3pd top 200 MOA

bind opioid receptors, resulting in altered pain perception

hydrocodone MOA

bind opioid receptors, resulting in altered pain perception

apap/hydrocodone MOA

Oxycodone is pure mu agonist. Mu receptors are responsible for analgesia, respiratory depression, miosis, decreased GI motility,

and euphoria

oxycodone MOA

3-methylmorphine, phenanthrene opioid with

very low affinity for opioid receptors. Analgesic activity

appears to result from conversion to morphine

APAP/Codeine MOA

Phenylpiperidine opioid agonist with predominant effects on mu-receptor

50-100x as potent as an analgesic than morphine

fentanyl MOA

a pure mu agonist. Mu receptors are responsible for analgesia, respiratory depression, miosis, decreased GI motility, and euphoria.

morphine MOA

a mu agonist and a weak inhibitor of serotonin and norepinephrine reuptake

tramadol MOA

mu-receptor partial agonist and kappa-

receptor antagonist, mu-receptor antagonist that causes opioid withdrawal when injected parenterally

buprenorphine/naloxone MOA

Inhibit monosynaptic and polysnaptic reflexes at spinal level; possibly by hyperpolarization of afferent terminals

although action at supraspinal sites may occur and contribute to effect. Analog of gamma-aminobutyric acid (GABA) but no evidence that actions on GABA systems involved

baclofen MOA

Relieve skeletal muscle spasm of local origin without interfering with muscle function. It is ineffective in muscle

spasm due to CNS disease. Net effect is a reduction in tonic motor activity, influencing both gamma and alpha motor systems

cyclobenzaprine MOA

not been established but may be due to general CNS depression. It has no direct action on the contractile mechanism of striated muscle, the motor end plate, or the

nerve fiber.

methocarbamol MOA

centrally acting muscle relaxant, imidazole derivative, agonist of α2- adrenergic receptors, which decreases spasticity by

increasing presynaptic inhibition

tizandine MOA

Block interneuronal activity in descending reticular formation and spinal cord, resulting in muscle relaxation

carisoprodol MOA

Nonselective inhibitor of cyclo-oxygenase-1 (COX-1) and cyclo-oxygenase-2 (COX-2), and reversibly alters platelet function and prolongs bleeding time.

ibuprofen MOA

Nonselective inhibitor of COX-1 and COX-2 which results in decreased formation of prostaglandin precursors; has antipyretic,

analgesic, and anti-inflammatory properties; reversibly alters platelet function and prolongs bleeding time.

meloxicam MOA

Nonselective inhibitor of COX-1 and COX-2

naproxen MOA

Inhibition of COX-2 enzyme isoform, thought to be responsible for the anti-inflammatory effects of NSAIDs

celecoxib MOA

Nonselective inhibitor of cyclo-oxygenase-1 (COX-1) and cyclo-oxygenase-2 (COX-2).

diclofenac sodium MOA

amide-type local anesthetic agent and is suggested to stabilize neuronal membranes by inhibiting the ionic fluxes required for the initiation and conduction of impulses.

lidocaine MOA

anti-inflammatory, antipruritic, and

vasoconstrictive properties. Corticosteroids are thought to act by the induction of phospholipase A2-inhibitory proteins,

lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as

prostaglandins and leukotrienes by inhibiting the release of their common precursor, arachidonic acid.

hydrocortisone MOA

naturally occurring and synthetic adrenocortical steroids that cause varied metabolic effects, modify the body's immune responses to diverse stimuli, and are used primarily for their anti-inflammatory effects in disorders of

many organ systems.

methylprednisolone MOA

naturally occurring and synthetic adrenocortical steroids that cause varied metabolic effects, modify the body's immune responses to diverse stimuli, and are used primarily for their anti inflammatory effects in disorders of

many organ systems.

prednisolone MOA

naturally occurring and synthetic

adrenocortical steroids that cause varied metabolic effects, modify the body's immune responses to diverse stimuli, and are used primarily for their anti-inflammatory effects in disorders of

many organ systems.

prednisone MOA

anti-inflammatory, antipruritic, and

vasoconstrictive properties, act by the induction of phospholipase A2 inhibitory proteins, lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as

prostaglandins and leukotrienes by inhibiting the release of their common precursor, arachidonic acid.

triamcinolone MOA

binds with high affinity to serotonin (5-HT)

subtypes 1B, 1D, and 1F receptors, vasoconstriction through activation of 5-HT1 receptors on sensory nerve endings in the

trigeminal system resulting in the inhibition of proinflammatory neuropeptide release.

sumatriptan MOA

binds to bone hydroxyapatite and, at the

cellular level, inhibits osteoclast activity, thereby inhibiting bone resorption and modulating bone metabolism.

alendronate

decreases the production of uric acid by inhibiting the action of xanthine oxidase, the enzyme that converts hypoxanthine to xanthine and xanthine to uric acid

allopurinol MOA

prostaglandin F2-alpha analog. It is believed to reduce IOP by increasing the outflow of aqueous humor. Studies

suggest that the main mechanism of action is increased uveoscleral outflow, but the exact mechanism is unknown.

lantanoprost MOA

relatively selective α-adrenergic agonist, reduces aqueous humor production and increases uveoscleral outflow.

brimonidine MOA

low-sedating, long-acting H1-receptor antagonist that is a metabolite of hydroxyzine, competitively inhibits the interaction of histamine with H1 receptors, thereby preventing the allergic response.

cetirizine MOA

required for the conversion of deoxyuridylate to thymidylate, which is a rate-limiting step in DNA synthesis.

folic acid MOA

unknown. It is effective in treating P. vivax, P. malariae, and susceptible strains of P. falciparum.

hydroxychloroquine MOA

antihistamine that suppresses the vasodepressor response to histamine while only slightly inhibiting acetylcholine

meclizine MOA

Reversibly inhibits dihydrofolate reductase (DHFR). Dihydrofolates are reduced to tetrahydrofolates by DHFR before they are used in DNA synthesis, interferes with DNA synthesis, repair, and cellular replication

methotrexate MOA

competitive muscarinic receptor antagonist.

Muscarinic receptors play an important role in several major cholinergically mediated functions, including contractions of the

urinary bladder smooth muscle and stimulation of salivary secretion.

oxybutynin MOA

competitive muscarinic receptor antagonist. Muscarinic receptors play an important role in several major cholinergically mediated functions, including contractions of the

urinary bladder smooth muscle and stimulation of salivary secretion.

solifenacin MOA

a competitive muscarinic receptor antagonist, has high binding affinity for the cholinergic muscarinic receptors that mediate contraction of the urinary bladder and salivation. The drug exerts its significant effects on the lower urinary tract by increasing the residual urine and decreasing detrusor pressure.

tolterodine MOA

a sympathomimetic amine with pharmacologic activity similar to amphetamines. Actions include CNS

stimulation and elevation of BP. Weight loss is due to anorectic effect, primarily one of appetite suppression, but may also have

other CNS or metabolic effects.

phentermine MOA

Inhibition of phosphodiesterase type 5 (PDE5) by sildenafil increases the amount of cyclic guanosine monophosphate (GMP)

enhancing erectile function and pulmonary vasculature relaxation.

sidenafil MOA

Inhibition of phosphodiesterase type 5 (PDE5) by sildenafil increases the amount of cyclic guanosine monophosphate (GMP)

enhancing erectile function and pulmonary vasculature relaxation.

tadalafil MOA

Forms a complex with positively charged proteins that forms a protective coating for local protection of the gastric lining

sucralfate MOA