Non-opioid (NSAIDs) analgesics Flashcards

1
Q

What are nociceptors?

A

Peripheral sensory neurons detecting temperature, pressure, and injury-related signals.

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2
Q

What is nociceptive pain?

A

Pain originating from nociceptive neurons, such as post-surgical pain, sports injuries, and arthritis.

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2
Q

What is neuropathic pain?

A

Chronic pain resulting from neuronal damage or dysfunction, such as diabetic neuropathy and chemotherapy-induced neuropathy.

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3
Q

What causes neuropathic pain?

A

Disrupted inhibitory pathways leading to pain without a direct stimulus.

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4
Q

What is allodynia?

A

Pain response to normally non-painful stimuli.

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5
Q

What is hyperalgesia?

A

Increased sensitivity to pain.

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6
Q

What is the treatment for mild to moderate acute nociceptive pain?

A

Nonsteroidal anti-inflammatory drugs or acetaminophen.

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7
Q

What is the treatment for moderate acute nociceptive pain?

A

Nonsteroidal anti-inflammatory drugs.

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8
Q

What are non-pharmacologic treatments for chronic nociceptive pain?

A

Exercise, massage, movement therapy, and heat.

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8
Q

What is the treatment for moderate to severe acute nociceptive pain?

A

Nonsteroidal anti-inflammatory drugs plus acetaminophen or opioids plus acetaminophen.

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8
Q

What are pharmacologic treatments for chronic nociceptive pain?

A

Nonsteroidal anti-inflammatory drugs or localized treatments like lidocaine, diclofenac, and capsaicin.

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9
Q

What are first-line medications for neuropathic pain?

A

Tricyclic antidepressants: Amitriptyline, nortriptyline, imipramine.
Serotonin-norepinephrine reuptake inhibitors: Venlafaxine, duloxetine, milnacipran.
Antiepileptics: Gabapentin, pregabalin, carbamazepine, oxcarbazepine.

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10
Q

What is used for localized neuropathic pain?

A

Topical lidocaine or capsaicin.

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11
Q

What are key NSAIDs used in dentistry?

A

Aspirin (salicylate), ibuprofen, naproxen, diclofenac.

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12
Q

Is acetaminophen an NSAID?

A

No, but it is commonly used for pain relief.

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13
Q

What is the mechanism of NSAIDs?

A

Inhibition of cyclooxygenase (COX) enzymes, reducing prostaglandin synthesis.

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14
Q

What are the functions of NSAIDs?

A

Analgesic, anti-inflammatory, antipyretic, antiplatelet.

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15
Q

What is the role of cyclooxygenase (COX) enzymes?

A

Convert arachidonic acid into prostaglandin H2 (PGH2), a precursor to prostaglandins and thromboxane.

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16
Q

What do prostaglandins and thromboxane regulate?

A

Inflammation, pain, fever, and clotting.

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17
Q

Where is COX-1 found?

A

Platelets, stomach lining, kidneys.

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18
Q

What does COX-1 produce?

A
  • Thromboxane A2 (TXA2), which promotes platelet activation and clotting.
  • Prostaglandin E2 (PGE2), which helps secrete protective mucus in the stomach and intestines.
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19
Q

What are the effects of COX-1 inhibition?

A

Reduced clotting (antiplatelet) but increased risk of stomach ulcers and bleeding.

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20
Q

Where is COX-2 found?

A

Inflamed tissues and kidneys.

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21
Q

What does COX-2 produce?

A

Pro-inflammatory prostaglandins that enhance the immune response.

22
What are the effects of COX-2 inhibition?
Anti-inflammatory effects but increased risk of kidney damage due to reduced blood flow in renal glomeruli.
23
What are the effects of aspirin?
Antiplatelet (10-14 days), analgesic, antipyretic, anti-inflammatory.
23
What makes aspirin's mechanism unique?
Irreversibly inhibits COX enzymes, permanently deactivating them.
24
What are the common uses of aspirin?
Analgesic for relief of mild to moderate pain (std. adult dose: 325mg, 1-2 tablets every 4 hours), can combine with opioid analgesics for moderate pain. Antipyretic: 325mg, 1-2 tablets every 4 hours. Anti-inflammatory in patients with rheumatoid arthritis, rheumatic fever, and inflammatory joint conditions (high dose, 3g/day). Prophylaxis of ischemic heart disease and ischemic stroke, to reduce incidence of coronary artery disease (typically low dose 81 mg daily)
25
How does naproxen compare to ibuprofen?
Similar but has a longer half-life (13 hours).
25
What are the major adverse effects of aspirin?
Gastrointestinal: Peptic ulcers, GI bleeding. Respiratory: Aspirin-exacerbated respiratory disease. Renal: Nephrotoxicity. Reye's Syndrome: Avoid in children with viral infections. Overdose: Salicylism (nausea, vomiting, tinnitus, confusion).
26
What are the adverse effects of ibuprofen?
GI bleeding (lower risk than aspirin), edema, nephrotoxicity.
26
What is the mechanism of ibuprofen?
Competitive, reversible COX inhibitor.
27
How does ibuprofen compare to aspirin?
More effective as an analgesic with reversible antiplatelet effects.
28
What is the maximum daily dose of ibuprofen?
3200 mg/day.
29
What is the maximum daily dose of naproxen?
1375 mg/day (prescription) or 660 mg/day (OTC).
30
How does diclofenac compare to ibuprofen?
More potent.
31
What are the common forms of diclofenac?
Oral (stronger than ibuprofen) and topical (Voltaren) for osteoarthritis.
32
What is the half-life of diclofenac?
~2 hours.
33
How selective is celecoxib for COX-2 compared to COX-1?
9 times more selective for COX-2.
34
What are the advantages of celecoxib?
Less GI irritation due to reduced COX-1 inhibition.
35
What are the risks of celecoxib?
Increased cardiovascular risks (heart attack, stroke).
36
How do NSAIDs affect antihypertensive medications?
Reduce antihypertensive efficacy by increasing water and sodium retention.
37
Why should NSAIDs not be combined with anticoagulants?
Increased bleeding risk due to platelet inhibition and GI ulceration.
38
What should be considered for chronic NSAID use in hypertensive patients?
Switching to a calcium channel blocker.
39
If a patient is allergic to aspirin, which medications should they avoid?
All NSAIDs except acetaminophen.
40
What populations have a higher renal risk with NSAIDs?
Elderly, heart failure patients, those on ACE inhibitors.
41
Why should aspirin be avoided in pregnancy?
It increases bleeding risks and complications.
42
Why should NSAIDs be avoided in the third trimester?
They can cause premature closure of the ductus arteriosus and increase preeclampsia risk.
43
How do non-aspirin NSAIDs affect cardiovascular health?
They increase the risk of heart attack and stroke.
44
How does acetaminophen work?
Inhibits COX at a distinct site, reducing fever and pain but not inflammation.
45
What are the advantages of acetaminophen over NSAIDs?
No significant gastrointestinal toxicity, no effect on platelets, and safe in pregnancy.
46
How does an acetaminophen overdose cause toxicity?
Saturates glucuronidation/sulfation pathways, leading to hepatotoxicity.
47
What is the leading cause of liver failure related to acetaminophen?
Combining acetaminophen with other medications containing it (opioids, cold remedies).
48
How is acetaminophen normally metabolized?
Via glucuronidation and sulfation.
49
What happens when acetaminophen is taken in excess?
It overwhelms normal pathways, shifting metabolism to CYP2E1, producing toxic NAPQI.
50
What does NAPQI do?
Depletes glutathione, leading to liver cell death.
51
What are symptoms of acetaminophen toxicity?
Nausea, vomiting, jaundice, liver failure.
52
What is the antidote for acetaminophen toxicity?
N-acetylcysteine (replenishes glutathione).
53
What are common over-the-counter doses of acetaminophen?
325-500 mg tablets (Tylenol, Datril).