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Pharm Unit 3 > General Anesthetics I and II > Flashcards

General Anesthetics I and II Flashcards

1
Q

What is the mechanism of Nitrous Oxide?

A

NMDA receptor antagonist

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2
Q

What is the therapeutic use of Nitrous Oxide?

A

Mask induction in children

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3
Q

What are important side-effects of Nitrous Oxide?

A

Post-operative nausea and vomiting, inactivates vit B (leading to abnormal embryonic development, abortion), accumulates in closed air-containing spaces (bowel, middle ear, pneumothoraces, air emboli) because N2O very insolube in blood

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4
Q

The anesthesiologist wants to use an anesthetic that causes muscle relaxation. Which anesthetic won’t she choose?

A

N2O because it does not relax muscles

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5
Q

What is the gold standard for maintenance of anesthesia?

A

Isoflurane

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6
Q

What are the 3 volatile anesthetics?

A

Isoflurane, Desflurane, and Sevoflurane

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7
Q

Which volatile anesthetic is the most potent?

A

Isoflurane

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8
Q

Which volatile anesthetic is the least soluble and and least potent? What is its benefit?

A

Deslurane; Allows for patients to rapidly emerge from anesthesia

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9
Q

In what therapeutic interventions is Sevoflurane used?

A

Mask induction in children and adults

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10
Q

What are common side effects of Isoflurane, Desflurane, and Sevoflurane use?

A

Dose dependent CNS depression, increase in cerebral blood flow and intracranial pressure, dose dependent decrease in systemic BP, decrease in respiratory function, skeletal muscle relaxation, increase in HR, malignant hyperthermia

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11
Q

The most pungent of the volatile anesthetics

A

Desflurane

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12
Q

Which of the volatile anesthetics can be metabolized into inorganic F- resulting in potential nephrotoxicity and form carbon monoxide when exposed to strong bases present in dry CO2 absorbers (canister fires!)?

A

Sevoflurane

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13
Q

What is the class of methohexital?

A

Barbiturate

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14
Q

Mechanism of Methohexital and what is the clinical use?

A

GABAa receptor binding producing hypnosis and sedation; Clinically used to induce general anesthesia

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15
Q

How is Methohexital dosed? How does it redistribute? How is it metabolized?

A

Dose based on lean body mass; Redistributes from brain to muscle and fat; Metabolized by the liver

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16
Q

What is the drug class of propofol?

A

Alkylphenol

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17
Q

What is the mechanism of propofol?

A

GABAa receptor agonist, NMDA-glutamate receptor antagonist, some a2 receptor activity, overall rapid onset and offset

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18
Q

What are the therapeutic uses of propofol?

A

Anti-emesis (at low doses), induction/maintenance of general anesthesia, ICU sedation, procedural sedation

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19
Q

What is a potentially severe side effect of propofol?

A

Propofol infusion syndrome after several days of administration (metabolic acidosis, myocardial failure, rhabdomyolysis, hyperkalemia, renal failure, lowered BP, bradycardia, death

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20
Q

When administering propofol, what should the anesthesiologist be cognizant of at the injection site?

A

The site is painful and supports bacterial growth

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21
Q

What in the patient’s history is a contraindication for propofol use?

A

Because propofol is administed in a yummy egg and soy emulsion, egg/soy allergies would contraindicate propofol use.

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22
Q

What class of anesthetic is Etomidate?

A

Carboxylated imidazole

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23
Q

What does the D isomer of Etomidate act on to induce anesthesia?

A

It is a GABAa receptor agonist

24
Q

What therapeutic effect does Etomidate have?

A

Hypnosis. NO analgesic effect

25
Q

George had a rough day. When he was administered the anesthetic, it was very painful. His astute wife noticed that he experienced myoclonic movements. After his surgery, George experienced nausea and vomiting. What anesthetic was used? What was its effect on cortisol synthesis? What caused the myoclonic movements?

A

Etomidate; Cortisol synthesis inhibition; Subcortical disinhibition

26
Q

Granny doesn’t have much cardiac reserve. What anesthetic will the doctor likely use?

A

Etomidate because it causes minimal cardiorespiratory depression!

27
Q

What is the drug class of Ketamine?

A

Phencyclidine

28
Q

What is the mechanism of Ketamine?

A

NMDA receptor antagonist and kappa opiate agonists which leads to dose-dependent unconsciousness, amnesia, and analgesia

29
Q

Ketamine has a significant laundry list of therapeutic uses. What are they? Ready, GO!

A

Sedative/anesthetic for pediatric/developmentally delayed patients
induction in patients w/ reactive airway disease
Hypovolemic patients (trauma)
Patients w/ cardiac disease

30
Q

What drug is combined with ketamine for IV procedural sedation?

A

Propofol!

31
Q

What drug is used as an adjuvant during and after surgery to reduce opioid use?

A

Ketamine!

32
Q

What are important side effect of Ketamine use?

A

It directly stimulates the SNS, causes increased cerebral blood flow, increased intracranial pressure, increased cardiac work, emergence delerium, nystagmus, lacrimation, salivation, and dissociative anesthesia

33
Q

Let’s bring back some organic chemistry! What isomers of Ketamine are administered? Which is more potent? How is it metabolized?

A

Racemic mixture (both isomers!); S isomer; P450

34
Q

What are contraindications for Ketamine use?

A

Coronary Artery Disease and Intracranial Lesions

35
Q

What class of anesthetic is Dexmedetomidine?

A

Alpha2 agonist

36
Q

What is the mechanism of Dexmedetomidine?

A

Binds Alpha2a and b in the locuse coeruleus and spinal cord resulting in sedation, sympatholysis, and analgesia!

37
Q

What are the therapeutic uses of Dexmedetomidine?

A

Awake intubations, awake craniotomies, adjunct to general anesthesia in patients susceptible to narcotic-induced post-op respiratory depression

38
Q

What makes Dexmedetomidine such a safe anesthetic?

A

Its use causes limited respiratory depression!

39
Q

What mechanism of action allows patients anesthetized with Dexmedetomidine to easily wake up?

A

Dexmedetomidine does not act on GABA and therefore the patient has an easier time waking up. It causes an effect similar to non-REM sleep too! Neat!

40
Q

Joe the new ICU intern needs help. He wants to keep his patient anesthetized for 1 week with Dexmedetomidine. What are your thoughts?

A

The FDA has only approved Dexmedetomidine use for ventilation of ICU patients for under 24 hours! He probably shouldn’t do that…

41
Q

To what drug class does Succinylcholine belong?

A

Depolarizing NMB

42
Q

What is the mechanism of action of Succinylcholine?

A

It stimulates and opens the nicotinic AChR at the NMJ causing depolarizations, disorganized muscular contractions and then paralysis. Weee!

43
Q

What is the most common therapeutic use of Succinylcholine?

A

Skeletal muscle relaxant used for intubations

44
Q

What are some potential side effects of Succinylcholine use?

A

Malignant hyperthermia, cardiac dysrhythmias, hyperkalemia, increased intraocular pressure, increased intracranial pressure, increased intragastric pressure, myalgias, masseter spasm

45
Q

How can a Succinylcholine NMB be reversed?

A

It can’t! It is hydrolyzed by pseudocholinesterase in the plasma and has a very quick onset and offset

46
Q

To what drug class do Pancuronium, Vecuronium and Rocuronium belong? Atracurium and cis-Atracurium? What is their mechanism of action? Therapeutic use?

A

Amino steroid non-depolarizing NMB; Isoquinoline non-depolarizing NMB; Competitive blockade of AChR; Muscle relaxant!

47
Q

What is the one important side effect of Pancuronium?

A

Increases HR

48
Q

What are the lengths of action of Pancuronium, Vercuronium, and Rocuronium, respectively?

A

Pan - longest acting, both Ver and Roc intermediate

49
Q

How do you reverse the actions of Pan, Ver, Rocuronium, Atracurium and Cisatracurium?

A

With an AChEsterase Inhibitor

50
Q

How are Pan, Ver, and Rocuronium excreted, respectively?

A

80% of Pan excreted unchanged in the liver, Ver and Roc primarily excreted via liver and kidney

51
Q

Jimmy the overly touchy intern wants to immediately reverse a Rocuronium blockade without effecting ACh Esterase. What non-FDA approved drug does Jimmy use and what are the possible side effects?

A

Sugammadex; Decrease in BP, N/V, Dry mouth

52
Q

What conditions would a patient have that would be indications to use Atracurium or cis-Atracurium to perform a NMB?

A

Liver or renal dysfunction

53
Q

What benefits are there to using cis-Atracurium instead of Atracurium?

A

Atracurium induces histamine release with resultant hypotension and tachycardia. cis-Atra does not induce histamine release or downstream effects

54
Q

Describe the process of elimination of Atracurium and Cisatracurium

A

Both undergo spontaneous non-enzymatic degradation via Hofman elimination

55
Q

What is the drug class of Edrophonium, Neostigmine, and Pyridostigmine? What are the therapeutic uses? Which is most commonly used?

A

AChesterase Inhibitor; Reverse NMB; Neostigmine

56
Q

Of the AChesterase Inhibitors, which has the longest duration of action? Which is the fastest and shortest acting? Which has even more antagonistic potential than edrophonium???

A

Pyridostigmine; Edrophonium; Neostigmined

57
Q

To what drug class does Glycopyrrolate belong? It’s therapeutic use? Important side effects?

A

Anti muscarinic; Reverse NMB; Diarrhea, urination, miosis/muscle weakness, bronchorrhea, bradycardia, emesis, lacrimation, salivation/sweating (DUMBELLS)

Pharm Unit 3 (14 decks)

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