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Pharm > Reversal Agents > Flashcards

Reversal Agents Flashcards

1
Q

What is the MOA of anticholinesterases?

A

increase concentration of acetylcholine at the nicotinic receptors through:
- inhibition of acetylcholinesterase leading to an increase in ACh concentration at both nicotinic and muscarinic receptors
- stimulation of presynaptic nicotinic ACh receptors causing release of additional ACh

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2
Q

What types of cholinesterase do anticholinesterases inhibit?

A

true cholinesterase
AND
pseudocholinesterase/plasma cholinesterase

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3
Q

What are the implications of inhibiting acetylcholinesterase?

A

increases ACh activity at nicotinic and muscarinic receptors

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4
Q

What are the implications of inhibiting pseudocholinesterase?

A

prolonged effect of succinylcholine, ester local anesthetics, and remifentanil

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5
Q

Give 2 examples of anticholinesterases that inhibit pseudocholinesterase:

A

organophosphates
echothiophate

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6
Q

What is the primary goal of reversing neuromuscular blocking agents?

A
  • maximize nicotinic transmission
  • minimize muscarinic side effects
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7
Q

Describe nicotinic cholinergic receptors:

A
  • ligand-gated ion channels
  • allow intracellular influx of Na+
  • located in the autonomic ganglia, skeletal muscle (NMJ), CNS
  • stimulated by nicotine, ACh, and succinylcholine
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8
Q

Describe muscarinic cholinergic receptors:

A
  • G-protein coupled receptors
  • 5 subtypes (M1-M5)
  • located in CNS, bronchial smooth muscle, salivary glands, SA node
  • stimulated by ACh and muscarine
  • blocked by atropine, scopolamine, pilocarpine
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9
Q

Stimulation of muscarinic receptors results in (4 things):

A

1) salivary and sweat gland secretion
2) pupillary constriction
3) increased GI peristalsis
4) slows conduction of SA and AV nodes

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10
Q

AChE inhibitors increase the concentration of ACh at the muscarinic receptor resulting in what predictable set of parasympathetic side effects?

A

Diarrhea
Urination
Miosis
Bradycardia
Bronchoconstriction
Emesis
Lacrimation
Laxation
Salivation

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11
Q

Which method of AChE inhibition results in a short-acting, reversible bond with a short DOA? Which drug acts in this way?

A

electrostatic attachment (Edrophonium)

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12
Q

Which method of AChE inhibition results in a slightly tighter, reversible bond with a moderate DOA? Which drug(s) act in this way?

A

formation of carbamyl esters (neostigmine, pyrido-, and physo-)

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13
Q

Which method of AChE inhibition results in an irreversible bond with a long DOA? Which drugs/substances act in this way?

A

phosphorylation (organophosphates and echothiophate)

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14
Q

Anticholinesterases have a prolonged effect in which patient population? Why?

A

renal and liver dz; they are conjugated, hydrolyzed and metabolized in the liver and have some degree of renal elimination

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15
Q

In general, anticholinesterases are _____ amines. Why is this relevant? What is the exception?

A

quaternary; they do not cross the BBB

exception: physostigmine is a tertiary amine and DOES cross the BBB

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16
Q

Give the dose/onset/duration of edrophonium. What drug is it paired with when used for reversal?

A
  • dose: 0.5-1.0 mg/kg (max 40mg)
  • onset: 1-2 min
  • duration: 30-60 min
  • paired with: atropine (0.014mg per 1mg edro)
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17
Q

Give the dose/onset/duration of neostigmine. What drug is it paired with when used for reversal?

A
  • dose: 0.05 mg/kg (max 5mg)
  • onset: <3 min
  • duration: 40-60min
  • paired with: glycopyrrolate (0.2mg per 1mg Neo)
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18
Q

Give the dose/onset/duration of pyridostigmine. What drug is it paired with when used for reversal?

A
  • dose: 0.1-0.3 mg/kg
  • onset: 10-20 min
  • duration: 60-120 min
  • paired with: glycopyrrolate (0.05mg per 1 pyrido)
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19
Q

What additional clinical issue is neostigmine used for?

A

treatment of myasthenia gravis

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20
Q

Give the dose/onset/duration of physostigmine.

A
  • dose: 0.5-2mg
  • onset: 3-8 min
  • duration: 30 min - 5 hours
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21
Q

What is the treatment of choice for anticholinergic syndrome?

A

physostigmine

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22
Q

What drug reverses the effects of scopolamine?

A

physostigmine

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23
Q

How is physostigmine metabolized?

A

plasma esterases

24
Q

Which anticholinesterase drug is used to treat glaucoma?

A

echothiophate

25
Q

What are the symptoms of anticholinesterase poisoning when it comes to nicotinic effects?

A
  • fasciculations
  • inability to repolarize cell membrane
  • weakness & paralysis
  • ventilatory failure
26
Q

What is the treatment for anticholinesterase poisoning?

A

1) atropine (1-2mg IV bolus, repeat Q3-5 mins)
2) pralidoxime (15mg/kg IV over 2 mins) - especially for organophosphate

need something that crosses the BBB

27
Q

What are other names for anticholinesterase poisoning? What does it mean?

A

central cholinergic syndrome
cholinergic crisis

means: excessive ACh in brain at nicotinic and muscarinic receptors

28
Q

Describe why we must give anticholinergic drugs in combination with anticholinesterases?

A
  • only the nicotinic cholinergic effects are needed for reversal of a NDMR
  • if unaddressed, the muscarinic effects would cause profound bradycardia and excessive salivation
29
Q

What is the MOA of anticholinergic drugs?

A
  • reversibly bind with muscarinic cholinergic receptors
  • prevent ACh from binding
  • results in excessive PNS effects
  • increasing amounts of ACh can overcome these drugs
30
Q

What tissues are most sensitive to anticholinergics?

A

salivary glands, sweat glands, bronchial tissue

31
Q

What effect to anticholinergics have on HR?

A

increase
atropine > glyco > scopolamine

32
Q

What effect do anticholinergics have on bronchial tissue?

A

bronchodilate

atropine = glyco > scopolamine

33
Q

What effect do anticholinergics have on sedation?

A

scopolamine&raquo_space; atropine
*glyco does not cross BBB d/t quaternary amine

34
Q

What effect do anticholinergics have on salivary glands?

A

inhibit salivation

scopolamine > glyco > atropine

35
Q

What effect do anticholinergics have on pupillary response?

A

mydriasis (dilation) and cycloplegia

scopolamine > atropine
glyco = no effect

36
Q

What effect do anticholinergics have on motion sickness?

A

prevent/reduce

scopolamine > atropine
*glyco = no effect

37
Q

What effect do anticholinergics have on the cardiovascular system?

A

increase rate of SA node (counteracts bradycardia)

38
Q

What effect do anticholinergics have on the GI tract?

A

decrease tone and motility

39
Q

What effect do anticholinergics have on the urinary system?

A

decreased tone (retention possible)

40
Q

Besides concomitant use with anticholinesterases, how else are anticholinergics used clinically?

A
  • Parkinson’s
  • motion sickness
  • ophthalmologic exams
  • CV disorders/bradycardia
  • cholinergic poisoning
41
Q

What is a major adverse effect of anticholinergics?

A

atropine poisoning/central anticholinergic syndrome

dry as a bone
blind as a bat
red as a beet
mad as a hatter

42
Q

List 2 contraindications to anticholinergic use:

A

glaucoma
gastric ulcer

43
Q

Give the dose/onset/duration of atropine:

A
  • dose: NDMR reversal 0.015 mg/kg
    sinus brady 0.4-0.8mg Q3-5min
  • onset: 45-60 sec
  • duration: 1 hour
44
Q

What are the minimum atropine doses for adult and pediatric bradycardia?

A

adult: no less than 0.4mg
peds: no less than 0.1mg

45
Q

What is the dose/onset/duration of glycopyrrolate?

A
  • dose: 0.1mg/kg
    (0.2mg for each 1mg of neo)
  • onset: <1min
  • duration: 2hr
46
Q

What is the dose/onset/duration of scopolamine for anticholinergic effects?

A
  • dose: 0.2-0.6 mg
  • onset: <1min
  • duration: 2-6 hours
47
Q

What is the MOA of sugammadex?

A
  • selectively binds to aminosteroid NDMRs (roc>vec>pan)
  • encapsulates NMBAs and renders them unable to engage with nicotinic receptors
48
Q

Sugammadex interacts with which receptors/NT?

A

NONE - and there are no systemic side effects

49
Q

How is sugammadex metabolized and excreted?

A

metab: none
excretion: unchanged by kidneys

50
Q

How long does sugammadex take to work? Does it depend on how deeply the pt is blocked?

A

fully restores muscle function to TOF >0.9 from any depth of NMB within 3 minutes

51
Q

List 3 advantages of sugammadex use:

A

1) no effect on anticholinesterase
2) no effect on any receptors
3) mechanism is independent of the depth of neuromuscular block

52
Q

What are the side effects of sugammadex?

A
  • bradycardia (1-5%)
  • anaphylaxis (0.3-1%)
  • bleeding
  • hormonal contraceptives ineffective x7 days
53
Q

Which 2 patient populations should not be given sugammadex?

A

kids
kidneys (dialysis or low creat clear)

54
Q

What dose of sugammadex should be given to patients with a moderate block? What does moderate block mean?

A

moderate block = 2 twitches
dose = 2mg/kg

55
Q

What dose of sugammadex should be given to patients with a deep block? What does deep block mean?

A

deep block = 0 twitches with TOF or 1-2 post-tetanic counts
dose = 4mg/kg

56
Q

What does of sugammadex should be administered to reverse a patient who received rocuronium 3-4 minutes ago?

A

16 mg/kg

57
Q

If a patient was reversed with sugammadex 5 mins to 4 hours ago, what dose of rocuronium is needed to re-paralyze? What about greater than 4 hours ago?

A

5 mins to 4 hours = 1.2 mg/kg (upper end)
>4 hours = 0.6 mg/kg

Pharm (19 decks)

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