WEEK 7 PHARM Flashcards
(190 cards)
1
Q
What is the purpose of the Induction Phase in anesthesia?
A
Achieve a state of unconsciousness and prepare the patient for surgery.
2
Q
What are the main techniques used during the Maintenance Phase of anesthesia?
A
Adjusting anesthetic dosage and using a combination of agents for optimal effect.
3
Q
What is the objective of the Emergence Phase in anesthesia?
A
Safely bring the patient out of anesthesia.
4
Q
What is Dexmedetomidine chemically described as?
A
(-)-4-[1-(2,3-dimethylphenyl)ethyl]-1H-imidazole monohydrochloride.
5
Q
What are the primary effects of Dexmedetomidine?
A
- Sedation
- Analgesia
- Anxiolysis
- Reduced postoperative shivering and agitation
- Cardiovascular sympatholytic actions
6
Q
What is the onset of action for Dexmedetomidine when administered via loading infusion?
A
10 to 20 minutes.
7
Q
True or False: Dexmedetomidine causes respiratory depression.
A
False.
8
Q
What are the cardiovascular effects of Dexmedetomidine?
A
- Hypotension
- Bradycardia
- Occasionally transient hypertension
9
Q
What is the chemical structure of Etomidate?
A
A carboxylated imidazole derivative.
10
Q
What is the primary use of Etomidate?
A
Induction in compromised patients where other anesthetics may be problematic.
11
Q
What significant adverse effect is associated with Etomidate?
A
Inhibition of adrenal steroidogenesis.
12
Q
What effect does Ketamine have on NMDA receptors?
A
Antagonism, resulting in a selective depressant effect on the medial thalamic nuclei.
13
Q
What is the primary site of analgesic action for Ketamine?
A
Thalamoneocortical system.
14
Q
What are the cardiovascular effects of Ketamine?
A
- Increases systemic blood pressure
- Increases heart rate
- Increases cardiac contractility and output
15
Q
Fill in the blank: The induction dose of Ketamine is typically _______.
A
2-4 mg/kg IV.
16
Q
What is a common adverse effect of Ketamine during emergence?
A
Vivid dreams and confusional disturbances.
17
Q
What is the primary formulation of Propofol?
A
2,6-diisopropylphenol.
18
Q
What is a unique advantage of Ketamine in airway management?
A
It is a potent bronchodilator, preserving airway reflexes.
19
Q
What is the potential concern regarding anesthetic neurotoxicity with Ketamine?
A
Neuroapoptosis in developing brains noted in animal models.
20
Q
What does the SPICE III trial suggest about Dexmedetomidine?
A
Early sedation with Dexmedetomidine is not associated with a reduction in mortality.
21
Q
What is the typical dosage range for Dexmedetomidine infusion?
A
0.2 to 0.7 μg/kg/hour.
22
Q
What percentage of Etomidate is excreted unchanged in urine?
A
Approximately 10%.
23
Q
True or False: Ketamine has minimal effects on the respiratory system.
A
True.
24
Q
What is the chemical structure of Propofol?
A
Propofol is a 2,6-diisopropylphenol
Propofol is prepared as a 1% solution in a lipid emulsion consisting of 10% soybean oil, 2.25% glycerol, and 1.2% purified egg lecithin.
25
What is the pH range of Propofol?
7 to 8.5
## Footnote
The pKa of Propofol is 11.
26
What is a significant concern regarding the pharmaceutics of Propofol?
It is particularly susceptible to bacterial contamination
## Footnote
The original trade product, Diprivan, contains disodium edetate (EDTA) as a preservative.
27
What neurotransmitter does Propofol primarily interact with?
Gamma-aminobutyric acid (GABA)
## Footnote
Propofol directly stimulates GABA_A receptors.
28
What is the typical induction dose of Propofol?
1-2 mg/kg
## Footnote
This is followed by a maintenance infusion of 100-200 μg/kg/min.
29
What are the central nervous system effects of Propofol?
Rapid and pleasant loss of consciousness, reduction in cerebral blood flow, and intracranial pressure
## Footnote
EEG data show a delta rhythm and burst suppression with higher doses.
30
What is a common cardiovascular effect of Propofol?
Mild to moderate transient decrease in blood pressure
## Footnote
Effects are more pronounced in select patients.
31
What syndrome is associated with high doses or prolonged infusions of Propofol?
Propofol Infusion Syndrome
## Footnote
Symptoms include metabolic acidosis, hyperkalemia, and elevated liver transaminases.
32
What unique structural feature does Midazolam have?
An imidazole ring
## Footnote
This allows for the preparation of water-soluble salts at a pH of 4.0.
33
What are the primary uses of Midazolam?
Preoperative medication, anxiolytic, sedative, and amnestic
## Footnote
It is commonly used due to its rapid onset and short duration.
34
What is the primary mechanism of action for opioids?
Inhibit ascending transmission of nociception and activate descending pain control pathways
## Footnote
This effect occurs in the spinal cord dorsal horn.
35
What is the typical respiratory effect of opioids?
Dose-dependent respiratory depression
## Footnote
This occurs through effects on mu and delta receptors in the brainstem.
36
What is Morphine primarily used for?
Abatement of moderate to severe pain
## Footnote
It is more effective for continuous dull pain than sharp intermittent pain.
37
What is the metabolism process of Morphine?
Phase 2 glucuronide conjugation in the liver
## Footnote
The active metabolite morphine-6-glucuronide (M6G) can prolong therapeutic effects.
38
What is the onset time for intravenous Morphine?
20 minutes
## Footnote
The peak effect is observed at 30-60 minutes with a duration of 4 to 5 hours.
39
What is the primary use of Fentanyl in anesthesia?
Opioid analgesic known for profound dose-dependent analgesia
## Footnote
It also provides ventilatory depression and sedation.
40
What is the duration of action for a single dose of Fentanyl?
Approximately 20-40 minutes
## Footnote
The action is terminated by redistribution.
41
What unique property does Alfentanil have compared to Fentanyl?
More rapid onset of action and shorter duration
## Footnote
Despite being less lipid-soluble.
42
What is a common adverse effect of Midazolam?
Unexpected respiratory depression
## Footnote
It can also contribute to postoperative cognitive dysfunction.
43
What is Flumazenil used for?
Reversal of benzodiazepine effects
## Footnote
It is a competitive antagonist with a high affinity for the receptor site.
44
What effects do opioids have on gastrointestinal function?
Constipation and urinary retention
## Footnote
These effects are common due to opioid action.
45
What is a common respiratory effect of Midazolam?
Dose-dependent respiratory depression
## Footnote
It is the most respiratory depressing among benzodiazepines.
46
What is Alfentanil's duration of analgesia?
Short duration of analgesia
## Footnote
Its short duration limits its popularity despite being effective epidurally.
47
How does Erythromycin interact with Alfentanil?
Prolongs metabolism and induces respiratory depression and sedation
## Footnote
Significant drug interactions can occur.
48
What is the recommended dose of Hydromorphone?
0.01 to 0.02 mg/kg
## Footnote
This dosage is important for effective pain management.
49
What is the half-life of Hydromorphone?
Approximately 1 to 3 hours
## Footnote
This range is significant for understanding its pharmacokinetics.
50
Why is Hydromorphone recommended for patients with renal failure?
Lack of active metabolites
## Footnote
This makes it a safer option compared to other opioids.
51
What structural similarity does Meperidine have?
Structurally similar to atropine
## Footnote
This contributes to its antispasmodic effect.
52
What is the elimination half-life of normeperidine?
Significantly longer than that of Meperidine
## Footnote
This can lead to CNS excitation and seizures.
53
What effect can accumulation of normeperidine have?
CNS excitation characterized by tremors, muscle twitches, and seizures
## Footnote
This is particularly concerning in specific patient populations.
54
What are the significant interactions of Meperidine?
Interactions with first-generation MAO-inhibiting drugs
## Footnote
Can lead to hyperthermia, seizures, and death.
55
What is a common use for Meperidine?
Effective in reducing shivering
## Footnote
This includes shivering from general and epidural anesthesia.
56
What is a distinctive feature of Remifentanil?
Rapid onset and ultrashort duration
## Footnote
This makes it convenient for modern clinical situations.
57
What is the elimination half-life of Remifentanil?
8 to 20 minutes
## Footnote
Its metabolism is not dependent on cholinesterase enzymes.
58
What is the commercial preparation of Remifentanil?
Water-soluble, lyophilized powder
## Footnote
Contains a free base and glycine as a vehicle.
59
What is the potency of Alfentanil compared to morphine?
Approximately 10-25 times more potent
## Footnote
This highlights its efficacy as an opioid.
60
How does Hydromorphone compare to morphine in terms of potency?
Roughly 5-7 times stronger than morphine
## Footnote
This is important for dosing considerations.
61
What is the ceiling effect in Buprenorphine?
Increased dose does not increase respiratory depression
## Footnote
This is due to the drug's antagonistic effects becoming more apparent at higher doses.
62
What is the duration of action of Naloxone?
Less than that of most opioid agonists
## Footnote
This can allow the return of respiratory depression in some patients.
63
What is the primary route for elimination of inhalation anesthetics?
Through the alveolar membrane
## Footnote
Particularly significant for nitrous oxide.
64
What is the mechanism of action for both Ketorolac and Ibuprofen?
Inhibition of cyclooxygenase enzymes
## Footnote
This is crucial for their analgesic properties.
65
What is the usual dose of intravenous Ibuprofen?
400 to 800 mg over 30 minutes
## Footnote
This has an onset of 30 minutes and a duration of 4 to 6 hours.
66
What is a significant side effect associated with Acetaminophen?
Hepatotoxicity at high doses
## Footnote
This is particularly a concern with doses over 4000 mg/day.
67
What is the primary use of Nalmefene?
Used in alcohol use disorder programs
## Footnote
Also recommended for acute opioid overdose.
68
What is the effect of ventilation/perfusion mismatch on arterial concentration?
Increases the alveolar-arterial difference
## Footnote
This leads to discrepancies in predicted arterial partial pressures.
69
What is the concentration effect in anesthesia?
Increasing inspired concentration increases the alveolar concentration
## Footnote
More significant with nitrous oxide.
70
What is the mechanism of action of Acetaminophen believed to involve?
Central inhibition of prostaglandin synthesis
## Footnote
Its exact mechanism is less clear compared to NSAIDs.
71
What is diffusion hypoxia?
A condition that can occur due to rapid elimination of nitrous oxide, leading to dilution of oxygen and carbon dioxide concentrations in the alveolar gas.
## Footnote
This state can cause relative hypoxia.
72
How can diffusion hypoxia be prevented?
By administering 100% oxygen for 5 to 10 minutes after discontinuing nitrous oxide.
## Footnote
This practice helps maintain adequate oxygen levels in the alveoli and bloodstream.
73
What is biotransformation in the context of anesthetics?
The metabolic process that can affect the elimination rate of soluble anesthetics, such as methoxyflurane and halothane.
## Footnote
Halothane's greater biotransformation compared to isoflurane accounts for its faster elimination.
74
What factors speed up recovery from anesthesia?
Factors include:
* Elimination of rebreathing
* High fresh gas flows
* Low anesthetic-circuit volume
* Low absorption by the anesthetic circuit
* Decreased solubility
* High cerebral blood flow
* Increased ventilation
75
What are the physical properties of nitrous oxide?
Nitrous oxide is a gas at room temperature and ambient pressure, but can be kept as a liquid under pressure. It is relatively inexpensive but has raised safety concerns.
## Footnote
Nitrous oxide is an NMDA receptor antagonist and has environmental impacts.
76
What are the cardiovascular effects of nitrous oxide?
It stimulates the sympathetic nervous system, potentially masking direct myocardial depressant effects in vivo.
## Footnote
Myocardial depression may be unmasked in patients with coronary artery disease.
77
What is the definition of Minimum Alveolar Concentration (MAC)?
MAC is the alveolar concentration of an inhaled anesthetic that prevents movement in 50% of patients in response to a standardized stimulus.
## Footnote
It reflects the partial pressure of the anesthetic in the brain.
78
What are the limitations of MAC?
MAC is a median value with limited utility in managing individual patients, especially during rapidly changing alveolar concentrations.
## Footnote
This is particularly relevant during induction and emergence from anesthesia.
79
What is the effect of combining anesthetic agents in terms of MAC values?
The MAC values for combinations of anesthetic agents are roughly additive.
## Footnote
For example, 0.5 MAC of nitrous oxide and 0.5 MAC of isoflurane produce similar effects as 1.0 MAC of isoflurane alone.
80
What physiological variable affects MAC, and by how much?
There is a 6% decrease in MAC per decade of age, regardless of the volatile anesthetic used.
## Footnote
MAC is relatively unaffected by species, sex, or duration of anesthesia.
81
What are the key cardiovascular effects of isoflurane?
Isoflurane dilates coronary arteries and may unmask potential myocardial depression in certain patients.
82
What are the respiratory effects of desflurane?
Desflurane is an airway irritant and may cause respiratory depression.
83
What are the renal effects of sevoflurane?
Sevoflurane slightly decreases renal blood flow but maintains total hepatic blood flow and oxygen delivery.
84
What is the preferred monitoring site for assessing neuromuscular block?
The ulnar nerve is preferred for determining the level of neuromuscular blockade.
85
What does the Train-of-Four (TOF) test measure?
TOF measures the degree of paralysis by delivering four stimuli at a frequency of 2 Hz every 0.5 seconds.
## Footnote
It is most sensitive between 70% and 100% paralysis.
86
What does a TOF ratio (TOFR) represent?
The size of the fourth twitch (T4) compared to the first twitch (T1).
## Footnote
A decreasing TOFR indicates increasing neuromuscular block.
87
What is succinylcholine, and what is its chemical structure?
Succinylcholine is formed by the joining of two acetylcholine molecules, with the chemical formula C14H30N2O4.
88
What is the onset time for succinylcholine?
Succinylcholine has an extremely rapid onset, usually within 3 minutes after administration.
89
What is the recommended dosage for succinylcholine for intubation?
A bolus of 0.5 to 1.5 mg/kg is recommended for adequate adult paralysis and relaxation for intubation.
90
What is the metabolism of succinylcholine?
Hydrolyzed by plasma cholinesterases into succinylmonocholine and choline, further into succinic acid and choline.
91
What percentage of the injected dose of succinylcholine reaches the neuromuscular junction?
10%.
92
What is the recommended bolus dosage of succinylcholine for adult paralysis?
0.5 to 1.5 mg/kg.
93
What is the effective dose for 95% of the population (ED95) of succinylcholine?
Approximately 0.30 mg/kg.
94
Does succinylcholine pass the blood-brain barrier?
No, it does not pass the blood-brain barrier.
95
What cardiovascular effects can succinylcholine cause?
Slight tachycardia or bradycardia, especially in children or with repeat dosing.
96
In which patients is succinylcholine contraindicated?
Patients with malignant hyperthermia (MH) or elevated preoperative potassium levels.
97
What is a Phase II block in neuromuscular blocking agents?
A desensitization block that occurs with high doses of depolarizing NMBAs like succinylcholine.
98
What characterizes a Phase II block?
Shows a fade in response to tetanic or train-of-four (TOF) stimulation.
99
How can a Phase II block be treated?
With anticholinesterase drugs.
100
What is the chemical structure of rocuronium bromide?
A monoquaternary aminosteroid neuromuscular blocker.
101
What is the primary method of elimination for rocuronium?
Biliary elimination of unchanged drug.
102
What is the typical intubating dose of rocuronium?
0.6 to 1.2 mg/kg.
103
What is the elimination half-life of rocuronium?
60 to 120 minutes.
104
What is vecuronium bromide derived from?
Pancuronium.
105
How does vecuronium act at the neuromuscular junction?
By competing with acetylcholine for binding to nicotinic receptors.
106
What is the induction dose of vecuronium?
0.1 mg/kg.
107
What is the elimination half-life of vecuronium in healthy adults?
51 to 90 minutes.
108
What is the primary advantage of cisatracurium over atracurium?
Three times more potent with a slower onset.
109
How does cisatracurium maintain cardiovascular stability?
By not causing histamine release.
110
What is the typical intubating dose of cisatracurium?
0.1 mg/kg.
111
What is a major benefit of cisatracurium for patients with renal or hepatic impairment?
Its elimination is non-organ-dependent.
112
What adverse effect is commonly associated with succinylcholine?
Myalgias and fasciculations.
113
What can be used to prevent myalgia after succinylcholine administration?
Small doses of nondepolarizing muscle relaxants or pretreatment with NSAIDs.
114
What condition can succinylcholine exacerbate in susceptible patients?
Hyperkalemia.
115
What is the risk of using succinylcholine in children under 8 years old?
Cardiac arrest from hyperkalemic rhabdomyolysis.
116
Which genetic variants can affect the response to succinylcholine?
Pseudocholinesterase variants such as F, S, and K.
117
In elderly patients, how does succinylcholine administration differ?
Onset may be slightly prolonged due to slower circulation time.
118
What is the effect of rocuronium on the cardiovascular system?
No significant cardiac effects at clinical doses.
119
How does vecuronium affect patients with hepatic disease?
The elimination half-life is prolonged.
120
What is the duration of action for vecuronium after a 0.1 mg/kg dose?
Approximately 36.2 ± 6.4 minutes.
121
What is the typical intubating dose of Cisatracurium?
0.1 mg/kg
122
What advantage does Cisatracurium provide in patients with ARDS?
Cardiovascular stability
123
How does Cisatracurium maintain cardiovascular stability?
It does not cause histamine release
124
What processes are involved in the elimination of Cisatracurium?
Hofmann elimination and ester hydrolysis
125
Why is Cisatracurium suitable for patients with renal or hepatic impairment?
Its elimination is not significantly affected by these conditions
126
How are dosing intervals and duration of action affected in elderly patients using Cisatracurium?
Not significantly changed
127
What is the half-life of Cisatracurium?
Approximately 26 to 36 minutes
128
What is the ED95 of Atracurium?
0.10 to 0.25 mg/kg
129
What happens to the potency of Atracurium when refrigerated at 5°C?
It loses potency at the rate of 6% per year
130
What is the action of Atracurium?
It is a competitive bisquaternary neuromuscular blocker
131
What is the onset time range for Atracurium?
1.2 to 2.8 minutes
132
What is the duration of action for Atracurium as an intermediate relaxant?
30 to 60 minutes
133
What are the two primary elimination processes for Atracurium?
Hofmann elimination and ester hydrolysis
134
What systemic effect can Atracurium cause due to histamine release?
Hypotension and tachycardia
135
In patients with hepatic and renal disease, how does the pharmacokinetics of Atracurium compare to nonimpaired subjects?
No differences in plasma elimination half-lives
136
What is recommended for dosing NMBAs in obese patients?
Dose at ideal body weight
137
True or False: The duration of Atracurium is affected by aging.
False
138
What is the primary response of the neuromuscular junction in neonates?
Incomplete at delivery
139
What is required for prophylaxis against histamine release caused by Atracurium?
Administration of both H1 and H2 receptor blockers
140
What is the importance of reversal in neuromuscular blocking agents?
Complete and effective reversal of muscle relaxants is crucial in clinical practice. Incomplete reversal leads to significant challenges.
141
What is the most commonly used anticholinesterase agent for reversal?
Neostigmine
142
What should the degree of spontaneous recovery be at the time of edrophonium administration?
At least a TOF count of 4
143
What is a key characteristic of sugammadex?
High efficacy in reversing neuromuscular blockade
144
What factors influence the incidence of postoperative residual neuromuscular blockade?
* Type of anesthesia used
* Type and dose of NMBD administered
* Type and dose of anticholinesterase reversal drug
* Duration of anesthesia
* Neuromuscular monitoring
* Patient factors
145
How do cholinesterase inhibitors primarily act?
By interacting with acetylcholinesterase (AChE) to prevent the hydrolysis of acetylcholine (ACh)
146
What is the pharmacokinetic difference between edrophonium and neostigmine?
Edrophonium binds reversibly, while neostigmine forms a stable carbamylated enzyme
147
What is the elimination half-life of neostigmine?
70 to 80 minutes
148
What adverse effect is commonly associated with neostigmine?
Increased incidence of postoperative nausea and vomiting
149
What is the recommended dose range for neostigmine?
25-75 mcg/kg
150
What are the pharmacokinetic properties of sugammadex?
* Biologically inactive
* Clearance of approximately 120 L/min
* Elimination half-life of 2.3 hours
* 80% eliminated in urine within 24 hours
151
What should be considered regarding sugammadex and renal function?
It should be avoided in patients with significant renal disease
152
What are common reactions associated with sugammadex?
* Nausea
* Vomiting
* Allergy
* Hypertension
* Headache
153
True or False: Sugammadex binds to oral contraceptives.
True
154
What two anticholinergics are commonly used with anticholinesterase agents?
* Atropine
* Glycopyrrolate
155
What is the primary action of atropine?
Induces vagolytic effects
156
What is the recommended dose of glycopyrrolate?
10-20 mcg/kg
157
What is ephedrine's pharmacological classification?
Synthetic noncatecholamine sympathomimetic
158
What are the effects of ephedrine?
* Increases blood pressure
* Increases cardiac output
* Increases heart rate
* Increases systemic vascular resistance
159
What is phenylephrine primarily used for?
* Prevent nosebleeds
* Reduce bleeding during ENT surgery
* Mydriatic in ophthalmology
160
What is esmolol and its primary pharmacological property?
A beta-blocker with a rapid onset and short duration of action
161
What is the elimination half-life of esmolol?
Approximately 9 minutes
162
What is the recommended IV loading dose of esmolol?
500 mcg/kg
163
What is the duration of action for esmolol?
10 to 15 minutes
164
What is the mechanism of action of Esmolol?
Esmolol is metabolized by nonspecific plasma esterases found in the cytosol of red blood cells.
165
What is the recommended intravenous loading dose of Esmolol?
500 mcg/kg
166
What is the infusion rate for Esmolol after the loading dose?
100 to 300 mcg/kg/min as needed
167
In which period is Esmolol particularly useful?
Perioperative period
168
What is the pharmacological classification of Metoprolol?
Beta-adrenergic blocking drug
169
What are the key actions of Metoprolol?
* Negative chronotropic
* Negative dromotropic
* Negative inotropic
* Antiarrhythmic
* Antiischemic
170
What is the usual intravenous administration dosage of Metoprolol?
5-mg doses at 5-minute intervals to a maximum dose of 15 mg
171
What is the typical oral dosage range for Metoprolol?
50-200 mg in one or two doses
172
What is the unique characteristic of Labetalol?
It possesses both beta-blocking and alpha-blocking properties.
173
What is the usual IV dose of Labetalol?
0.25 mg/kg
174
In which patients is Labetalol particularly recommended?
Obstetric patients for hypertensive episodes
175
What are the three anticholinergics used in anesthesia practice?
* Atropine
* Scopolamine
* Glycopyrrolate
176
What is the primary use of Atropine in anesthesia?
It is used for antisialagogue effects and prevention or treatment of bradycardia.
177
What is the usual adult IV dose of Atropine?
0.4 to 0.6 mg
178
What is the purpose of Scopolamine in anesthesia?
Used for sedation and amnesia preoperatively
179
What is the typical duration of action for a Scopolamine patch?
3 days
180
What is Glycopyrrolate primarily used for in anesthesia?
Preventing bradycardia without significant levels of tachycardia.
181
What is the typical dosage of Cefazolin for surgical procedures?
2g IV
182
Which pathogens is Cefazolin effective against?
* Staphylococcus aureus
* Enteric gram-negative bacilli
183
What is the recommended timing for administering Cefazolin?
As a single IV dose within 60 minutes before incision
184
What is the mechanism of action for Cefazolin?
Time-dependent killing
185
What is the recommended dose of Dexamethasone for PONV prevention?
4 mg IV after anesthesia induction
186
What is Ondansetron primarily used for?
Anti-emetic, effective for vomiting
187
What is the standard dose of Ondansetron?
4 mg IV at the end of the procedure
188
What are the side effects of Droperidol?
May cause extrapyramidal side effects
189
What is the role of Midazolam in antiemetic therapy?
Has significant antiemetic effects and decreases dopamine's emetic effect.
190
What should be considered for patients at moderate to high risk for PONV?
Multimodal PONV and PDNV prophylaxis
