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Pharmacology > Antidepressants > Flashcards

Antidepressants Flashcards

1
Q

What is reactive (secondary) depression?

A
  • temporary reaction to real stimuli such as grief or illness
  • tx is mostly by psychotherapy
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2
Q

What is considered major depression?

A
  • one or more major depressive episodes free of manic, mixed or hypomanic episodes
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3
Q

What is the lifetime prevalence of depression? When foes it usually onset?

A
  1. 6% in males and 20.4% in females

- onset is frequently 25-44 years of age

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4
Q

What are the emotional sx of major depression?

A
  • inability to experience pleasure
  • loss of interest in usual activities
  • pessimistic outlook
  • anxiety
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5
Q

What are the physical sx of depression?

A
  • chronic fatigue, terminal insomnia, appetite disturbances
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6
Q

What are the cognitive symptoms of depression?

A

poor concentration, slow thinking, poor short term memory

- confusion

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7
Q

What are the psychomotor sx of depression?

A
  • slowed physical movements and speech

- agitation

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8
Q

What are the common non-pharm therapies for depression?

A

psychotherapy and ECT

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9
Q

What is the amine hypothesis?

A
    • depression is related to reduces synaptic levels of NE and 5HT
  • autopsy showed reduced NE and 5HT metabolism in depressed suicide victims
  • – this predicts that the amine NT are not being synthesized sufficiently
  • most antidepressant drugs work by enhancing synaptic monoamines - do this by blocking normal neurotransmitter reuptake processes
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10
Q

What are the 2 phases of drug action in the synapse?

A

Phase 1- amine enhancement
- short term (min-hours); uptake inhibition
Phase 2- amine enhancement
- long term (weeks) effects of phase 1 enhancement - produces further enhances amine levels to reach therapeutic significance

— longer term effects cause presynaptic auto-receptor down regulation

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11
Q

Understanding phase 2..

A
  • normal scenario: presynaptic receptors feedback inhibit to stop the release of amines
  • phase 1 causes homeostatic down regulation of these receptors to maintain “normal” agonist: receptor interaction levels- you have fewer inhibitory auto receptors here
  • results in negative feedback and phase 2 amine release
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12
Q

What is the cellular feature that can be seem to correlate with improved mood?

A

presynaptic receptor down regulation directly correlates with improved mood
- down regulation occurs on a timescale that is quite common to the time that you get improvement in mood

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13
Q

What are the different classes of antidepressants?

A
  • MAO inhibitors
  • TCAs
  • SSRIs
  • SNRIs and atypicals
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14
Q

Tricyclic Antidepressants

A

examples: amitriptyline, Imipramine, clomipramine, doxepin, protriptylline, desipramine
- Mechanism: mixed NE and 5HT reuptake inhibitors
- great variation in relative NE:5HT reuptake blockade potencies
- also used in neuropathic pain(NET effect)
- ALSO blocks cholinergic, histaminergic, a1 adrenergic receptors

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15
Q

What are the adverse effects of TCAs?

A
  • antimuscarinic, cardiovascular (orthostatic hypotension, conduction defects), sedation, sympathomimetic (tremor, insomnia), neurologic (seizures), metabolic (weight gain, sexual disturbances), overdose (dangerous cardiac arrhythmias)
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16
Q

What are the drug interactions associated with TCAs?

A
  • pharmacokinetic: CYP 2D6 inhibitors, highly protein bound

- pharmacodynamic: sedatives, sympathomimetics, antimuscarinics

17
Q

What are the drug interactions associated with SSRIs?

A
  • ex: fluoxetine, paroxetine, sertraline, citalopram
  • MOA: block serotonin reuptake more effectively than NE
  • no more effective than TCAs
  • fluoxetine was used first - paroxetine and sertraline have shorter half lives- citalopram is the most SERT selective
  • also drug interaction differences
18
Q

What are the adverse effects of SSRIs?

A
  • much less cholinergic, histaminergic, adrenergic receptor blockade than TCAs- more tolerable side effect profile
  • safer than o/d
  • associate with mild, short lived GI symptoms, headache
  • sexual dysfunction, fatigue, insomnia can be problems
  • paroxetine withdrawal - dizziness, nausea, tremor, anxiety
  • platelet inhibition
19
Q

What are the drug interactions associated with SSRIs?

A

Pharmacokinetic: strong CYP 2D6 inhibitors, TCAs, antipsychotics, beta blockers interfere with metabolism.
Pharmacodynamic: low non SERT interactions

20
Q

What is the advantage of using SSRIs over TCAs?

A
  • have equal efficacy with milder side effect profile
  • much more favourable TI
  • smaller chance of having additive drug interactions
21
Q

SNRIs?

A
  • examples: venlafaxine, duloxetine, desvenlafaxine
  • MOA: inhibits both serotonin and NE reuptake, but NOT TCA
  • also weak dopamine reuptake inhibitors
  • no affinity for muscarinic, a1 adrenergic or histaminergic receptors
22
Q

What are the adverse effects of SNRIs?

A
  • much lower incidence than TCAs, similar to SSRIs

- can include nausea, sweating, dizziness, anxiety, sexual dysfunction, hypertension

23
Q

What are the drug interactions?

A
  • limited pharmacodynamic
  • protein binding varies: venlafaxine 30%, duloxetine >90%
  • CYP 2D6 substrate
24
Q

What is the advantage of SNRIs over SSRIs/TCAs?

A
  • have a milder side effect profile over SSRIs?
  • may be useful for depression with neuropathic pain
  • fewer drug interactions
  • potentially lower safety margin than SSRIs in O/D
25
Q

Mirtazapine is considered what?

A

atypical antidepressants

26
Q

What is the mechanism of action of mirtazapine?

A
  • structurally a tetracyclic compound
  • blocks a2 adrenergic receptors, thus increasing NE release
  • low affinity for muscarinic, a1 adrenergic receptors
  • potent blocker of histamine receptors
27
Q

What are the adverse effects of mirtazepine?

A
  • sedation, weight gain
  • no anticholinergic effects
  • less propensity for sexual side effects than SSRIs and TCAs
28
Q

What are the advantages of mirtazapine?

A
  • as tolerable as SSRIs
  • anxiolytic/sedative effects can be useful (antihistamine)
  • minimal cholinergic/ adrenergic drug interactions
  • weight gain is a major drawback
    • this is a good drug to use when someone is concerned about sexual dysfunction!
29
Q

What is the MOA of buproprion?

A
  • does not inhibit NE or serotonin reuptake
  • blocks DA reuptake weakly
  • mild stimulant - treat comorbid fatigue/poor concentration, ADHD
  • low affinity or muscarinic, a1 adrenergic or histaminergic receptors
30
Q

What are the adverse effects of buproprion?

A
  • much lower incidence than TCAs

- can include nausea, headache, dizziness, seizures.. no sexual dysfunction, weight gain and sedation

31
Q

What drug interactions are involved with buproprion?

A
  • meds that lower seizure threshold, L-dopa
  • CYP 2D6 inhibitor

—- good option for a drug for people experiencing sexual dysfunction and also don’t want weight gain

32
Q

What are the first line therapies for treating depression?

A

SSRIs and SNRIs

Pharmacology (23 decks)

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