Non-opioid and Opioid Analgesics Flashcards
1
Q
What is the only non-opioid analgesic that is also NOT a NSAID?
A
Acetaminophen
NO anti-inflammatory effect
2
Q
What are the subclasses of NSAIDs?
A
Non-acetylated salicylates
Acetylated salicylates (ASA)
Selective COX-2 inhibitor (Celecoxib)
Traditional NSAIDs
3
Q
Traditional NSAIDs include:
A
Ibuprofen Naproxen Oxaprozin Diclofenac Etodolac Indomethacin Ketorolac Nabumetone Sulindac Tolmetin Proxicam Meloxicam Flurbiprofen
4
Q
Between what dose does a ceiling effect happen in ASA and APAP?
A
650-1300mg
NSAIDs other than ASA may have higher ceiling doses
5
Q
Does tolerance develop to Non-Opioid Analgesics?
A
No
6
Q
APAP has a similar efficacy and potency as _______ .
A
ASA
7
Q
APAP should be used in caution with what type of patients and why?
A
Pts on isoniazid (TB med)
Heavy ETOH users
Serious or fatal hepatic injury (same with overdose)
8
Q
Why may inadvertent overdoses of APA occur? (2)
A
- Patients may be taking multiple products with APAP in them
- Wrong dose of highly concentrated product (ex-infant drops)
9
Q
Maximum safe dose of APAP in children >12yrs is:
A
4grams/day
OTC= 3grams unless directed by MD/NP
10
Q
Non-opioid analgesics are the first line for what type of pain?
A
Mild to moderate
11
Q
Hows is ASA (acetylated salicylate) different from other NSAIDs?
A
ASA causes irreversible inhibition of COX. A single dose inhibits platelet function for lifetime of the plt (4-7days)
12
Q
What AE does ASA cause (like other NSAIDs)?
A
GI bleeding
PUD
13
Q
Unlike other NSAIDs, ASA is not commonly used for its _______ _______ .
A
anti-inflammatory effects
d/t high doses necessary and increased risk for GI bleed
14
Q
What is the difference is dosing for ASA used as an analgesic/antipyretic vs an anti-inflammatory?
A
Analgesic/antipyretic: 325-650mg
Anti-inflam: 1000mg (3-5g/day)
15
Q
When using ASA as an anti-inflammatory how much a patient be dosed/monitored?
A
Increase dose gradually
Assess serum salicylate levels
16
Q
How is ASA cleared?
A
Hepatic clearance
17
Q
S/s of ASA overdose:
A
Metabolic acidosis
Tinnitus
18
Q
When should ASA never be used and it what age patient? Why?
A
Viral syndromes in children and teens
Can causes Reye’s Syndrome and lead to multi-organ failure
19
Q
Why are non-acetylated salicylates more favorable than ASA and what are some examples?
A
Less AE-
Do not interfere with plt aggregation
Rarely associated with GI bleeding
Well tolerated by asthmatics
Examples:Choline Mag trisalicylate, Diflunisal, Mag salicylate
20
Q
How do traditional NSAIDs analgesia compare to ASA or APAP and an opioid combined with APAP?
A
More effective than ASA or APAP
Equal or more effective than opioid and APAP
21
Q
Different NSAIDs have _______ efficacy at _______ doses.
A
Similar
Equipotent
22
Q
What is the MOA of NSAIDs?
A
Inhibition of COX 1 and 2
Conversion of A.A. to prostaglandins is blocked
Decreased release of prostglandins causes analgesia, anti-inflammatory effects and antipyretic activity
23
Q
Why is a traditional NSAID more appropriate than ASA for an asthmatic to take?
A
NSAID inhibition of the COX pathway is reversible and less likely to push the pathway to the lipooxygenase side
24
Q
What are NSAIDs effect on platelets?
A
Reversible inhibition of COX which blocks synthesis of thromboxane A2 inhibiting platelet aggregation
25
What are s/s of salicylate build up?
Tinnitis
| Hearing loss
26
NSAIDs are considered what Category in the third trimester and why?
Category D
premature closure of ductus arteriousus
(Category B in 1st and 2nd trimester)
27
GI AE of NSAIDs include:
Dyspepsia
GI bleeding
PUD
28
How do NSAIDs cause GI upset?
Inhibiting PGs that maintain normal gastric and duodenal mucosa increased acid production, decreases mucus production, and decreases gastric blood flow
Local irritation occurs d/t NSAIDs being lipid soluble at a low pH allowing them to enter gastric mucosal cells where they lose lipid solubility and become trapped in the cell
29
Risk factors for GI AE of NSAIDs include:
```
High doses
Prolonged use
Hx of GI ulcer or bleeding
Excessive ETOH intake
Elderly
Corticosteroid use (may also cause PUD)
```
30
How can the GI effects of NSAIDs be prevented?
- PG analog- misoprostil (replenish the PGs that are reduced) or Diclofenac/misoprostol
- PPI
- H2 receptor antagonists
- Sucralfate (s/s management)
- Take with food
31
What are the highest risk NSAIDs and why?
```
Tolmetin
Piroxicam
ASA
Indomethacin
Ketorolac
```
More COX1 inhibition increases risk
32
What are the low risk NSAIDs and why?
Ibuprofen and Naproxen at low doses
Etodolac, sulindac
Celcoxib
More COX2 inhibition over COX1
33
In addition to GI AE what other AE do NSAIDs cause and how?
Renal AE
Decreased synthesis of renal vasodilator PGE (PGE2) leads to decreased RBF, Na and H2O retention, renal failure, HTN, interstitial nephritis
34
What are risk factors for renal AE of NSAIDs?
```
Old age
CHF
HTN
Renal Insufficiency
Ascites
Volume depletion
Diuretic therapy
```
Type of NSAIDs
Longer half-life, highly potent COX inhibitors (ketorolac, indomethacin)
High doses
35
Which NSAIDs are considered 'renal sparing'
Sulindac
Nabumetone
Celecoxib
36
What drug increases levels of most NSAIDs?
Probenicid
Not always clinically significant because NSAIDs have wide TI
*Avoid with ketorolac
37
How do NSAIDs causes many DI?
-Displace other highly protein bound agents
(Increases levels of warfarin, phenytoin, sulfonylureas, sulfonamides, and dig)
-Suppression of renal PGs
(Reduces effects of diuretics, beta-blockers, ACEIs)
38
What is the effect of NSAIDs on lithium?
Increases levels
39
Which NSAIDs are less likely to interact with warfarin?
Ibuprofen
Diclofenac
Tolmetin
Naproxen
40
What is the only NSAID given IV/IM and how long can it be used for?
Ketorolac
| No more than 5 days of use
41
What are the serious risk associated with Ketorolac?
```
GI bleeding
Ulceration
Perforation
Renal toxicity
(increased risk in elderly)
```
42
What is the only selective COX2 inhibitor NSAID on the market today and why were the others withdrawn?
Celecoxib
Other withdrawn d/t increased risk of MI (inhibition of COX 2 only disrupts balance in contrast to nonselective NSAIDs that inhibit both and create a new balance)
43
What is the potential benefit to using a COX2 inhibitor?
Less GI effects
| COX 1 in responsible for gastric production and is not inhibited
44
What AE is not avoided by using a COX2 inhibitor?
Renal AE
45
Celecoxib should be used at the lowest effective dose, this dose should not exceed:
200mg/day
| equivalent to 500mg BID of naproxen
46
What should be considered when prescribing a patient Celecoxib
Risk for CV events
47
What is the Black Box warning for all NSAID related to CV risk?
Increased risk of serious CV thrombotic events, MI, stroke
| CI for tx of peri-operative pain in setting of CABG
48
What is the Black Box warning for all NSAID related to GI risk?
Increased risk of bleeding, ulceration, perforation of the stomach or intestines
49
What desirable effects does PG suppression create?
Antipyretic
Analgesic
Anti-inflamm
50
What drugs mainly act as agonist on Mu receptors (some kappa and sigma)?
Morphine
Heroin
Codeine
Fentanyl
51
What drug is an agonist at kappa receptors and a partial antagonist at the Mu receptor?
Pentazocine
52
Which drugs act as an antagonist at the Mu, kappa, and sigma receptors?
Naloxone
| Naltrexone
53
Opioids are prescribed for what type of pain?
Moderate to severe
54
Which type of opioids have a ceiling effect?
```
Partial agonist
(full agonists have no max dose)
```
55
How are opioids metabolized?
Hepatically
| inactive or active metabolites are renally excreted
56
Tolerance means:
Decreased effect of drug that develops with continued use
57
______ tolerance can occur with opioids?
Cross
58
Full agonist opioids that are most effective include:
```
Morphine
Oxycodone
Hydromorphone
Methadone
Meperidine
Fentanyl
Oxymorphone
```
59
Full agonist opioids that are considered to have more mild effects include:
Codeine
Hydrocodone
Propoxyphene
60
What is the difference between an opiate and an opioid?
An opiate is a naturally occurring drug, like morphine or codeine, and an opioid is a drug that acts like an opiate (synthetic).
61
Partial agonists, mixed agonist-antagonists include:
Pentazocine
Butorphanol
Nalbuphine
Buprenorphine
62
Why is morphine not as effective orally?
First pass metabolism
63
Morphine's two main active metabolites are:
Morphine 6-glucuronide
| Morphine 3-glucoronide
64
SE causes by a build of morphine's active metabolites include?
Nausea
Myoclonus
Hallucinations
65
What off target effect can morphine cause and what does it result in?
Histamine release
| Pruritis
66
Morphine's routes of administration include:
PO, IM, IV, SubQ, rectal, epidural, intrathecal
67
Codeine is what type of drug?
Prodrug
| Only about 10% is metabolized by CYP2D6 to its active form
68
What is codeine's active form?
Morphine
69
Without conversion to morphine what is codeine's effect?
Antitussive
70
10% of Caucasians and 30% of Asians lack ______ prevent codeine from having any analgesia effect.
2D6
71
Hydrocodone's route of administration:
PO
72
Hydrocodone is always combined with what four drugs:
APAP
ASA
Ibuprofen
Antihistamine
73
Which two opioids are used as cough suppressants?
Codeine
| Hydrocodone
74
Oxycodone is available in combination with what two drugs?
APAP
| ASA
75
Why is oxycodone often the drug of choice in patients with renal dysfunction?
No active metabolites
76
Hydromorphone:
Available PO, IM, IV, SubQ, rectal, epidural
Semi-synthetic
No major metabolites (safer in patients with renal dysfxn)
77
How is methadone doses differently when given to treat addiction vs neuropathic pain management?
Addiction: once daily
| Pain management: BID or TID
78
What type of opioid is methadone?
Synthetic
79
Why is methadone used for opioid addiction?
Longer half-life elimination
80
Morphine has no ______ _______, so is safer in patients with renal dysfunction.
active metabolites
81
How is meperidine usually used?
Post-op shakes/chills, caused by anesthetic agents, epidurals, and spinal anesthesia
(short term, 24-48hrs)
82
What is meperidine's main metabolite and the AEs associated with it?
Normeperidine (long half-life, 15-20hrs)
Accumulation can cause CNS excitation/anxiety and convulsions
Caution in elderly and pts with renal dysfunction
83
Why was propoxyphene removed from the market in 2010?
Cardiac toxicity
84
Propoxyphene: Route, combined with, metabolized to
PO
Combined with APAP
Metabolized to norpropoxyphene, long half life (30-36hrs) can causes stupor, coma, convulsions
85
How much more potent than morphine is fentanyl?
80-100x
86
When would a transdermal fentanyl patch be used?
Chronic pain
| Only after titration with short-acting opioid
87
Which type of administration route is used for fentanyl for breakthrough pain?
Transmucosal lozenge
| 35-50% bioavailability
88
Buprenoprhine is a ____ _____ .
partial agonist
89
Route of administration of buprenorphine include:
SL (dependence), parenteral (pain)
90
If buprenorphine is given while a patient is taking a full agonist what may occur?
Withdrawal symptoms
Buprenorphine will take the place of the full agonist at the receptor but does not elicit a full effect d/t ceiling effect
91
Buprenorphine is less likely to cause ________ than a full agonist?
Dependency
92
How is buprenorphine used for opioid dependence?
SL tablets
alone=Subutex
combined with naloxone=Suboxone
93
Why is heroin 3x more potent than morphine?
Greater lipid solubility
| metabolized to morphine
94
3-methylfentanyl is also known as ________ .
China white
1000x more potent than morphine
Metabolites can accumulate with chronic use
95
Most common opioid effects:
```
Sedation
Dizziness
N/V
Itching (histamine release)
Sweating
Constipation
```
96
Most serious opioid AE is:
Respiratory depression
| esp. chronic COPD, or pts with decreased resp reserve
97
Patients become tolerate to most AE of opioids except:
Constipation
98
Opioids have no minimum or maximum dosing unless:
combined with APAP or ASA
99
Which type of formulation of opioid should be used in chronic pain?
Sustained release
100
Which type of formulation should be used for breakthrough pain?
```
Immediate release
(10-15% of total daily sustained does can be given as immediate)
```
101
Tramadol is considered a __-_____ .
Non-opioid
102
How does tramadol work?
Block reuptake of NE and 5HT
| Metabolite has 200x greater affinity for Mu receptor and 6x more potent than its parent compound
103
What type of pain is tramadol indicated for?
Moderate to severe
104
T or F: Tramadol is reversed with naloxone.
False, only partially reversed. Drug targets other receptors than just Mu
105
What type of drugs should be avoided when giving tramadol?
MAOIs and antipsychotics (d/t to blocking of NE and 5HT)
106
Tramadol can be combined with:
APAP and ASA
| effectiveness comparable to codeine and propoxyphene combos
107
30mg of immediate release morphine orally is equivalent to how much IV?
10mg
108
When a patient has acquired a tolerance to one opioid what should the next opioid dose be changed to when switching?
10-50% less
109
Naloxone and Naltrexone are what type of drugs?
Pure competitive opioid antagonists
110
_______ and ______ are prodrugs of morphine.
Codeine and Heroin
111
Tolerance to _______ and _______ effects of opioids develop rapidly.
Sedative and emetic
112
Which pure competitive opioid antagonist is available PO and approved for maintaining an opioid free state and alcoholism?
Naltrexone
113
Naloxone is only available in what form?
IV
114
Common uses of naloxone include:
Reversal of opioid overdose
| Reversal of opioid induced anesthesia
115
How is naloxone used for opioid free state maintenance?
Blocks receptors so opioids have no effect if taken
| Patients must be detoxed from opioids for 7-10days or severe withdrawal s/s could occur
116
What type of drug is Nalmephine, what is it used for and how is it different from Naloxone?
Pure opioid antagonist
Post op reversal of opioids or opioid overdoes
Longer half life than naloxone (10hrs vs 30-90mins)
117
The boxed warning for NSAIDs applied to all NSAIDs, except ______ .
ASA
