Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Anesthesiology > Pharm > Flashcards

Pharm Flashcards

1
Q

Pros of IV induction agents

A

rapid induction, sedation with low doses, can be continuous infusion that is also used for maintenance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cons of IV induction agents

A

once it is in, you cannot remove it; difficulty in measuring how much anesthesia is given (no ET concentration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Propofol use and mechanism

A

Used for induction and maintenance. Mechanism: facilitation of inhibitory neurotransmission at GABA receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Advantages of propofol

A

i. Rapid onset due to high lipid solubility
ii. Quick recovery with minimal residual CNS effects
iii. Specifically suppresses upper airway reflexes and bronchodilates
iv. Antiemetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Disavantages of propofol

A

i. Burning pain on injection (precede with lidocaine injection)
ii. Cardiovascular depression: Drop in arterial blood pressure (20-30%) from a decrease in systemic vascular resistance, cardiac contractility, and preload
iii. Impairs baroreceptor response to hypotension
iv. Respiratory depressant: causes apnea and decreases the normal response to hypercarbia and inhibits hypoxic respiratory drive
v. Decreases cerebral blood flow
vi. Intralipid emulsion can support growth of microorganisms causing sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does propofol affect BP, SVR, contractility and preload?

A

Drop BP (20-30%) from decrease in SVR, contractility, and preload.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the pulm effects of propofol?

A

iv. Respiratory depressant: causes apnea and decreases the normal response to hypercarbia and inhibits hypoxic respiratory drive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is propofol metabolized and excreted?

A

Intra and extra hepatic metabolism. Excreted by kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some common IV induction agents?

A

propofol, thiopental, methoxexital, etomidate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Mechanism of thiopental?

A

mimics GABA by acting on Cl channels and increasing their duration of opening; suppresses excitatory ACh; depresses RAS (reticular activating system)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Uses of thiopental

A

rapid sequence induction (RSI), continuous infusion to decrease intracranial pressure; (no analgesic effects)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Advantages of thiopental

A

i. Rapid induction, well tolerated
ii. Cheap
iii. Less likely to cause apnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Disadvantages of thiopental

A

i. Slow recovery, with CNS suppression
ii. Decrease in BP and CO and increased HR (central vagolytic)
iii. Increased CV depression (hypotension) in hypovolemic, elderly pts or those on beta-blockers of with chronic HTN (inadequate baroreceptor responses)
iv. Can cause histamine release which could lead to bronchospasm (or from cholinergic stimulation)
v. Depresses medullary ventilation center , doesn’t completely suppress airway reflexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens to BP, CO, and HR with thiopental? Why?

A

BP decreases, CO decreases, HR increases. Because Central vagolytic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What patient populations should you be particularly careful with for thiopental? Why?

A

Increased hypotension in the hypovolemic, elderly, or those on beta-blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How can thiopental cause brochospasm?

A

histamine release or from cholinergic stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

For whom is thiopental contraindicated?

A

asthmatics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

pharmokinetics

A

renal excretion of water soluble hepatic metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Mechanism of methohexital?

A

Same as thiopental: mimics GABA by acting on Cl channels and increasing their duration of opening; suppresses excitatory ACh; depresses RAS (reticular activating system)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Uses of methohexital?

A

drug of choice for ECT; induction of anesthesia, (no analgesic effects)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Advantages of methohexital?

A

i. Minimal impact on seizure threshold
ii. Rapid recovery with minimal CNS suppression
iii. No histamine release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Disadvantages of methohexital

A

i. May stimulate seizure foci causeing myoclonic movement

ii. Depresses medullary ventilation center , doesn’t completely suppress airway reflexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

metabolism and excretion of methohexital?

A

metabolized quickly by the liver; excreted in feces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Mechanism of etomidate?

A

mimics inhibitory effects of GABA and depresses RAS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Use of etomidate
Rapid induction in patients with cardiovascular disease (no analgesia)
26
Advantages of etomidate
i. No or minimal cardiovascular effects (good for CAD, shock, valvular dz, cardiomyopathy) ii. Rapid induction and recovery with minimal residual CNS depression iii. Bronchodilator
27
Disadvantages of etomidate
i. Adrenocortical suppression of the 1-beta-hydroxylase (necessary for cholesterol  cortisol); decreases cortisol and aldosterone (increases mortality in critically ill pts) ii. Induction dose causes resp depression iii. Post-op nausea and vomiting iv. Myoclonic mvt on injection (without EEG changes) v. Can activate seizure foci
28
pharmokinetics of etomidate
highly protein bound, rapid onset of action (highly lipid soluble) Hepatic metabolism to a product excreted in urine
29
Which IV induction anesthetic is used for ECT?
methohexital
30
Which IV induction anesthetic is best for a patient with cardiovascular disease?
etomidate. also very rapid induction.
31
Which IV induction anesthetic has the greatest CNS suppression?
thiopental
32
Which IV induction agents are barbituates?
thiopental, methohexital, etomidate
33
Mechanism of ketamine
NMDA receptor agonist, muscarinic antagonist, and opioid agonist; causes functional dissociation of the thalamus from the RAS from the limbic cortex (decreases awareness)
34
Use of ketamine
dissociative anesthesia (pt appears to be conscious with eyes open and nystagmus, but doesn’t respond), analgesia, and amnesia
35
Which IV induction agent is the only central cardiovascular simulant? What does this mean?
ketamine. It increases HR, BP, CO
36
Which IV induction agents should be used for hypovolemic or cardiogenic shock?
ketamine, etomidate, midazolam. improves perfusion
37
Advantages of ketamine
i. Only IV induction agent that is a central CV stimulant  increases HR, BP, CO ii. Good for cardiogenic or hypovolemic shock (improves perfusion) iii. Potent somatic analgesia, iv. Minimal respiratory depression, potent bronchodilator (good in asthmatics)
38
Which IV induction agent is a potent bronchodilator? what does this mean?
ketamine. good for asthmatics
39
Disadvantages of ketamine
i. Respiratory depression with rapid administration ii. Normal airway reflexes remain intact iii. Can get excess respiratory secretions (necessitating antiChl drug-glycopyrrolate) iv. Increased BP and HR causes increased myocardial O2 demand (not good in CAD) v. cerebral vasodilationincreases ICP; bad with intracranial problems vi. emergent reactions with unpleasant dreams or hallucinations or delirium
40
pharmokinetics of ketamine
metabolized by liver, excreted renally
41
Which IV induction agent is contraindicated for epileptics?
methohexital
42
Common benzodiazepines used for IV induction
midazolam (Versed), diazepam, lorazepam
43
Uses of benzodiazepines
anxiolysis and sedation | not as fast as others for induction, NO analgesia
44
Mechanism of benzodiazepines
GABA Agonist - increase frequency of Cl opening
45
Advantages of benzos
i. minimal CV depression (slight increase HR and decrease in BP, CO and SVR) ii. anterograde amnesia iii. reduce cerebral O2 use, decrease ICP, prevent seizures
46
Disadvantages of benzos
respiratory depressant at medullary respiratory center (esp with concurrent opioids)
47
pharm of benzos
inactive metabolites, highly lipid soluble and high VD with high hepatic metabolism and clearance (t1/2 2 hr); renal excretion
48
Reversal agent of benzos
Flumazenil - benzo receptor antagonist. strong affinity short half life so resedation can occur after initial dose - repeat as needed
49
Which drug inhibits the metabolism of midazolam? What does this cause?
Erythromycin. Prolongs action of midazolam
50
Which drug increases diazepam concentration? How?
Heparin. By competing for protein binding.
51
Which drug class acts synergistically with benzos to cause respiratory depression and hypotention, and decreased SVR?
opioids
52
How do benzos affect volatile anesthetics?
Benzos reduce MAC up to 30%
53
What is the order of recovery speed for the IV induction agents, fastest to slowest?
propofol > methohexital > etomidate > thiopental > midazolam > ketamine > diazepam
54
Commonly used perioperative opioids
Morphine, fentanyl, hydromorphone (Dilaudid), remifentanil, sufentanil, alfentanil, meperidine
55
Opioid mechanism
a. bind mu (and kappa, delta and sigma) receptors in the CNS and peripheral tissues, which inhibits the presynaptic release and postsynaptic response to excitatory neurotransmitters from sensory neurons
56
Opioid use and effect on MAC
analgesia, some with sedation. Reduce MAC requirements
57
Which opioid increases HR and decreases contractility?
meperidine
58
Which opioids cause histamine release, causing bradycardia?
morphine, meperidine
59
Cardiovascular effects of opioids
Induce bradycardia via stimulation of medullary vagal nucleus
60
Respiratory effects of opioids
i. depresses respiratory rate; increases resting PCO2; decreases vent response to CO2 and hypoxia ii. can induce skeletal muscle chest wall rigidity which prevents PPV (mostly fentanyl, alfentanil, and sufentanil) iii. blunts bronchoconstrictive response to airway stimulus (intubation)
61
CNS effects of opioids
If not hypoventilating, decreases cerebral blood flow and ICP. Pinpoint pupils - CN III
62
GI effects of opioids
slows gastric emptying time, can cause biliary spasm or ileus (but tolerance develops long-term); constipation, nausea and vomiting
63
Endocrine effects of opioids
block the stress response during surgery by blocking release of catecholamines, ADH, and cortisol; good for those with ischemic heart dz
64
Which opioid is most effective at decreasing post-op shivering
meperidine
65
Shortest acting opioid
remifentanil
66
fast onset, short acting opioids
fentanyl: highly lipid soluble alfentanyl: less lipid soluble but high nonionized fraction and small Vd
67
slower onset, longer acting opioid
morphine - low lipid solubility
68
Overdose/narcotization signs
respiratory rate slowing/apnea; desaturation to cyanosis; bradycardia, hypotension, decreased CNS response or coma, pinpoint pupils
69
Treatment of opioid overdose
Naloxone - competative inhibitor, side effects are tachycardia, ventricular irritability, HTN, pulm edema, vomiting. Can cause acute opioid withdrawal syndrome in opioid dependent ppl Oxygenate/ventilate, CV support
70
Depolarizing muscle relaxant
succinylcholine. Intraoperative paralysis- rapid onset, lasts ~5 min
71
Mechanism of action of succinylcholine
composed of 2 ACh; binds Ach receptor and acts as agonist (generates AP) but does not dissociate off then prolonged depolarization of motor endplate and inability to generate new AP (can’t repolarize) =Phase I block; Then after prolonged infusion of sux, ionic and conformational changes at ACh receptor cause Phase II Block
72
Metabolism of succinylcholine
must diffuse away from NMJ to get to plasma cholinesterase located in blood and liver (not AChE)
73
Side effects of succinylcholine
1. fasciculations 2. profound bradycardia with multiple doses or in kids 3. malignant hyperthermia 4. hyperkalemia (dangerous for pts with burns, trauma, stroke, imobilized, myopathies, GBS...) 5. CV: low does is neg. chronotropic and inotropic; high dose is opposite NO dry mouth
74
Reversal of succinylcholine
by diffusion away from NM junction over time; can’t use ACHE inhibitors (they increase duration of depolarizing blockade by preventing sux metabolism)
75
Contraindications for succinylcholine
Kids: due to risk of hyperkalemia, rhabdomyolysis, and cardiac arrest in kids with undiagnosed myopathies Pts with burns, trauma, stroke, imobilized, myopathies, GBS...
76
Nondepolarizing muscle relaxants and use
Rocuronium, Cisatracurium, vecuronium | Use: intraoperative paralysis
77
Mechanism of nondeplarizing muscle relaxants
bind ACh receptors as competitive antagonists; cannot cause conf change necessary for ion channel opening so they prevent AP; only needs one alpha subunit bound to produce NM blockade
78
Speed of onset and duration of action of nondepolarizing m. relaxants
i. Speed of onset: roc 1.5 min, cisatra and vec 2-3 min | ii. Duration of action: roc 35-75 min
79
What potentiates block for nondepolarizing m. relaxants?
i. Hypothermia prolongs block by decreasing metabolism and excretion ii. Hypokalemia, hypoCa, and hyperMg potentiates block iii. Volatile inhalation anesthetics potentiate block
80
Reversal of nondepolarizing m. relaxants?
i. Neostigmine: acetylcholinesterase inhibitors can cause increased ACh in the NM junction and compete away the NDMR ii. Anticholinergic agents (glycopyrrolate, atropine) must be given with the cholinesterase inhibitor to prevent increased ACh at muscarinic receptors (bradycardia, increased secretions)
81
Metabolism of nondepolarizing m. relaxants?
i. Rocuronium: no metabolism, elim mostly by liver, slightly by kidneys; ii. Cisatracurium: degradation in plasma at physiologic pH and temp by Hofmann elimination (good in liver or renal failure) iii. Vecuronium: metabolized by liver, biliary excretion (primarily with 25% renal); prolonged action in renal failure
82
Risks of neuromuscular blockade
a. Difficult airway: must ensure adequate mask ventilation after induction of general anesthetic and before giving muscle relaxant; otherwise may need to emergently establish airway by LMA or trach b. Post-extubation residual NM blockade so cannot breathe; must mask or use LMA
83
Perioperative hemodynamic support drugs
Ephedrine | Phenylephrine
84
How does ephedrine work?
Indirect and direct Adrenergic Agonist (noncatecholamine): alpha 1, beta1, beta2. Increases BP, HR, contractility, CO. Bronchodilates.
85
How does phenylephrine work?
Direct noncatecholamine Adrenergic Agonist - alpha1 . Increases SVR which increases BP, decreases HR and CO.
86
Anti-emetic drugs
1. Odansetron (Zofran) 5HT3 (seratonin) antag in brain and abdominal vagal afferents. can cause headache and prolonged QTc 2. Metoclopramide - ACh agonist peripherally and DA antag centrally (CTZ region) 3. Droperidol - DA antag in CTZ 4. Diphenhydramine - H1 antag 5. Scopalamine - antimuscarinic - dryness and mystriasis
87
Sedative drug
Dexmeditomidate: selective alpha2 agonist that causes sedation/hypnosis (easy to arouse), anxiolysis, amnesia, mild analgesia, and sympatholytic (decreases HR and BP) i. No respiratory depression ii. Bradycardia and hypotension if given too rapidly or in hypovolemic pt

Anesthesiology (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions