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PHARMACOLOGY I > EXAM II > Flashcards

EXAM II Flashcards

1
Q

what is the greatest concern when using pyridostigmine

A

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

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2
Q

what is the greatest concern when using Neostigmine

A

cholinergic crisis

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3
Q

if you are treating a dog or cat for MSG like syndrome, would you reach for neostigmine or pyridostigmine first and why?

A

pyridostigmine is labeled for use of canine MSG like syndrome
and is ELU for cats

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4
Q

what animals is neostrigmine labeled for use in

A

sheep, cattle, swine, equine

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5
Q

what is neostigmine primarily used to treat

A

GI or bladder atony esp. post Sx

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6
Q

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

A

compounding is required :(

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7
Q

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?

A

equine - constantly producing acid to breakdown feed
SA - only produce acid when eating

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8
Q

why might u look like an absolute fool if you give a horse atropine to dilate their eyes

A

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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9
Q

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

A

Tropicamide
effects are much shorter lasting

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10
Q

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)

A

Glycopyrrolate

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11
Q

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

A

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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12
Q

what cholinergic antagonist has no use in livestock

A

Glycopyrrolate

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13
Q

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

A

Oxybutynin chloride

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14
Q

what are the 4 main uses for atropine

A
  1. pre anesthetic (decreases secretions)
  2. sinus bradycardia, SA arrest or incomplete AV blocks
  3. differentiation of vagally mediated vs primary bradycardia
  4. treatment for cholinergic agonist toxicity
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15
Q

what cholinergic antagonists blocks the iris sphincter and ciliary muscles, and what result does this have

A

atropine
block iris sphincter = dilation (mydriasis)
block ciliary muscles = can’t accommodate, can’t focus

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16
Q

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

A
  1. treatment of pain from uveal/corneal disease
  2. dilation for sx
  3. synechiae during uveitis
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17
Q

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

A

triple bond = NP

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18
Q

what drug can NEVER BE GIVEN ALONE or else you’re doing some fucked up torture

A

Atracurium
- only induced flaccid paralysis
- NO analgesia
- NO pain relief
THE ANIMAL IS FULLY CONSICOUS AND CAN FEEL EVERYTHING

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19
Q

what might be the use of Atracurium in male cats

A

intraurethral administration to help relaxation for unblocking

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20
Q

how is atracurium metabolized and what is wacky about it

A

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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21
Q

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

A

Pancuronium bromide and vecuronium bromide

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22
Q

what is the order of paralysis induced by an NMJ blockade

A
  • 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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23
Q

you have just administered a patient atracurium and are waiting for signs of paralysis, what do you expect to go limp first

A

head, neck, tail

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24
Q

how can you reverse NMJ blockade

A

AChE inhibitors
neostigmine is DOC

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25
Q

does atropine have much of an affect on arterioles and veins?

A

no b/c those are mostly sympathetic and atropine works to increase parasympathetics

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26
Q

why might giving cholinergic antagonists to a glucoma patient not be a very slay choice

A

cholinergic antagonists increase aqeous humor = increased IOP

27
Q

why is high dose epinephrine required for anaphylaxis

A

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

28
Q

why is a low dose of epinephrine used in asystole patients

A
  • low dose epinephrine effects vasculature β2 most strongly
  • increases HR and contractility
29
Q

adrenergic agonists share the same mechanism of metabolism and elimination which is…?

A

metabolism: hepatic breakdown into catechol
elimination: catechol is reasborbed

30
Q

all use of Epi is considered ELDU, but what are its main indicated uses?

A
  • anaphylaxis (at high dose)
  • asystole (at low dose)
  • vasoconstriction to extend the effects of local anesthetics (often used w/ lidocaine)
31
Q

which receptor type is more sensitive to NE Bitartrate compared to β1

A

α1&raquo_space;>

32
Q

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

A

Phenylephrine (α1 agonist)

33
Q

what type of cardiac patient might be a candidate for phenylephrine IV/CRI

A

patient with severe caridac insufficiency in which you don’t want to increase CO by increasing contractility

ex: hypertorpic cardiomyopathy, R sided heart failure

34
Q

what are the indicates uses (all of which are ELDU) of phenylephrine?

A
  • 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)
35
Q

drug given to induce mydriasis prior to phagoemulsification procedure in canines

A

Phenylephrine

36
Q

what is the indication for Dobutamine HCl use (ELDU)

A

Dobutamine = β1 agonist
short term treatment of heart failure
increases HR and contractility

37
Q

mixed acting adrenergic agonist used to treat urinary incontinence in dogs (ELDU in cats)

A

Phenylpropanolamine HCl

38
Q

mixed acting adrenergic agonists are able to act directly on adrenergic receptors AND induce _____ release from _____ neurons

A

NE from post-ganglionic neurons

39
Q

what is the indicated use for all direct acting β2 agonists

Albuterol, Clenbuterol, Terbutaline

A
  • bronchoconstriction
  • increased HR, increased contractility
  • vasodilation, decreased pressure
40
Q

what drug is a better option instead of ephedrine sulfate for treatment of urinary incontinence in dogs and cats and why?

A

Phenylpropanolamine HCl
better b/c actually labeled for this use

41
Q

what is important to know about the elimination of ephedrine sulfate

A

it is pH dependent

42
Q

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

A

Phenoxybenzamine

43
Q

α1 competitive inhibitor used in the treatment of functional urethrospasm in dogs and cats ONLY

A

Prazosin

44
Q

what is the only class III β antagonist

A

sotalol (β1+β2)

45
Q

drugs ending in - “olol” are ?

A

adrenergic antagonists

46
Q

β1 antagonist that is primarily used in diagnostics due to its fast acting, short duration

A

Esmolol

47
Q

adrenergic antagonist associated with thryotoxicosis due to its super vasoconstrictive abilities

A

Propranolol (β1+β2 antagonist)

48
Q

adrenergic antagonist used for the treatment of glaucomas; decreases IOP by reducing production of aqeous humor

A

Timilol (β1+β2)

49
Q

all uses of β-antagonists are considered ELDU, why?

A

human drugs

50
Q

why is it important to taper off β-antagonists rahter than stopping cold turkey

A

abrupt discontinuation may lead to tachycardia and arrythmias due to an upregulation of β receptors (data from humans)

51
Q

what drugs can reverse an epinephrine mediated increase in BP

A

alpha blockers (adrenergic antagonists)
* phenoxybenzamine
* prazosin

52
Q

what β antagonists have mild local anesthetic activity?

A

propranolol and metoprolol
mechanism = Na+ channel blockade “membrane stabilizing”

53
Q

why would it be a bad idea to use β-antagonists in the eye?

A

risk of injury induced corneal ulceration - can’t feel if you hurt your eye

54
Q

if you stimulate the vagus nerve what do you expect to happen in the respiratory and GI

A

resp: bronchoconstriction and increased mucus secretions
GI: relaxation of sphnicters, stimulates GI motility, increased gastric acid productin

55
Q

explain the reflex bradycardia that occurs with NE use

A

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

56
Q

why doesn’t Epinephrine cause as large of an increase in BP as seen w/ NE

A

Epi stimulates both α1 and β2 receptors. α1 causes an increased BP (vasoconstriction) while β2 casuses vasodilation (decreased BP)

57
Q

why might a patient given high dose Epi for anaphylaxis exhibit bronchoconstriction

A

high dose of Epi causes α1 receptors to override β2

58
Q

what is the main GI concern when giving Pyridostigmine

A

intussuception

59
Q

what drug is labeled for treatment of Myasthenia gravis like syndrome in dogs (ELU:cats)

A

Pyridostigmine

60
Q

what are the clinic signs of cholinergic crisis and what drug can cause this

A

bradycardia, hella salivation, dyspnea and tremors
caused by Neostigmine

61
Q

what adrenergic agonist has pH dependent elimination

A

Ephedrine sulfate

62
Q

why does atropine prevent a decrease in HR

A

blocks the M receptors in the heart, leaving sympathetic innervation unopposed

63
Q

what drug could be administered to increase the strength of skeletal muscle contraction

A

Neostigmine (or Pyridostigmine)
AChE inhibitors; they stimulate neuromuscular nicotinic receptors

PHARMACOLOGY I (21 decks)

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