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Pharmacology > Lecture # 06_Fall > Flashcards

Lecture # 06_Fall Flashcards

1
Q

When a nerve depolarizes, ___ ions enter the neuron and ___ is released from vesicles and binds to ___ receptors on the motor-end plate of the muscle fiber

A

Ca ions enter, Ach is released, binds to nicotinic cholinergic receptors

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2
Q

Ach is hydrolyzed by ____ into ____ and ____.

A

Acetylcholinesterase, acetate and choline

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3
Q

Select the correct option.

Depolarizing NMBAs act as Ach receptor _____ (agonist or competitive antagonist).

A

agonist

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4
Q

Select the correct option.

Non-depolarizing NMBAs act as Ach receptor _____ (agonist or competitive antagonist).

A

competitive antagonist

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5
Q

T or F. Phase I and Phase II blocks are seen with non-depolarizing NMBAs.

A

False. They refer to the blocks seen with depolarizing NMBAs.

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6
Q

NMBAs are quaternary ______ compounds with afinity for _____ Ach receptors.

A

ammonium, nicotinic

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7
Q

A Phase II block resembles a ___ block.

A

non-depolarizing

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8
Q

What % of receptors must be blocked before you observe fade with a twitch monitor?

A

> 70%

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9
Q

What % of receptors must be blocked for complete twitch suppression?

A

> 90%

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10
Q

What is responsible for the metabolism of sux?

A

plasma pseudocholinesterase

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11
Q

What happens if you try to reverse a Phase I block with an AchE inhibitor?

A

can lead to prolonged depolarization

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12
Q

What is Dibucaine

A

it is a local anesthetic that inhibits pseudocholinesterase

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13
Q

What is A Dibucaine Number?

A

It is the % of pseudocholinesterase that is inhibited by dibucaine

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14
Q

What is a normal Dibucaine number?

A

80 = normal

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15
Q

What would a dibucaine number of 0-20 indicate?

A

a homozygous abnormal pseudocholinesterase gene that will result in prolonged NMB with Sux, lasting 4-8hrs

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16
Q

What would a dibucaine number of 40-60 indicate?

A

a homoheterozygous abnormal pseudocholinesterase gene that will result in prolonged NMB with Sux, lasting 20-30min

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17
Q

Pesticide toxicity resembles the effects of what drugs?

A

resembles the SLUDGE effects of AchE Inhibitors like Neostigmine

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18
Q

T or F. Pancuronium can prolong the depolarizing block of Sux.

A

True - Pancuronium inhibits pseudocholinesterase

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19
Q

T or F. Low doses of Sux causes tachycardia.

A

False. It binds to muscarinic cardiac Ach receptors - causes bradycardia and decreased myocardial contractility. Opposite at high doses

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20
Q

Why is hyperkalemia a side effect of Sux?

A

Due to the sustained opening of ion channels and membrane depolarization

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21
Q

Sux increases serum K+ levels by ___ mEq/L

A

0.5 mEq/L

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22
Q

How does neural injury lead to significant K+ release with Sux?

A

Rapid proliferation of extrajunctional ACh receptors with neural injury (trauma, denervation) - Widespread depolarization leads significant K+ release

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23
Q

Which of the following side effects associated with Sux can be attenuated with a defasciculating does of non-depolarizering MRs? (select all that apply)

A. Myalgias
B. Increased ICP
C. Increased IOP
D. Hyperkalemia
E. Increased Gastric Pressure
A 
A. Myalgias - Yes
B. Increased ICP - Yes
C. Increased IOP - NO!!
D. Hyperkalemia - NO!!
E. Increased Gastric Pressure - Yes
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24
Q

A Phase II block will be seen after ___mg/kg IV Sux.

A

7-10 mg/kg or 30-60 min

  • or after a single dose in pts with atypical plasma cholinesterase
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25
Q

Which of the following increases risk of succinylcholine induced hyperkalemia (Potential risk within 96 hours, peaks ~7-10 days after injury, lasts 6 months or longer)?

A. 3rd degree burn injury
B. Massive skeletal trauma
C. Upper motor neuron injury
D. Denervation  muscle atrophy
E. Myopathies (myotonia, muscular dystrophy)
A

All of them

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26
Q

Inhalational anesthetics ____ the onset of a Phase II block.

A

accelerate

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27
Q

Succinylcholine-induced MMR can lead to _____.

A

rhabdomyolysis

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28
Q

What are the 6 ABSOLUTE contraindications for succinylcholine?

A 
ABSOLUTE contraindications include: 
1, MH
2. dangerously elevated serum K+
3. known myotonia or muscular dystrophy
4. >2-4 days after CNS injury (stroke, cord injury)
5. massive musculoskeletal injury
6. major burn
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29
Q

What are 2 signs of rhabdomyolysis?

A

myoglobinuria and myoglobinemia

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30
Q

What are the 2 classes of Non-Depolarizing Neuromuscular Blocking Agents?

A

Benzoisoquinolines (“-acurium”) or steroidals (“-curonium”)

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31
Q

What is the Priming dose of Non-Depolarizing Neuromuscular Blocking Agents?

A

Priming dose: give 10% of intubating dose 5 min before induction

32
Q

What is the Defasciculating dose of Non-Depolarizing Neuromuscular Blocking Agents?

A

Defasciculating dose: give 10% of intubating dose 5 minutes before succinylcholine

33
Q

___, ____, ___, and ___ potentiate the action of Non-Depolarizing NMBAs.

A
  1. inhalational anesthetics (DES > SEVO > ISO > HAL)
  2. antibiotics (aminoglycosides – prolong
    steroidal NMBs)
  3. phenytoin
  4. Mg
34
Q

___, ____, ___, and ___ prolong the action of Non-Depolarizing NMBAs.

A

hypothermia, acidosis, hypokalemia, and hypocalcemia

35
Q

Muscles of glottis, face, airway, diaphragm are ___ sensitive to NMB than the thumb (adductor pollicis) so the dose to block diaphragm is ___ the dose needed to block adductor pollicis.

A

less, twice

36
Q

Cisatracurium is metabolized by _____.

A

Hoffman Elimination

37
Q

Atracurium (isomer of cisatracurium) is degraded by ___ AND _____ by
non-specific plasma esterases

A

Hoffman elimination AND ester hydrolysis

38
Q

What is the must common paralytic used in renal failure patietns and for ICU infusions?

A

Cistatracurium

39
Q

Which paralyzing agent is metabolized by pseudocholinesterase but no longer available?

A

Mivacurium

40
Q

Which paralyzing agent should be used with caution in renal failure patients and why?

A

Pancuronium - 40% renally cleared – caution in renal failure

41
Q

What CV effect does Pancuronium have?

A

Increases in HR, BP, CO (block cardiac

muscarinic ACh receptors)

42
Q

What is the best non-depolarizer for rapid sequence intubation?

A

Rocuronium

43
Q

What is the onset time and duration of Vecuronium?

A 
Onset = 3-4 min
Duration = 35-45min
44
Q

What is the onset time and duration of Rocuronium?

A 
Onset = 2 min
Duration = 30-40min
45
Q

What is the onset time and duration of Nimbex

A 
Onset = 2-4 minutes
Duration =  35-40 minutes
46
Q

What percent of Vecuronium is renally cleared?

A

25%

47
Q

How do reversal agents work?

A

Cholinesterase (AChE) Inhibitors (“Anticholinesterases”) - Indirectly increase amount of ACh in the NMJ which can compete with the non-depolarizing NMB agent

48
Q

T or F> Organophosphates (pesticides) are also anticholinesterases.

A

True

49
Q

AChE inhibitors are used in the diagnosis of ____.

A

myasthenia gravis

50
Q

In excessive doses, AChE inhibitors can cause_____ leading to ____.

A

ACh-mediated blockade, weakness

51
Q

T or F. Bronchospasm is a side effect of AChE inhibitors.

A

True

52
Q

___ is the only AChE inhibitor that crosses the Blood-Brain Barrier.

A

physostigmine

53
Q

Which anticholinergic agent crosses the BBB?

A

Atropine

54
Q

A pt with TOF with fade should get a ___ reversal dose.

A

Full

55
Q

A pt with TOF without fade should get a ___ reversal dose

A

partial

56
Q

When would you consider giving no reversal?

A

If the pt has sustained 5 sec tetanus or clinical evidence of adequate strength

57
Q

List the clinical signs of adequate strength in order from best to least acceptable.

A

Sustained head lift / leg lift > negative inspiratory force > vital capacity > tidal volume

58
Q

A p with post-tetanic twitch or no tetanic response should get a ___ reversal dose.

A

They should not get any reversal - they are unreversible at this point

59
Q

Post-tetanic count correlates with ____.

A

time until spontaneous recovery

60
Q

Reversal agents have ____% Hepatic and ____% renal clearance.

A

Hepatic (25-50%) and Renal (50-75%)

61
Q

What is the max dose of Neostigmine for adults?

A

5mg

62
Q

Which reversal agent should be given with atropine and why?

A

Edrophonium: rapid onset of action (1-2 minutes) and short duration of effect - Give with atropine – better match with onset, duration

63
Q

When would you consider using atropine with neostgmine instead of glycopyrrolate?

A

When you are concerned about it crossing the placenta

64
Q

_____ is a tertiary amine that crosses blood-brain barrier and is used as treatment for central cholinergic toxicity

A

Physostigmine

65
Q

T or F. You do not have to give atropine / glycopyrrolate with Physostigmine.

A

True

66
Q

Physostigmine is metabolized by ____.

A

plasma esterases

67
Q

_____ can be used to reverse deep NMB from non-depolarizing agents, although it is not currently approved for use in the US.

A

Sugammadex

68
Q

Sugammadex only works on non-depolarizing NMBAs with a ____ nucleus, such as ___, ____, and ___.

A

Steroid, Rocuronium, Vecuronium, and Pancuronium

69
Q

______ could be used with rocuronium for RSI – replace succinylcholine- which would be a huge benefit due to all the contraindications associated wit Sux.

A

Sugammadex

If you couldn’t tell by my 3 flashcards, this is sort of important to know!

70
Q

___is an autoimmune neuromuscular disease where circulating antibodies block Ach receptors at the postsynaptic NMJ and cause muscle weakness.

A

Myasthenia Gravis

71
Q

What should you remember about NMBAs in patients with Myasthenia Gravis?

A

They are Resistant to Sux and Sensitive to non-depolarizers (like Roc)

so you can remember this with:
“R to S and S to R”

72
Q

What is Myotonia?

A

abnormal delay in muscle relaxation after contraction

73
Q

What should you remember about NMBAs in patients with Myotonia (many types)?

A

They will have:

SUSTAINED contracture leading to hyperkalemia with SUX

A Normal response to Non-depolarizers

so you can remember this with:
“S with S and N with N”

74
Q

What should you remember about NMBAs in patients with Muscular Dystrophy, a disease that causes loss of muscle mass?

A

First, it is often latent and undiagnosed in patients <10y old (esp. males)

They have a normal response to non-depolarizers

BUT Sux can cause hyperkalemic cardiac arrest

This is why we avoid using sux in children

75
Q

What should you remember about NMBAs in patients with Upper Motor Neuron Lesions: hemiplegia, quadriplegia?

A

starting ~2-4 days after injury for up to 6-12 months use of Sux will cause hyperK

And they have a resistance to non-depolarizers below the level of the lesion

76
Q

What should you remember about NMBAs in burn patients?

A

They are Sensitive to Sux b/c they have a proliferation of extra-junctional Ach receptors
(sux will cause hyperK starting ~2-4 days after the burn for at least 12 months)

They are Resistance to non-depolarizing agents (Roc)

so you can remember this with:
“S to S and R to R”

Pharmacology (22 decks)

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