Psychopharmacology/Stimulants Flashcards
When Cl- (exits/enters), cells are less likely to fire
enters
When K+ (exits/enters), cells are less likely to fire
exits
Neurotransmitters, like Ach, NE, Serotonin, Dopamine, etc., are STIMULATORY by what mechanism (what ion and which direction)
Stimulate Na+ influx
Neurotransmitters, like GABA and Glycine, are INHIBITORY by what mechanism (what ion and which direction)
Stimulate Cl- influx
Examples of Inhibitory neurotransmitters (2 total)
GABA
Glycine
Which serotonin receptors inhibit the signaling pathway (2 total)
5-HT1
5-HT5
Which neurotransmitters are “Monoamines” and thus key to all anti-depressant drugs
NE
Serotonin
Dopamine
*thus reuptake inhibitors for these are essential treatments (SSRIs, DNRIs, etc.)
Monoamines are NTs that are key to treating…
depression (so monoamine oxidase inhibitors are crucial for treatment)
Serotonin Receptor Antagonists (5HT2 & a1/2 antagonists)
Trazodone
Mirtazapine
How do serotonin antagonists (Trazodone and Mirtazapine) cause anti-depressant effects?
Not clear how. They also antagonize NE receptors, which may play a role
Examples of Tricyclic Anti-Depressants (SSRIs/SNRIs) (2 total)
Amitriptyline
Imipramine
All Tricyclic Anti-depresants (Amitriptyline, Impiramine) are what class?
SSRIs/SNRIs
Toxicities of anti-cholinergic effects (especially Tricyclics) (7 total)
"Red as a beet" (flushing) "Hot as hades" (fever) "Mad as a hatter" (delerium) "Blind as a bat" (blurred vision) "Dry as a bone" (xerostomia) "Heart runs alone" (tachycardia) "Bowel and bladder lose their tone" (constipation and urinary retention)
Why are BOTH depression and anxiety treated with SSRIs and SNRIs (would think anxiety would be worsened with more serotonin and NE)?
Those with anxiety typically have underlying depression because they are closely linked (fear, panic, worry, agitation, etc.) (treating one can treat the other)
Classes of drugs to treat anxiety
SSRIs/SNRIs (counter-intuitive)
Buspirone (5-HT1 agonist)
Benzodiazepines (GABA)
_______________ is a 5-HT1 agonist (serotonin) that inhibits signaling at serotonergic synapses, thus helping to relieve anxiety
Buspirone
Inhibitory receptor that acts as a Cl- channel in order to hyperpolarize the post-synaptic neuron; acted on by benzodiazepines to be anxiolytics
GABA receptor
_____________________________ are GABA-a receptor positive modulators (NOT agonists, don’t open), increasing the potency of GABA receptors; cause anxiolysis but can also produce sedation/hypnosis
Benzodiazepines
Benzodiazepines increase the (potency/effectiveness) of GABA
Potency; does NOT increase effectiveness, so BZs can NEVER have more of an effect than GABA itself (difficult to overdose on BY THEMSELVES)
Examples of Benzodiazepines (anxiolytics) (5 total)
Diazepam Lorazepam Midazolam Alprazolam Chlordiazepoxide
(-pams, -lams)
2 Benzodiazepines that are best known for their sedative effects via “active metabolites”
Diazepam
Chlorodiazepoxide
The “active metabolites” of BZ metabolism act on (a1/a2) containing GABA receptors to produce sedation
a2
Anxiety is typically treated with what two categories of drugs?
BZ (anxiolytic via hyperpolarization)
SSRIs and SNRIs (treat underlying depression)
“Schizo-“ meaning
“split from”
Schizophrenia= split from “mind” (-phrenia)
What are the two main “positive” symptoms of Schizophrenia
Delusions (false beliefs)
Hallucinations (false perceptions)
Treatments for Schizophrenia by the action of what NT antagonism
D2 receptor antagonists (Dopamine)
5-HT2A receptor antagonists (Serotonin)
(1st/2nd) Generation drugs have VERY potent D2 receptor antagonists and thus have more extrapyramidal symptoms and hormonal changes because of inhibition of the Nigrostriatal pathway (EP) and Tuberoinfundibular pathway (hormones)
1st Generation
(1st/2nd) Generation drugs have VERY potent 5-HT receptor antagonists and thus have more prominent side effects, like weight gain
2nd Generation
The EXTRAPYRAMIDAL symptoms from D2 receptor antagonism are due to the inhibition of what portion of the brain
Nigrostriatal pathway (motor control of skeletal muscles) (Parkinsonism)
The HORMONAL effects from D2 receptor antagonism (breast tissue and lactation) are due to the inhibition of what portion of the brain
Tuberoinfundibular pathway
Hormonal effects of D2 receptor antagonism in psychotic treatments
Prolactin–> breast tissue and lactation (dopamine normally inhibits)
Side effects of serotonin receptor antagonism in psychotic treatments
weight gain
The psychotic treatment that blocks a1 receptors (ex: ________________________) can result in orthostatic hypotention with low potency and 2nd Generation drugs
Norepinephrine
(low/high) potency and 2nd Generation a1 receptor antagonists like NE more commonly cause Orthostatic Hypotension
Low
Antipsychotic treatment that can cause prolonged QT intervals
K+ channel blockers (Haloperidol)
Why are 1st generation Antihistamines more likely to cause sedation than 2nd generation
Cross the BBB moreso, allowing for direct effects
Atypical antipsychotic medication; mainly used when psychosis does not improve following the use of other antipsychotic medications; can cause agranulocytosis/neutropenia (potentially fatal)
Clozapine
What percent of occupancy of D2 receptors is required for therapeutic effects on “positive” symptoms (can titrate to reduce side effects while maintaining efficacy)
60%
ADHD is caused by deficiencies in what NTs
Dopamine
NE
- is actually a loss of stimulants, go figure
- thus reuptake inhibitors and agonists for each should treat
Examples of stimulants used in ADHD treatment (3 total)
Methylphenidate (MPH)
Dextroamphetamine
Amphetamine salts
Stimulant used for ADHD; blocks the reuptake of NE and Dopamine, inc. concentrations in synaptic space
Methylphenidate
Stimulant used for ADHD; acts to BOTH block the reuptake and to release additional NE and Dopamine into synaptic space
Amphetamines
Side effects of stimulant use (Methylphenidate, Amphetamines)
Tachycardia Arrhythmias Diaphroesis Insomnia Euphoria Agitation Paranoia
Simulants, like Amphetamines, are contraindicated with _________________ __________________
Monoamine Oxidase Inhibitors (would make too much) (main mech is already to inc. levels of monoamines)
Non-stimulant used for ADHD; inhibits reuptake of NE; can initially cause sedation and fatigue because it takes time to become effective; can inc. suicidal ideations
Atomoxetine
Alpha-2 agonists used for ADHD; modulate noradrenergic tone; can result in hypotension and sedation
Clonidine and Guanfacine
Anti-depressants inc. neuronal firing by what two mechanisms
1) Inc. synaptic levels (reuptake inhibitors)
2) inhibit enzymatic breakdown (monoamine oxidase)
Anxiolytics decrease neuronal firing by what mechanism
Cl- influx (Benzodiazepines)
SSRIs/SNRIs (treat underlying depression)
NT receptors located on PRE-synaptic neuron that INHIBIT NT release, thus reducing signaling through that particular pathway
Autoreceptors
