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59 Cards in this Set

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