sense of impeding danger, panic or doom
Palpitations
Hyperventilation
Sweating
Tremor
Feeling weak or tired trouble concentrating or thinking about anything other than the present worry/overthinking

27
Q

What is the approach to management of anxiety disorders?

A

Non pharmacological - CBT
Pharmacological:
- acute: benzodiazepines
- chronic: SSRI/TCA

28
Q

Describe the mechanism of action of benzodiazepines.

A

Benzodiazepines act by potentiating the actions of GABA (primary inhibitory neurotransmitter in CNS)
When GABA binds to GABA-A receptor it increases the influx of chloride into the neuron, causing hyperpolarization of the cell membrane and decreased cell excitability.

Benzodiazepines bind to the site closely related to the GABA-A receptor, inducing a conformational change in the GABA receptor that enhances its affinity for the GABA neurotransmitter.

29
Q

What are the different groups of benzodiazepines? Indicate their elimination half life and an example of each.

A

Ultra short acting: < 6 hours (midazolam)
Short acting: 6-12 (oxazepam)
Intermediate acting: 12-24 hours (lorazepam)
Long acting: > 24 hours (diazepam)

30
Q

What are the indication for use with benzodiazepines?

A

Alcohol withdrawal states
Seizures
Muscle relaxant
Acute sedation
Perioperatively

31
Q

What is the antidote for benzodiazepine poisoning?

A

Flumazenil

  • short acting GABA A receptor antagonist
  • reversal of procedural sedation
32
Q

What is the antidote for benzodiazepine poisoning?

A

Flumazenil

  • short acting GABA A receptor antagonist
  • reversal of procedural sedation
33
Q

What are the adverse effects of benzodiazepines?

A

Sedation
Respiratory depression
Amnesia
Tolerance and dependence
Potentiation of sedative effects when given with other CNS depressants
Paradoxical increase in aggression

34
Q

Which group of benzodiazepines have a greater tendency to produce overt dependence and withdrawal?

A

Short acting agents

Clinical Pharmacology & Applied Therapeutics (3 decks)

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