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Psychiatry > Anti-Depressants > Flashcards

Anti-Depressants Flashcards

1
Q

What is the monoamine theory of depression

A

The monoamine theory (1965) depression results from functionally deficient monoamine (NE and/or 5-HT) transmission in the CNS • The theory was based on pharmacological evidence o the ability of known antidepressant drugs (TCAs and MAO inhibitors) to facilitate monaminergic transmission o drugs such as reserpine that depletes amines to cause depression

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2
Q

Does the monoamine theory of depression still hold up?

A

• Simple monoamine hypothesis no longer tenable as an explanation of depression, BUT pharmacological manipulation of monoamine transmission remains the most successful approach to treating depression.

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3
Q

Neurons containing norepinephrine are located in the ______ and innervate nearly every part of the CNS.

A

locus coeruleus

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4
Q

Neurons containing serotonin are located in two groups of _____and project to most of the brain.

A

raphe nuclei

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5
Q

Neurons containing dopamine are located in the ____(and these project to the striatum) and the _____ area of the midbrain (and these project to the prefrontal cortex and parts of the limbic syste

A

substantia nigra ventral tegmental

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6
Q

Neurons containing ACh are located in the _____, which includes the septal nuclei and nucleus basalis and project to the hippocampus and the neocortex.

A

basal forebrain complex

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7
Q

Where are the cell bodies of neurons that contain Nepi located in the brain?

A

locus coerules: innervate the forebrain and neolimbic cortex

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8
Q

Where are the cell bodies containing Serotonin located?

A

Raphe nulcei to cortex + basal ganglia

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9
Q

What is the funciton of the Alpha 2 receptor on the presynaptic neuron?

A

Its a NE sensor; detects amount of Nepi in the synapse adn will regulate how much is made and released

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10
Q

What is the function of the Post juntional alpha receptor

A

stimulates; its on muscles and autonomic systems

both alpha and beta are terminated by neuronal uptake and blocked by certain drugs

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11
Q

How is the action of Nepi terminated?

A

Neuronal uptake or degraded by MAO

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12
Q

How is Nepi made?

A
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13
Q

What do we see in the post synaptic terminal in acute TCA use

A

TCA blocks Nepi release from presynaptic terminal

we see More Nepi made and relased into the synpase dt loss of negative feedback

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14
Q

What do we see in chronic TCA use in regards to postynaptic neuron

A

see lots more NE but decrease in the post synpatic receptors: this leads to decreased cAMP activity.

As drug builds up we see less signal tranduciton but more NE

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15
Q

DEscribe how Seratonin is made

A

Tryptophan–> 5-OH tryptophan –> 5HT

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16
Q

How do SSRIs work?

A

Block SERT reuptake

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17
Q

How does Mirtazapine work

A

Blocks seratonin and Nepi pre-synpatic receptors thus sends the message of “hey, we have plenty of seratonin” message never gets sent and you make more

this is at the alpha-2 autoreceptor

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18
Q

What is a common MAO-I and what is the mechanism of action

A

Monoamine oxidase is found in the mitochondria; we block MAO so we increase intrneuronal conc of NTs and increase receptor binding as well and end up with same result

Phenelzine

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19
Q

What is the restated monamine hypothesis?

A

Depression is due to a biogenic amine receptor or transmission imbalance. The various drugs that we are discussing today, act to change the imbalance and restore a more normal affect.

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20
Q

______ prevent presynaptic reuptake of the amines noradrenaline and seratonin

_____ predominately block seratonin reuptake

____ recude amount of MAO in breaking down presynaptic amines

A

TCAs

SSRIs

MAOIs

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21
Q

Why have SSRIs replaced TCAs as drug of choice for first line therapy against major depressive disorder

A

more desirable side effect profile

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22
Q

What are five common SSRI examples and what is there side effect profile

A

Fluoxetine, Fluvaximine, paroxetine, sertraline, citalopram

sides = nausea, insomnia, sexual dysfunction

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23
Q

Why are SSRIs prefered over TCAS? what is still dangeorus about SSRIs?

A

less risk for overdose, less acute toxicity

Seratonin reaction: hyperthermia, msucle ridgitidy, CV collapse when given with MAOIs!

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24
Q

What is something we need to consider when prescribing antidepressants to younger pts

A

suicidal thinking; need to watch pts that just start therapy very closely

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25
Q

What are some symptoms of SSRI withdrawl

A

dizzy, lightheaded, vertigo, shock like sensations, parethesia, anxiety, diarrhea, fatigue, gait issues, headace, insomnia

26
Q

Approved uses of SSRIS

A
  • Major Depression
  • Obsessive-Compulsive disorder
  • Panic disorder
  • Social Anxiety Disorder
  • PTSD
  • Generalized Anxiety disorder
  • PMS – Now PDD (Premenstrual Dysphoric Disorder)

• Hot flashes associated with menopause

27
Q

Fluoxitine(Prozac) is an ______ with a _____ half life

Lots of inteactions with ____

A

SSRI

long half live

drug metabolism via CYP 2D6

28
Q

has simular action to Fluoxetine with less effects on drug metabolism

used for OCD, PTSD and Panic attacks

short 1/2 life

A

Sertraline (Zoloft)

29
Q

Parozetine is an SSRI with additional approval for ______

A

hot flashes post menopause

least muscarininc effects of all drugs

30
Q

Fluvovazimine is a ____ approved for ____

A

SSRI

OCD

31
Q
  • Drugs block both 5-HT and NE reuptake
  • Side effect profile is more SSRI-like than TCA- Like.
A

Serotonin-Norepinephrine Reuptake Inhibitors (SNRI)

32
Q

SNRI approved for Major Depressive Disorder and anxiety.

  • Also approved for neuropathic pain syndromes, fibromyalgia, back pain and osteoarthritis pain.
  • Use with caution in patients with liver disease
A

• Duloxetine (Cymbalta®)

33
Q

SNRI approved for Major Depressive Disorder and anxiety.

A

Venlafaxine (Effexor®)

34
Q

SNRI approved for fibromyalgia

A

Milnacipran (Savella)

35
Q

Duloxetine, Venlafaxine and Milnaciprin are all examples of

A

SRNIs

36
Q

What is Duloxetine and what can it treat

A

SNRI, for antidepression but also fibromyalgia

37
Q

o Weakly blocks NE and dopamine uptake.
o also approved for nicotine withdrawal and seasonal affective disorder.

o No weight gain or sexual dysfunction.

A

Buproprion

38
Q

blocks presynaptic alpha2 receptors in brain

Increases appetite ***AIDS patients.

A

Mirtazapine (Remeron®)

39
Q

o Weak SSRI-like effect. Sedating
o also used for insomnia.
o low incidence of cardiovascular side effects,

o can cause priapism.

A

Trazodone (Oleptro®)

40
Q

o The newest drug approved to treat MDD. Has a SSRI-like action in addition to 5- HT1A agonist and 5-HT3 antagonist activity.

A

Vortioxetine (Brintellix®)

41
Q

What are my atypical antidepressant drugs

A

Buprioprion

Mirtazapine

Trazadone

Vortioxetine

42
Q

Amitriptyline, Timipromine, Nortryptiline, Protriptyline are all examples of

A

TCAs

43
Q

What is the volume of distribution like in TCAs?

What about half life?

A

Very large volume of distribution, very lipophilic

long half life thus high risk for overdose

see high concentrations in heart and brain

44
Q

Mechanism of action of TCAs

A

Block NE and 5-HT reuptake

(now second line to SSRIS for depression)

45
Q

Effect of TCAs on mood and sleep

A

MOod is elevated in 2-3 weeks

DECREASED REM and Increased stage 4

46
Q

What type of anticholinergic effects do we see from TCAs?

A

Dry mouth, blurred vision, urniary retention

(as well as orthostatic hypotension, cardiac abnormalities)

47
Q

What cardiac side effects are seen d/t TCAs

A
  • Due to anticholinergic effects and increased NE concentrations
  • Palpitations, tachycardia and arrhythmias
  • EKG changes such as lengthened QRS intervals and flattened or inverted T-waves reflect a slowed conduction time and significant alterations in the electrophysiology of the heart.
48
Q

What do we see as a result of TCA overdose

A

Symptoms include hyperpyrexia, changes in blood pressure, seizures, coma and cardiac conduction defects.

Treatment is symptomatic. Observe for at least 3 days because of long half-lives.

49
Q

What type of drug interactions do we see with TCAs?

A
  • Guanethidine - blocks guanethidine uptake
  • Sympathomimetic drugs - particularly indirect acting agents
  • Effects absorption and metabolism of other drugs.
50
Q

Therapeutic uses for TCAs

A
  • Major depressive disorder
  • Enuresis in childhood - imipramine
  • Chronic pain - amitriptyline
  • OCD – clomipramine and SSRIs
51
Q

What is the MOA for Phenelzine and Tranylcypromine

A

Both are MAO-Is

Phenelzine is irreverislbe inhibitor

Tranylcypromine is reversible

52
Q

How long does MAO-Is take to work?

What affect does it have on mood?

sleep?

A
  • Antidepressant action takes about 2 weeks.
  • Produces mood elevation in depressed patients. Mayprogress to hypomania particularly in bipolar disease.

• Corrects sleep disorders in depressed patient.

53
Q

How do ‘Normals’ respond to MAOIs?

what do we see with BP?

Acute toxicity from MAOIs

A
  • May produce stimulation in normals.
  • Lowers blood pressure; often produces orthostatic hypotension.
  • Acute toxicity can produce agitation, hallucinations, hyperpyrexia, convulsions and changes in blood pressure.
54
Q

What food needs to be avoided when on MAOIs?

A

Tyramine foods: can cause Hypertensive crisis; tyramine goes through liver and is usually metabolized to inactivce metabolite but MAOIs block that thus you ahve active tyramine which stimulates dumping of NE–> to areterioles of heart == hypertensive crisis!

55
Q

Uses of MAOIS

A

Major depression (NOT first choice)

Narcolepsy

56
Q

What are some options if Antidepressants alone aren’t enough?

A
  • Augmentation with antipsychotic agents.
  • Approved drugs for treatment resistant major depressive disorder include:

Olanzapine (Zyprexa)

Aripiprazole (Abilify)

Quetiapine (Seroquel

  • Ketamine – experimental treatment
  • Physiological treatments

ECT (Electroconvulsive therapy)

TMS (Transcranial Magnetic Stimulation)

(Experimental) Deep Brain Stimulation

57
Q

Why does St. Johns wort work for depression?

A

Has Ypericin which causes MAOI activity; but it upregulates Cyp3A4 thus lowers effectiveness of BC, protease inhibitors in AIDS pts and Cyclosporine

58
Q

MOA for Imipramine and Amitryptyline

A

Nonspecific blockers of NE and 5-HT: dirty drugs with bad side effect profile

59
Q

MAO of Fluoxetine, Sertraline, Paroxetine, Citalopram and Escitalopram

A

SSRIs

60
Q

MOA of Venlafaxine and Duloxetine

A

SNRIs

61
Q

Phenelzine is a

A

MAOI

Psychiatry (19 decks)

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