EXAM II Flashcards
what is the greatest concern when using pyridostigmine
intussuception
(and tolerance caused by down regulation of Nm receptos)
what is the greatest concern when using Neostigmine
cholinergic crisis
if you are treating a dog or cat for MSG like syndrome, would you reach for neostigmine or pyridostigmine first and why?
pyridostigmine is labeled for use of canine MSG like syndrome
and is ELU for cats
what animals is neostrigmine labeled for use in
sheep, cattle, swine, equine
what is neostigmine primarily used to treat
GI or bladder atony esp. post Sx
why is bethanecol not a great choice for treatment of GI issues in LAs
compounding is required :(
why is bethanecol used for treatment of gastric ulcer syndrome in equines but gastric ulcers in small animals is a contraindication of the same drug?
equine - constantly producing acid to breakdown feed
SA - only produce acid when eating
why might u look like an absolute fool if you give a horse atropine to dilate their eyes
effects of dilation last DAYS in horses and atropine causes decreased GI motility so you are putting that horse at risk for colic
what drug should be used over atropine for fundoscopic exams and why
Tropicamide
effects are much shorter lasting
what cholinergic antagonist is labeled as a pre-med for dogs and cats but can also be used in ferrets and other small animals (ELDU)
Glycopyrrolate
Glycopyrrolate is a quaternary amine, how does this affect its distribution/absorption and why might it be a better choice for a pregnant animal over atropine as a cholinergic antagonist
quaternary amines have low Vd, therefore they stay around long because less asborbed
- glycopyrrolate does NOT cross CNS, placenta or milk like how atropine does
what cholinergic antagonist has no use in livestock
Glycopyrrolate
what cholinergic antagonist is ELDU for detrusor hyperreflexia in dogs and cats
Oxybutynin chloride
what are the 4 main uses for atropine
- pre anesthetic (decreases secretions)
- sinus bradycardia, SA arrest or incomplete AV blocks
- differentiation of vagally mediated vs primary bradycardia
- treatment for cholinergic agonist toxicity
what cholinergic antagonists blocks the iris sphincter and ciliary muscles, and what result does this have
atropine
block iris sphincter = dilation (mydriasis)
block ciliary muscles = can’t accommodate, can’t focus
why might you use atropine in the eyes (3 reasons)
- treatment of pain from uveal/corneal disease
- dilation for sx
- synechiae during uveitis
structural characteristic of oxybutynin chloride that makes it able to go essentially everywhere
triple bond = NP
what drug can NEVER BE GIVEN ALONE or else you’re doing some fucked up torture
Atracurium
- only induced flaccid paralysis
- NO analgesia
- NO pain relief
THE ANIMAL IS FULLY CONSICOUS AND CAN FEEL EVERYTHING
what might be the use of Atracurium in male cats
intraurethral administration to help relaxation for unblocking
how is atracurium metabolized and what is wacky about it
via plasma esterases = still gets broken down even if liver/renal issues
breakdown is pH dependent and spontaneous = highly variable and irregular
what are the two other ‘flavors’ of atracurium that are only used in cats and dogs
Pancuronium bromide and vecuronium bromide
what is the order of paralysis induced by an NMJ blockade
- small muscles first (head, neck, tail)
- then larger muscles (limbs)
- deglutition, laryngeal and abdominal intercostal muscles
- respiratory goes last
recovery starts in opposite direction
you have just administered a patient atracurium and are waiting for signs of paralysis, what do you expect to go limp first
head, neck, tail
how can you reverse NMJ blockade
AChE inhibitors
neostigmine is DOC
does atropine have much of an affect on arterioles and veins?
no b/c those are mostly sympathetic and atropine works to increase parasympathetics
why might giving cholinergic antagonists to a glucoma patient not be a very slay choice
cholinergic antagonists increase aqeous humor = increased IOP
why is high dose epinephrine required for anaphylaxis
at high doses, the alpha receptors take effect and cause vasoconstriction whereas at low doses, the effects are predominately on the heart (increase HR + contractility)
this is b/c vasculature β2 receptors are more sensitive than α1
why is a low dose of epinephrine used in asystole patients
- low dose epinephrine effects vasculature β2 most strongly
- increases HR and contractility
adrenergic agonists share the same mechanism of metabolism and elimination which is…?
metabolism: hepatic breakdown into catechol
elimination: catechol is reasborbed
all use of Epi is considered ELDU, but what are its main indicated uses?
- anaphylaxis (at high dose)
- asystole (at low dose)
- vasoconstriction to extend the effects of local anesthetics (often used w/ lidocaine)
which receptor type is more sensitive to NE Bitartrate compared to β1
α1»_space;>
what drug might you use in a patient who has already been administered atropine and fluid boluses, neither of which have raised their blood pressure enough
Phenylephrine (α1 agonist)
what type of cardiac patient might be a candidate for phenylephrine IV/CRI
patient with severe caridac insufficiency in which you don’t want to increase CO by increasing contractility
ex: hypertorpic cardiomyopathy, R sided heart failure
what are the indicates uses (all of which are ELDU) of phenylephrine?
- low bp (hypotension) in dogs and cats
- opthalamic solution to induce mydriasis without loss of accommodation; used in canine phagoemulsification
- ascending colon displacement in horses (not really used tho)
drug given to induce mydriasis prior to phagoemulsification procedure in canines
Phenylephrine
what is the indication for Dobutamine HCl use (ELDU)
Dobutamine = β1 agonist
short term treatment of heart failure
increases HR and contractility
mixed acting adrenergic agonist used to treat urinary incontinence in dogs (ELDU in cats)
Phenylpropanolamine HCl
mixed acting adrenergic agonists are able to act directly on adrenergic receptors AND induce _____ release from _____ neurons
NE from post-ganglionic neurons
what is the indicated use for all direct acting β2 agonists
Albuterol, Clenbuterol, Terbutaline
- bronchoconstriction
- increased HR, increased contractility
- vasodilation, decreased pressure
what drug is a better option instead of ephedrine sulfate for treatment of urinary incontinence in dogs and cats and why?
Phenylpropanolamine HCl
better b/c actually labeled for this use
what is important to know about the elimination of ephedrine sulfate
it is pH dependent
α1 non-competitive inhibitor used in the treatment of functional urethrospasm in dogs,cats,horses as well as treatment of pheochromocytoma
all use is ELDU
Phenoxybenzamine
α1 competitive inhibitor used in the treatment of functional urethrospasm in dogs and cats ONLY
Prazosin
what is the only class III β antagonist
sotalol (β1+β2)
drugs ending in - “olol” are ?
adrenergic antagonists
β1 antagonist that is primarily used in diagnostics due to its fast acting, short duration
Esmolol
adrenergic antagonist associated with thryotoxicosis due to its super vasoconstrictive abilities
Propranolol (β1+β2 antagonist)
adrenergic antagonist used for the treatment of glaucomas; decreases IOP by reducing production of aqeous humor
Timilol (β1+β2)
all uses of β-antagonists are considered ELDU, why?
human drugs
why is it important to taper off β-antagonists rahter than stopping cold turkey
abrupt discontinuation may lead to tachycardia and arrythmias due to an upregulation of β receptors (data from humans)
what drugs can reverse an epinephrine mediated increase in BP
alpha blockers (adrenergic antagonists)
* phenoxybenzamine
* prazosin
what β antagonists have mild local anesthetic activity?
propranolol and metoprolol
mechanism = Na+ channel blockade “membrane stabilizing”
why would it be a bad idea to use β-antagonists in the eye?
risk of injury induced corneal ulceration - can’t feel if you hurt your eye
if you stimulate the vagus nerve what do you expect to happen in the respiratory and GI
resp: bronchoconstriction and increased mucus secretions
GI: relaxation of sphnicters, stimulates GI motility, increased gastric acid productin
explain the reflex bradycardia that occurs with NE use
NE causes a strong increase in BP from α1 vasoconstriction being unchecked (no β2 to vasodilate like w/ Epi)
to counteract the high rise in pressure, the heart rate drops
why doesn’t Epinephrine cause as large of an increase in BP as seen w/ NE
Epi stimulates both α1 and β2 receptors. α1 causes an increased BP (vasoconstriction) while β2 casuses vasodilation (decreased BP)
why might a patient given high dose Epi for anaphylaxis exhibit bronchoconstriction
high dose of Epi causes α1 receptors to override β2
what is the main GI concern when giving Pyridostigmine
intussuception
what drug is labeled for treatment of Myasthenia gravis like syndrome in dogs (ELU:cats)
Pyridostigmine
what are the clinic signs of cholinergic crisis and what drug can cause this
bradycardia, hella salivation, dyspnea and tremors
caused by Neostigmine
what adrenergic agonist has pH dependent elimination
Ephedrine sulfate
why does atropine prevent a decrease in HR
blocks the M receptors in the heart, leaving sympathetic innervation unopposed
what drug could be administered to increase the strength of skeletal muscle contraction
Neostigmine (or Pyridostigmine)
AChE inhibitors; they stimulate neuromuscular nicotinic receptors
