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3rd Quarter > Pharm Quiz#6 > Flashcards

Pharm Quiz#6 Flashcards

1
Q

What is the definition of postoperative residual neuromuscular blockade

A

Train of four < 0.9 after reversal

Clinical weakness

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2
Q

What is recurarization?

A

Not “re-paralysis” but residual paralysis

Residual paralysis may persist up to 4 hours after rocuronium/vecuronium/cisatracurium

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3
Q

When do you reverse a patient?

A

TOFR > 0.9, statistical reduction in morbidity

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4
Q

What does the ability to reverse depend on

A

Ability to revere depends on amount of spontaneous recovery before reversing

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5
Q

How much time should be given for anticholinesterases to antagonize block?

A

at least 15 to 30 minutes

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6
Q

What is the safest approach for residual paralysis?

A

Sedation/mechanical ventilation

“Keep the tube in”

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7
Q

List qualitative monitoring for paralysis

A

Train of four, single twitch, tetanus

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8
Q

List quantitative monitoring for paralysis

A

Electromyography

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9
Q

What will potentiate neuromuscular blockers?

A

inhalation agents

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10
Q

What are metabolic issues related to paralysis?

A

Acidosis, hypercarbia, hypoxia, hypothermia

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11
Q

What class of antibiotic will potentiate NMBs?

A

Aminoglycosides

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12
Q

What is the most common cholinesterase inhibitor?

A

Neostigmine

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13
Q

Cholinesterase inhibitors hydrolyze ___ molecules of acetylcholine per minute.

A

300,000

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14
Q

Acetylcholine is a protein with molecular weight of approximately ___

A

320,000

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15
Q

Explain the ionized centers of cholinesterase inhibitors. List three cholinesterase inhibitors.

A

Cholinesterase inhibitors have ionized centers that combine at AChE active center or site removed from active center of AChE.

Neostigmine
Pyridostigmine
Edrophonium

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16
Q

List the three mechanisms of action for cholinesterase inhibitors

A

Direct influences on neuromuscular transmission along with enzyme inhibition.

MOA

  • weak agonist action
  • formation for desensitized receptor complex intermediates
  • alteration of conductance properties of active channels
17
Q

All cholinesterase inhibitors act by the same mechanism, what is it?

A

They prevent the hydrolysis of acetylcholine in the neuromuscular junction

18
Q

What is the class of cholinesterase inhibitors? How lipid soluble is it?

A

Quaternary ammonium compounds

Poorly lipid soluble

19
Q

Neostigmine and pyridostigmine, describe the structure and function of these drugs

A

Carbamic acid esters of alcohols containing quarternary or tertiary ammonium groups

Form carbamyl-ester complexes at esteratic sites of cholinesterase

20
Q

Neostigmine and pyridostigmine increase ACh ___ and ___ by changing the agonist-antagonist ratio and amount of free ACh available.

A

concentration, duration of effect

21
Q

Neostigmine and pyridostigmine form ___ bonds with AChE resulting in carbamylated enzyme. Carbamylated AChE won’t work.

A

covalent

22
Q

Give details for Neostigmine

A 
Onset IV - 4 to 8 minutes
Duration - 0.5 to 2 hr
50% glomerular filtration excretion
50% hydrolyzed by plasma esterases and hepatic metabolism
- 3-hydroxyphenyltrimethyl ammonium
- conjugated 3-OH PPM
Metabolites 1/10 activity of neostigmine
23
Q

How are metabolites of neostigmine eliminated?

A

Renal elimination

  • Elimination 1/2 of neostigmine 70 to 80 min. Increase to 181 to 183 min in anephric patients
  • Vd of 0.7 L/kg in healthy patients increases to 0.8 L/kg with renal failure
24
Q

Pyridostigmine, give details

A 
Longest onset and duration
Onset - 2 to 5 min
Duration - 90 min to 3 to 6 hours
75% renal elimination
25% metabolized by hepatic microsomal enzymes 
- 3-hydroxy-methyl pyridinium
- six others
25
Q

How are pyridostigmine metabolites eliminated?

A

Urine excretion

Elimination 1/2 time - 113 minutes, Vd 1.1 L/kg

26
Q

Edrophonium, explain how it works

A

Binds reversibly with negatively charged enzyme sites by electrostatic attraction of positively charged nitrogen.

Prevents catalytic binding with ACh for the short time that edrophonium occupies binding sites.

27
Q

What is the chemical composition of edrophonium

A

Simple alcohol containing quarternary ammonium group
Electorstatically attaches to anionic site of AChE, stabilized with hydrogen bones.
True chemical bond not formed.

28
Q

Edrophonium, give chemical information

A

Competitive inhibition for binding sites with ACh
Short duration - 5 to 10 min
Onset - 30 to 60 seconds
IM onset 2 to 10 min

29
Q

Edrophonium, how is it eliminated?

A

75% renal elimination
Without renal function - hepatic metabolism inactivates 30% of the dose via conjugation to edrophonium glucuronide
1/2 life 110 min with Vd 1.1 L/kg
1/2 life 304 min in anephric patient with Vd 0.7 L/kg

30
Q

List clinical signs of NMB recovery

A 
Adequate tidal volume and rate
Respirations smooth and unlabored
Opens eyes widely on command
No diplopia
Tongue protrusion and purposeful movement
Effective swallowing and sustained bite
Sustained head or leg lift for 5 seconds
Arm lift and touch opposite shoulder
Strong, constant hand grip
Effective cough
Adequate vital capacity of at least 15 ml/kg
Adequate inspiratory force of at least 25 to 30 cm H2O negative pressure
Sustained tetanic response
Train of four ratio greater than 0.9
No fade to double burst stimulation
31
Q

Factors prolonging paralysis

A 
Acid maltase deficiency
Adrenocortical dysfunction
Acute intermittent porphyria
Amyotrophic lateral sclerosis
Anoxia and ischemia
Carcinomatous polyneuropathy
Cholinesterase deficiency of genetic variance
Compressive neuropathy
Critical illness polyneuropathy
Diphtheria
Eaton-Lambert syndrome
Guillain-Barre syndrome
32
Q

Electrolyte imbalances associated with factors prolonging paralysis

A 
Hypokalemia
Hypocalcemia
Hypomagnesemia
Hypophosphatemia
Hypothermia
Motor neuron disease
33
Q

More factors prolonging paralysis

A 
multiple sclerosis
muscular dystrophy
myasthenia gravis
myotonic syndromes
neurofibromatosis
nonspecific nutritional deficiency
Poliomyelitis
Pyridoxine abuse
Polymyositis
Renal failure
Respiratory acidosis
Sepsis
Thiamine deficiency
Tike bite
Trauma
Vitamin E deficiency
Wound botulism
34
Q

Pharmacologic causes of prolonged paralysis

A 
Aminoglycoside toxicity
Penicillin toxicity 
Steroid myopathy
Antihypertensives
- Calcium channel blockers
- beta blockers
- Furosemide
35
Q

Continued pharmacologic causes of prolonged paralysis (antidysrhthmics, aminoglycosides)

A

Quinidine
Porcainamide
Local anesthetics in large doses

Polymyxin B
Clindamycin
Tetracycline

36
Q

Continued pharmacologic causes of prolonged paralysis (miscellaneous drugs)

A 
Cyclosporine
Steroids
Volatile anesthetics
Dantrolene
Magnesium - OB
Lithium
Azathioprine
Organophosphate (Poisoning) ***
37
Q

Typical doses and duration of Neostigmine

A 
Neostigmine
Dose - 25-75 mcg/kg
Onset - 5-15 min
Duration - 45-90 min
Side effects - +PONV
38
Q

Typical doses and side effects of Pyridostigmine

A

Dose - 100-300 mcg/kg
Onset - 10-20 min
Duration - 60-120 min
Side effects - slow onset, long duration

39
Q

Typical doses and side effects to Edrophonium

A

Dose - 50-1,000 mcg/kg
Onset - 5-10 min
Duration - 30-60 min
Side effects - Not for deep block, rapid

3rd Quarter (22 decks)

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