Week 4 (Quiz 3) (Pain, Nausea and Anesthesia) Flashcards
1
Q
Local analgesics end in
A
“-caine”; lidocaine
2
Q
Mechanism of local analgesics
A
blockade of Na+ and therefore the action potential
3
Q
Order of pain block
A
pain –> cold –> warmth –> touch –> deep pressure –> motor [recovery in reverse]
4
Q
Two types of pain fibers
A
Type A Delta
Type C
5
Q
Type A Delta pain fibers
A
sense pain and temperature; larger, myelinated, faster signal velocity
6
Q
Type C pain fibers
A
sense pain; smaller, unmyelinated, slower signal velocity
7
Q
Ceiling effect and NSAIDS
A
no further effect on pain above a particular dosage level
8
Q
NSAIDs agents
A
Ibuprofen, Naproxen, ASA, indomethacin, etc.
9
Q
NSAIDs work on pain in PNS or CNS?
A
PNS
10
Q
What inhibits substance P?
A
5-HT and NE
11
Q
Agents for neuropathic pain
A
TCAs (imipramine, doxepin); gabapentin, carbamazepine
12
Q
What is neuropathic pain?
A
shooting, burning, stabbing, electric shock-like pain
13
Q
Disadvantages of agents for neuropathic pain?
A
severe side effects possible; anticholinergics –> sedation
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)
15
Q
What G protein do opioids act on?
A
Gi on presynaptic terminal
16
Q
What are the three types of receptors in opioids?
A
Mu, Delta, Kappa
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]
18
Q
Delta receptors
A
modulates mu activity
19
Q
Kappa receptors
A
analgesia with little/no resp.
depression
20
Q
Opioids work in PNS or CNS
A
CNS
21
Q
Do opioids have a ceiling effect?
A
No
22
Q
Major SE of Opioids
A
Respiratory depression
23
Q
Buprenorphine receptor
A
partial Mu
24
Q
Nalbuphine receptor
A
moderate Kappa
25
Butorphenol receptor
partial Mu, full Kappa
26
What are partial agonist opioids good for?
good for hyper-reactivity to opioids - can be used for partial reversal (competes with full agonists)
27
Example of a weak agonist
Propoxyphene
28
Opioid antagonist
Naloxone (all receptors)
29
What can sudden, complete antagonism cause (Naloxone)?
sudden complete antagonism can cause severe hypertension, ventricular dysrhythmias, acute/fatal PE
30
Benzodiazepines mechanism
modulate GABA receptor activity --> ↑Cl- channel opening (hyperpolarization) --> ↓ excitability of neuron
31
Benzodiazepines advantage
good anxiolytics and amnestics
32
What should you not use benzodiazepines for?
Pain management
33
Morphine (morphine sulfate)/Hydromorphone receptor
Mu, weak Kappa
34
Morphine (morphine sulfate)/Hydromorphone administration
IV, IM, PO, rectal, subQ
35
Morphine (morphine sulfate)/Hydromorphone onset
onset = 5 min; peak = 30 min; duration = 3-4 hrs. via IV
36
Morphine (morphine sulfate)/Hydromorphone advantages
maintenance of acute and chronic pain; good for post MI
37
Morphine (morphine sulfate)/Hydromorphone disadvantages
long onset
38
Fentanyl receptor
Mu only
39
Fentanyl administration
IV, IM, PO, transdermal (patch)
40
Fentanyl action
onset = 1-2 min; peak = 5-7min/(24hrs transdermally); duration =30-60 hrs. via IV
41
Fentanyl advantages
give to pts with morphine allergy; effective; rapid onset
42
Fentanyl disadvantages
chest wall rigidity after rapid IV administration
43
Methadone administration
IV, IM, PO
44
Methadone use
severe pain; opioid withdrawal
45
Methadone advantages
long half-life (good for pain and withdrawal); NMDA antagonist effects = lowers tolerance
46
Methadone disadvantages
accumulates (bad PK profile); not for routine pain management
47
Oxycodone, Hydrocodone, Codeine advantages
good first-line if NSAIDs are ineffective/pt has breakthrough pain
48
Oxycodone, Hydrocodone, Codeine disadvantages
CYP2D6 metabolism; nausea (esp. codeine PO); use caution when concomitantly given with acetaminophen
49
Meperidine administration
IV, IM, SQ, PO
50
Meperidine action
onset = 5 min; peak = 15-30 min; duration = 2-4 hrs. via IV
51
Meperidine advantages
give to pts with morphine allergy; good for chills; ↓ biliary spasm
52
Meperidine disadvantages
long onset; metabolite accumulates (PO)
53
Tramadol administration
PO
54
Tramadol receptor
Mu
55
Tramadol mechanism
inhibits 5-HT and NE reuptake
56
Tramadol advantages
alternative to opioids; not controlled substance
57
Tramadol disadvantages
no more effective than APAP with codeine (acetaminophen); seizures
58
Emesis happens when you stimulate:
Chemoreceptor Trigger Zone
59
What receptors does the Chemoreceptor Trigger Zone contain?
Dopamine and 5-HT
60
What can the Chemoreceptor Trigger Zone be stimulated by?
```
○ vestibulocochlear nerve (CN 8)
○ dopamine, serotonin, histamine
○ opioids, muscarinics
○ S. aureus enterotoxin
○physicaltriggers: pharynx, coronary vessels, bile
ducts, vestibular apparatus
```
61
Patient risk factors for PONV
```
○ female, age (11-14 y/o is peak)
○ obesity
○ hx of migraines, PONV, motion sickness ○ postop eating patterns
○ gastroparesis
○ anxiety
```
62
Procedural risk factors for PONV
○ gynecological; abdominal (GI)
○ laparoscopy
○ ENT; Ophthalmic
63
Anesthetic risks for PONV
○ premedication
○ opioids, NO
○ duration/depth of anesthesia
64
Post-op risks for PONV
○ pain, dizziness, early ambulation
○ hypotension
○ premature oral intake
65
Antihistimine agents that can be used for nausea and vomiting
Diphenhydramine; dimenhydrinate; meclizine
66
Anticolinergic agents that can be used for nausea and vomiting
Scopolamine
67
Mixed agents for nausea and vomiting
Promethazine; Metoclopramide
68
Serotonin agents for nausea and vomiting
Ondansetron; Dolasetron; Granisetron; Palonosetron
69
What is the most efficacious for single agent for PONV treatment?
Serotonin
70
Dopamine agents for nausea and vomiting
Droperidol*; Haloperidol; Prochlorperazine
71
What is the "gold standard" for PONV treatment?
Dopamine
72
Black box warning for Dopamine
cardiac rhythm abnormalities
73
What can low dose steroids be used to prevent?
Prophylaxis for nausea and vomiting (e.g. Dexamethasone)
74
What prevents PONV
Aprepitant
75
Aprepitant mechanism
selective, high-affinity antagonist of substance P/neurokinin 1 (NK1) receptors
76
Pros of ether
circulatory stability, spontaneous breathing/patent airway, muscular relaxation
77
Cons of ether
explosive, vomiting, slow/unpleasant induction
78
N2O is used for:
sedation or as component of general anesthesia
79
N2O pros
rapid onset/offset, minimal CV/resp. function effects, minimal toxicity
80
N2O cons
not potent enough to produce general anesthesia on its own
81
Minimal alveolar concentration
measure of potency of anesthetic based on the concentration 50% of inhaled drug that patients still move at (like ED50)
82
Increased MAC = ___ potency
decreased
83
Meyer-Overton Rule
anesthetic potency is directly correlated with lipid solubility
84
Increased lipid solubility = ____ potency
Increased
85
Why can we use lungs as a measure of partial pressure of anesthetics?
partial pressure of anesthetics in brain doesn't exceed partial pressure of anesthetics in lungs
86
Partial pressure in lungs depends on balance between
Delivery via airway and uptake via blood
87
Steady state for less lipophilic anesthetics
quick!
88
Steady state for highly lipophilic anesthetics
slower
89
Inhaled anesthetics use
Pediatric induction, maintenance of anesthesia
90
Pros of inhaled anesthetics
predictable and measurable pharmacodynamics; safe use; reliable
91
Halothane is metabolized via:
Cytochrome P450
92
Halothane can cause what side effect
halothane hepatitis
93
Inhaled anesthetics CV side effects
↓ mean arterial pressure
94
Inhaled anesthetics respiratory side effects
↓pump function (↓ventilation↑ PCO2);
↓response to hypercarbia and hypoxia;
↓ activity/coordination of upper airway muscles
95
What is malignant hyperthermia?
(very rare) intraoperatively and postoperatively, pts with abnormality of ryanodine receptor in sarcoplasmic reticulum
96
What do you treat malignant hyperthermia with?
Dantrolene
97
What are 5 inhaled anesthetics?
- NO
- Halothane
- Sevoflurane
- Isoflurane
- Desflurane
98
Thiopental mechanism
may act on GABA receptors?; highly lipid soluble
99
Thiopental metabolism
slow hepatic (12 hour half-life) - not good for maintenance of anesthesia
100
Thiopental use
Obsolete
101
Thiopental SE
triggers porphyria
102
Propofol mechanism
may act on GABA receptors and/or NMDA receptors
103
Propofol delivery
IV in lipid emulsion (not very water soluble; very lipid soluble)
104
Propofol metabolism
relatively rapid metabolism (1-3 hr. half-life) - rapid onset and offset
105
Propofol use
as bolus/emergent or continuous infusion (maintenance); popular for sedation
106
Propofol SE
similar to thiopental (potent CV and resp); respiratory depression; pain at IV site
107
Ketamine is a derivative of
PCP
108
Ketamine mechanism
NMDA receptor antagonist
109
Ketamine delivery
IV or IM (fairly water soluble)
110
Ketamine metabolism
relatively rapid metabolism (1-3 hr. half-life); circulatory stability
111
Ketamine use
IM makes it ideal for difficult anesthesia scenarios (unstable pt); maintains spontaneous breathing
112
Ketamine SE
hallucinations; relatively little CV and resp. depression; ↑sympathetic nervous system; bronchodilator; slowest recovery
113
Drugs used for analgesia in anesthesia
opioids (fentanyl, morphine)
114
Drugs used for amnesia in anesthesia
benzodiazepines (midazolam)
115
Drugs used for hypnosis in anesthesia
IV agents (propofol)
116
Drugs used for immobility in anesthesia
neuromuscular agents (vecuronium)
