Pharm Quiz#5 Flashcards Preview

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Flashcards in Pharm Quiz#5 Deck (38):
1

Of the phase I and Phase II blocks associated with succinylcholine administration, which is the desirable block?

Phase I

2

What causes a phase I block with succinylcholine administration?

due to prolonged stimulation of acetylcholine receptors--->results in disorganized muscle contractions(fasciculation's)

3

What is occurring at the cellular level during fasciculation?

acetylcholine receptors become an ion channel, so there is a high flux of K+ out of the cell, and Na+ into the cell, resulting in a membrane potential less than the action potential. After the initial firing, the cells remain refractory.

4

What should be used to diagnose Phase II block due to prolonged NMB? What response will be seen with Phase II block?

PNS prior to giving anti cholinesterase drugs, presence of Phase II block indicated by fade of responses to successive stimuli(preferably "train-of-four")

5

Reversel of a Phase II block should not be attempted unless(2)?

1. a peripheral nerve stimulator is used
2. spontaneous recovery of muscle twitch has been observed for at least 20 minutes and has reached a plateau with further recovery proceeding slowly.

6

Should the type of block be misdiagnosed, Phase I block will be _____ by an anti cholinesterase agent.

prolonged

7

What are characteristics of Phase II block seen with a PNS?(5)

1. fade of ToF
2. decreased single twitch response
3. fade on tetanus
4. TOF ratio < 0.7
5. post-tetanic facilitation(post-tetanic potentiation)

*Phase I ToF ratio-no difference*

8

Can a Phase II block be reversed by anticholinesterase drugs?

yup

9

Transition between Phase I and Phase II block is abrupt, occurring with doses > _____.

2-4 mg/kg

10

What is the initial sign of transition from Phase II block to Phase I block?

tachyphylaxis

11

Anticholinesterase drugs _____ Phase II blocks but _____ Phase I blocks.

reverse, worsen

12

What is the anticholinesterase medication typically used to reverse Phase II blocks and why?

edrophonium because its short duration of action

*if bock is reversed a longer acting reversal should be considered--->post-op ventilation*

13

What is the best reversal agent of a phase II block?

time

14

Patients with genetic resistance to succinylcholine have a shorter duration of action caused by?

accelerated hydrolysis

15

Obese patients require larger doses of succinylcholine due to?

greater plasma cholinesterase activity

16

Myasthenia graves patients may be up to _____ times more resistant to succinylcholine, due to?

2.6, decreased numbers of functional acetylcholine endplate receptors.

17

Atypical plasma cholinesterase is often found after typical succinylcholine doses and cause?

longer than expected duration of action

18

The important variety of atypical plasma cholinesterase are the?

dubucaine related variants

19

What is dubucaine?

an amide local anesthetic that inhibits normal plasma cholinesterase activity 80% and atypical activity 20%

20

What does a Dibucaine # of 80 indicate?

80% inhibition of plasma cholinesterase activity-NORMAL

21

What does a Dibucaine # of 20 mean?

20% inhibition of plasma cholinesterase activity(found in 1 of 3200 patients), means they are HOMOZYGOUS for an atypical plasma cholinesterase variant.

22

In patients with Homozygous atypical plasma cholinesterase variant, how long does succinylcholine usually last?

up to 3 hours in normal doses

23

What does a Dibucaine # of 40-60 indicate?

1/480 patients are heterozygous for atypical plasma cholinesterase. These patients may have prolonged succinylcholine blocks lasting up to 30 minutes.

24

What does a Dibucaine # indicate about plasma cholinesterase?

Indicates quality of plasma cholinesterase not quantity

25

Diminished plasma cholinesterase activity causes....

prolonged duration of action with a single dose of succinylcholine

26

What types of patients have diminished plasma cholinesterase activity?

-patients with heterozygous/homozygous atypical plasma cholinesterase
-pregnancy
-severe liver/kidney disease
-malignant tumors
-infections
-burns
-anemia
-decompensated heart disease
-peptic ulcer
-myxedema
-chronic admin of oral contraceptives
-glucocorticoids
-MAO inhibitors
-irreversible inhibitors of plasma cholinesterase
-echothiophate
-antineoplastic drugs

27

With plasma cholinesterase, slow to absent succinylcholine hydrolysis and prolongation of NMB is see with?(3)

1. decreased hepatic production of plasma cholinesterase
2. drug induced decreases in plasma cholinesterase
3. genetically atypical plasma cholinesterase

*only with severe liver disease is plasma cholinesterase production too low to prolong succinylcholine*

28

What is the incidence of low plasma cholinesterase?

6% resulting in a longer duration of action

29

Neostigmine lowers plasma cholinesterase {} up to _____ after administration

30 minutes

30

If you reverse, extubate, laryngospasm, give succinylcholine, expect what?

longer duration of action

31

Plasma cholinesterase levels are reduces with(4)

1. insecticides
2. glaucoma
3. myasthenia gravis drugs
4. chemotherapy

32

In younger patients undergoing minor surgery particularly in outpatient setting, what symptoms can be seen?

post-op myalgia in the neck, back and abdomen can occur post succinylcholine, especially with early ambulation

*myalgia localized to neck may be wrongly attributed to intubation*

33

What attenuates the myalgia sometimes seen with succ administration?

pre-treatment of a non-depolarizer

34

What are the concerns of succinylcholine administration and pregnancy?

-should only be given if absolutely required
-plasma cholinesterase levels are decreased by 24% during pregnancy and for several days postpartum
-a higher proportion of patients will have increased sensitivity to succinylcholine when pregnant than when not pregnant.

35

Factors influencing development of phase II block:

-duration of exposure to drug
-drug concentration
-muscle type(i.e., fast or slow)
-interaction with anesthetics

36

Does the K+/Na+ ATP pump continue while muscle is depolarized?

yup, it increases with increasing intracellular Na+(pumps Na+ out and K+ in)
-pump restores normal inonic balance and membrane potential
-if depolarizing drug present, receptor channels remain open and ion flux through them remains high

37

In a phase II block, the NMJ is _____.

depolarized by a depolarizing relaxant, but membrane potential gradually recovers toward normal, even though junction is still exposed to depolarizers.

*NM transmission remains blocked throughout exposure*

38

In a phase II block, reversal by a cholinesterase inhibitor is best.......

not attempted, although response to tetanus or ToF sim resembles non-depolarizers.