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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
Prototype barbiturate drug:
Thiopental
26
Anesthetic uses of barbiturates:
Sedation/hypnosis Cerebral protection Anticonvulsive Induction of GA
27
In which patients is a barbiturate induction beneficial?
Pts with increased ICP or focal brain ischemia
28
Are benzos or barbiturates more effective anticonvulsants?
Benzos
29
Adverse cardiopulmonary effects of barbiturates:
``` SNS depressant (peripheral vasodilation, BP/CO decrease) Ventilatory depression ```
30
Under what circumstances will barbiturates cause significant cardiac depression?
SNS not intact Hypovolemia Large doses
31
What occurs if barbiturates are injected intra-arterially?
Very high pH (10-11) - drug precipitates quickly if injected arterially, causes vasoconstriction, gangrene, nerve damage
32
Adverse metabolic effects of barbiturates:
Potent hepatic enzyme inducers Accelerates production of heme
33
Drugs that barbiturates increase the metabolism of:
``` Muscle relaxers Oral anticoagulants Phenytoin TCAs Corticosteroids Vitamin K ```
34
What condition is a strong contraindication to use of barbiturates?
Porphyria
35
Barbiturate allergies:
1 in 30,000 | High mortality
36
Barbiturates and pregnancy:
Readily crosses the placenta
37
Propofol is supplied as:
1% solution in egg, soy, glycerol base
38
Preservatives used in propofol and related caution:
EDTA | Sodium metabisulfite - can cause rxn in asthmatics
39
Special care in drawing up propofol:
Highly susceptible to contamination All vials are single-use; do not spike a bottle twice
40
Propofol mechanism of action:
Potentiates binding of GABA to B1 subunit of receptor Decreases rate of GABA dissociation from receptor
41
Effects (5) of propofol:
``` Sedation/hypnosis Antiemetic Antipruritic Anticonvulsant Reduction in bronchoconstriction ```
42
Anesthetic uses of propofol:
``` IV sedation Induction Maintenance (TIVA) Part of maintenance (combined technique) Antiemetic ```
43
Consideration with injection of propofol:
Very painful - use lidocaine + opioid before propofol
44
Cardiopulmonary effects of propofol:
Ventilatory depression Myocardial depression Vasodilation No reflex tachycardia (baroreceptor inhibition)
45
Muscular/tissue/hematologic effects of propofol:
Myoclonus (esp. with large induction doses) Painful injection Lipidemia with long-term infusion
46
Pre-synaptic events at the neuromuscular junction:
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
Post-synaptic events at the neuromuscular junction:
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
Structure of ACh receptor:
5 protein subunits | Central cation channel
49
Which subunits on the ACh receptor must be bound to ACh to activate it?
Both alpha subunits
50
Succinylcholine class:
Depolarizing neuromuscular blockade
51
Succinylcholine mechanism of action:
Binds to nicotinic receptors Causes a single contraction then muscles stay relaxed until drug diffuses back into circulation
52
Metabolism of succinylcholine:
Plasma esterases - NOT acetylcholine esterases in the synapse
53
Anesthetic uses of succinylcholine:
Optimize intubating conditions RSI Treatment of laryngospasm
54
Adverse effects of succinylcholine:
``` Cardiac dysrhythmias Hyperkalemia Muscle pain Increased ICP, IOP MH triggering agent ```
55
Conditions that predispose pts to hyperkalemia with succs:
``` Burns Trauma Nerve damage Neuromuscular disease Renal failure ```
56
Pts that should not receive succinylcholine:
Atypical acetylcholinesterase | Head injury patients
57
Vecuronium class of drugs:
Non-depolarizing muscle relaxant Monoquaternary aminosteroid
58
Vecuronium mechanism of action:
Competitive antagonist at pre- and post-synaptic ACh receptors (occupies alpha subunit without conformational change)
59
Anesthetic uses for vecuronium:
Facilitate intubation | Optimize surgical conditions (abdominal surgeries)
60
Condition(s) that make effects of vecuronium prolonged/unpredictable:
``` Liver/kidney disease Neuromuscular disease Hypothermia Electrolyte imbalances Aminoglycoside antibiotics ```
61
Condition(s) that make patients resistant to vecuronium:
Burns
62
Signs of residual neuromuscular blockage:
"Floppy fish" appearance | TOF twitches not equally strong
63
Isoflurane class of drug:
Inhalational anesthetic Halogenated methyl ethyl ester
64
What characteristic of isoflurane determines onset, duration, etc?
Lipid solubility
65
Isoflurane eliminated almost entirely via:
Lungs
66
Contemporary inhaled anesthetics eliminated via:
Minimal hepatic metabolism and renal excretion
67
Anesthetic uses of isoflurane:
``` Bronchodilation General anesthesia (maintenance - Sevo best for induction) ```
68
Adverse effects of isoflurane:
Respiratory depression Cardiac depression/vasodilation Malignant hyperthermia
69
Physiology of malignant hyperthermia:
Ca++ channel interference Muscle rigidity Increased temperature Increased CO2
70
Characteristics of isoflurane respiratory depression:
Increased rate | Decreased volume
71
Define MAC:
Mean alveolar concentration Concentration at which 50% of patients do not move to noxious stimulus
72
MAC of isoflurane:
1.2%
73
MAC of nitrous oxide:
104%
74
Local anesthetic mechanism of action:
Inhibits Na+ channels during inactivated closed state and blocks impulse conduction during depolarizing phase
75
Prototype local anesthetic:
Lidocaine
76
Pharmacologic effects of local anesthetics:
Block afferent nerve transmission; analgesic/anesthesia without effect on consciousness
77
Three modalities that local anesthetics block:
Autonomic Somatic sensory Somatic motor
78
Classification of lidocaine:
Amide local anesthetic
79
Structure of local anesthetic molecule:
``` Lipophilic head (aromatic ring) Intermediate chain (amide NH or ester COO-) Hydrophilic tail (tertiary amine) ```
80
CNS s/s of local anesthetic toxicity:
``` Circumoral/tongue numbness, tinnitus, vision changes Dizziness, slurred speech Restlessness Seizure CNS depression Apnea Hypotension ```
81
Cardiac s/s of local anesthetic toxicity:
Hypotension Myocardial depression Reduced SVR/CO
82
Cardiac s/s of bupivicaine toxicity:
Arrythmias AV heart block Hypotension Arrest
83
Cardiac s/s of cocaine toxicity:
Massive SNS outflow Coronary vasospasm MI Dysrhythmias (v-fib)

ARCHIVED: Pharmacology for Nurse Anesthesia (20 decks)

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