MOAs for Test 4 Flashcards
(Lecture 1) This class of drugs blocks the reuptake of norepinephrine and serotonin (precursors to SNRI) into the presynaptic neuron which increases [monoamine] in the synaptic cleft (debated); also blocks alpha adrenergic, histamine, and muscarinic receptors.
Tricyclic Antidepressants
(Lecture 1)
This drug class Inhibits serotonin reuptake, without affecting reuptake of norepinephrine or dopamine into the presynaptic neuron;
they DO NOT SIGNIFICANTLY EFFECT histamine, muscarinic, or other receptors
SSRIs
(Lecture 1)
These drugs/classes carry a risk of serotonin syndrome because they INHIBIT SEROTONIN REUPTAKE
- Cocaine
- Dextromethorphan (DM)
- Meperidine
- SSRIs
- TCAs
- Trazodone
- Venlafaxine
(Lecture 1) This drug/class carries a risk of serotonin syndrome because it is a DOPAMINE AGONIST
L- dopamine
(Lecture 1) This drug/class carries a risk of serotonin syndrome because it is a SEROTONIN PRECURSOR
L-tryptophan
(Lecture 1) These drug/class carries a risk of serotonin syndrome because it INHIBITS SEROTONIN METABOLISM
MAOIs
(Lecture 1)
These drugs/classes carry a risk of serotonin syndrome because they INCREASE SEROTONIN RELEASE
- Amphetimines
- Lithium
- MDMA (ecstacy)
(Lecture 1)
These drugs/classes carry a risk of serotonin syndrome because they are SEROTONIN RECEPTOR AGONISTS
- Triptans
- Buspirone
- Lysergic Acid Diethylamide
(Lecture 1)
This drug class inhibits the reuptake of 5HT and NE, increasing their levels (may be dose-related);
it displays LITTLE activity for alpha-adrenergic, cholinergic, or histamine receptors
SNRIs
(Lecture 1)
This drug inhibits dopamine AND Norepinephrine (at high doses) with minimal activity on serotonin
Bupropion (an NDRI)
(Lecture 1)
This drug modestly inhibits serotonin uptake (less than SSRIs); are antagonist for pre-synaptic 5HT(2A), H(1), and alpha(1) receptors
Trazodone
a serotonin receptor antagonist
(Lecture 1)
This drug inhibits 5HT(2A), H(1), and alpha(1) receptors AND ALPHA 2 receptors, but does not have reuptake inhibition effect.
Mirtazapine
a serotonin Receptor Antagonist
(Lecture 1)
This drug inhibits 5HT(2) family of receptors, alpha(1) receptors, and reuptake of serotonin and norepinephrine
Nefazodone
a serotonin receptor antagonist
(Lecture 1) This drug class blocks the enzyme responsible for the breakdown of NE, dopamine, and serotonin which increases the stores of these neurotransmitters in the neurons
MAOIs
Two forms: MAO-A, MAO-B
Foods that interact with these medications occur because they inhibit MAO in the GI tract that normally breaks down tyramine, resulting in increased levels of catecholamines.
(Lecture 1)
These drugs are non-selective MAOIs which are considered last line agents in antidepression
Phenelzine
Tranylcypromine
(Lecture 1)
This MAO-B INHIBITOR is used in the treatment of MDD (and Parkinson’s) and claims to exhibit longer time to relapse and less sexual dysfunction and weight gain
Selegiline Transdermal System
(Lecture 1)
The MOA of this drug is unknown, but may inhibit 2 signal transduction pathways; it is used in the tx of the manic phase for bi-polar patients and anti-manic effects can occur in 1-2 weeks; it appears to be neuroprotective.
Lithium
(Lecture 2) This drug class acts directly on postsynaptic dopamine receptors and do not require enzymatic conversion. Specifically, D2 receptor stimulation improves rigidity and bradykinesia in Parkinson's
Dopamine agonists
(Lecture 2)
This short-acting dopamine agonist stimulates post-synaptic D2-type receptors
Apomorphine
Will probably cause severe N/V… prophylax with trimethobenzamide
(Lecture 2)
This Aromatic L-amino Acid Decarboxylase (AAAD) inhibitor DOES NOT CROSS THE BBB; prevents peripheral conversion and metabolism of levopdopa to dopamine in the peripheral tissues, thereby allowing increased availability of levodopa to cross into the CNS
Carbidopa
(Lecture 2)
This precursor to dopamine HAS THE ABILITY TO CROSS THE BBB and replenish depleted dopamine in the brain; it is CONVERTED TO DOPAMINE IN THE PERIPHERY
Levodopa
(Lecture 2)
This drug irreversibly inhibits the metabolism of dopamine by MAO-B (ONLY!! -> lower risk of HTN CRISIS) which results in increased dopamine levels in the brain
Selegiline
LAST DOSE SOULD BE EARLY AFTERNOON TO PREVENT INSOMNIA
(Lecture 2)
This MAOI has not yet had selectivity for MAO-B definitively established, but provides sx relief to PTs suffering from Parkinson’s and has possible neuroprotective effects
Rosagiline
- 5X MORE POTENT THAN SELEGILINE
- NOT METABOLIZED TO AMPHETAMINE
- HTN CRISIS POTENTIAL needs ADDITIONAL TESTING
- DO NOT take with TYRAMINE-containing foods
(Lecture 2) This class of drugs blocks the excitatory neurotransmitter ACTH to try and restore balance with dopamine
Anticholinergics
EX: Benzatropine; Trihexyphenidyl
(Lecture 2)
This NMDA Receptor Inhibitor’s MOA is not completely understood, does not work if dopamine release is already at maximum and has an adverse risk of LIVEDO RETICULARIS
Amantadine
(Lecture 2) This class of drug prevents the dreakdown of dopamine, leaving more levodopa available to cross the BBB
COMT Inhibitors
EX: Tolcapone, Entacapone, Stalevo
(Lecture 3)
These drugs work by blocking/preventing the spead of electrical discharge by one of several mechanisms:
- Enhancement of GABAnergic transmission
-Diminution of excitatory transmission
-Modification of ionic conductance through ion channels
Anticonvulsants
(Lecture 3)
This drug is a fast sodium channel blocker used as part of Tx in status epilepticus; DO NOT USE in absence seizures
Phenytoin
PREGNANCY CAT D
(Lecture 3)
This drug is also a fast sodium blocker and is the PRODRUG for another drug with a similar name and is preferred when parenteral administration is needed
Fosphenitoin
1mg PHENYTOIN = 1.5mg FOSPHENYTOIN
(Lecture 3)
This drug is a fast sodium channel blocker, a CYP3A4 INDUCER and AUTO-INDUCER, used to tx primary gen. tonic-clonic simple, or complex partial seizures as well as TGN and bipolar disease
Carbamazepine
(Lecture 3)
This drug is a fast sodium channel blocker, is a CYP inducer, and used similarly to carbamazepine (but less potent) and reserved for PTs who do not tolerate it well
Oxcarbazepine
(Lecture 3)
This drug’s MOA is to increase GABA mediated chloride influx (inhibitory neurons)
Primidone
-IS METABOLIZED TO PHENOBARBITAL AND PHENYLETHYLMALONAMIDE
(Phenobarbital has the same basic MOA)
(Lecture 3)
This drug and its derivatives block t-type CALCIUM currents, blocks SODIUM channels, INCREASES GABA PRODUCTION and DECREASES GABA DEGRADATION
Valproic acid
(Lecture 3)
This drug inhibits the a2delta subunit of voltage-dependent ALCIUM channels and is an analog of GABA, but does not directly impact the GABA receptor
Gabapentin
ADEs include DROWSINESS, FATIGUE, DIZZINESS, and WEIGHT GAIN
(Lecture 3)
This drug is a GABA derivative similar to Gabapentin that binds pre-synaptically to the a2deltasubunit of the voltage-gated calcium channel AND BLOCKS INFLUX OF Ca2+ IN HYPER-EXCITED NEURONS
Pregabalin
ADEs include DIZZINESS and WEIGHT GAIN
(Lecture 3)
The way this drug is used is mostly unknown, but is thought to block T-type calcium channels; it is the DOC in absence seizures.
Ethosuximide
(Lecture 3)
This drug acts by decreasing glutamate and aspartate release, delays repetitive firing of neurons, and blocks fast sodium channels
Lamotrigine
(Lecture 3)
This drug acts by blocking fast sodium channels, enhancing GABA activity, antagonizing AMPA/kainate activity, and is a weak carbonic anhydrase inhibitor
Topiramate
(Lecture 3)
This drug binds at voltage gated POTASSIUM CHANNELS and may also exert therapeutic effects through augmentation of GABA-MEDIATED CURRENTS
Ezogabine
ADEs include URINARY RETENTION, UTI, QT PROLONGATION, PSYCHOSIS, RETINAL ABNORMALITIES and VISION LOSS (req. periodic vision tests), and SKIN DISCOLORATION
(Lecture 3)
This drug works by ENHANCING THE SLOW INACTIVATION OF SODIUM CHANNELS
Lacosamide
ADEs include Prolonged PR INTERVAL, AV BLOCKS, MULTIORGAN HYPERSENSITIVITY, NEUTROPENIA
(Lecture 3)
This drug IRREVERSIBLY INHIBITS GABA-T and is a MONOTHERAPY FOR INFANTILE SPASMS
Vigabactrin
ADEs include VISION LOSS (needs periodic vision testing); RESTRICTED DISTRIBUTION PROGRAM, MRI ABNORMALITIES, DEPRESSION, and WEIGHT GAIN
(Lecture 3)
This drug works at BOTH SODIUM AND CALCIUM CHANNELS, is used in the tx of BIPOLAR D/O, and is a SULFONAMIDE
Zonisamide
ADEs include RASH, SJS/TEN, APLASTIC ANEMIA, AGRANULOCYTOSIS, NEPHROLITHIASIS
CHILDREN MAY ALSO HAVE FEVER AND HYPERHIDROSIS when using it
(Lecture 3)
This drug has WEAK INHIBITORY EFFECTS ON GABA-RECEPTOR BINDING, benzo receptor binding, is a adjunct for Lennox Gastaut
Felbamate
ADEs include APLASTIC ANEMIA, LIVER FAILURE
(Lecture 3)
This drug ENHANCES THE ACTIVITY OF GABA and is an ADJUNCTIVE therapy for partial seizures, but has a potential ADE of NONCONVULSIVE STATUS EPILEPTICUS
Tiagabine
Other ADEs include SJS/TEN
(Lecture 3)
This drug is used in the tx of Eclampsia; possibly works by potent cerebral vasodilator properties which reduce the chance of seizures caused by vasospasm decreasing cerebral blood flow
MAGNESIUM SULFATE
