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ARCHIVED: Pharmacology for Nurse Anesthesia > Exam 2: Basic Pharmacology of Anesthetics > Flashcards

Exam 2: Basic Pharmacology of Anesthetics Flashcards

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1
Q

What functions are impaired in minimal sedation/anxiolysis?

A

Cognitive

Coordination

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2
Q

What additional functions are impaired in moderate/conscious sedation?

A

Level of awareness; pts respond purposefully to verbal command

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3
Q

What additional functions are impaired in deep sedation?

A

Level of awareness; pts respond purposefully to pain stimulus

Airway/ventilatory function (may need assistance)

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4
Q

What additional functions are impaired in general anesthesia?

A

Level of awareness (nonresponsive)

Airway/ventilatory function (will need airway assistance)

Cardiovascular function

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5
Q

Define general anesthesia:

A

Generalized, reversible central nervous system depression

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6
Q

Four characteristics of general anesthesia:

A

No sensory perception
Loss of consciousness
No recall of events
Immobility

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7
Q

Seven types of drugs used in general anesthesia:

A 
Pre-op/sedation
Induction
NMB
Inhalational
Opioids/LA
Antiemetic
Reversal
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8
Q

Prototype benzodiazepine:

A

Diazepam

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9
Q

5 effects of all benzos:

A 
Anxiolysis
Sedation
Anterograde amnesia
Anticonvulsant
Muscle relaxation
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10
Q

At what level do benzos cause muscle relaxation?

A

Spinal level

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11
Q

Benzo mechanism of action:

A

Potentiates binding of GABA to receptor

Increases GABA potency 3x

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12
Q

What changes do benzos cause in the neuronal membrane?

A

Increased Cl- influx
Hyperpolarization
Decreased excitability

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13
Q

During what perioperative stage(s) are benzos used? Why?

A

Pre-operative; very long half-life

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14
Q

Adverse effects of benzos:

A

Ventilatory decrease, especially with opioids; potential hypoxemia

Decreased SVR (high dose) and resulting hypotension

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15
Q

Contraindication(s) for benzos:

A

Pregnancy

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16
Q

At what level(s) do opioids suppress pain?

A

Spinal and supraspinal

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17
Q

What system do opioids activate?

A

Endogenous pain suppression system

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18
Q

Opioid mechanism of action:

A

Agonist at stereospecific opioid receptors

Increased K+ outflow - hyperpolarization

Ca++ channel inactivation

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19
Q

Where are the receptors that opioids affect?

A

Pre- and post-synaptic sites in the brainstem, spinal cord, and peripheral tissues

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20
Q

During which perioperative stage(s) are opioids used?

A

All of them

Pre-medication
Intra-op pain management
General anesthesia
Post-op pain management

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21
Q

Adverse effects of opiates:

A 
Bradycardia
Respiratory depression
Miosis
Urinary retention
Constipation
Dependence
Sedation
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22
Q

Characteristics of opioid-induced respiratory depression:

A 
Rate decreases
TV increases (but not enough to overcome)
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23
Q

Barbiturate mechanism of action:

A

Decreases rate at which GABA dissociates from receptors (prolongs Cl- channel opening)

Mimics GABA (activates Cl- channels)

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24
Q

What system do barbiturates depress?

A

Reticular activating system (thus inducing sleep)

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25
Q

Prototype barbiturate drug:

A

Thiopental

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26
Q

Anesthetic uses of barbiturates:

A

Sedation/hypnosis
Cerebral protection
Anticonvulsive
Induction of GA

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27
Q

In which patients is a barbiturate induction beneficial?

A

Pts with increased ICP or focal brain ischemia

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28
Q

Are benzos or barbiturates more effective anticonvulsants?

A

Benzos

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29
Q

Adverse cardiopulmonary effects of barbiturates:

A 
SNS depressant (peripheral vasodilation, BP/CO decrease)
Ventilatory depression
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30
Q

Under what circumstances will barbiturates cause significant cardiac depression?

A

SNS not intact
Hypovolemia
Large doses

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31
Q

What occurs if barbiturates are injected intra-arterially?

A

Very high pH (10-11) - drug precipitates quickly if injected arterially, causes vasoconstriction, gangrene, nerve damage

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32
Q

Adverse metabolic effects of barbiturates:

A

Potent hepatic enzyme inducers

Accelerates production of heme

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33
Q

Drugs that barbiturates increase the metabolism of:

A 
Muscle relaxers
Oral anticoagulants
Phenytoin
TCAs
Corticosteroids
Vitamin K
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34
Q

What condition is a strong contraindication to use of barbiturates?

A

Porphyria

35
Q

Barbiturate allergies:

A

1 in 30,000

High mortality

36
Q

Barbiturates and pregnancy:

A

Readily crosses the placenta

37
Q

Propofol is supplied as:

A

1% solution in egg, soy, glycerol base

38
Q

Preservatives used in propofol and related caution:

A

EDTA

Sodium metabisulfite - can cause rxn in asthmatics

39
Q

Special care in drawing up propofol:

A

Highly susceptible to contamination

All vials are single-use; do not spike a bottle twice

40
Q

Propofol mechanism of action:

A

Potentiates binding of GABA to B1 subunit of receptor

Decreases rate of GABA dissociation from receptor

41
Q

Effects (5) of propofol:

A 
Sedation/hypnosis
Antiemetic
Antipruritic
Anticonvulsant
Reduction in bronchoconstriction
42
Q

Anesthetic uses of propofol:

A 
IV sedation
Induction
Maintenance (TIVA)
Part of maintenance (combined technique)
Antiemetic
43
Q

Consideration with injection of propofol:

A

Very painful - use lidocaine + opioid before propofol

44
Q

Cardiopulmonary effects of propofol:

A

Ventilatory depression
Myocardial depression
Vasodilation
No reflex tachycardia (baroreceptor inhibition)

45
Q

Muscular/tissue/hematologic effects of propofol:

A

Myoclonus (esp. with large induction doses)
Painful injection
Lipidemia with long-term infusion

46
Q

Pre-synaptic events at the neuromuscular junction:

A
  1. Action potential depolarizes nerve terminal
  2. Ca++ channels open
  3. Ca++ diffuses down gradient to nerve terminal
  4. ACh spills into synaptic cleft
47
Q

Post-synaptic events at the neuromuscular junction:

A
  1. ACh combines with nicotinic receptors (both must be occupied)
  2. Na+, Ca++ diffuse into cell, K+ diffuses out
  3. Motor end plate depolarizes
  4. Action potential
  5. Contraction
48
Q

Structure of ACh receptor:

A

5 protein subunits

Central cation channel

49
Q

Which subunits on the ACh receptor must be bound to ACh to activate it?

A

Both alpha subunits

50
Q

Succinylcholine class:

A

Depolarizing neuromuscular blockade

51
Q

Succinylcholine mechanism of action:

A

Binds to nicotinic receptors

Causes a single contraction then muscles stay relaxed until drug diffuses back into circulation

52
Q

Metabolism of succinylcholine:

A

Plasma esterases - NOT acetylcholine esterases in the synapse

53
Q

Anesthetic uses of succinylcholine:

A

Optimize intubating conditions
RSI
Treatment of laryngospasm

54
Q

Adverse effects of succinylcholine:

A 
Cardiac dysrhythmias
Hyperkalemia
Muscle pain
Increased ICP, IOP
MH triggering agent
55
Q

Conditions that predispose pts to hyperkalemia with succs:

A 
Burns
Trauma
Nerve damage
Neuromuscular disease
Renal failure
56
Q

Pts that should not receive succinylcholine:

A

Atypical acetylcholinesterase

Head injury patients

57
Q

Vecuronium class of drugs:

A

Non-depolarizing muscle relaxant

Monoquaternary aminosteroid

58
Q

Vecuronium mechanism of action:

A

Competitive antagonist at pre- and post-synaptic ACh receptors (occupies alpha subunit without conformational change)

59
Q

Anesthetic uses for vecuronium:

A

Facilitate intubation

Optimize surgical conditions (abdominal surgeries)

60
Q

Condition(s) that make effects of vecuronium prolonged/unpredictable:

A 
Liver/kidney disease
Neuromuscular disease
Hypothermia
Electrolyte imbalances
Aminoglycoside antibiotics
61
Q

Condition(s) that make patients resistant to vecuronium:

A

Burns

62
Q

Signs of residual neuromuscular blockage:

A

“Floppy fish” appearance

TOF twitches not equally strong

63
Q

Isoflurane class of drug:

A

Inhalational anesthetic

Halogenated methyl ethyl ester

64
Q

What characteristic of isoflurane determines onset, duration, etc?

A

Lipid solubility

65
Q

Isoflurane eliminated almost entirely via:

A

Lungs

66
Q

Contemporary inhaled anesthetics eliminated via:

A

Minimal hepatic metabolism and renal excretion

67
Q

Anesthetic uses of isoflurane:

A 
Bronchodilation
General anesthesia (maintenance - Sevo best for induction)
68
Q

Adverse effects of isoflurane:

A

Respiratory depression
Cardiac depression/vasodilation
Malignant hyperthermia

69
Q

Physiology of malignant hyperthermia:

A

Ca++ channel interference
Muscle rigidity
Increased temperature
Increased CO2

70
Q

Characteristics of isoflurane respiratory depression:

A

Increased rate

Decreased volume

71
Q

Define MAC:

A

Mean alveolar concentration

Concentration at which 50% of patients do not move to noxious stimulus

72
Q

MAC of isoflurane:

A

1.2%

73
Q

MAC of nitrous oxide:

A

104%

74
Q

Local anesthetic mechanism of action:

A

Inhibits Na+ channels during inactivated closed state and blocks impulse conduction during depolarizing phase

75
Q

Prototype local anesthetic:

A

Lidocaine

76
Q

Pharmacologic effects of local anesthetics:

A

Block afferent nerve transmission; analgesic/anesthesia without effect on consciousness

77
Q

Three modalities that local anesthetics block:

A

Autonomic
Somatic sensory
Somatic motor

78
Q

Classification of lidocaine:

A

Amide local anesthetic

79
Q

Structure of local anesthetic molecule:

A 
Lipophilic head (aromatic ring)
Intermediate chain (amide NH or ester COO-)
Hydrophilic tail (tertiary amine)
80
Q

CNS s/s of local anesthetic toxicity:

A 
Circumoral/tongue numbness, tinnitus, vision changes
Dizziness, slurred speech
Restlessness
Seizure
CNS depression
Apnea
Hypotension
81
Q

Cardiac s/s of local anesthetic toxicity:

A

Hypotension
Myocardial depression
Reduced SVR/CO

82
Q

Cardiac s/s of bupivicaine toxicity:

A

Arrythmias
AV heart block
Hypotension
Arrest

83
Q

Cardiac s/s of cocaine toxicity:

A

Massive SNS outflow
Coronary vasospasm
MI
Dysrhythmias (v-fib)

ARCHIVED: Pharmacology for Nurse Anesthesia (20 decks)

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