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My Pharm 1 > Quiz 7 > Flashcards

Quiz 7 Flashcards

1
Q

Which receptor does NMB work on? how do the normally work?

A

Nicotinic

  • ACH binds to both alpha channels (ligand gated)
  • Na moves through
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2
Q

What part of ACH reacts with subunit at receptor?

A

N+

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3
Q

ACH deactivated by? made of?

A

Acetylcholinesterase

choline and acetate

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4
Q

ACH facts

A

can activate rest/digest or fight/flight response b/c activates both parasympathetic/sympathetic pathways

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5
Q

receptor that activates fight/flight

A

nicotinic

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6
Q

receptor that activates rest/digest

A

muscarinic

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7
Q

how much twitch response suppression adequate for surgery?

A

90%

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8
Q

tracheal intubation dose = ?

A

2x ED95 dose

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9
Q

how are muscles effected by NMB

A

small muscles first (eyes, fingers)

large muscles last (abdomen, diaphragm)

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10
Q

More rapid/ less intense at _______ muscles than ________ muscles. Whats a good predictor?

A

laryngeal

peripheral

(Adductor pollicis response poor indicator of laryngeal relaxation
Orbicularis oculi better prediction)

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11
Q

which type NDMNB has a higher incidence of histamine release? whats the other type of NDNMB?

A
  • Benzylisoquinolinium
  • Aminosteroid

(different reversals b/w the 2)

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12
Q

does albumin levels effect NMB action?

A

No bc not highly protein bound

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13
Q

CYP interference is what type of interaction?

A

Pharmacokinetic

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14
Q

membrane stabilization or receptor site action is what type of interaction?

A

Pharmacodynamic

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15
Q

Long acting NDNMB and class? (3)

A

Pancuronium (A)
Doxacurium (B)
Pipecuronium (A)

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16
Q

Intermediate acting NDNMB and class? (4)

A

Atracurium (B)
Vecuronium (A)
Rocuronium (A)
Cisatracurium (B)

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17
Q

Short acting NDNMB and class? (1)

A

Mivacurium (B)

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18
Q

Succ action on receptor site?

Succ specific on formulary level?

A
  • only needs to bind to 1 site (nicotinic receptor)

- two N+ in chemical formula

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19
Q

Why does Succ. have a longer duration than ACH?

A

Slower hydrolysis

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20
Q

any pre or post synaptic effects in Succ?

A

Pre - minor effects

Post - leakage of K+ out of cell for increase serum K+ of 0.5 mEq/L

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21
Q

Phase I Blockade:

A
  • Depolarizing block- receptor stimulation
  • Decreased contraction in response to single twitch stimulation
  • Decreased amplitude by sustained response to continuous stimulation
  • TOF ratio >0.7
  • Absence of posttetanic facilitation
  • Augmentation of neuromuscular blockade after reversal agent
  • Accompanied by fasiculations at onset
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22
Q

Phase II Blockade:

A
  • Desensitization: Similar to non-depolarizers
  • May be antagonized by a reversal agent
  • Manifests as tachyphylaxis
23
Q

Metabolites of Succ? what breaks Succ. down?

A
  • succinic acid and choline
  • Plasma Cholinesterase

(Must diffuse away from the NMJ to plasma to be metabolized)

24
Q

what reduces amounts of plasma cholinesterase? what increases?

A
  • Severe liver disease
  • neostigmine
  • high estrogen levels
  • Reglan (inhibits enzyme)

-Obesity

25
Q

What tests for atypical pseudocholinesterase?

A

Dibucaine test

26
Q

how to reduce Succ side effects?

A

treat with NDNMB

doesn’t treat s/e of hyperkalemia

27
Q

what increases arrhythmia risk in Succ use? What to do for arrythmias?

A
  • 2nd dose within 5 minutes

- Atropine will not work, need B1 agonist (epi, dopamine)

28
Q

What arrythmias can you get with Succ?

A
  • Sinus bradycardia
  • junctional rhythm
  • sinus arrest
  • May increase heart rate and BP due to ANS ganglia stimulation
29
Q

increased risk pts for hyperkalemia? VERY high risk? How long can last?

A
  • Muscular dystrophy
  • Third degree burns
  • Skeletal muscle atrophy or severe trauma
  • Upper motor neuron lesions

VERY HIGH RISK - male children with undiagnosed myopathy

-May develop within 96 hours, last up to 6 months or more

30
Q

Succ s/e of increased pressure - most common? biggest risk?

A
  • increased intragastric pressure

- aspiration

31
Q

NDNMB characteristics:

A
  • Antagonism by anticholinesterases
  • Decreased twitch response to single stimulus
  • TOF ratio <0.7
  • Unsustained response during continuous stimulation
  • Posttetanic potentiation
  • Potentiation of other nondepolarizers
32
Q

NDNMB cardiac effects

A
  • Histamine release (Atracurium, Mivacurium)* vasodilation, drops bp
  • Cardiac muscarinic receptors (Pancuronium)
  • Nicotinic autonomic ganglia (mostly SCh)
33
Q

what type of receptor competition for NDNMB?

A

Competitive antagonist

34
Q

who has higher risk of allergic reaction to NDNMB

A

women

35
Q

what enhances NMBs

A
  • Volatile anesthetics
  • Aminoglycosides ( tobramycin, gentamicin, and amikacin)
  • Local anesthetics
  • Antiarrhythmics
  • Diuretics
  • Mg++, Li+ (Ca inhibition with too much Mg. Li tricking body believe its Na)
  • hypothermia
36
Q

Temp and NMB

A

Every degree C in each direction can delay/quicken response by 5-15 mins

37
Q

Pancuronium:

A
  • Renal failure: clearance reduced up to 50%
  • Metabolite: 3-desacetylpancuronium Half as potent as pancuronium
  • Total billiary obstruction, hepatic cirrhosis - prolonged half life d/t fluid dynamic changes (larger vD) bc hydrophilic
  • Enhanced by respiratory acidosis
38
Q

Pancuronium cardiovascular effects:

A

Increase heart rate
Increased MAP
Increased cardiac output

Mechanism: vagal blockade; SNS activation; muscarinic interference (block)
Dysrhythmias, esp. in combo with Digoxin

39
Q

NMB with no CV changes

A

Doxacurium

pipecuronium

40
Q

Infants: increased potency, shorter duration

A

pipecuronium

41
Q

Priming Principle:

A 
Alternative to SCh for intubation
1: Small dose binds spare receptors
no clinical effect
2: 4 minutes later deliver the rest
deepens the neuromuscular blockade rapidly
42
Q

Which drug is protein bound?

A

Atracurium (higher effect in low albumin levels)

43
Q

what effects Hoffmans elimination and what drugs effected?

A
  • Accelerated by alkalosis, slowed by acidosis
  • Atracurium and Cisatracurium

(Independent of renal and hepatic function)

44
Q

What NMB good for pts with organ issues?

A

-Atracurium and Cisatracurium

45
Q

what metabolite of Hoffman elimination that can increase MAC values?

A

Laudanosine

46
Q

Atracurium CV s/e?

A
  • Histamine release (H1 and H2 blockers help (combo))

- long term H2 blocker use may exacerbate CV effects due to histamine

47
Q

cisatricurium difference?

A

NO HISTAMINE release

48
Q

Vecuronium:

A
  • Both hepatic metabolism and renal clearance
  • Higher lipid solubility to enter hepatocytes
  • Lipid solubility for billiary excretion (40% unchanged in the bile)
  • Exaggerated response with hepatic cirrhosis
  • 30% unchanged in the urine (Half life prolonged in renal failure)
49
Q

what enhances vecuronium?

A

-Hypercarbia post injection enhances effects (avoid hypoventilation post-op)

50
Q

Vecuronium - Pediatric:

A
  • Onset more rapid for infants

- Duration longest in infants shortest in children

51
Q

NDNMB with quickest onset?

A

Rocuronium

52
Q

NDNMB with shortest duration?

A

Mivacurium

53
Q

NMB with 1 N+ base?

A

Rocuronium

Vecuronium

54
Q

most potent NMB

A

Doxacurium

My Pharm 1 (10 decks)

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