Test 1 MOAs Flashcards
Acepromazine MOA
Inhibits central dopaminergic and is antimuscarinic and blocks norepinephring at adrenergic receptors (alpha receptors). Sedation and vasodialation.
Acetaminophen MOA
Analgesic: Inhibits centrally mediated pain transmission by inhibition of COX 3, inhibit prostaglandins in tissues low in arachidonic acid. Site of action is peroxidase enzyme on prostaglandin H2 synthase. Stimulate inhibitory pain pathwasy mediated by serotonin (5HT3)
Altrenogest MOA
Synthetic progestin thus progesterone agonist. Suppresses estrus, predictable estrous activity once discontinued. Useful to induce syncronized normal cycle of estrous.
Apomorphine MOA
Emetic; potent lipophilic agent that crosses the blood brain barrier to stimulate dopamine receptors in the vomiting center. Not absorbed orally due to first pass effect.
Aspirin MOA
NSAID: Binds irreversibly to COX enzyme in tissues to inhibits synthesis of prostaglandins. Inhibition of NF kappa-B.
Azathioprine MOA
Inhibits T-cell lymphocyte function specifically purine metabolism
Benzocaine MOA
Inhibits Na channels on neurons thus inhibiting depolarization and conduction of nerve impulses.
Betamethasone MOA
Corticosteroid (no glucocorticoid effects) that inhibits inflammatory cells, suppresses expression of inflammatory mediators. Anti-inflammatory and immunosuppressive.
Budesonide MOA
Corticosteroid. High glucocorticoid and weak mineralocorticoid
Bupivacain MOA
Inhibits Na channels on neurons thus inhibiting depolarization and conduction of nerve impulses. Binds to prostaglandin E2 receptors to inhibit production of prostaglandins thus reduce fever, inflammation, and hyperalgesia
Carprofen MOA
NSAID: inhibits COX, relatively COX 1 sparing
Chlorambucil MOA
Cytotoxic agent: nitrogen mustard
Ciclesonide MOA
Affinity for glucocorticoid receptor that has anti-inflammatory activity
Cisapride MOA
Increase GI motility: Agonist for 5-hydroxytryptamine (5-HT4) recetors on myenteric neurons, antagonist for 5-HT3 receptor, thus enhanses the release of acetylcholine at the myenteric plexus thereby increasing motility of the stomach, SI, and colon.
Cloprostenol MOA
Synthetic prostaglandin (PGF2-alpha) provides PGF2 alpha effects. Direct luteolytic action on CL. In non-cycling cows induces etrus in 2-5 days. Terminates pregnancy. Resolution of pyometra, mummified fetus, or luteal cyst.
Cyclophosphamide MOA
Cytotoxic and anticancer agent. Nitrogen mustards that alkylate various macromolecules (guanine of DNA), toxic to rapidly proliferating cells
Cyclosporine MOA
Binds to receptor on calcineurin and inhibits the t cell receptor activated signal transduction pathway. Blocks cytokines (IL 2) and block proliferation of activated T lymphocytes
Cyproheptadine MOA
Antiserotonin properties that alter serotonin activity in appetite center.
Deracoxib MOA
NSAID: inhibits COX, relatively COX 1 sparing
Desoxycorticosterone pivalate MOA
Mineralocorticoid without glucocorticoid activity, mimics the effects of aldosterone by retaining Na.
Dexamethasone MOA
Corticosteroid that inhibits inflammatory cells, suppresses expression of inflammatory mediators. Anti-inflammatory and immunosuppressive. Glucocorticoid effects.
Diazepam MOA
Potentiation of GABA-receptor-mediated effects in CNS.
Diclofenac MOA
NSAID: inhibits COX thus inhibiting prostaglanding formation
Dinoprost MOA
Synthetic prostaglandin (PGF2-alpha) provides PGF2 alpha effects. Direct luteolytic action on CL. In non-cycling cows induces etrus in 2-5 days. Terminates pregnancy. Resolution of pyometra, mummified fetus, or luteal cyst.
Diphenhydramine MOA
Antihistamine: blocks H1 receptor and suppresses inflammation caused by histamine.Antiemetic: block histamine in vomiting control centers.
Diphenoxylate MOA
Binds to mu-opiate receptors to stimulate smooth muscle segmentation, decrease peristalsis, enhance fluid and electrolyte.
eCG MOA
Mare: LH like action causing ovulation/luteinization of follicles. All other animals: FSH like action.
Erythromycin MOA
GI motility: stimulation of motilin receptors. Antibiotics: binds 50S ribosome in bacteria to inhibit protein synthesis. Spectrum: gram positive aerobic bacteria and mycoplasma. Cattle: Pasteurella multocida, Mannheimia haemolytica, Histophilus somni.
Etodolac MOA
NSAID: inhibits COX, relatively COX 1 sparing in horses but not in dogs
Famotidine MOA
Antiulcer agent; inhibit histamine on H2 receptors of parietal cells, inhibits gastric parietal cell thus dec gastric acid secretion thus increases stomach pH.
Finasteride MOA
Synthetic steroid type II 5 alpha reductase inhibitor. Inhibits conversion of testosterone to dihydrotestosterone.
Firocoxib MOA
NSAID: inhibits COX, relatively COX 1 sparing
Flumethasone MOA
Potent glucocorticoid that inhibits inflammatory cells, suppresses expression of inflammatory mediators. Anti-inflammatory and immunosuppressive.
Flunixin MOA
NSAID: inhibits COX thus inhibiting prostaglanding formation
Flurbiprofen MOA
NSAID: inhibits COX thus inhibiting prostaglanding formation
Fluticasone MOA
Glucocorticoids that inhibit gene transcription for production of mediators involved in airway inflammation as well as prostaglandins, leukotrienes, and platelet activtating factors.Enhance action of adrenergic agonists on beta 2 receptors
FSH MOA
Follicular growth and stimulates OV.
Gonadorelin MOA
Stimulates the release of LH to cause OV and luteinization.
hCG MOA
Induces luteinization in animals to stimulate ovulation.
Hydrocortisone MOA
Glucocorticoid with weak anti-inflammatory effect and greater mineralocorticoid effect. Inhibits inflammatory cells, suppresses expression of inflammatory mediators. Anti-inflammatory and immunosuppressive.
Hydrocortisone MOA
Glucocorticoid: Inhibition of inflammatory cells and supress the gene expression of inflammatory mediators
Ibuprofen MOA
NSAID: inhibits COX thus inhibiting prostaglanding formation
Insulin MOA
Replace deficient insulin
isoflupredone MOA
Corticosteroid with gluco- and mineralocorticoid effects. Inhibits inflammatory cells, suppresses expression of inflammatory mediators. Anti-inflammatory and immunosuppressive.
Ketoprofen MOA
NSAID: inhibits COX thus inhibiting prostaglanding formation
Lidocaine MOA
Increase GI motility: suppression of painful stimuli, anti-inflammatory effects on neutrophils. Local anesthetic: inhibits nerve conduction by blocking the Na channel
Loperamide MOA
Binds to mu-opiate receptors to stimulate smooth muscle segmentation, decrease peristalsis, enhance fluid and electrolyte, antisecretory, increase tone of GI sphincters.
Maropitant MOA
Antiemetic for central and peripheral sources: blocks neurokinin-1 receptor in the emetic center.
Megestrol MOA
Progestin hormone mimics the effects of progesterone. It feeds back on the pituitary to inhibit LH thus stopping maturation of follicles and ovulation.
Melengesterol MOA
Progestin hormone mimics the effects of progesterone. It feeds back on the pituitary to inhibit LH thus stopping maturation of follicles and ovulation.
Meloxicam MOA
NSAID: inhibits COX, relatively COX 1 sparing
Mepivacaine MOA
Antagonist of Na channels in nerves thus inhibiting neural conduction
Methimazole MOA
Antithyroid drug serves as a substrate for thyroid peroxidase to inhibit it and decrease incorporation of iodide into T4 and T3. Also inhibits coupling of residues to T4 and T3.
Methylprednisolone MOA
Corticosteroid with glucocorticoid effects. Inhibits inflammatory cells, suppresses expression of inflammatory mediators. Anti-inflammatory and immunosuppressive.
Metoclopramide MOA
Antiemetic: stimulates motility of upper GI by stimulating 5-HT4 (serotonin) receptors, increase release of ACh in GI tract, anti-dopamine inhibits gastric relaxation
Misoprostol MOA
Synthetic analogue of PGE1 causing a cytoprotective effect on GI mucosa thus decreasing the damage to GI mucosa by NSAIDs.Anti-inflammatory effects.
Mitotane MOA
Cytotoxic agent that binds to adrenal proteins is converted to a reactive metabolite then destroys the cells of the zona fasciculata and reticularis of adrenal cortex.
Mycophenolate MOA
Inhibits inosine monophosphate dehydrogenase which is used for gene creation
Naproxen MOA
NSAID: inhibits COX thus inhibiting prostaglanding formation
N-butylscopolammonium bromide MOA
Blocks cholinergic receptort decreasing parasympathetic actions. Antispasmotic, antimuscarinic, anticholinergic. Inhibits secretions and motility of GI.
Neostigmine MOA
Cholinesterase inhibitor.
Oclacitinib MOA
Inhibits a variety of pruritogenic cytokines and pro-inflammatory cytokines and cytokinse (JAK1 or JAK3 dependent) and involved in allergies.
Omeprazole MOA
Antiulcer: Increases stomach pH by inhibiting gastric acid secretion by inhibiting K+/H+ pump.
Ondansetron MOA
Antiemetic: inhibits serotonin type 3 receptors (5-HT3),
Oxytocin MOA
Stimulates oxytocin receptors to stimulate uterine muscle contractions. When admin near luteolysis it stimulates PGF2 alpha secretions and disrupts luteolysis.
Pergolide MOA
Dopamin agonist that stimulates postsynaptic dopamine receptors (D1, D2). Dopamine then antagonises ACTH release which helps Cushing’s dz expessially in horses.
Phenylbutazone MOA
NSAID: inhibits COX thus inhibiting prostaglanding formation
Physostigmine MOA
Cholinesterase inhibitor. Crosses the blood brain barrier.
Piroxicam MOA
NSAID: inhibits COX, relatively COX 1 sparing
Prednisolone MOA
Corticosteroid with glucocorticoid effects. Inhibits inflammatory cells, suppresses expression of inflammatory mediators. Anti-inflammatory and immunosuppressive.
Prednisone MOA
Corticosteroid with glucocorticoid effects. Inhibits inflammatory cells, suppresses expression of inflammatory mediators. Anti-inflammatory and immunosuppressive.
Progesterone CIDR MOA
Synthetic progesterone removal results in predictable return to estrus
Proparacaine MOA
Antagonist of Na channels in nerves thus inhibiting neural conduction
Pyridostigmine MOA
Cholinesterase inhibitor.
Ranitidine MOA
Increase GI motility: Anticholinesterase. Increase stomach pH: Antagonist of H2 in gastric parietal cell.
Robenacoxib MOA
NSAID: inhibits COX, relatively COX 1 sparing
Sucralfate MOA
Antiulcer: Gastric mucosa protectant: forms sucrose octasulfate and aluminum hydroxide in the stomach which binds to the damaged mucosa.
Tacrolimus MOA
Binds to intracellular receptor and to calcineurin and inhibits that pathway to prevent stimulation of the nuclear factor (NFAT transcription factor for IL 2)
Thyroxine MOA
Replace deficiency in thyroid
Tramadol MOA
Some mu-opioid receptor action, inhibits reuptake norepinephrine and serotonin 5 HT thus effects alpha 2 adrenergic receptors in pain paths
Triamcinolone MOA
glucocorticoid. Anti inflammator via inhibition of inflammatory cells and suppression of DNA expression of inflammatory mediators.
Triamcinolone MOA
Corticosteroid with glucocorticoid effects. Inhibits inflammatory cells, suppresses expression of inflammatory mediators. Anti-inflammatory and immunosuppressive.
Trilostane MOA
Inhibits synthesis of cortisol in dogs. Inhibits 3-beta-hydroxysteroid dehydrogenate thus interferring with cortisol secretion from adrenal cortex. Used for pituitary dependent hyperadrenocorticism in dogs.