Paralytics Flashcards

1
Q

What receptors are the receptors for ACh on the neuromuscular end plate of skeletal muscle and preganglionic autonomics?

A

Nicotinic

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2
Q

What do drugs that cross the BBB result in? How about drugs that dont?

A

Central side effects, drugs that do not result in paralysis only

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3
Q

What are the two types of MOAs for drugs acting on the nicotinic receptor?

A

Direct = stimulate or block the receptor; Indirect = AChE inh increase the ACh at the receptors

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4
Q

What is the nicotinic ACh receptor?

A

A ligand gated Na+ channel that leads to membrane depolarization, 2 AChs required for activation

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5
Q

What are NMDs used for?

A

Muscle paralysis, NOT ANALGESIA therefore use for intubation or orthopedic procedures, also IV only

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6
Q

How do you test the extent of paralysis/durability of drug action?

A

By sending a current down the ulnar nerve and monitoring the electrical activity of the muscle twitch of the Adductor Pollicis (Or twitch of the eyebrow if facial nerve stimulated; or plantar flexion of great toe if Posteror Tibial stimulated)

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7
Q

Describe what happens during peripheral nerve stimulation and what fade is.

A

A train of four of sequential stimuli are sent and each causes a release of ACh; in absesne of NMB the first is as strong as the last; with NMB the fourth will be less than the first until eventually it does not twitch with the fourth stimulation. This is fade.

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8
Q

At what percent occupation will only the first twitch happen?

A

85-90%

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9
Q

At what percent occupation will 2-4 twitches happen?

A

70-85%

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10
Q

What is the desired number of twitches?

A

2-3; NMBs are titrated to this goal

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11
Q

What does use of Peripheral nerve stimulators do for ICU?

A

Reduces the amount of drugs used

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12
Q

What is Post-tetanic Potentiation (PTP)?

A

It is caused by prolonged stimulation which results in Ca2+ depended activation of PKC that can overcome paralysis by increased ACh vesicle release but it fades rapidly

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13
Q

What are the off target effects of paralytics?

A

Autonomic ganglionic effects (N, Cardiac M2, and Histamine release)

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14
Q

What is malignant hyperthermia?

A

It is genetic and AD, caused by uncontrolled release of Ca2+ from SR that causes rigor, increased CO2, increased lactic acidosis, very increased body temp and caused by succinylcholine and volatile anesthetics

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15
Q

How do you treat malignant hyperthermia?

A

Give the patient Dantrolene

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16
Q

What are some DDRs with NMBs?

A

Can interact with local and general anesthetics (malignant hyperthermia), ABX can cause prolonged blockade (aminoglycosides)

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17
Q

What is the MOA of all the Nondepolarizing paralytics? and what are they derived from?

A

They prevent the opening of the ACh receptor Na channel preventing the depolarization from occuring; it is competitive antagonist and are derived from Isoquinolone and Steroids

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18
Q

What drugs are classified as nondepolarizing?

A

Atracurium, Pancuronium, Vecuronium

19
Q

What do nondepolarizing parylitics show on peripheral nerve stimulation?

A

With TOF stimulation these cause stepwise diminution of muscle twitch = fade, titrated to 2-3 twitches

20
Q

How are nondepolarizing paralytics (other than DTC) distributed and eliminated?

A

Rapid distrubution, slow elimination (nonenzymatic elimination) and about 20-45 minutes

21
Q

What drug are the potencies of all the other NMBs based off of?

A

D-Tubcurarine

22
Q

How is DTC eliminated?

A

Renally, >50 minutes

23
Q

What are the off-target effects of DTC?

A

Weak autonomic ganglion blockade and moderate histamine release

24
Q

How is Atracurium metabolized/eliminated? and what are the consequences of it’s metabolite?

A

Hepatically metabolized into Laudanosine = seizures and histamine release and Hofmann elimination

25
Q

What are the Nondepolarizing paralytics and what are they derived from? How are they all eliminated?

A

Pancuronium, Vecuronium; steroid derived; Hepatically and Renally

26
Q

What is the off target effect of Atracurium?

A

Slight histamine release

27
Q

What are the elimination time/route potency, elimination, and side effects of Pancuronium?

A

> 35 min, 6x DTC, 80% renal, and Moderate M2 cardiac blocking

28
Q

What are the elimination time/route, potency, and side effects of vecuronium?

A

20-35 min, 90% hepatic, 6x DTC, and no off target effects

29
Q

What is the MOA of the depolarizing paralytics?

A

Activates the channel causing a depolarization (contraction); but the drug persists on the binding site and blocks the channel from closing; inhibits repolarization which leads to paralysis

30
Q

What will be seen with Peripheral nerve stimulation and depolarizing agents?

A

Phase 1: causes initial fasciculation (depol) that shows no fade then Phase 2 is a fade like non-depolarizing with flaccid paralysis

31
Q

What do you not give depolarizing paralytics with?

A

A non-depolarizing agent

32
Q

What is the sole depolarizing paralytic and what is it’s duration of action?

A

Succinylcholine; 5-10 minute duration

33
Q

How is Succinylcholine metabolized?

A

Rapid hydrolysis by butyrylcholinesterase in liver and high capacity pseudocholinesterase in plasma therefore genetic variations in these cause changes in duration

34
Q

How do you test the enzymes that metabolize Succinylcholine?

A

Dibucaine test

35
Q

What is the potency of Succinylcholine and what are the off target effects?

A

.4x DTC and stimulation of autonomic nicotinic N-receptors and cardiac M2, slight histamine release

36
Q

What are the ADE of Succinylcholine?

A

Arrythmias, HTN, hyperkalemia in large traume and neuromuscular dz (increase ACh receptor), prolonged paralysis (dibucaine test) increase ocular/cranial pressure (mannitol), Myalgia/Myoglobinuria, Anaphylaxis, and Malignant hyperthermia

37
Q

What are the reversal agents MOA?

A

They are AChE inhibitors so ACh increases so it can outcompete the blockers.

38
Q

What do you give reversal agents with?

A

Anti-cholinergic so you dont get SLUDGEBBB

39
Q

What are the reversal agents?

A

Pyridostigmine, Neostigmine

40
Q

What is the onset, duration, and coadministered drug with pyridostigmine?

A

20 min onset; 2 hr duration; Glycopyrrolate; NO BBB

41
Q

What is the onset, duration, and coadministered drug with Neostigmine?

A

10 min onset; 1 hr duration; Glycopyrrolate; NO BBB

42
Q

What do paralytic agents actually do and not do?

A

They only paralyze muscles by blockade of Nm receptor, they DO NOT provide pain or anxiety relief

43
Q

How does succinylcholine differ from all of the other drugs?

A

It produces initial muscle contraction then flaccid paralysis and has distinct adverse effects

44
Q

What are the two ways reversal is achieved?

A

Inhibition of AchE or through encapsulation of steroids (Sugammedex) which shifts the balance in favor of restoration of skeletal muscle function