Drugs Flashcards
List category and actions of each drug listed
Diphenhydramine
1st gen. H1 histamine blocker
Competitive antagonist/inverse agonist
^ free intracellular Ca2+
Chlorpheniramine
1st gen. H1 histamine blocker
Competitive antagonist/inverse agonist
^ free intracellular Ca2+
phrilamine
1st gen. H1 histamine blocker
Competitive antagonist/inverse agonist
^ free intracellular Ca2+
Meclizine
1st gen. H1 histamine blocker
Competitive antagonist/inverse agonist
^ free intracellular Ca2+
hydroxyzine
1st gen. H1 histamine blocker
Competitive antagonist/inverse agonist
^ free intracellular Ca2+
Cetirizine
2nd gen H1 histamine blocker
Competitive antagonist/inverse agonist
^ free intracellular Ca2+
Pumped out of BBB by P glycoprotein
Loratidine
2nd gen H1 histamine blocker
Competitive antagonist/inverse agonist
^ free intracellular Ca2+
Pumped out of BBB by P glycoprotein
Fexofenadine
2nd gen H1 histamine blocker
Competitive antagonist/inverse agonist
^ free intracellular Ca2+
Pumped out of BBB by P glycoprotein
Epinepherine
Functional antagonist of histamine effects
Agonizes all ARs
A: vasoconstriction –> ^ BP
B1: ^ HR and CO –> ^ systolic BP
B2: skeletal muscle vasodilation –> decreased systolic BP –> widening in pulse
Vc, decreased allergic response
Use in anaphylactic shock, heaves, hypotensive states, cardiac arrest, + hemostasis, local anesthesia, can produce cardiac dysrhythmias
Misoprostil
H2-histamine antagonist, PGE derivative
Decrease acid secretion, increase GI mucosal cytoprotection, decrease mast cell degranulation
Highly effective, long lasting
Dinoprost
PGF-2a derivative
Estrus synchronization
Increase uterine contractions (expel uterus pus, abortion)
Travoprost
PGF-2a derivative
Glaucoma, ocular fluid drainage (decr. ocular pressure)
latanoprost
PGF-2a derivative
Glaucoma, ocular fluid drainage (decr. ocular pressure)
Carprofen
Proprionic acid derived Inhibits COX-2 > COX-1 No TxA2 inhibition Low ulcer formation Anti-inflammatory analgesic > aspirin, phenylbutazone
Deracoxib
Coxib
Inhibits COX-2 > COX-1
No TxA2 inhibition
GI ulcers and changes in renal function at high doses
Tepoxalin
Dual COX/5-LOX inhibitor (block both sides of arachadonic acid pathway)
Inhibits COX-2 > COX-1, 5-LOX, NF-kB, TxA2
Phenylbutazone –> oxyphenbutazone
anti-inflammatory/analgesic
inhibits prostanoid biosynthesis, COX-1 and COX-2, and 5-LOX
Chondrodestructive effects
Flunixin/Flunixin Meglumide
Non-selective COX inhibitor (both COX-1 and COX-2)
May inhibit NF-kB
anti-inflammatory, analgesic, antipyretic
Used for skeletal muscle pain (horses) and visceral pain (dogs)
Aspirin/salicylate ions
Irreversibly acetylates/inhibits COX
–> decreases TxA2 formation
Can change properties of COX-2 favoring production of anti-inflammatory lipoxins
anticoagulant, analgesic, anti-pyretic, anti-inflammatory
Cloprostenol
PGF-2a derivative
Estrus synchronization
Increase uterine contractions (expel uterus pus, abortion)
Cromoglycate
Mast cell stabilizer
Mifepristone
GcR antagonist
Inhibits dissociation of HSP90
Changes interaction of GcR with accessory proteins to inhibit GC-GcR effects on gene transcription
Hydrocortisone
Full GC agonist
Short duration
Low anti-inflammatory and Na+ retention potency
Act at GcRs and mineralocorticoid receptors
Dexamethasone
Full GC agonist
Long duration
High potency
No mineralocorticoid activity
Prednisone ( –> prednisolone)
Medium duration and potency
Works both at GcR and MC receptors (more so at GcR)
Prednisolone is more bioavailable in dogs and cats
Triamcinolone
Medium duration and potency
Aldosterone
High mineralocorticoid potency
^ Na+ retention and K+ secretion
Can lead to hypertension and hypokalemic alkalosis
Betamethasone
Long duration
Highly potent GcR agonist
Less mineralocorticoid effects
Cortisone –> hydrocortisone
Greatest MC side effects
Binds both GcRs and MCRs
Fludrocortisone
short duration medium potency (esp. Na+ retention potency)
SEGRAs
Selective GcR agonists
Trans-repress pro-inflammatory genes
trans-activate anti-inflammatory genes
no catabolism-related gene TS –> less side effects
Cyclosporine
Calcineurin inhibitor: binds cyclophilin
Inhibits gene transcription in activated Th cells
Inhibits mast cells and eosinophils as well
Uses for CsA: ocular inflammation, dry eye, atopic dermatitis, graft vs. host defense
CsA increases digoxin plasma levels
Most effective if given before T cell activation has occurred
Tacrolimus
Calcineurin inhibitor: FKBP Inhibits gene transcription in activated Th cells atopic dermatitis More potent Use topically
Bethanechol
Cholinomimetic (alkaloid)
mAChR agonist (contracts smooth m.)
Contract detrusor m. and relax trigone/sphincter m.
GI motility
Carbachol
Cholinomimetic (alkaloid)
mAChR agonist (contracts smooth m)
Rumen/colonic motility
Pilocarpine
Cholinomimetic alkaloid tertiary amine - less ionized mAChR agonist (NOT nAChR) Topical (eye): pupillary constriction Glaucoma: miosis decreases intraocular P Lens ciliary m. accommodation for near vision Dry eye (KCS): increases lacrimation
Edrophonium
Cholinesterase inhibitor
Quaternary ammonium compound: N+ slowly unbinds from (-) anionic site (minutes)
Increases Ach in synaptic zone
Ionized - poor GI absorption
Neostigmine
Carbamate: reversible carbomylates esteratic site (15-30m)
Ionized: poor GI absorption
Can increase Ach at NMJ and surmount nicotinic cholinergic antagonist
mAChR blockers co-administered to prevent adverse muscarinic effects of ACE
Potentiates relaxation of depolarizing agents like succinylcholine
Organophosphates
Irreversibly phosphorylate esteratic site (must be replaced)
Lipid soluble
With all cholinergic agonists: watch for SLID and cardiorespiratory effects (bradycardia)
Cholinergic toxidrome
Solanaceous (belladonna)
mAChR antagonist
alkaloid, tertiary amine ~atropine
mydriasis
increases ocular P, cycloplegia, decreased tear formation
Increased HR and AV conduction
Bronchodilation, decreased tracheobronchiolar secretions
Decreased salivation, GI motility, urinary bladder relaxation and retention
Antiemetic
Sedation (only tertiary amines)
Scopolamine
tertiary amine ~atropine
mydriasis
increases ocular P, cycloplegia, decreased tear formation
Increased HR and AV conduction
Bronchodilation, decreased tracheobronchiolar secretions
Decreased salivation, GI motility, urinary bladder relaxation and retention
Antiemetic
Sedation (only tertiary amines)
Tropicamide
shorter duration and less cycloplegic effects than atropine
can use as short-acting non-cycloplegic a1-Ar agonists
mydriasis
increases ocular P, cycloplegia, decreased tear formation
Increased HR and AV conduction
Bronchodilation, decreased tracheobronchiolar secretions
Decreased salivation, GI motility, urinary bladder relaxation and retention
Antiemetic
Sedation (only tertiary amines)
Quaternary amines and atropine are more peripherally selective
Trimethaphan
nN-AChR blocker (ANS ganglia, some peripheral N-terminals)
Inhibits both sympathetic and parasympathetic neurotransmission
Blocks ganglia without skeletal muscle paralysis
Causes tachycardia, mydriasis, cycloplegia, urine retention, dry mouth, decrease in GI motility (constipation), decreased sweating, decreased cardiac contractility/CO, increased vasodilation, hypotension
Use as hypotensive agent
Pancuronium
nMAChR blocker (skeletal ms. endplates)
Non-depolarizing NM blocker = curariform
Long duration of action (>35m)
Use as skeletal ms. relaxants/paralyzing agents
Also blocks mAChR –> tachycardia (~atropine)
Vecuronium
intermediate duration (20-30m)
No CV side effects
Elim in bile rather than urine
Atracurium
~vecuronium
spontaneously decomposes in plasma
Levamisole
non-depolarizing NM blocker = curariform
antiparasitic