MOA Flashcards
low to moderate noncompetitive antagonist at NMDA receptors, persistent stimulation of NMDA receptors by glutamate is thought to possibly contribute to the symptomology of AD
NMDA Receptor Antagonist; Memantine (Namenda) MOA?
reversibly and non-competitively inhibits centrally active acetylcholinesterase, which results in increased levels of Ach available for synaptic transmission in the CNS
AD drugs Donepezil and Rivastigmine MOA?
may inhibit burst firing without affecting normal neuronal excitability
Levetiracetam MOA?
may block sodium channels or potentiate GABA
Topirimate MOA?
increases GABA availability, enhances action of GABA, mimics action at postsynaptic sites
Valproic acid MOA?
exact MOA is unk, but blocks voltage dependent sodium and chloride channels
Zonisamide MOA?
thought to affect voltage sensitive sodium channels and inhibit presynaptic release of glutamate and aspartate in the neuron
Lamotrigine MOA?
exact MOA is unclear, but thought to affect the NA+ channels, slowing influx of NA+ in the cortical neurons and slowing spread of abnormal activity
Carbamazepine (Tegretol) MOA?
inhibit and stabilize electrical discharges in the motor cortex of the brain by affecting the influx of sodium ions during generation of nerve impulses
Phenytoin (Dilantin) MOA?
binding the circulating TNF-alpha, rendering it inactive; reduces chemostatic affect of TNF alpha by reducing IL-6 and CRP, resulting in reduced infiltration of inflammatory cells into the joint; cell lysis also occurs
Biologic DMARDS (Non-TNF Biologics) Rituximab and Abatacept MOA?
folic acid antagonist, thought to affect leukocyte suppression, decreasing inflammation, decreasing inflammation that results from immunological byproducts
Disease modifying anti-rheumatic drugs (DMARDS) like Methotrexate?
inhibits conversion of arachidonic acid to prostaglandin, prostacyclin, and thromboxanes, all of which are mediators of pain and inflammation
NSAIDS MOA?
decreases inflammation by suppressing migration of polymorphonuclear leukocytes (neutrophils, eosinophils, and basophils) and reversing increased capillary permeability
Corticosteroids (Prednisone) MOA?
inhibits activation, degranulation and migration of neutrophils to area of gout attack, decreases inflammation and pain associated with gout attack; takes 18-24 to work and full effect is at 48 hours
Colchicine MOA?
increases excretion of serum uric acid by competitively inhibiting reabsorption of uric acid in kidney
Probenecid MOA?
decrease uric acid by selectively inhibiting xanthine oxidase, uric acid decreases, reducing risk of crystallization and gout attack
Antigouts (Allopurinol and Febuxostat) MOA?
inhibit bone reabsorption by reducing osteoclast number and fxn
Bisphosphonates MOA?
thickens cervical mucus to inhibit sperm mitigation, suppresses ovulation, lower mid-cycle peak of FSH and LH; slow egg movement through fallopian tube; thins endometrium
Progesterone MOA?
primary effects are maturation and function of female reproductive system; in addition to breast, ovaries, and uterus, estrogen receptors also present in bone, CNS, GI tract and CV tissue
Estrogens and Anti-Estrogens MOA?
luteinizing hormone (LH)- releasing hormone antagonists; creates reversible chemical orchiectomy state in males; creates reversible chemical oophorectomy state in females
GnRH Analogues (Leuprolide, Lupron) MOA?
inhibits enzyme that converts testosterone to DHT
Finasteride (Proscar, Propecia) MOA?
principle endogenous androgen responsible for promoting the growth and development of male sex organs and maintaining secondary sex characteristics
Testosterone MOA?
after diffusing into the organism, it is thought that tinidazole causes cytotoxicity by damaging DNA and preventing additional DNA synthesis
Tinidazole MOA?
diffuses into the organism and interacts with DNA to cause a loss of helical DNA structure and strand breakage, results in inhibition of protein synthesis and cell death
Metronidazole MOA?
synthetic allylamine derivative that inhibits squalene epoxidase, a key enzyme in sterol biosynthesis in fungi, resulting in fungal cell death
Terbinafine MOA?
interferes with fungal cytochrome p450 activity, decreasing ergosterol synthesis (principle sterol in fungal cell membrane), and inhibiting cell membrane formation
Fluconazole and itraconazole MOA?
dependent endonuclease inhibitor that interferes with viral RNA transcription, resulting in inhibition of flu virus replication
Baloxavir marboxil MOA?
neuraminidase is a viral enzyme responsible for cleaving viral attachment to the host cell surface, allowing for viral circulation, inhibiting this enzyme prevents release of virus and halts the spread of infection
Neuraminidase inhibitors (Oseltamivir, zanamivir, peramivir) MOA?
inhibit HCV protein necessary for viral replication
Hep C Tx (Ledipasvir/Sofosbuvir) and (Sofosbuvir/Velpatasvir) MOA?
interferes with DNA synthesis and inhibit viral replication
Nucleoside analogues (Acyclovir, Famiciclovir, and Valacyclovir) MOA?
activated by bacteria to re-activate intermediates that inactivate or alter bacterial ribosomes, leading to inhibition of protein synthesis, aerobic energy metabolism, DNA, RNA, and cell wall synthesis
Nitrofurantoin MOA?
competitively inhibit dihydrofolate synthetase, which is necessary for the conversion of para-aminobenzoic acid (PABA) to dihydrofolate acid, inhibiting this pathway prevents folic acid synthesis, which is important for some bacteria to survive
Sulfonamides and Trimethroprim (Bactrim) MOA?
bactericidal through interference with enzymes required for the synthesis and repair of bacterial DNA and promote breakage of DNA strands
Fluoroquinolones (Cipro and Levo) MOA?
inhibit protein synthesis by reversibly binding to the 30S subunit of the bacterial ribosome
What is the MOA of Tetracyclines?
binds to the 50s subunit of the bacterial ribosome and suppresses protein synthesis
What is the MOA of both lincosamides (clindamycin) and macrolides (erythromycin, azithromycin, and clarithromycin)?
inhibit bacterial cell wall synthesis by blocking glycopeptide polymerization through binding tightly to the D-A1a-D-A1a portion of cell wall precursor
What is the MOA of glycopeptides (vancomycin)?
prevent bacterial cell wall synthesis during active multiplication, causing cell wall death; bactericidal against susceptible bacteria
What is the MOA of Penicillins and Cephalosporins
competitively inhibits postsynaptic alpha 1 receptors which results in vasodilation of veins and arterioles and a decrease in total peripheral resistance and BP
Alpha 1 selective antagonists (doxazosin, tamsulosin, or terazosin) Hypertension MOA
competitively inhibits postsynaptic alpha-1 receptors in prostatic stromal and bladder neck tissues, which reduces the sympathetic tone induced urethral stricture causing BPH sxs
Alpha 1 selective antagonists (doxazosin, tamsulosin, or terazosin) BPH MOA?
stimulates alpha-2 receptors in the brain stem, activating an inhibitory neuron, resulting in reduced sympathetic outflow from the CNS, decreasing peripheral resistance, HR, BP, & renal vascular resistance; * this all occurs due to down regulation of alpha-2 receptors after chronic use
Alpha 2 agonists: central (Clonidine/Catapres)
HTN MOA?
MOA unknown; thought that it regulates activity in the prefrontal cortex responsible for emotions, attention & behaviors
Alpha 2 receptors: central (Clonidine/Catapres)
MOA ADHD?
stimulation of central alpha-2 receptors by methyldopa’s metabolite alpha-methylnorepinephrine, which produces a decrease in sympathetic outflow to the heart, kidneys, & blood vessels; can build tolerance over 2-3 months & may have to increase dose or add on diuretic
Alpha 2 agonists: central
Methyldopa MOA?
block beta-1 receptors at the SA node to decrease HR, decrease contractility in the atria & ventricles and conduction velocity, and slow conduction at the AV node
Selective BBs: Metoprolol and Atenolol MOA
competitively block response to beta-1 & beta-2 stimulation, which results in decreased HR, myocardial contractility, BP & myocardial oxygen demand
Nonselective BBs: Propanolol (Inderal) MOA
nonselective beta receptor blockade & alpha-1 receptor blockade thereby decreasing BP & peripheral resistance; these combined effects decrease myocardial oxygen demand & lower cardiac workload
Combined Alpha and Beta-Adrenergic Agonists and Antagonists: Carvedilol MOA
nonselective beta receptor blockade & alpha-1 receptor blockade thereby decreases BP & peripheral resistance; these combined effects decrease myocardial oxygen demand & lower cardiac workload
Combined Alpha and Beta-Adrenergic Agonists and Antagonists: Labetalol MOA
decreases the vasodilation & vascular permeability that occur during anaphylaxis; relaxes smooth muscles, relieves bronchospasm, wheezing, dyspnea, pruritus, angioedema, & urticaria
Combined Alpha and Beta-Adrenergic Agonists and Antagonists: Epinephrine MOA
