drug class Flashcards
Thioxanthenes
FGAs.
Similar to phenothiazines in that they are also D2 antagonists, but have 5-HT, NE, H effects as well
FGAs vs SGAs
1st gen: motor problems / 2nd gen: metabolic issues (weight gain, diabetes, hyperglycemia, QT)
FGAs better for positive symptoms of schizophrenia, SGAs better for negative symptoms
All SGAs differ from FGAs by having less affinity for D2 receptors and greater affinity for 5-HT receptors.
Phenothiazines
FGAs.
Chlorpromazine (Thorazine)
primarily blocks DA D2, but also AChM1, H1, NEα1
Side Effects
(EPS), (TD)
Affinity of AChM, H and NE predicts sympathetic effects, memory impairment, sedation and hypotensive effects.
Neuroleptic Malignant Syndrome (NMS): fever, muscle rigidity, autonomic fluctuations, alterations in consciousness. Can lead to death
EPS vs TD
antipsychotics, more so FGAs.
EPS: rapid onset, reversible
TD: late-onset and irreversible
Butyrophenones
FGAs.
very similar to phenothiazines: block DA D2, but also AChM1, H1, NEα1
Side effects:
Have highest incidence of EPS, particularly PD-like symptoms, dystonia, TD*
Examples:
Haloperidol (Haldol)
Droperidol (Inapsine)
SNRIs
selective norepinephrine reuptake inhibitors
reboxetine (Edronax)
Atomoxetine (Strattera)
Not showing much promise as antidepressants; use for treatment of ADHD
Tetracyclics
mirtazepine (Remeron)
antidepressant
Does not block reuptake transporters; increases release of 5-HT and NE.
only stimulates 5-HT1 receptors
–> does not produce the side effects of SSRIs (especially anxiety, insomnia, agitation, nausea, and sexual dysfunction).
Very few sexual side effects
Side effect - increased appetite/weight gain
Good for txting pxts with eating or wasting disorders (for example, cancers and AIDS), and elderly pxts
SSNRIs
(dual-action - selective serotonin and norepinephrine reuptake inhibitors)
Analgesic
Should probably not be a first choice unless have treatment resistant anxiety / depression
Highly selective for NT and 5-HT, with little binding to other receptors
Inhibit the active presynaptic reuptake of both serotonin and norepinephrine
Fewer side effects, particularly ones related to increased serotonergic tone
SSRIs
highest incidence of sexual dysfunction is SSRIs
first choice for anxiety disorders
seem to be better for OCD and PTSD (BZDs are not); first choice for all except for possibly social anxiety
Serotonin syndrome
Do not bind to 5-HT receptors but make 5-HT more available to bind to receptors due to blocking its reuptake
Do not bind to other receptor systems, so few anticholinergic or antihistaminic side effects.
Safer than TCAs; no cardiac effects
Differences in efficaciousness between SSRIs mainly due to different metabolic, particularly CYP-450 liver enzymes
FINISH
Withdrawal syndrome:
-Flu-like symptoms
-Insomnia
-Nausea
-Imbalance (dizziness, vertigo, ataxia)
-Sensory disturbances (sensations of electric shocks)
-Hyperarousal (anxiety, agitation)
Anxiolytic Drugs
Target GABA receptors
hippocampus has a high density of GABA receptors, leading to amnesic effects of antianxiety meds
Not recommended in pxts with decreased GABA function (i.e., in the elderly, dementia patients)
Barbiturates
Anxiolytics
GABAA agonists: Hold Cl- channels open longer to increase efficacy of GABA
Low TI: very dangerous; death usually results from respiratory depression
No txt for OD
cognitive inhibitor
Shorter ½ lives used primarily for anesthesia: Amytal, Nembutal
Not used today because:
strong sedative effects
the low dose required for anxiolytic effects also cause amnesiac and sedative effects
super addictive
Serious withdrawal syndrome
Non-barbiturate Sedatives
Commonly known as “date rape” drugs: Placidyl, Noludar, Equanil, Soma, Quaalude, Noctec, GHB
Benzodiazepines (BZDs)
Benzodiazepine receptor agonist (BZRAs)
BZR is found on GABAA receptors → increases affinity of GABA binding site for GABA
Benzos work off of GABA - in the absence of GABA, do not have an effect
Mental confusion and amnesia follow action on GABA neurons located in the cerebral cortex and the hippocampus.
High TIs, low toxicity UNLESS combined with other NS depressants (alcohol)
OD txt with flumazenil (BZD antagonist - can kick BZDs off of the receptor)
High rates of dependence limit use
should only be used for short periods - 1 month
cognitive impairments + potential for dependency limit therapeutic use to relatively short periods of time
Side Effects of sedation, ataxia, confusion, cognitive/motor impairment, and amnesia are especially problematic in children/adolescents and elderly
Some evidence that impairments are semi-permanent (for everyone, not just these populations)
The elderly have a reduced ability to metabolize long-acting benzos and their active metabolites.
Because all benzos can produce cognitive dysfunction, elderly patients can become clinically demented as a result.
long-term benzodiazepine use was associated with a more than twofold-increased risk of dementia
Pregnancy category D
first trimester: does not seem to be associated with increased risk of congenital malformations
Near time of delivery, if a mother is on high dose, fetus can develop dependence or “floppy-infant syndrome”
Nonbenzodiazepine BZRAs
Different molecular structure than BZDs, but same effect at BZD receptor
Zolpidem (Ambien), zaleplon (Sonata), eszopliclone (Lunesta)
Shorter half-lives
Insomnia
CBT equally effective
