EXAM 2 Review Flashcards

1
Q
  1. What is the mechanism of action of succinylcholine?
A

Ach agonist, mimics Ach binding to Ach receptors at ALPHA subunit causing sustained depolarization (opening of receptor ion channels)

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2
Q

2.What is the mechanism for the metabolism of succinylcholine?

A

Marjority metabolized before reaching NMJ
Hydrolysis by plasma cholinesterase (pseudocholinesterase)
Metabolism on dependent of DIFFUSION away from the NMJ

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3
Q

3.What metabolites are formed from the metabolism of succinylcholine?

A

Broken down into Acetate and Choline

or NO metabolites

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4
Q

4.What inhalation agent is associated with diffusion hypoxia?

A

Nitrous Oxide

occurs when N2O d/c abruptly leading to reversal of partial pressure gradients, leave blood to enter alveoli

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5
Q

5.What steps can be done to prevent diffusion hypoxia caused by ______?

A

Giving 100% oxygen for several minutes at the end of the case can help avoid diffusion hypoxia from occurring

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6
Q

6.What anticholinesterase inhibitor can be used to treat psychosis due to anticholinergic drugs?

A

Physostigmine 15-60mck/kg/IV

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7
Q

7.What drug characteristic is responsible for this effect of diffusion Hypoxia

A

Low Blood gas coefficient 0.46 so rapidly reversible with rapid onset. Leaves blood 34 times more rapidly

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8
Q

8.What condition can result in an exaggerated long duration of action with the use of succinylcholine?

A

Atypical Plasma Cholinesterase

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9
Q

9.Explain the difference between heterozygous and homozygous genetic alterations?

A

Heterozygous dibucaine #40-60 slightly prolonged block, 20-30 mns, only 1 ABNORMAL GENE
Homozygous dibucaine #20, very LONG block 6-8 hours due to 2 ABNORMAL GENES

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10
Q

10.What test can be used to diagnosis this condition of heterozygous and homozygous?

A

Dibucaine Test

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11
Q

11.What steps can the anesthesia care provider use to prevent an exaggerated long duration of action with the use of succinylcholine?

A
DIbucaine test
Check twitches before giving NMB
Avoid in pseudocholinesterase deficiency
Use TOF
Reversal agents
Neogstimine before SCH can prolong block (don't do this ) if in phase 1 can go to phase 2
Obtain hx of patient.
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12
Q

12.Do all volatile anesthetics blunt the ventilatory stimulation evoked by arterial hypoxemia?

A

yes; all anesthetics including nitrous oxide profoundly depress the ventilatory response to arterial hypoxemia that is normally mediated by carotid bodies

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13
Q

13.What are the recommended steps used to avoid residual paralysis with the use of NDNMB?

A

Avoid long acting NDNMB (Pancuronium)
Use intermediate acting
Do not use unreliable indicators such as head lift, jaw clenching, grip strength and tidal volume leg lift
Use quantitative and objective (AMG, KMG, EMG) better legal ground in court

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14
Q

14.What volatile agents undergo the least amount of metabolism?

A

N2O

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15
Q

15.Which Inhalation agent undergoes the least amount of metabolism?

A

Nitrous Oxide (0.004%) –> Des 0.02, ISo 0.2 sevo 3-5% HALOTHANE –>20%

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16
Q

16.What is the clinical significance VA that undergoes the least amount of metabolism?

A

Produces less free fluorides and is therefore safer for the kidneys
Sevo does not produce TFA

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17
Q

17.What steps can the anesthesia care provider take to prevent myopathy associated with the use of succinylcholine?

A

may be prevented by prior administration of a NON paralyzing dose of NDNMB agent or by going to high dose Sch 3mg/kg straight to Block II

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18
Q

18.What is the intubation dose for each NDNMB agent?

A
Atracurium 0.5mg/kg IV over 60 seconds
Cisatracurium 0.1mg/kg
Mivacurium 0.15 mg/kg
Pancuronium 0.08-0.12 mg/kg 
Rocuronium 0.6 - 1.0 mg/kg
Vecuronium 0.08-0.12mg/kg
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19
Q

19.What would the expected result be from the use of succinycholine and a patient with myastenia gravis?

A

Resistant to Sch due to destruction of ACh receptors by antibodies

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20
Q

20.What would the expected result be from the use of NDNMB agents and a patient with myastenia gravis?

A

Very sensitive to NDNMB

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21
Q
  1. How should the neuromuscular blocker dosage to cause adequate muscle relaxation be altered when you administer volatile anesthetics?
A

Volatiles dose dependent increases in neuromuscular blockade
volatile enhances effects of NMB
DECREASE THE Dose

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22
Q

22.Which volatile anesthetic agent causes the greatest/least degree of bonchodilation?

A

Great –> SEVOFLURANE

Least –> DESFLURANE

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23
Q

23.What clinical scenarios may lead to a phase block with the use of succinylcholine?

A

low dose 0.5 - 1mg/kg phase I fasciculations 5 minutes duration
high dose 2-4 mg/kg phase II rapid 20-30 minutes,

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24
Q

24.What volatile anesthetic is most likely to cause nephrotoxicity?

A

Sevoflurane and Enflurane

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25
25.Which volatile anesthetics are non-pungent and can be used for a mask induction?
SEVOFLURANE
26
26.What volatile agent is considered to be the most pungent?
DESFLURANE
27
27. What are the volume of distribution for neuromuscular blocking agents? smallest --Cisatracurium
``` Quarternary ammonium Vd 200ml/kg Atracurium 182-282 ml/kg Cisatracurium 31 ml/kg Mivacurium 211-278ml/kg Rocuronium 194-207 ml/kg Pancuronium 261 ml/kg ``` Succinylcholine
28
29. Which induction agent has the highest context sensitive half life?
Halothane Isoflurane 86 min sevoflurane 65 min Desflurane 14 min
29
30. What is the onset of action for each NDNMB agent? | fastest? longest?
``` 3-5 minutes PVAC Atracurium 3-5 minutes Cisatracurium 3-5 minutes Vecuronium 3-5 minutes Pancuronium 3-5 minutes ``` 1-2 minutes Rocuronium 1-2 minutes
30
31. What are the absolute contraindications for nitrous oxide? (VPIAP)
``` Venous or arterial air embolism Pneumothorax Intraocular air / surgeries Acute INTESTINAL OBSTRUCTION Pernicious anemia B12 deficiency , N2O decrease B12 in liver. ```
31
32.At different times during the case, what is the predicted percentage of receptors occupied by NDNMB agent?
See other
32
33.How many receptor occupied right after administration with 0/4?
>95% , no fade
33
34. How many receptor occupied right after administration with 1/4?
90% no fade
34
35. How many receptor occupied right after administration with 2/4?
85%, no fade
35
36. How many receptor occupied right after administration with 3/4?
80% no fade
36
37. How many receptor occupied right after administration with 4/4?
75% receptors blocked (recovery), 4th twitch is 0.2 (20%) of the 1st twitch , 4 twitches then there is FADE
37
38. How many receptor occupied right after admin? with/without fade?
75% with fade
38
39. What volatile anesthetic has a chloride in its molecular structure?
Isoflurane (1 fluoride substituated with chloride)
39
40. What volatile anesthetic has a bromine in its molecular structure?
Halothane
40
41. What effect does each of the volatile agents have on hepatic blood flow?
Hepatic blood flow decrease | or inhibition of drug metabolizing enzymes
41
42. Do NMBA have sedative/analgesic effects?
ABSOLUTELY NO
42
43. What are the potentially toxic compounds produced by the breakdown of volatile
TFA Sevo --> Compound A at low flow, no TFA Desflurane> ISo = CO Des and ISO can be metabolized to acyl halides which are hepatotoxic
43
44. What is the least amount of twitch required before attempting reversal for NDNMBA blockade?
During anesthetic techniques that do not enhance the effects of muscle relaxants (TIVA) a minimum TOF count of 2 should be present before administration of anticholinesterases During anesthetic techniques that enhance the effects of muscle relaxants (such as inhaled Volatile anesthesia) a TOF count of 4 should be present before administration of anticholinesterases
44
45. What is responsible for the faster onset of rocuronium?
The lack of potency of rocuronium to vecuronium is the Important reason for RAPID onset large number of molecules given with a LESS potent agent are available to occupy a greater number of receptors
45
46. What NMBA is recommended for rapid sequence intubation?
DNMB : RSI succinylcholine | NDNMB : Roc can also be used
46
47. What volatile agent has the greatest effect on EEG?
Enflurane
47
48. What pathological conditions may result in up-regulation of acetylcholine receptors?
Muscular dystrophies GBS Burns
48
49. What patient characteristics can prolong the effects of atracurium?
Hypothermia | Acidosis
49
lack vec roc cis have atracurium miva Histamine release - What NDNMBA would be best for a patient with liver failure?
Atracurium | Cisatracurium
50
52. How does each Sevoflurane affect CVP?
NO INCREASE in RAP or CVP
51
53.How does Desflurane affect CVP?
INCREASE CVP
52
54.How does Isoflurane affect CVP ?
INCREASE CVP
53
55.What are absolute contraindications for the use of succinylcholine?
Hx MALIGNANT hyperthermia Myotonia congenita and dystrophica Duschenne muscular dystrophy
54
56.In a patient with renal failure, what agent would have the greatest degree of duration of action prolongation?
Pancuronium, Vecuronium
55
57.In a patient with renal failure, what agent would have the LEAST degree of duration of action prolongation?
Atracurium and Cisatracurium (undergoes Hoffman)
56
58.What are the clinical characteristics of nitrous oxide?
``` INCREASE in CMRO2 Produces either NO effect or MODEST increase in BP CO modestly increased by Nitrous oxide Increase RAP Does not increase PaCO2 ```
57
59.What drugs will prolong the duration of action of NMBA?
``` VA ABT LA Cardiac dysrhythmias Diuretics Mag Lithium Ganglionic Blockers Cyclosporin ```
58
60. Which volatile anesthetic can be safely used above 1.5MAC without causing apnea?
Isoflurane
59
61.Which volatile agent can cause an isoelectric EEG at 2 MAC?
Isoflurane produces isoelectric EEG at 1.5 MAC and 2 MAC
60
62.What is the best way to manage a patient that has a significantly long prolonged block from succinycholine?
Keep them sedated and ventilated
61
63.What inhalation agents have greatest least degree of muscle paralysis?
Most -->Desflurane | Least --> NITROUS
62
64.What are triggers for MH?
Volatile anesthetics | SUCCINYLCHOLINE
63
65.What anticholinesterase agent can be used to treat CNS side effects from anticholinergic agents?
Physostigmine 15-60mcg/kg IV, increased risk of NV though
64
66.What anticholinergic agent is classified an a quatinary ammonium compound? What about their VD?
Glycopyrrolate Quarternary ammonium compound; DOES NOT CROSS CNS and Is highly ionized DECREASED VD
65
67.How does this change the volume of distribution of quaternary compared to tertiary ammonium compounds.
Quarternary - Decreased Vd | Tertiary - Increased Vd
66
68.How does VD affect the clinical effects of this agent of quaternary compound?
Does not Cross CNS, no sedation
67
69.What are all of the clinical effects anticipated after the administration of any anticholinergic agent?
Increase HR Smooth Muscle Relaxation Decrease gastric H+ Ions (increase pH) Antisialalogue
68
70. What anticholinergic agent has greatest antisialagogue effects?
SCOPOLAMINE then glycol -> Atropine
69
71.What anticholinergic agent has fastest onset of action?
Atropine
70
72.What anticholinergic agent has slowest onset of action?
Glycopyrrolate
71
73.Which anticholinergic agent is the most sedating?
SCOPOLAMINE
72
74.Which anticholinergic agent is the LEAST sedating?
GLYCOPYRROLATE
73
75. Do any of the anti-cholinergic agents effect fetal heart rate?
No
74
76.What anticholinergic agent causes greatest amount of mydriasis?
SCOPOLAMINE
75
77.What anticholinergic agent causes LEAST amount of mydriasis?
GLYCOPYRROLATE
76
78.What is the mechanism by which each of the anticholinesterase agents attaches to cholinesterase?
Reversible Electrostatic attachment to anticholinesterase by EDROPHONIUM
77
79.What is the mechanism of action of suggamadex?
- Modified gamma cyclodextrin, selective relaxant binding agent specifically designed to encapsulate the STEROIDAL NMBAs vec and Roc - Work by forming a complex with the NMBs by preventing their binding to nicotinic receptors at the NMJ, resulting in reversal of NMB
78
80.What are the indications for suggamadex?
Indicated for reversal of blockade done by STEROIDAL NMBA
79
81.What are major precautions/contraindications with the use of suggamadex?
Clearance decrease in RENAL IMPAIRMENT | Avoided in patients with a creatinine clearance of <30ml/min
80
Conscious memory is suppressed by
Volatile anesthetics
81
How much of MAC of ISOFlurANE suppresses memory
0.45 MAC
82
How much of MAC of Nitrous suppresses memory
0.6 MAC