Quiz 7

Question 1

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

Answer 1

Nicotinic

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

Question 2

What part of ACH reacts with subunit at receptor?

Answer 2

N+

Question 3

ACH deactivated by? made of?

Answer 3

Acetylcholinesterase

choline and acetate

Question 4

ACH facts

Answer 4

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

Question 5

receptor that activates fight/flight

Answer 5

nicotinic

Question 6

receptor that activates rest/digest

Answer 6

muscarinic

Question 7

how much twitch response suppression adequate for surgery?

Answer 7

90%

Question 8

tracheal intubation dose = ?

Answer 8

2x ED95 dose

Question 9

how are muscles effected by NMB

Answer 9

small muscles first (eyes, fingers)

large muscles last (abdomen, diaphragm)

Question 10

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

Answer 10

laryngeal

peripheral

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

Question 11

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

Answer 11

• Benzylisoquinolinium
• Aminosteroid

(different reversals b/w the 2)

Question 12

does albumin levels effect NMB action?

Answer 12

No bc not highly protein bound

Question 13

CYP interference is what type of interaction?

Answer 13

Pharmacokinetic

Question 14

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

Answer 14

Pharmacodynamic

Question 15

Long acting NDNMB and class? (3)

Answer 15

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

Question 16

Intermediate acting NDNMB and class? (4)

Answer 16

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

Question 17

Short acting NDNMB and class? (1)

Answer 17

Mivacurium (B)

Question 18

Succ action on receptor site?

Succ specific on formulary level?

Answer 18

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

- two N+ in chemical formula

Question 19

Why does Succ. have a longer duration than ACH?

Answer 19

Slower hydrolysis

Question 20

any pre or post synaptic effects in Succ?

Answer 20

Pre - minor effects

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

Question 21

Phase I Blockade:

Answer 21

• 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

Question 22

Phase II Blockade:

Answer 22

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

Question 23

Metabolites of Succ? what breaks Succ. down?

Answer 23

• succinic acid and choline
• Plasma Cholinesterase

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

Question 24

what reduces amounts of plasma cholinesterase? what increases?

Answer 24

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

-Obesity

Question 25

What tests for atypical pseudocholinesterase?

Answer 25

Dibucaine test

Question 26

how to reduce Succ side effects?

Answer 26

treat with NDNMB | doesn't treat s/e of hyperkalemia

Question 27

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

Answer 27

- 2nd dose within 5 minutes | - Atropine will not work, need B1 agonist (epi, dopamine)

Question 28

What arrythmias can you get with Succ?

Answer 28

- Sinus bradycardia - junctional rhythm - sinus arrest - May increase heart rate and BP due to ANS ganglia stimulation

Question 29

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

Answer 29

- 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

Question 30

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

Answer 30

- increased intragastric pressure | - aspiration

Question 31

NDNMB characteristics:

Answer 31

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

Question 32

NDNMB cardiac effects

Answer 32

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

Question 33

what type of receptor competition for NDNMB?

Answer 33

Competitive antagonist

Question 34

who has higher risk of allergic reaction to NDNMB

Answer 34

women

Question 35

what enhances NMBs

Answer 35

- 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

Question 36

Temp and NMB

Answer 36

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

Question 37

Pancuronium:

Answer 37

- 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

Question 38

Pancuronium cardiovascular effects:

Answer 38

Increase heart rate Increased MAP Increased cardiac output Mechanism: vagal blockade; SNS activation; muscarinic interference (block) Dysrhythmias, esp. in combo with Digoxin

Question 39

NMB with no CV changes

Answer 39

Doxacurium | pipecuronium

Question 40

Infants: increased potency, shorter duration

Answer 40

pipecuronium

Question 41

Priming Principle:

Answer 41

``` 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 ```

Question 42

Which drug is protein bound?

Answer 42

Atracurium (higher effect in low albumin levels)

Question 43

what effects Hoffmans elimination and what drugs effected?

Answer 43

- Accelerated by alkalosis, slowed by acidosis - Atracurium and Cisatracurium (Independent of renal and hepatic function)

Question 44

What NMB good for pts with organ issues?

Answer 44

-Atracurium and Cisatracurium

Question 45

what metabolite of Hoffman elimination that can increase MAC values?

Answer 45

Laudanosine

Question 46

Atracurium CV s/e?

Answer 46

- Histamine release (H1 and H2 blockers help (combo)) | - long term H2 blocker use may exacerbate CV effects due to histamine

Question 47

cisatricurium difference?

Answer 47

NO HISTAMINE release

Question 48

Vecuronium:

Answer 48

- 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)

Question 49

what enhances vecuronium?

Answer 49

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

Question 50

Vecuronium - Pediatric:

Answer 50

- Onset more rapid for infants | - Duration longest in infants shortest in children

Question 51

NDNMB with quickest onset?

Answer 51

Rocuronium

Question 52

NDNMB with shortest duration?

Answer 52

Mivacurium

Question 53

NMB with 1 N+ base?

Answer 53

Rocuronium | Vecuronium

Question 54

most potent NMB

Answer 54

Doxacurium