Week 4 (Quiz 3) (Pain, Nausea and Anesthesia) Flashcards

1
Q

Local analgesics end in

A

“-caine”; lidocaine

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

Mechanism of local analgesics

A

blockade of Na+ and therefore the action potential

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

Order of pain block

A

pain –> cold –> warmth –> touch –> deep pressure –> motor [recovery in reverse]

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

Two types of pain fibers

A

Type A Delta

Type C

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

Type A Delta pain fibers

A

sense pain and temperature; larger, myelinated, faster signal velocity

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

Type C pain fibers

A

sense pain; smaller, unmyelinated, slower signal velocity

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

Ceiling effect and NSAIDS

A

no further effect on pain above a particular dosage level

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

NSAIDs agents

A

Ibuprofen, Naproxen, ASA, indomethacin, etc.

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

NSAIDs work on pain in PNS or CNS?

A

PNS

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

What inhibits substance P?

A

5-HT and NE

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

Agents for neuropathic pain

A

TCAs (imipramine, doxepin); gabapentin, carbamazepine

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

What is neuropathic pain?

A

shooting, burning, stabbing, electric shock-like pain

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

Disadvantages of agents for neuropathic pain?

A

severe side effects possible; anticholinergics –> sedation

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

Mechanism of opioids

A
  • mimics endorphins; activates pain modulating system –>
  • binds opioid receptors on presynaptic terminal of primary
    afferent fibers (at the synapse between primary afferents and spinal pain-transmission neurons)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What G protein do opioids act on?

A

Gi on presynaptic terminal

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

What are the three types of receptors in opioids?

A

Mu, Delta, Kappa

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

Mu receptors

A

supraspinal analgesia, euphoria, resp. depression, ↓ HR, dependence

Also increased K+ efflux creating an inhibitory postsynaptic potential (IPSP) on postsynaptic neuron [hyperpolarizes]

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

Delta receptors

A

modulates mu activity

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

Kappa receptors

A

analgesia with little/no resp.

depression

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

Opioids work in PNS or CNS

A

CNS

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

Do opioids have a ceiling effect?

A

No

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

Major SE of Opioids

A

Respiratory depression

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

Buprenorphine receptor

A

partial Mu

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

Nalbuphine receptor

A

moderate Kappa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Butorphenol receptor

A

partial Mu, full Kappa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are partial agonist opioids good for?

A

good for hyper-reactivity to opioids - can be used for partial reversal (competes with full agonists)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Example of a weak agonist

A

Propoxyphene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Opioid antagonist

A

Naloxone (all receptors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What can sudden, complete antagonism cause (Naloxone)?

A

sudden complete antagonism can cause severe hypertension, ventricular dysrhythmias, acute/fatal PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Benzodiazepines mechanism

A

modulate GABA receptor activity –> ↑Cl- channel opening (hyperpolarization) –> ↓ excitability of neuron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Benzodiazepines advantage

A

good anxiolytics and amnestics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What should you not use benzodiazepines for?

A

Pain management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Morphine (morphine sulfate)/Hydromorphone receptor

A

Mu, weak Kappa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Morphine (morphine sulfate)/Hydromorphone administration

A

IV, IM, PO, rectal, subQ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Morphine (morphine sulfate)/Hydromorphone onset

A

onset = 5 min; peak = 30 min; duration = 3-4 hrs. via IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Morphine (morphine sulfate)/Hydromorphone advantages

A

maintenance of acute and chronic pain; good for post MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Morphine (morphine sulfate)/Hydromorphone disadvantages

A

long onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Fentanyl receptor

A

Mu only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Fentanyl administration

A

IV, IM, PO, transdermal (patch)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Fentanyl action

A

onset = 1-2 min; peak = 5-7min/(24hrs transdermally); duration =30-60 hrs. via IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Fentanyl advantages

A

give to pts with morphine allergy; effective; rapid onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Fentanyl disadvantages

A

chest wall rigidity after rapid IV administration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Methadone administration

A

IV, IM, PO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Methadone use

A

severe pain; opioid withdrawal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Methadone advantages

A

long half-life (good for pain and withdrawal); NMDA antagonist effects = lowers tolerance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Methadone disadvantages

A

accumulates (bad PK profile); not for routine pain management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Oxycodone, Hydrocodone, Codeine advantages

A

good first-line if NSAIDs are ineffective/pt has breakthrough pain

48
Q

Oxycodone, Hydrocodone, Codeine disadvantages

A

CYP2D6 metabolism; nausea (esp. codeine PO); use caution when concomitantly given with acetaminophen

49
Q

Meperidine administration

A

IV, IM, SQ, PO

50
Q

Meperidine action

A

onset = 5 min; peak = 15-30 min; duration = 2-4 hrs. via IV

51
Q

Meperidine advantages

A

give to pts with morphine allergy; good for chills; ↓ biliary spasm

52
Q

Meperidine disadvantages

A

long onset; metabolite accumulates (PO)

53
Q

Tramadol administration

54
Q

Tramadol receptor

55
Q

Tramadol mechanism

A

inhibits 5-HT and NE reuptake

56
Q

Tramadol advantages

A

alternative to opioids; not controlled substance

57
Q

Tramadol disadvantages

A

no more effective than APAP with codeine (acetaminophen); seizures

58
Q

Emesis happens when you stimulate:

A

Chemoreceptor Trigger Zone

59
Q

What receptors does the Chemoreceptor Trigger Zone contain?

A

Dopamine and 5-HT

60
Q

What can the Chemoreceptor Trigger Zone be stimulated by?

A
○ vestibulocochlear nerve (CN 8)
○ dopamine, serotonin, histamine
○ opioids, muscarinics
○ S. aureus enterotoxin
○physicaltriggers: pharynx, coronary vessels, bile
ducts, vestibular apparatus
61
Q

Patient risk factors for PONV

A
○ female, age (11-14 y/o is peak)
○ obesity
○ hx of migraines, PONV, motion sickness ○ postop eating patterns
○ gastroparesis
○ anxiety
62
Q

Procedural risk factors for PONV

A

○ gynecological; abdominal (GI)
○ laparoscopy
○ ENT; Ophthalmic

63
Q

Anesthetic risks for PONV

A

○ premedication
○ opioids, NO
○ duration/depth of anesthesia

64
Q

Post-op risks for PONV

A

○ pain, dizziness, early ambulation
○ hypotension
○ premature oral intake

65
Q

Antihistimine agents that can be used for nausea and vomiting

A

Diphenhydramine; dimenhydrinate; meclizine

66
Q

Anticolinergic agents that can be used for nausea and vomiting

A

Scopolamine

67
Q

Mixed agents for nausea and vomiting

A

Promethazine; Metoclopramide

68
Q

Serotonin agents for nausea and vomiting

A

Ondansetron; Dolasetron; Granisetron; Palonosetron

69
Q

What is the most efficacious for single agent for PONV treatment?

70
Q

Dopamine agents for nausea and vomiting

A

Droperidol*; Haloperidol; Prochlorperazine

71
Q

What is the “gold standard” for PONV treatment?

72
Q

Black box warning for Dopamine

A

cardiac rhythm abnormalities

73
Q

What can low dose steroids be used to prevent?

A

Prophylaxis for nausea and vomiting (e.g. Dexamethasone)

74
Q

What prevents PONV

A

Aprepitant

75
Q

Aprepitant mechanism

A

selective, high-affinity antagonist of substance P/neurokinin 1 (NK1) receptors

76
Q

Pros of ether

A

circulatory stability, spontaneous breathing/patent airway, muscular relaxation

77
Q

Cons of ether

A

explosive, vomiting, slow/unpleasant induction

78
Q

N2O is used for:

A

sedation or as component of general anesthesia

79
Q

N2O pros

A

rapid onset/offset, minimal CV/resp. function effects, minimal toxicity

80
Q

N2O cons

A

not potent enough to produce general anesthesia on its own

81
Q

Minimal alveolar concentration

A

measure of potency of anesthetic based on the concentration 50% of inhaled drug that patients still move at (like ED50)

82
Q

Increased MAC = ___ potency

83
Q

Meyer-Overton Rule

A

anesthetic potency is directly correlated with lipid solubility

84
Q

Increased lipid solubility = ____ potency

85
Q

Why can we use lungs as a measure of partial pressure of anesthetics?

A

partial pressure of anesthetics in brain doesn’t exceed partial pressure of anesthetics in lungs

86
Q

Partial pressure in lungs depends on balance between

A

Delivery via airway and uptake via blood

87
Q

Steady state for less lipophilic anesthetics

88
Q

Steady state for highly lipophilic anesthetics

89
Q

Inhaled anesthetics use

A

Pediatric induction, maintenance of anesthesia

90
Q

Pros of inhaled anesthetics

A

predictable and measurable pharmacodynamics; safe use; reliable

91
Q

Halothane is metabolized via:

A

Cytochrome P450

92
Q

Halothane can cause what side effect

A

halothane hepatitis

93
Q

Inhaled anesthetics CV side effects

A

↓ mean arterial pressure

94
Q

Inhaled anesthetics respiratory side effects

A

↓pump function (↓ventilation↑ PCO2);
↓response to hypercarbia and hypoxia;
↓ activity/coordination of upper airway muscles

95
Q

What is malignant hyperthermia?

A

(very rare) intraoperatively and postoperatively, pts with abnormality of ryanodine receptor in sarcoplasmic reticulum

96
Q

What do you treat malignant hyperthermia with?

A

Dantrolene

97
Q

What are 5 inhaled anesthetics?

A
  • NO
  • Halothane
  • Sevoflurane
  • Isoflurane
  • Desflurane
98
Q

Thiopental mechanism

A

may act on GABA receptors?; highly lipid soluble

99
Q

Thiopental metabolism

A

slow hepatic (12 hour half-life) - not good for maintenance of anesthesia

100
Q

Thiopental use

101
Q

Thiopental SE

A

triggers porphyria

102
Q

Propofol mechanism

A

may act on GABA receptors and/or NMDA receptors

103
Q

Propofol delivery

A

IV in lipid emulsion (not very water soluble; very lipid soluble)

104
Q

Propofol metabolism

A

relatively rapid metabolism (1-3 hr. half-life) - rapid onset and offset

105
Q

Propofol use

A

as bolus/emergent or continuous infusion (maintenance); popular for sedation

106
Q

Propofol SE

A

similar to thiopental (potent CV and resp); respiratory depression; pain at IV site

107
Q

Ketamine is a derivative of

108
Q

Ketamine mechanism

A

NMDA receptor antagonist

109
Q

Ketamine delivery

A

IV or IM (fairly water soluble)

110
Q

Ketamine metabolism

A

relatively rapid metabolism (1-3 hr. half-life); circulatory stability

111
Q

Ketamine use

A

IM makes it ideal for difficult anesthesia scenarios (unstable pt); maintains spontaneous breathing

112
Q

Ketamine SE

A

hallucinations; relatively little CV and resp. depression; ↑sympathetic nervous system; bronchodilator; slowest recovery

113
Q

Drugs used for analgesia in anesthesia

A

opioids (fentanyl, morphine)

114
Q

Drugs used for amnesia in anesthesia

A

benzodiazepines (midazolam)

115
Q

Drugs used for hypnosis in anesthesia

A

IV agents (propofol)

116
Q

Drugs used for immobility in anesthesia

A

neuromuscular agents (vecuronium)