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59 Cards in this Set
- Front
- Back
histamine is chemical mediator of
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inflammatory rxns, allergy, anaphylaxis, gastic secretion and neurotransmission
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what stimulates histamine release?
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1) mast cells/basophils can be sensitized by IgE Abs which cause degranulation upon appropriate Ag exposure 2) certain drugs 3) physical injury
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what opiate stimulates histamine release?
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morphine
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what rc can histamine bind?
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h1 and h2 (also 3 and 4)
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where are h1 rc?
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smooth m, endothelium, CNS, peripheral nerves
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where are h2 rc?
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parietal cells
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histamine h1 rc effects (PLC pathway)
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increase perm of capillaries, recruit eosinophils, pruritis/pain, emetic response, sleep regulation, smooth m/bronchial contraction, smooth m/intestal contraction
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histamine h2 rc effects (camp patheay)
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stimulate HCL release
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how are h1 antihistamines eliminated
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hepatic metabolism
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are h1 antihistamines absorbed orally?
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yes
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h1 antihist side effects
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CNS effects, anticholinergic effeects
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1st generation
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sedative effects (or ataxia), anticholinergic effects (dry mouth, pupillary dilation, tachycardia)
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2nd generation
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less/non sedating antihist, lack antimuscarinic properties, do not cross BBB as easily as 1st (less lipid soluble)
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atopic dermatitis
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chronic pruritic skin dz, genetic predisposition, IgE abs against environmental allergens
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do oral antihists tx atopic dermatitis?
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no conclusive evidnce about efficacy
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drugs that evelate camp / improve allergic symptoms
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epi, theophylline
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why is epi first choice for acute anaphylaxis
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its major action is to reverse vasodilatory effects of histamine
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drugs that lower camp /worsen allergic symptoms
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propranolol, acetycholine
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serotonin comes from
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dietary tryptophan
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where are serotonic rc
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cns
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serotonin storage sites
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cns, gi, platelets
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prostaglandin production
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arachidonic acid --> oxidative enzyme pathways --> PGs
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what is an nsaid?
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drugs that inhibit prostaglandin and/or leukotriene synthesis
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four aspects of an NSAID
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anti inflammatory, analgesis, anti pyretic, anti thrombotoc
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what has an action that opposes prostacyclin?
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thromboxane
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two isoforms of the cox pathway
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cytoprotective Pgs and proinflammatory Pgs
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COX1
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membrane bound enzyme in ER. Expressed consititutively in many tissues and platelets. Blood clotting, renoprotection, gastroprotection
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COX2
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both inducible and constitutive, induced by proinflammatory mediators. Consitituve in brain, kidney and uterus
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PGs play important roles in
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normal physiology and inflammation
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NSAIDS ____ PG production
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inhibit
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nonselective COX inhibitor
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inhibits both COX1 and 2
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preferential COX inhibitor
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prefers to inhibit 1 isoform
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selective cox inhibitor
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selectively inhibits one isoform much more than the other isoform
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dual inhibotir
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inhibits cox and lox
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three major points to nsaid pharmokinetics
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weak organic acids (bioavailibility), lipid soluble (bioavailabiliy), highly bound to plasma protein (distribution)
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what do weak organic acids favor?
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movement from acidic environment of stomach into plasma
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nsaids accumulate in
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inflammatory exudate
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how are most nsaids eliminated
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hepatic metabolism into less active/inactive metabolites. Often infolves glucuronidation (except cats)
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aspirin is antithrombic via
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blocking COX1 (irreversible effect on platelet aggregation)
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some cancers overexpress COX_
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2
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nsaid for mastitis/endotoxemia in cattle
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flunixin
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aspirin, phenylbute and flunixin are ____ nsaids
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nonselective
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carprofen, piroxicam and meloxicam are ____ nsaids
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preferential
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robenacoxib, deracoxib and firocoxib are ___ nsaids
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selective
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dual nsaid
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tepoxalin
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Diphenhydramine
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H1 blocker -Antihistamine, motion sickness in small animals, laminitis in cattle = ++Sedation, anticholin
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Dimenhydrinate
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H1 blocker -Motion sickness in small animals - ++Sedation, anticholin
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Pyrilamine
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H1 blocker -Antihistamine in horses - +Sedation, anticholin
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Tripelennamine
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H1 blocker -CNS stimulant in Downer cows- + sedation, anticholin
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Cromolyn
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mast cell stabilizer / adjunct therapy for airway allergy (asthma) prevention in horse
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Cyproheptadine
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5HT blocker - Antihistamine, photic head shake - Appetite stimulant
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Aspirin
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Nonsel COX inhib, COX-1 specific in platelet - low dose = Anti-thrombotic = GI irritation;cats sensitive b/c lower ability to metabolize
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Phenylbutazone
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Nonsel COX inhib -Potent anti-inflamm, lameness in horses = Rt dorsal colitis, renal papill, ulcers; more toxic than other nonse
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Flunixin
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Nonsel COX inhib -Anti-inflamm, “anti-endotoxic” LESS TOXIC THAN BUTE
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Carprofen
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Pref COX-2 inhib -Manage pain, inflamm, some cancers (canine prostatic) -- GI effects (but less than Nonsel COX inhib)
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Piroxicam
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Pref COX-2 inhib - Anti-cancer (canine TCC-bladder; oral, equine squamous) --GI effects; narrow therapeutic window
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Meloxicam
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Pref COX-2 inhib -Canine osteoarthritis, periop for cats (single sc dose only!) -- GI, renal; was the only NSAID (cats) until 2011
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Robenacoxib
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Sel COX-2 inhib -Only NSAID apprv for cats, oral - Control postop pain, 3 d
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Deracoxib
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Sel COX-2 inhib -Canine post op – high dose; osteoarthritis – low dose - -Little GI & renal b/c sel COX-2 inhib; caution if hypercoag b/c “tip bal”
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