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Sketchy Pharmacology Notecards > Antidepressants & Anxiolytics > Flashcards

Antidepressants & Anxiolytics Flashcards

1
Q

What is the first line pharmacological therapy for depression?

A

SSRIs and SNRIs

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2
Q

MOA of SSRIs and SNRIs

A

Both work to increase dopamine transmission in the CNS

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3
Q

What are the other uses of SSRIs and SNRIs

A

SSRIs and SNRIs are first line therapy for:Generalized Anxiety DisorderPanic DisorderPTSDSSRIs management of OCD, depression, bulimia and social anxiety disorder

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4
Q

What is bulimia?Is it related to anorexia?

A

Bing eating and then purging out food either by vomiting or diarrheaNot related to anorexia

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5
Q

Explain the treatment of generalized anxiety disorder. What drugs are used for this?

A

Benzodiazepines provide much more rapid relief of anxiety, but SSRIs and SNRIs are just as effective for long-term treatment and do not carry the same risk of physical dependence & addiction that benzodiazepines do

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6
Q

What is a disadvantage of using SSRIs or SNRIs for treatment of anxiety disorder

A

Don’t provide acute relief, have to wait at least 1 to 2 months to determine if they are effective or not

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7
Q

What do we use for pain management? SSRIs or SNRIs?What kind of pain can be managed with this agent?

A

SNRIs are used for neuropathic pain disorder (such as back pain etc)

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8
Q

Name SNRIs used for pain management

A

Venlafaxine and duloxetine

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9
Q

What specific pain management can be achieved with SNRIs?

A

Both can be used for painful sensation associated with diabetic neuropathy, duloxetine specifically is used for pain associated with fibromyalgia

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10
Q

Name SSRIs

A

“Fly out” Fluoxitine, “Parrot Air” Paroxetine, “Desert Airline” Sertraline, and “The City” Citalopram

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11
Q

Name SNRIs

A

“Fax Machine” Venlafaxine, Duloxetine “Duel copy scanner”

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12
Q

MOA of SSRIs

A

Work by inhibiting the presynaptic Serotonin Reuptake Transporter (SERT)

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13
Q

MOA of SNRIs

A

Work by inhibiting the presynaptic reuptake of norepinephrine (NET) and serotonin (SERT)

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14
Q

What are the side effects of SSRIs

A
  1. Hyponatremia due to excessive ADH release2. Decreased libido, disrupted arousal, inorgasmia, and increased ejeculation latency 3. Weight gain4. Drowsiness
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15
Q

What are the side effects of SNRIs

A

SNRIs can cause hypertension d/t increasing norepinephrine in the synaptic cleft or just autonomic malfunction in general such as tachycardia, excessive sweating etc

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16
Q

What is a common side effect of SSRIs and SNRIs

A

Serotonin syndrome

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17
Q

What causes neuroleptic malignant syndrome?

A

Dopamine blockers such as anti psychotics

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18
Q

Explain serotonin syndrome and NMS and how do they differ

A

Serotonin syndrome shares many of the characteristics as neuroleptic malignant syndrome or NMS, however there is a subtle difference in the 2. Just like in NMS serotonin syndrome can present with (1) agitation, (2) autonomic instability, (3) hyperthermia and (4) hypertension but there is one thing that should clue us into thinking serotonin syndrome specifically, look for hyper reflexia and clonus whereas in NMS we see hyporeflexia and rigidity.NMS ALSO has Rhabdomyolysis

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19
Q

How do you treat serotonin syndrome

A

Involves discontinuation of the offending drug, stabilizing vitals, and possibly administration of a Serotonin inhibitor such as Cyproheptadine

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20
Q

What is cyprohepatidine

A

5HT-2 blocker

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21
Q

What happens when someone being treated with SSRIs or SNRIs suddenly stops taking their medication

A

Withdrawal symptoms from SSRIs and SNRIs include flu-like symptoms 1-2 days after stopping the medication - so you need to slowly taper patients of the medication

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22
Q

What are tricyclics used for

A

They have numerous side effects so are used as 2nd or 3rd line for treatment of depression

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23
Q

Tricyclics MOA

A

Tricyclic Antidepressants work by inhibiting the reuptake of Norepinephrine (NET) and Serotonin (SERT)

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24
Q

Explain the pathophysiology of depression

A

One of the leading hypothesis for the pathophysiology of depression is the monoamine hypothesis that suggests that depression is related to a deficiency in monoamines (central serotonin, norepinephrine, and dopamine)

25
Q

Name tricyclics

A

Imipramine, desipramine, and clomipramineAmitriptyline, nortriptyline

26
Q

What are other uses of TCAs

A

All TCAs have been used historically for neuropathic pain.

27
Q

What is a specific use of Amitriptyline other than to treat depression

A

Migraine prophylaxis

28
Q

What is a specific use of Clomipramine other than to treat depression

A

Treats OCD

29
Q

Most important AE of TCAs

A

By far the most important side effect is the anti cholinergic effectDry mouth, constipation, blurred vision, and urinary retention

30
Q

Which TCA is most closely associated with anti cholinergic effects.What TCAs have less of this side effect?

A

Amitripline has the most anti-cholinergic effects out of the Tricyclic AntidepressantsNortriptyline and desipramine are secondary amines that are associated with less anticholinergic effects than Amitripiline

31
Q

What are the other major AE of TCAs.What is a clinical concequence of these AE?

A
  1. Blocks histamine receptors = sedation, increased appetite, weight gain and drowsiness2. Block alpha 1 receptors - orthostatic hypotension, can cause falls in the elderly and a fatal ↓CO3. Sexual dysfunction4. Can cause serotonin syndromeTCAs are relatively contraindicated in elderly patients due to severe anticholinergic and antihistamine effects -> increased risk of sedation, delerium, urinary retention, and falls.
32
Q

What is the most common cause of death in patients with TCA overdose

A

The most common cause of death is fatal cardiac arrhythmia by blocking cardiac fast Na+ channels -> decreased slope of P1 -> QRS & QT prolongation -> QT prolongation can cause torsades

33
Q

Treatment of TCAs overdose

A

Sodium-bicarb Therapy, it increases the pH of the blood and provides Na to increase conductance

34
Q

What are the 3 Cs side effects of TCAs and how are they caused?

A

Tricyclic Antidepressants can cause 3 C’s: Cardiac, Coma, Convulsions (likely d/t antagonistic effect on GABA-A receptors).

35
Q

Name monoamines

A

NE, dopamine, serotonin

36
Q

What breaks down monoamines?

A

Monoamine oxidase (MOA)

37
Q

How many types of MOA are there? What do they break down?

A

MAO-A - breaks down serotonin, norepinephrine, and dopamine MAO-B - breaks down dopamine

38
Q

When are MOA inhibitors used?Are these reversible or irreversible?

A

ALL are irreversibleUsed for Parkinson’s supplementary to L dopa and atypical depression, can treat major depressive disorder but used as a last resort

39
Q

Name MAO inhibitors

A

Tranylcypromine “try a sip of wine” Phenelzine “funnel” Isocarboxazid “boxed wine”These are non selective MAO inhibitors so they inhibit both MAO-A and B

40
Q

Name MAO-B specific inhibitor

A

Selegiline “sledge hammer” - a selective irreversible MAO-B inhibitor

41
Q

What is a use of Selegiline

A

Useful in treating the cogwheel rigidity of Parkinson’s in patients that are not responding well to Levodopa

42
Q

AE of MAO inhibitors?

A

Similar side effects as SSRIs and SNRIs, highest rate of sexual dysfunction

43
Q

What food should be avoided while on MOA inhibitors?

A

Tyramine containing foods so aged meats, fermented dairy products, and alcohol

44
Q

MOA of tyramine

A

Release of stored catecholamines

45
Q

What happens when tyramine is taken with MOA inhibitors

A

Tyramine is normally broken down by MAO-A in the GI tract - with inhibition of MAO-A, the Tyramine flows into the general circulation where it acts as a sympathomimetic agent, displacing NE from neuronal storage vesicles and sending an absurd amount of NE into the synapse -> can cause a hypertensive crisis (HTN, blurry vission, diaphoresis, stroke, and even MI).

46
Q

What can be used to treat tyramine toxicity

A

Phentolamine

47
Q

When do we use atypical antidepressants

A

Used for treatment in patients who have failed to respond to other therapy, these can also be 1st line agents in patients that are looking for specific drug results

48
Q

Bupropione drug type and MOA

A

Atypical antidepressant, inhibits NET and DAT so it has no effect on serotonin

49
Q

What are the uses of bupropione?

A

Resembles amphetamine structure so it has CNS activating effects, useful for treating depression associated with hyper somnolence and low energy. Can also be used to treat tobacco dependence, smoking.

50
Q

What makes bupropion especially useful as an antidepressant?

A

Bupropion does not affect serotonin - so it does not cause sexual dysfunction, making it useful for patients that are distressed/anxious about lack of libidoBupropion also causes less weight gain than other antidepressants - it can even be used for weight maintenance

51
Q

AE of bupropione

A

Can induce seizures especially at high doses and in older patients. Contraindicated in patients with history of bulimia and anorexia due to the drug’s ability to induce seizures

52
Q

What is mirtazapine?

A

Alpha 2 blocker

53
Q

What are the other MOA of mirtazapine?

A

Blocks 5HT-2 & 5HT-3 and H1 Histamine receptors

54
Q

What does alpha 2 blockade by mirtazapine specifically lead to?

A

Mirtazapine blockage of α-2 receptors causes an increase in presynaptic release of Serotonin and NE

55
Q

What are the 3 clinical scenarios where mirtazapine is especially useful?

A

(1) Blockage of H1-receptors can cause sedation -> making it one of the 1st-line options for patients with depression and insomnia. (2) Blockage of H1-receptors is assoicated with weight gain -> can be used in patients w/ depression and anorexia. (3) Does not cause sexual dysfunction -> can be preferred as a 1st-line treatment for depression due to its lack of sexual side effects

56
Q

What is trazodone?

A

Atypical anti depressant, Inhibits serotonin by blocking 5HT 2 and 5HT3 receptors. It has NO effects of NE or dopamine.Also an H1-receptor antagonist -> useful for treating insomnia associated with depression

57
Q

What is a major side effect associated with trazodone due to which it is colloquially called ‘trazo-bone’?

A

Antagonizes alpha 1 receptors, causes priapism (persistant erection lasting >4hrs) d/t vasodilatory effects.It is not a first line agent.

58
Q

Explain in what condition is priapism more likely with trozadone?What does priapism lead to?

A

Patients with SCD or multiple myeloma are more likely to develop priapism It can lead to permanent damage to penile tissue and erectile dysfunction if left untreated

59
Q

What are other AE of trozadone?

A

Orthostatic hypotension due to alpha 1 blockade, also blocks H1 receptor so can cause drowsiness, can cause sexual dysfunction and finally it can cause serotonin syndrome

Sketchy Pharmacology Notecards (14 decks)

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