Term
| What are the 3 Classifications of Depression? |
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Definition
1. Reactive (secondary)
2. Major Depressive Disorder (Endogenous)
3. Bipolar Disorder (Manic Deprission) |
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Term
| What is thought to be involved in the pathophysiology of depression? What Evidence supports this? |
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Definition
A Functional deficit of monoamines(NE) and Serotonin (5-HT)
Reserpine disrupts monoamine storage, causes depression
Antidepressants act to increase monoamines |
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Term
| What are the 4 major classes of antidepressants? |
|
Definition
Tricyclic antidepressants
2nd and 3rd Generation Drugs (heterocyclics or atypical antidepressants)
Selective Serotonin Reuptake Inhibitors
Monoamine Oxidase Inhibitors |
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Term
| What natural supplement did the FDA issue a warning about because it interferes with medications, particularly for HIV infection? |
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Definition
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Term
| What are the Tricyclic antidepressants? |
|
Definition
Amitriptyline
Imipramine
Desipramine |
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Term
| What group of anti-depressants is considered the "gold standard"? |
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Definition
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Term
| What are TCAs indicated for? |
|
Definition
Major Depression
Also...
Pain, anxiety disorders, ADHD, nocturnal enuresis, depression associated with schizophrenia |
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Term
| What is the mechanism of TCAs? |
|
Definition
| Inhibit reuptake of serotonin and norepinephrine into presynaptic terminals --> Potentiate and prolong the neurotransmitters actions --> Receptor and transporter requlation with repeated treatment |
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Term
| What receptors do TCAs block? |
|
Definition
mACh
5-HT
Histamine receptors |
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|
Term
| What clinical effects do TCAs have acutely? Chronicly? |
|
Definition
Acute: Drowsy, Dysphoric, Anxious, cognition impaired
Chronic: clinical symptoms improve, Not Euphoria |
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Term
| What does TCAs antagonism of alpha-AR cause? |
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Definition
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Term
| What can TCAs antagonism of mAch receptors cause? |
|
Definition
Blurred vision
Worsening narrow-angle glaucoma
Dry mouth
Constipation
Urinary retention
Tachycardia
Confusion |
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Term
| How do TCAs cause sedation? |
|
Definition
| Antagonism of histamine and alpha-ARs |
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|
Term
| What is the pharmacokinetics of TCAs? |
|
Definition
Incompletely absorbed - High 1st pass
High Lipid solubility --> distribution to Brain and Fat
Highly bound to plasma proteins -> limits excretion -> t1/2 >1day |
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|
Term
| What Drugs do TCAs interact with? |
|
Definition
Alcohol and other sedatives
Antiparkinson drugs
Antipsychotic drugs
biogenic amines
Clonidine |
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Term
| What are the Atypical antidepressants? |
|
Definition
Bupropion
Mirtazepine
Nefazodone |
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Term
| What mechanisma of action are the Atypical antidepressants similar to? |
|
Definition
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Term
| What are all the atypical antidepressants indicated for? |
|
Definition
| treatment of major depression |
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Term
| What drug is useful in the treatment of depression characterized by anxiety and sleep disturbances? |
|
Definition
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|
Term
| What atypical drug is an analogy of mianserin? |
|
Definition
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|
Term
| What Atypical drug enhances the release of serotonin and norepinephrine? |
|
Definition
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Term
| How does Mirtazepine enhance the release of serotonin? |
|
Definition
| antagonizing presynaptic alpha-2ARs |
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Term
| What receptors does Mirtazepine antagonize? |
|
Definition
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|
Term
| Why does Mirtazepin have a side effect of sedation? |
|
Definition
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Term
| What Atypical drug has a side effect of increased weight gain, but less GI and sexual problems than SSRIs? |
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Definition
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Term
| What Atypical drug is a weak blocker of DAT, SERT, and NET, and has an active metabolite that is a NE reuptake blocker? |
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Definition
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|
Term
| What atypical drug is also used as an aid in smoking cessation? |
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Definition
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Term
| What are the side effects of Bupropion? |
|
Definition
Anxiety
restlessness
seizures |
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|
Term
What are the Selective Serotonin reuptake inhibitors?
(SSRIs) |
|
Definition
|
|
Term
| What is the first-line therapy in patients diagnosed with major depression? |
|
Definition
|
|
Term
| What are the indications for SSRIs? |
|
Definition
Major Depression
Also...
Panic, OCD, social-anxiety disorder, ADHD, some eating disorders |
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|
Term
| Why is there typically better compliance to SSRIs? |
|
Definition
More Tolerable Side Effects
(Negligible activity at mACh and Histamine receptors) |
|
|
Term
| What is the mechanism of SSRIs? |
|
Definition
| Selective inhibition of serotonin reuptake --> Potentiates and prolongs the action of 5-HT |
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|
Term
| What acute clinical effects of SSRIs improve after 2-6 weeks? |
|
Definition
anxiety, agitation
CNS stimulation remains |
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|
Term
| What Adverse effects are associated with SSRIs? |
|
Definition
Nausea
Decreased libido
Sexual dysfunction |
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Term
| Which SSRI has a t1/2 ~7-9days, and can be formulated for weekly administration? |
|
Definition
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|
Term
| What drugs are SSRIs contraindicated with? |
|
Definition
MAOIs
Must wait at least 2 weeks |
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|
Term
| What is Serotonin Syndrome? |
|
Definition
overstimulation of 5-HT1A receptors in central grey (midbrain) and medulla
Onset within 24hrs of Overdose
Hyperpyrexia, Hyperreflexia, tremor, shivering, myoclonus, agitation, seizures, confusion and delirium, cardiovascular collapse and coma |
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|
Term
| What is the Monoamine Oxidase Inhibitor? |
|
Definition
|
|
Term
| Who are MAOIs indicated for? |
|
Definition
patients who are unresponsive to other antidepressants and ECT is not suitable
Also...
used for panic disorder, agoraphobia |
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|
Term
| What is the mechanism of MAOIs? |
|
Definition
| Blocks oxidative metabolism of monoamines by irreversible inhibition of MAO-A and MAO-B in nerve terminials |
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|
Term
| What does MAO-A and MAO-B do? |
|
Definition
MAO-A -> metabolizes NE, 5-HT, and Tyramine
MAO-B -> metabolizes DA selectively |
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|
Term
| What are the pharmacokinetics of MAOIs? |
|
Definition
well absorbed from GI
Daily dosing, even though irreversible inhibition
Inactivated by acetylation |
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|
Term
| What drug interactions do MAOIs have? |
|
Definition
Sympathomimetic drugs -> acute hypertensive reaction
Meperidine, Dextromethorpham -> hyperpyrexia, delirium, convulsions, coma, death.
SSRIs -> Serotonin Syndrome |
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Term
| What are the Mood-stabilizing drugs? |
|
Definition
Lithium
Valproate
Carbamazepine |
|
|
Term
| What are the mood-stabilizers indicated for? |
|
Definition
maintenance of manic depression
(Bipolar affective disorder) |
|
|
Term
| What mood-stabilizer has a very narrow therapeutic window? What are toxic effects observed? |
|
Definition
Lithium
Neurologic/psychiatric: tremor, ataxia, hyperactivity, aphasia, sedation, fatigue
Glandular: edema, hypothyroidism
Renal: polydipsia, polyuria
Cardiac: bradycardia-tachycardia
acne, folliculitis, exacerbates psoriasis |
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Term
| What drugs should be avoided with Lithium use? |
|
Definition
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Term
| What 2 mood-stabilizers are Anticonvulsants? |
|
Definition
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|
Term
| What is first-line treatment for bipolar disorder? |
|
Definition
|
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Term
| What are advantages and disadvantages to using Anticonvulsants over Lithium? |
|
Definition
Advantages: increase dose faster, quicker response, better TI
Disadvantages: less experience, efficacy questionable in severe disease |
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Term
| What anticonvulsant is the drug of choice when absence seizures are also accompanied with tonic-clonic seizures? |
|
Definition
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|
Term
| What 3 mechanism of action does Valproic Acid have? |
|
Definition
1.Inhibits voltage-gated Na channels by stabilizing the inactivated state of the channel.
2. Blocks Ca channels slightly
3. Stimulates GABA synthesis and inhibits degredation. |
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Term
| What is the drug of choice for partial seizures? |
|
Definition
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Term
| What mood-stabilizer is effectrive for trigeminal neuralgia? |
|
Definition
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|
Term
| What is the mechanism of Carbamazepine? |
|
Definition
Na channel inhibition
prolongs recovery from inactivation |
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|
Term
| How is Carbamazepine metabolized? |
|
Definition
| by CYP3A4 to an active metabolite |
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|
Term
| What mood-stabilizer affects the metabolism of oral contraceptives? |
|
Definition
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Term
| Toxicity of what mood-stabilizer can cause Diplopia and ataxia? |
|
Definition
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