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Pharmacology > Non-opioid and Opioid Analgesics > Flashcards

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

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2
Q

What are the subclasses of NSAIDs?

A

Non-acetylated salicylates
Acetylated salicylates (ASA)
Selective COX-2 inhibitor (Celecoxib)
Traditional NSAIDs

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3
Q

Traditional NSAIDs include:

A 
Ibuprofen 
Naproxen
Oxaprozin
Diclofenac
Etodolac
Indomethacin 
Ketorolac 
Nabumetone 
Sulindac 
Tolmetin 
Proxicam
Meloxicam
Flurbiprofen
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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

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5
Q

Does tolerance develop to Non-Opioid Analgesics?

A

No

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6
Q

APAP has a similar efficacy and potency as _______ .

A

ASA

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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)

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8
Q

Why may inadvertent overdoses of APA occur? (2)

A
  1. Patients may be taking multiple products with APAP in them
  2. Wrong dose of highly concentrated product (ex-infant drops)
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9
Q

Maximum safe dose of APAP in children >12yrs is:

A

4grams/day

OTC= 3grams unless directed by MD/NP

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10
Q

Non-opioid analgesics are the first line for what type of pain?

A

Mild to moderate

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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)

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12
Q

What AE does ASA cause (like other NSAIDs)?

A

GI bleeding

PUD

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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

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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)

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15
Q

When using ASA as an anti-inflammatory how much a patient be dosed/monitored?

A

Increase dose gradually

Assess serum salicylate levels

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16
Q

How is ASA cleared?

A

Hepatic clearance

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17
Q

S/s of ASA overdose:

A

Metabolic acidosis

Tinnitus

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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

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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

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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

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21
Q

Different NSAIDs have _______ efficacy at _______ doses.

A

Similar

Equipotent

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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

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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

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24
Q

What are NSAIDs effect on platelets?

A

Reversible inhibition of COX which blocks synthesis of thromboxane A2 inhibiting platelet aggregation

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25
Q

What are s/s of salicylate build up?

A

Tinnitis

Hearing loss

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26
Q

NSAIDs are considered what Category in the third trimester and why?

A

Category D
premature closure of ductus arteriousus

(Category B in 1st and 2nd trimester)

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27
Q

GI AE of NSAIDs include:

A

Dyspepsia
GI bleeding
PUD

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28
Q

How do NSAIDs cause GI upset?

A

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

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29
Q

Risk factors for GI AE of NSAIDs include:

A 
High doses 
Prolonged use 
Hx of GI ulcer or bleeding 
Excessive ETOH intake 
Elderly 
Corticosteroid use (may also cause PUD)
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30
Q

How can the GI effects of NSAIDs be prevented?

A
  • PG analog- misoprostil (replenish the PGs that are reduced) or Diclofenac/misoprostol
  • PPI
  • H2 receptor antagonists
  • Sucralfate (s/s management)
  • Take with food
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31
Q

What are the highest risk NSAIDs and why?

A 
Tolmetin
Piroxicam
ASA
Indomethacin
Ketorolac

More COX1 inhibition increases risk

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32
Q

What are the low risk NSAIDs and why?

A

Ibuprofen and Naproxen at low doses
Etodolac, sulindac
Celcoxib

More COX2 inhibition over COX1

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33
Q

In addition to GI AE what other AE do NSAIDs cause and how?

A

Renal AE

Decreased synthesis of renal vasodilator PGE (PGE2) leads to decreased RBF, Na and H2O retention, renal failure, HTN, interstitial nephritis

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34
Q

What are risk factors for renal AE of NSAIDs?

A 
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

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35
Q

Which NSAIDs are considered ‘renal sparing’

A

Sulindac
Nabumetone
Celecoxib

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36
Q

What drug increases levels of most NSAIDs?

A

Probenicid

Not always clinically significant because NSAIDs have wide TI
*Avoid with ketorolac

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37
Q

How do NSAIDs causes many DI?

A

-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)

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38
Q

What is the effect of NSAIDs on lithium?

A

Increases levels

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39
Q

Which NSAIDs are less likely to interact with warfarin?

A

Ibuprofen
Diclofenac
Tolmetin
Naproxen

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40
Q

What is the only NSAID given IV/IM and how long can it be used for?

A

Ketorolac

No more than 5 days of use

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41
Q

What are the serious risk associated with Ketorolac?

A 
GI bleeding 
Ulceration
Perforation
Renal toxicity 
(increased risk in elderly)
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42
Q

What is the only selective COX2 inhibitor NSAID on the market today and why were the others withdrawn?

A

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)

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43
Q

What is the potential benefit to using a COX2 inhibitor?

A

Less GI effects

COX 1 in responsible for gastric production and is not inhibited

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44
Q

What AE is not avoided by using a COX2 inhibitor?

A

Renal AE

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45
Q

Celecoxib should be used at the lowest effective dose, this dose should not exceed:

A

200mg/day

equivalent to 500mg BID of naproxen

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46
Q

What should be considered when prescribing a patient Celecoxib

A

Risk for CV events

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47
Q

What is the Black Box warning for all NSAID related to CV risk?

A

Increased risk of serious CV thrombotic events, MI, stroke

CI for tx of peri-operative pain in setting of CABG

48
Q

What is the Black Box warning for all NSAID related to GI risk?

A

Increased risk of bleeding, ulceration, perforation of the stomach or intestines

49
Q

What desirable effects does PG suppression create?

A

Antipyretic
Analgesic
Anti-inflamm

50
Q

What drugs mainly act as agonist on Mu receptors (some kappa and sigma)?

A

Morphine
Heroin
Codeine
Fentanyl

51
Q

What drug is an agonist at kappa receptors and a partial antagonist at the Mu receptor?

A

Pentazocine

52
Q

Which drugs act as an antagonist at the Mu, kappa, and sigma receptors?

A

Naloxone

Naltrexone

53
Q

Opioids are prescribed for what type of pain?

A

Moderate to severe

54
Q

Which type of opioids have a ceiling effect?

A 
Partial agonist 
(full agonists have no max dose)
55
Q

How are opioids metabolized?

A

Hepatically

inactive or active metabolites are renally excreted

56
Q

Tolerance means:

A

Decreased effect of drug that develops with continued use

57
Q

______ tolerance can occur with opioids?

A

Cross

58
Q

Full agonist opioids that are most effective include:

A 
Morphine 
Oxycodone 
Hydromorphone
Methadone 
Meperidine 
Fentanyl 
Oxymorphone
59
Q

Full agonist opioids that are considered to have more mild effects include:

A

Codeine
Hydrocodone
Propoxyphene

60
Q

What is the difference between an opiate and an opioid?

A

An opiate is a naturally occurring drug, like morphine or codeine, and an opioid is a drug that acts like an opiate (synthetic).

61
Q

Partial agonists, mixed agonist-antagonists include:

A

Pentazocine
Butorphanol
Nalbuphine
Buprenorphine

62
Q

Why is morphine not as effective orally?

A

First pass metabolism

63
Q

Morphine’s two main active metabolites are:

A

Morphine 6-glucuronide

Morphine 3-glucoronide

64
Q

SE causes by a build of morphine’s active metabolites include?

A

Nausea
Myoclonus
Hallucinations

65
Q

What off target effect can morphine cause and what does it result in?

A

Histamine release

Pruritis

66
Q

Morphine’s routes of administration include:

A

PO, IM, IV, SubQ, rectal, epidural, intrathecal

67
Q

Codeine is what type of drug?

A

Prodrug

Only about 10% is metabolized by CYP2D6 to its active form

68
Q

What is codeine’s active form?

A

Morphine

69
Q

Without conversion to morphine what is codeine’s effect?

A

Antitussive

70
Q

10% of Caucasians and 30% of Asians lack ______ prevent codeine from having any analgesia effect.

A

2D6

71
Q

Hydrocodone’s route of administration:

A

PO

72
Q

Hydrocodone is always combined with what four drugs:

A

APAP
ASA
Ibuprofen
Antihistamine

73
Q

Which two opioids are used as cough suppressants?

A

Codeine

Hydrocodone

74
Q

Oxycodone is available in combination with what two drugs?

A

APAP

ASA

75
Q

Why is oxycodone often the drug of choice in patients with renal dysfunction?

A

No active metabolites

76
Q

Hydromorphone:

A

Available PO, IM, IV, SubQ, rectal, epidural
Semi-synthetic
No major metabolites (safer in patients with renal dysfxn)

77
Q

How is methadone doses differently when given to treat addiction vs neuropathic pain management?

A

Addiction: once daily

Pain management: BID or TID

78
Q

What type of opioid is methadone?

A

Synthetic

79
Q

Why is methadone used for opioid addiction?

A

Longer half-life elimination

80
Q

Morphine has no ______ _______, so is safer in patients with renal dysfunction.

A

active metabolites

81
Q

How is meperidine usually used?

A

Post-op shakes/chills, caused by anesthetic agents, epidurals, and spinal anesthesia
(short term, 24-48hrs)

82
Q

What is meperidine’s main metabolite and the AEs associated with it?

A

Normeperidine (long half-life, 15-20hrs)
Accumulation can cause CNS excitation/anxiety and convulsions
Caution in elderly and pts with renal dysfunction

83
Q

Why was propoxyphene removed from the market in 2010?

A

Cardiac toxicity

84
Q

Propoxyphene: Route, combined with, metabolized to

A

PO
Combined with APAP
Metabolized to norpropoxyphene, long half life (30-36hrs) can causes stupor, coma, convulsions

85
Q

How much more potent than morphine is fentanyl?

A

80-100x

86
Q

When would a transdermal fentanyl patch be used?

A

Chronic pain

Only after titration with short-acting opioid

87
Q

Which type of administration route is used for fentanyl for breakthrough pain?

A

Transmucosal lozenge

35-50% bioavailability

88
Q

Buprenoprhine is a ____ _____ .

A

partial agonist

89
Q

Route of administration of buprenorphine include:

A

SL (dependence), parenteral (pain)

90
Q

If buprenorphine is given while a patient is taking a full agonist what may occur?

A

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
Q

Buprenorphine is less likely to cause ________ than a full agonist?

A

Dependency

92
Q

How is buprenorphine used for opioid dependence?

A

SL tablets
alone=Subutex
combined with naloxone=Suboxone

93
Q

Why is heroin 3x more potent than morphine?

A

Greater lipid solubility

metabolized to morphine

94
Q

3-methylfentanyl is also known as ________ .

A

China white
1000x more potent than morphine
Metabolites can accumulate with chronic use

95
Q

Most common opioid effects:

A 
Sedation 
Dizziness
N/V
Itching (histamine release)
Sweating 
Constipation
96
Q

Most serious opioid AE is:

A

Respiratory depression

esp. chronic COPD, or pts with decreased resp reserve

97
Q

Patients become tolerate to most AE of opioids except:

A

Constipation

98
Q

Opioids have no minimum or maximum dosing unless:

A

combined with APAP or ASA

99
Q

Which type of formulation of opioid should be used in chronic pain?

A

Sustained release

100
Q

Which type of formulation should be used for breakthrough pain?

A 
Immediate release
(10-15% of total daily sustained does can be given as immediate)
101
Q

Tramadol is considered a __-_____ .

A

Non-opioid

102
Q

How does tramadol work?

A

Block reuptake of NE and 5HT

Metabolite has 200x greater affinity for Mu receptor and 6x more potent than its parent compound

103
Q

What type of pain is tramadol indicated for?

A

Moderate to severe

104
Q

T or F: Tramadol is reversed with naloxone.

A

False, only partially reversed. Drug targets other receptors than just Mu

105
Q

What type of drugs should be avoided when giving tramadol?

A

MAOIs and antipsychotics (d/t to blocking of NE and 5HT)

106
Q

Tramadol can be combined with:

A

APAP and ASA

effectiveness comparable to codeine and propoxyphene combos

107
Q

30mg of immediate release morphine orally is equivalent to how much IV?

A

10mg

108
Q

When a patient has acquired a tolerance to one opioid what should the next opioid dose be changed to when switching?

A

10-50% less

109
Q

Naloxone and Naltrexone are what type of drugs?

A

Pure competitive opioid antagonists

110
Q

_______ and ______ are prodrugs of morphine.

A

Codeine and Heroin

111
Q

Tolerance to _______ and _______ effects of opioids develop rapidly.

A

Sedative and emetic

112
Q

Which pure competitive opioid antagonist is available PO and approved for maintaining an opioid free state and alcoholism?

A

Naltrexone

113
Q

Naloxone is only available in what form?

A

IV

114
Q

Common uses of naloxone include:

A

Reversal of opioid overdose

Reversal of opioid induced anesthesia

115
Q

How is naloxone used for opioid free state maintenance?

A

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
Q

What type of drug is Nalmephine, what is it used for and how is it different from Naloxone?

A

Pure opioid antagonist
Post op reversal of opioids or opioid overdoes
Longer half life than naloxone (10hrs vs 30-90mins)

117
Q

The boxed warning for NSAIDs applied to all NSAIDs, except ______ .

A

ASA

Pharmacology (48 decks)

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