Anti-depressants & Mood Stabilizers (TCAs & Atypicals) Flashcards
Definition of depression?
Affective disorder w/ emotional, cognitive, behavioral, somatic regulation
Definition of depression?
Affective disorder w/ emotional, cognitive, behavioral, somatic regulation
Core syndrome?
Persistent emotion, guilt, untreatable physical symptoms
Pathophys of depression?
Decrease of monoamines (NE & serotonin)
When do anti-depressants take clinical effect?
Takes weeks
BBW for all anti-depressants & mood disorders?
<24 y/o you should monitor changes in depression, suicidal thinking, unusual behavior
What is reactive or secondary depression? What are its symptoms? What is its tx?
it is secondary to loss, drugs, alcohol, other psychiatric disorders. Symptoms: Core syndrome. Tx: remits spontaneously + responds to Rx
What is major depressive disorder? Symptoms? Tx?
Recurrent. Symptoms: core syndrome + vital signs. Tx: anti-depressants + ECT
What is bipolar disorder (manic depression)? Symptoms? Tx?
Mania + depression episodes. Symptoms: increased elation, irritable, less sleep needed, grandiose notions, increased talking. Tx: mood stabilizers + anti-depressants
What are the issues with pharmacogenomics?
ABC (MDR1/P-gp) @ BBB –> decreased access to brain
What drugs are substrates for MDR1?
Citalopram, Paroxetine, Amitriptyline, Venlafaxine
Non-substrates for MDR1?
Mirtazapine, fluoxetine
What are the TCAs?
Amitriphyline, Imipramine, Nortriptyline
What do the TCAs treat?
- Major depression
- Bedwetting (Imipramine)
- OCD (Clomipramine)
MOA of TCAs?
decrease reuptake of 5HT and NE into presynaptic terminals –> increased actions of neuroTx + change receptor profile with treatment
What else do the TCAs do?
block ACh, 5-HT, histamine receptors (these are the basis of ADEs)
Are the TCAs highly lipid soluble?
Yes, the get into the brain and into fat
Are the TCAs protein bound?
Yes, they have a high volume of distribution and a long half life
Describe the metabolism of TCAs?
Tertiary amines –> secondary amines via demethylation (imipramine –> desipramine; amitriptyline –> nortriptyline)
-Metabolized via CYP2D6
What are the acute effects of TCAs?
drowsy + decreased cognition
chronic effects of TCAs?
increased cognition; NOT euphoria
DDIs w/ TCAs?
EtOH, other sedatives; TCAs block clonidine
ADEs of TCAs?
- Orthostatic hypoTN (antagonism of alpha-adrenergic receptors)
- Anti-DUMBBELLS + CI Glaucoma (antagonism of ACh receptors)
- Sedations (antagonism of histamine + alpha adrenergic receptors)
- Metabolic/Endocrine: gain weight + sexual disturbance
TCAs have a low TI. What does OD cause?
Arrhythmia, cardiac failure, CHF
- Acidosis, delirium, seizure
- FA says Tri-C’s: Coma, Convulsions, Cardiotoxicity