EXAM II Flashcards by Riley Hrasky

what is the greatest concern when using pyridostigmine

intussuception
(and tolerance caused by down regulation of Nm receptos)

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what is the greatest concern when using Neostigmine

cholinergic crisis

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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

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what animals is neostrigmine labeled for use in

sheep, cattle, swine, equine

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what is neostigmine primarily used to treat

GI or bladder atony esp. post Sx

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why is bethanecol not a great choice for treatment of GI issues in LAs

compounding is required :(

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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

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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

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what drug should be used over atropine for fundoscopic exams and why

Tropicamide
effects are much shorter lasting

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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

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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

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what cholinergic antagonist has no use in livestock

Glycopyrrolate

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what cholinergic antagonist is ELDU for detrusor hyperreflexia in dogs and cats

Oxybutynin chloride

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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

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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

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why might you use atropine in the eyes (3 reasons)

treatment of pain from uveal/corneal disease
dilation for sx
synechiae during uveitis

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structural characteristic of oxybutynin chloride that makes it able to go essentially everywhere

triple bond = NP

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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

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what might be the use of Atracurium in male cats

intraurethral administration to help relaxation for unblocking

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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

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what are the two other ‘flavors’ of atracurium that are only used in cats and dogs

Pancuronium bromide and vecuronium bromide

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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

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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

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how can you reverse NMJ blockade

AChE inhibitors
neostigmine is DOC

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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 >>>

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

EXAM II Flashcards

(63 cards)