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Drugs > Paralytics > Flashcards

Paralytics Flashcards

1
Q

In the neuromuscular junction, how is acetylcholine synthesized?

A

It is synthesized from choline and acetate in the presence of acetylcholine transferase

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2
Q

How is acetylcholine released?

A

It’s released from nerve endings in response to an impulse traveling down a motor nerve. Calcium enters the nerve terminal, combines with calmodulin, and facilitates discharge of acetylcholine

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3
Q

What happens after acetylcholine is discharged in the neuromuscular junction?

A

it stimulates nicotinic cholinergic receptors on post-junctional skeletal muscle membranes to initiate excitation-contraction coupling. It’s then hydrolyzed by acetylcholinesterase

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4
Q

What are the two types of paralytics?

A

depolarizing and non-depolarizing

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5
Q

List the popular depolarizing paralytics

A

succinylcholine and decamethonium

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6
Q

What are the two sub groups of non-depolarizing paralytics?

A

benzylisoquinoliniums and aminosteroids

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7
Q

List two examples of a benzylisoquinolinium

A

atracurium, cisatracurium

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8
Q

List three examples of an aminosteroid

A

pancuronium, rocuronium, vecuronium

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9
Q

What is the order of muscle relaxation sequence with a paralytic?

A

OUTER TO INNER!

oculomotor –> palpebral and facial –> tongue and pharynx –> jaw and tail –> limbs –> pelvic –> caudal abdominal –> cranial abdominal –> intercostal –> larynx –> diaphragm

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10
Q

What is the molecular structure of succinylcholine?

A

two acetylcholine molecules joined back to back

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11
Q

What is the mechanism of action of succinylcholine?

A

succinylcholine attaches to one or both of the alpha subunits of the nicotinic acetylcholinergic receptors and mimics action of acetylcholine

The hydrolysis of succinylcholine is slower than that of acetylcholine causing sustained depolarization of receptor ion channels

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12
Q

Why does neuromuscular blockade develop with succinylcholine?

A

because the depolarized postjunctional membrane is unable to respond to a subsequent release of acetylcholine. There is a depolarizing, or Phase 1, neuromuscular blockade

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13
Q

What is a phase II block?

A

with repeated doses, CRIs, or a large dose of succinylcholine, postjunctional membranes may not respond normally to acetylcholine even after repolarization. The mechanism is not known, however

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14
Q

How is succinylcholine metabolized and excreted?

A

duration of action id depending on hydrolysis of succinylcholine by plasma cholinesterase (pseudocholinesterase) enzyme. The initial metabolite is succinylmonocholine which is hydrolyzed to succinic acid and choline

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15
Q

What are the CNS effects of succinylcholine?

A

none

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16
Q

What are the CV effects of succinylcholine?

A

sinus bradycardia, junctional rhythm, and sinus arrest (IN PEOPLE) d/t the cardiac muscarinic effects.

Heart rate can also increase d/t ganglionic stimulation at autonomic nervous system ganglia

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17
Q

What are the respiratory effects of succinylcholine?

A

Respiratory arrest occurs d/t the paralysis of skeletal muscle

18
Q

What are the musculoskeletal effects of succinylcholine?

A
  1. initial muscle contraction
  2. flaccid skeletal muscle paralysis
19
Q

What are the gastrointestinal effects of succinylcholine?

A

inconsistent increases in gastric pressure

20
Q

What are the urinary effects of succinylcholine?

A

myoglobinuria may occur d/t skeletal muscle damage associated with the muscle fasciculations

21
Q

Anything weird about eyes and succinylcholine?

A

Yes, an increase in IOP has occurred after administration of succinylcholine, likely due to contraction of extraocular muscles

22
Q

When is succinylcholine contraindicated?

A

patients predisposed to malignant hyperthermia

23
Q

What is the molecular structure of a non-depolarizing paralytic?

A

variable based on classification but, all are quaternary ammonium compounds with at least one positively charged nitrogen atom that binds to alpha subunit of postsynaptic cholinergic receptors

24
Q

What is the specificity of the drugs for the NMJ versus the autonomic ganglia nicotinic receptors dependent on? (non-depolarizing)

A

the length of the carbon chains separating the 2 positively charged ammonia groups. Neuromuscular blockade occurs when 10 carbon atoms are present. Maximal autonomic ganglion blockade occurs when 6 carbon atoms are present

25
Q

What is the mechanism of action for a non-depolarizing paralytic?

A

combine with nicotinic acetylcholine receptors without activating them. THey can act competitively with acetylcholine at the alpha subunits of the post-junctional acetylcholine receptors without changing their configuration. They can also act by blocking the ion receptor channels. They can also act at prejunctinoal acetylcholine receptors

26
Q

How is atracurium metabolized and excreted?

A

hydroysis in plasma and Hoffman elimination

27
Q

What is Hoffman elimination?

A

spontaneous degradation in plasma and tissue at normal body pH and temperature

28
Q

How is cisatracurium metabolized and excreted?

A

Hoffman elimination

29
Q

How is pancuronium excreted?

A

renal, 80% unchanged

30
Q

How is rocuronium excreted?

A

biliary excretion (50-70% unchanged) and renal excretion (10-25% unchanged)

31
Q

How is vecuronium excreted?

A

biliary excretion 40-75% unchanged and renal excretion (15-25%) unchanged

32
Q

How is vecuronium excreted?

A

biliary excretion 40-75% unchanged and renal excretion (15-25%) unchanged

33
Q

What is something that all nondepolarizing NMBs are dependent on for degradation?

A

temperature!!

atracurium and cisatracurium are also dependent on pH

34
Q

What is the elimination of pancuronium, rocuronium, and vecuronium dependent on?

A

Renal function

rocuronium and vecuronium are also dependent on liver function

35
Q

What CNS effects to nondepolarizing paralytics have?

A

none

36
Q

What CV effects do nondepolarizing paralytics have?

A
  • pancuronium increases HR, MAP, and CO d/t selective vagal blockade and increases in cardiac dysrhythmias when also receiving digitalis
  • atracurium can result in decreased BP and increased HR d/t histamine release
37
Q

what are the respiratory effects of nondepolarizing paralytics?

A

none directly. respiratory arrest occurs d/t paralysis of skeletal muscle

38
Q

What musculoskeletal effects do nondepolarizing paralytics have?

A

flaccid skeletal muscle paralysis

39
Q

What GI effects do nondepolarizing paralytics have?

A

none

40
Q

What are the urinary effects of a nondepolarizing paralytic?

A

none

41
Q

What are the drug interactions of nondepolarizing paralytics to be aware of?

A

volatile anesthetics - dose dependent enhancement of magnitude and duration of NMB

Antibiotics - aminoglycosides enhance NMB, reversal of paralytics can be unpredictable

Diuretics - furosemide enhances NMB, mannitol does NOT have an effect

Local anesthetics - small doses can enhance NMB

Magnesium - enhances NMB

42
Q

What is a particular side effect of atracurium to be aware of?

A

histamine release!!

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