Antidepressants/antipsychotics

Front 1

What is the MOA of Reserpine?

Back 1

-decreases serotonin & NE levels in brain
-found associated w/ depression

Front 2

What does the theory say about depression?

Back 2

depression is caused by decreased amine-dependent synaptic transmission

Front 3

Amitriptyline

Back 3

-cleared by first-pass metabolism of liver
-half-lives range from 12-76hrs
-5 half-lives to reach steady-state
-takes wks to months to see any clinical benefit (probably has to due w/ remodeling of neuronal networks)
-VERY lipid soluble

Front 4

What is the MOA of tricyclic antidepressants?

Back 4

-non-specifically inhibit storage of serotonin & NE in the CNS
-accounts for therapeutic effects
-binds to alpha-adrenergic, histaminergic & cholinergic receptors
-accounts for ADVERSE effects
alpha-adrenergic=hypOtension
histaminergic=drowsiness
cholinergic=SLUD

Front 5

What are the uses of TCAs?

Back 5

secondary agents to SSRIs & SNRIs

Front 6

Trazodone

Back 6

MOA:
-serotonin antagonist & reuptake inhibitor
Use:
-depression & insomnia
ADR:
-overall less than TCAs; drowsiness

Front 7

What are the SSRI drug agents?

Back 7

fluoxetine (Prozac)
paroxetine (Paxil)
citalopram (Celexa)
sertraline (Zoloft)

Front 8

How are SSRIs metabolized?

Back 8

metabolized by p450s

Front 9

What is the MOA, uses &* ADR of SSRIs?

Back 9

MOA:
-decreased serotonin reuptake=increased serotonin levels in CNS
Use:
-Drug of CHOICE for initial treatment of depression
ADR:
-similar to TCAs but MUCH LESS severe & frequent
-N/V, dry mouth, insomnia, drowsiness, sexual dysfunction

Front 10

What are the SNRI drug agents?

Back 10

bupropion (Wellbutrin) - prototypical agent
venlafaxine (Effexor)
duloxetine (Cymbalta)

Front 11

What is the MOA & uses of SNRIs?

Back 11

MOA:
-decreases reuptake of both NE & serotonin at synapse
Use:
-may be more effective in depression w/ anxiety
-also used for chronic pain syndromes & neuropathies

Front 12

Lithium

Back 12

*Drug of choice for BIPOLAR DISORDER
MOA:
-decreases overactivity of neurotransmitters in CNS
ADR:
-dizziness, lethargy, memory loss, metallic taste, hand tremors, muscle weakness
Interactions:
-NSAIDs, tetracycline: decrease clearance of lithium

Front 13

What are the positive & negative symptoms of schizophrenia?

Back 13

Positive: (exaggeration of normal parameters)
-hallucinations, delusions, though disorders, insomnia, bizarre behavior
Negative: (decrease from normal)
-apathy, a motivation, anhedonia (lack of pleasure from normal pleasurable experiences), asocial behavior

Front 14

What are the 3 dopamine pathways?

Back 14

Mesolimbic
-reward pathway
-affects emotions, behavior
Mesocortical
-affects cognition & processing info
Nigrostriatal

Front 15

What are the traditional antipsychotic agents?

Back 15

chlorpromazine (Thorazine) - prototypical agent
haloperidol (Haldol)
MOA:
-non-specifically inhibit dopamine at level of its D2 receptor
-true MOA is a mystery
Use:
-reserved for pts not responding to other agents

Front 16

What are the ADRs for antipsychotics?

Back 16

Extrapyramidal symptoms:
-due to dopamine effects on tracts OTHER than mesocorticolimbic
Early onset:
-dystonia: muscle spasms (facial muscles_
-pseudoparkinsonism
-more due to BLOCK of DA
Intermediate onset:
-akathisia (restlessness)
Neuroleptic malignant syndrome
-EPS leading to death

Front 17

What are the newer generation antipsychotic agents?

Back 17

risperidone (Risperdal)
quetiapine (Seroquel)
olanzapine (Zyprexa)
aripiprazole (Abilify)

Front 18

What is the MOA of newer generation antipsychotic agents?

Back 18

MOA:
-inhibit serotonin at receptor
-also inhibit D2 receptors

Front 19

What are the implications for dentistry?

Back 19

-Neuroleptic facial movements
-increase sedation when given w/ opioids
-increase oral candidiasis
-decrease salivation
-NSAIDs - interaction w/ lithium