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Anes Pharm Spring 25’ > Exam 3 Drugs > Flashcards

Exam 3 Drugs Flashcards

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1
Q

What are the commonly used inhaled anesthetics?
Try to list the Generic and trade name :)

A
  • Desflurane (Suprane)
  • Nitrous Oxide (Entonox)
  • Sevoflurane (Ultane)
  • Isoflurane (Forane)
  • Enflurane (Ethrane)
  • Halothane (Fluothane)

These agents vary in their pharmacokinetic and pharmacodynamic properties.

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2
Q

What does the Blood/Gas Solubility Coefficient indicate?

A

The speed of onset and offset of the anesthetic.

A lower coefficient indicates poorer solubility in blood, leading to faster induction and emergence.

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3
Q

What is the Blood/Gas Solubility Coefficient of Desflurane?

A

0.42

This indicates that Desflurane has a relatively low solubility in blood.

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4
Q

What is MAC (Minimum Alveolar Concentration)?

A

The concentration of anesthetic at 1 atmosphere that prevents movement in 50% of subjects in response to a surgical stimulus.

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5
Q

What is the MAC value of Sevoflurane?

A

1.8%

This value is based on a 30-55 year old population at 37°C and 1 ATM.

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6
Q

Which inhaled anesthetic has the highest vapor pressure?

A

Desflurane: 669 mmHg

This high vapor pressure allows for rapid delivery of the anesthetic.

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7
Q

What is the boiling point of Nitrous Oxide?

A

-88.5 °C

This low boiling point indicates that it is a gas at room temperature.

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8
Q

Which inhaled anesthetic is considered the least pungent?

A

Sevoflurane

Its sweet smell and lack of airway irritation make it ideal for inhalation induction.

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9
Q

True or False: Sevoflurane is the preferred anesthetic for patients with irritable airways.

A

True

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10
Q

How is Desflurane metabolized?

A

Resistant to metabolism, unlikely to cause organ toxicity.

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11
Q

What compounds are produced from the metabolism of Sevoflurane?

A

Vinyl halides and inorganic fluoride.

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12
Q

Which inhaled anesthetic is known to produce antibody reactions due to prior sensitization?

A
  • Isoflurane
  • Enflurane
  • Halothane
  • Nitrous Oxide

These anesthetics can be oxidized by P450 to acetyl halides.

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13
Q

What is the effect of Nitrous Oxide on cerebral blood flow (CBF)?

A

Increases CBF; it is the drug of choice for increased ICP cases.

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14
Q

Which inhaled anesthetic is most likely to cause bronchospasm?

A

Desflurane

Its pungency can worsen bronchospasms, especially in smokers.

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15
Q

What effect does Nitrous Oxide have on the hypoxic ventilatory response?

A

No blunting of hypercarbic response; it won’t increase PaCO2.

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16
Q

What cardiovascular effect is associated with Halothane?

A

Increased pulmonary vascular resistance and potential bradyarrhythmias in pediatrics.

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17
Q

Which inhaled anesthetics potentiate the effects of neuromuscular blocking drugs?

A

All except Nitrous Oxide

This includes both depolarizing and non-depolarizing neuromuscular blockers.

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18
Q

What is the potential renal effect of inhaled anesthetics?

A

Dose-dependent decrease in renal blood flow (RBF), glomerular filtration rate (GFR), and urine output (U/O).

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19
Q

Fill in the blank: All inhaled anesthetics are _______.

A

emetogenic

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20
Q

What is a clinical implication of using Sevoflurane in patients with liver disease?

A

It is considered the best option due to its minimal metabolism and lack of antibody reactions.

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21
Q

What is the effect of inhaled anesthetics on uterine contractility?

A

Dose-dependent decrease in uterine contractility

This can be useful with retained placenta but may worsen blood loss with uterine atony.

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22
Q

What is the clinical significance of vasodilation in 20-50 µm meter vessels?

A

Not significant clinically.

This indicates that the vasodilation effect in this vessel size range does not impact clinical outcomes.

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23
Q

What does QT interval prolongation indicate in relation to K+ current?

A

Increased risk of torsades.

QT prolongation can lead to life-threatening arrhythmias.

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24
Q

How does dose dependency affect uterine contractility during OB procedures?

A

0.5-1.0 MAC decreases uterine contractility.

This can be useful in managing retained placenta but may worsen blood loss with uterine atony.

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25
What effect does nitrous oxide have on uterine contractility?
No effect on uterine contractility. ## Footnote Nitrous oxide is often used for analgesia without impacting uterine function.
26
How does nitrous oxide compare to other volatiles in terms of analgesia and depression?
Increases analgesia without BZD/opioid depression faster than other volatiles. ## Footnote This makes nitrous oxide a favorable choice for pain management.
27
What are the unique properties of desflurane?
Lowest blood/gas solubility, rapid onset and offset, high vapor pressure requiring a special heated vaporizer. ## Footnote These properties make desflurane suitable for certain surgical scenarios.
28
What are the clinical considerations for desflurane?
Pungent, can cause airway irritation and laryngospasm, not ideal for mask induction. ## Footnote Rapid concentration increases can stimulate the sympathetic nervous system.
29
What are the contraindications for using desflurane?
Patients with increased ICP due to increased CBF. ## Footnote This is due to the potential for further increasing intracranial pressure.
30
What are the unique properties of nitrous oxide?
Rapid onset and offset, potent analgesic, cannot achieve surgical anesthesia alone (MAC > 100%). ## Footnote It is often used for sedation and pain relief.
31
What are the clinical considerations regarding nitrous oxide?
Can cause megaloblastic bone marrow suppression with prolonged exposure. ## Footnote It's contraindicated in certain surgical procedures where air-filled spaces are present.
32
What are the contraindications for nitrous oxide?
First trimester of pregnancy due to B12 deficiency risk. ## Footnote This is important for the safety of the developing fetus.
33
What are the unique properties of sevoflurane?
Low pungency, suitable for mask induction, relatively stable, can degrade in desiccated CO2 absorbents to produce Compound A. ## Footnote This makes sevoflurane a good choice for patients with reactive airways.
34
What are the clinical considerations for sevoflurane?
Good choice for patients at risk for bronchospasm. ## Footnote Additional water is added to sevo for safety.
35
What are the unique properties of isoflurane?
Intermediate solubility, potent anesthetic, relatively stable. ## Footnote Isoflurane is commonly used in various surgical settings.
36
What are the clinical considerations for isoflurane?
Can cause coronary steal in susceptible patients. ## Footnote This can have significant implications for patients with coronary artery disease.
37
What are the unique properties of enflurane?
Intermediate solubility, potent anesthetic, can cause seizure activity at high doses or with hypocarbia. ## Footnote This limits its use in certain patient populations.
38
What are the unique properties of halothane?
High potency, intermediate solubility, associated with hepatotoxicity. ## Footnote Its use is rarely seen in modern practice due to these risks.
39
What is malignant hyperthermia?
A rare but life-threatening pharmacogenetic disorder triggered by volatile anesthetics and succinylcholine. ## Footnote It is crucial to recognize and treat this condition promptly.
40
What is the etiology of malignant hyperthermia?
Inherited genetic disorder caused by dysfunction with RyR receptor causing excessive release of Ca+. ## Footnote This leads to severe metabolic disturbances.
41
What are the signs of malignant hyperthermia?
Increased body temperature, increased ETCO2, increased O2 consumption, muscle rigidity, rhabdomyolysis. ## Footnote Early recognition is key to effective treatment.
42
What is the treatment for malignant hyperthermia?
Dantrolene is the antidote, blocking intracellular Ca+ release. ## Footnote Timely administration can significantly reduce mortality.
43
What is the mortality rate of untreated malignant hyperthermia?
80% mortality if untreated. ## Footnote This highlights the critical nature of swift diagnosis and intervention.
44
What is the mechanism of action of depolarizing neuromuscular blocking agents (NMBAs)?
Mimics acetylcholine by binding to nicotinic ACh receptors, causing sustained depolarization. ## Footnote Succinylcholine is the only clinically used depolarizing NMBA.
45
What is the metabolism of succinylcholine?
Hydrolyzed by butylcholinesterase. ## Footnote This slower hydrolysis than ACh leads to increased potassium levels.
46
What is the onset and duration of succinylcholine?
Onset: 30-60 seconds; Duration: 3-5 minutes. ## Footnote This rapid action makes it useful for rapid sequence intubation.
47
What are the side effects of succinylcholine?
* Hyperkalemia * Increased ICP * Sympathomimetic effects * Increased intragastric pressure * Myalgia * Malignant hyperthermia concern ## Footnote These effects necessitate careful patient selection.
48
What is the typical presentation of a phase 1 block with depolarizing NMBAs?
Decreased contraction to single twitch stimulation, TOF ratio > 0.7. ## Footnote This indicates a typical response to succinylcholine.
49
What can cause a phase 2 block in depolarizing NMBAs?
Overdose or pseudocholinesterase deficiency. ## Footnote This can enhance non-depolarizing drug effects.
50
What is the effect of decreased pseudocholinesterase activity?
Causes prolonged succinylcholine effects. ## Footnote This can be due to various factors including genetics and certain medications.
51
What are the mechanisms of action for non-depolarizing NMBAs?
Competitive antagonists of nAChRs, preventing ACh from binding. ## Footnote This leads to muscle paralysis without initial fasciculations.
52
What are examples of aminosteroid non-depolarizing NMBAs?
* Pancuronium * Vecuronium * Rocuronium ## Footnote Each has distinct properties regarding duration and metabolism.
53
What is the metabolism of vecuronium?
Hepatic and renal metabolism with active metabolites. ## Footnote This can lead to prolonged effects in patients with renal dysfunction.
54
What are factors influencing NMBA action?
* Electrolyte imbalances * Acid-base balance * Temperature * Volatile anesthetics * Other drugs ## Footnote These factors can significantly alter the effectiveness of NMBAs.
55
What is the Train-of-Four (TOF) monitoring method?
A series of four supramaximal stimuli delivered to a peripheral nerve. ## Footnote The TOF ratio indicates the degree of neuromuscular blockade.
56
What is the mechanism of action for anticholinesterase inhibitors?
Inhibit acetylcholinesterase, increasing ACh concentration at the neuromuscular junction. ## Footnote This facilitates the reversal of non-depolarizing NMBAs.
57
What is sugammadex used for?
A selective relaxant binding agent that inactivates rocuronium and vecuronium. ## Footnote It allows for rapid and predictable reversal of neuromuscular blockade.
58
What is dantrolene's mechanism of action?
Inhibits calcium release from the sarcoplasmic reticulum. ## Footnote This is crucial for treating malignant hyperthermia.
59
What are Depolarizing NMBAs?
Competitively bind to ACh receptors without causing depolarization, preventing ACh binding and subsequent muscle contraction.
60
What does ED95 represent?
Effective dose required to achieve 95% depression of baseline muscle contraction.
61
What is Rapid Sequence Induction and Intubation (RSII)?
A technique used for emergency intubation, often requiring rapid-onset NMBAs.
62
What is Hoffman Elimination?
A spontaneous chemical degradation process independent of liver or kidney function.
63
What is the role of Plasma Cholinesterase (Pseudocholinesterase)?
Enzyme responsible for the metabolism of succinylcholine and mivacurium.
64
What are Active Metabolites in the context of NMBAs?
Some NMBAs are metabolized into compounds with significant neuromuscular blocking activity, prolonging the duration of action.
65
What type of NMBA is Vecuronium?
Non-depolarizing (curare derivative) with intermediate duration of action.
66
What is the potency (ED95) of Vecuronium?
0.04 mg/kg.
67
What is the intubating dose for Vecuronium?
0.10 to 0.20 mg/kg.
68
What is the elimination half-life of Vecuronium?
50 to 60 minutes (normal organ function).
69
What are the side effects of Vecuronium?
Vagal blockade with large doses.
70
What is the primary metabolism route for Vecuronium?
Renal (10 to 50%), hepatic (30 to 50%).
71
What is the duration of action of Rocuronium?
Intermediate.
72
What is the potency (ED95) of Rocuronium?
0.3 mg/kg.
73
What is the onset time for Rocuronium?
1 to 2 minutes.
74
What are the side effects of Rocuronium?
Minimal.
75
What is the elimination half-life of Pancuronium?
100 to 130 minutes (normal organ function).
76
What are the side effects of Pancuronium?
Vagal block (tachycardia), catecholamine release.
77
What is the type of Mivacurium?
Non-depolarizing (benzylisoquinoline).
78
What is the duration of action of Mivacurium?
Short.
79
What is the elimination half-life of Mivacurium?
2 to 2.5 minutes.
80
What are the side effects of Mivacurium?
Histamine release.
81
What is the primary metabolism route for Mivacurium?
Plasma cholinesterase.
82
What is the type of Atracurium?
Non-depolarizing (benzylisoquinoline).
83
What is the elimination route for Atracurium?
Hoffman elimination (30%), ester hydrolysis (60%).
84
What are the side effects of Atracurium?
Histamine release.
85
What is the type of Cisatracurium?
Non-depolarizing (benzylisoquinoline).
86
What is the duration of action of Cisatracurium?
Intermediate.
87
What is the potency (ED95) of Cisatracurium?
0.04 to 0.05 mg/kg.
88
What is the type of Succinylcholine?
Depolarizing (ACh analog).
89
What is the duration of action of Succinylcholine?
Ultrashort.
90
What are the contraindications for Succinylcholine?
High K+, MH, muscular dystrophy, children, receptor up-regulation settings, pseudocholinesterase deficiency.
91
What is the role of Cholinesterase Inhibitors in NMBA reversal?
Inhibit acetylcholinesterase, increasing ACh levels at the neuromuscular junction.
92
What is Sugammadex used for?
Rapidly reverses the effects of rocuronium and vecuronium.
93
What is the Train-of-Four (TOF)?
A method of monitoring neuromuscular function using peripheral nerve stimulation.
94
What is Malignant Hyperthermia (MH)?
A known trigger for MH in susceptible individuals, associated with succinylcholine.
95
What is NMBA-Induced Critical Illness Myopathy (CIM)?
Severe muscle weakness due to prolonged NMBA use, particularly with corticosteroids.
96
What are the risk factors for CIM?
Prolonged NMBA use, high-dose corticosteroids, sepsis, multi-organ failure.
97
What is the mechanism of Phase II Block with Succinylcholine?
Changes in the ACh receptor conformation and ion channel kinetics.

Anes Pharm Spring 25’ (22 decks)

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