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Pharm 512 Drugs > Non-Opioid Analgesics Factoids > Flashcards

Non-Opioid Analgesics Factoids Flashcards

1
Q

What are the Types/Classes of Non-Opioid analgesics?

A 
Salicylates
Acetic acid derivatives
Propionic acid derivatives
Cox-2 selective drugs
Non traditional medications
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2
Q

What are the functions of prostaglandins?

A 
Inflammatory responses
Pain signal transduction
Central pyretic effects
Gastric mucosal protection
Platelet aggregation
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3
Q

What is the MOA for NSAIDS?

A

Interfering with prostaglandin production.

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4
Q

What are the general pharmacokinetic profiles of Tylenol, Ibuprofen, Ketorolac, Celebrex, and ASA?

A

Weak acids with pKa < 5
Predominantly protein bound
Most are rapidly absorbed orally
Primary mode of metabolism is CYP 450

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5
Q

Which specific NSAIDS treat what types of pain?

A

Acetaminophen (headaches and toothaches)

Aspirin (back pain, sore muscles and long term to reduce heart attach risk)

Naproxen (arthritis, bursitis, joint pain, tendinitis, menstral cramps)

Ibuprofen (aches, fever, and minor muscle pains)

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6
Q

What are NSAIDS commonly used to treat?

A

Mild to moderate pain, Fever, Thrombosis prevention

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7
Q

T/F NSAIDS can increase the risk of thrombotic events?

A

True

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8
Q

Thromboxane A2 is responsible for…?

A

platelet aggregation, prothrombosis, vasoconstriction

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9
Q

Prostaglandin (PGI2) are responsible for…?

A

antithrombotic and vasodilation

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10
Q

T/F COX-2 affect platelet aggregation?

A

False

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11
Q

What are the effects of NSAIDS on the renal system?

A

Inhibition of prostaglandins will decrease GFR by causing afferent arteriole vasoconstriction

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12
Q

What type of NSAID is Celecoxib and what are the risks and benefits?

A

COX-2 (increased risk for CV events, decreased risk for GI side effects)

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13
Q

What type of NSAIDS are Meloxicam, diclofenac, etodolac, indomethacin, piroxicam, nabumetone, sulindac and what are the risks and benefits?

A

Semiselective NSAIDS (Increased affinity for COX-2 but still retain activity for COX-1, Use with caution in patients with increased CV risk)

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14
Q

What type of NSAID is Ibuprofen and naproxen and what are the risk and benefits?

A

Nonselective NSAIDS (Decrease risk for CV events, Increased risk for GI side effects)

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15
Q

What type of NSAID is Aspirin and what are the risks and benefits?

A

Nonselective NSAID (Cardioprotective at low doses, Increased risk for GI side effects)

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16
Q

What special populations are NSAIDS commonly avoided in?

A

Renal failure (Decreased GFR), Liver Disease (tylenol), and under 19 (ASA- Reyes syndrome)

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17
Q

What class of NSAID is Ketorolac and what is its MOA?

A

Acetic acid derivative, Non selective COX enzyme inhibitor

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18
Q

What drugs efficacy is similar to morphine?

A

Ketorolac

19
Q

What NSAID may cause tubular necrosis?

A

Ketorolac

20
Q

What class of NSAID is Acetaminophen and what is its MOA?

A

Para-aminophenal derivative, MOA not well understood (maybe COX-1 and COX-3)

21
Q

Does acetaminophen act centrally or peripherally?

A

Centrally. (No CV affects and minimal renal effects)

22
Q

How is Acetaminophen metabolized?

A

By the liver and the metabolite is responsible for toxicity

23
Q

Acetaminophen dose should never exceed what in a day?

A

4 g/day

24
Q

What type of NSAID is Ibuprofen and what is the MOA?

A

Propionic Acid derivative, Non-selective COX inhibitor

25
Q

Chronic use of which NSAID has shown increase risk for HTN, Renal disease, MI an Stroke, and GI bleeding?

A

Ibuprofen

26
Q

What type of NSAID is Aspirin and what is the MOA?

A

Salicylate drug. Irreversible non-selective NSAID

27
Q

All NSAIDS are highly protein bound accept?

A

ASA and Tylenol

28
Q

What is the main clinical use of ASA?

A

Anti platelet effects (irreversibly inhibits thromboxane production)

29
Q

What is the MOA of Celebrex (Celecoxib)?

A

COX-2 selective

30
Q

Which NSAID theoretically has no platelet interaction?

A

Celebrex (Celecoxib)

31
Q

Which NSAID should be avoided in patients with a sulfa allergy?

A

Celebrex (Celecoxib)

32
Q

What type of drug is Neurontin and what is the MOA?

A

Gabapentinoid. Chemical analogue of GABA (Binds to pre-synaptic voltage gated sodium channels in the CNS)

33
Q

What are the key points of Non-Opioid analgesics?

A

Inhibit conversion of arachidonic acid to prostaglandins, thromboxane, and prosotocyclins
COX-2 selective do not affect platelet function
GI complications are rarely associated with short term use
Avoid COX-1 and COX-2 in renal failure
NSAIDS can contribute to MI/Stroke, and HTN
Gabapentin used for multimodal pain treatment

34
Q

Why can’t platelets make new proteins?

A

Platelets do not have nuclei

35
Q

How does ASA prevent platelet aggregation?

A

ASA irreversibly binds to the platelet inhibiting the production of thromboxane (stops arachidonic acid from converting to Prostaglandin)

36
Q

What type of renal failure could NSAIDs cause?

A

Pre-renal failure from vasoconstriction of afferent arteriole

37
Q

What are special concerns of NSAID use and kidney function?

A

Intraoperative Oliguria
Volume depletion
Pre-exisiting renal disease

38
Q

When should Ketorolac be avoided post operatively?

A

If the patient is oozing from incision

39
Q

What drug is acetaminophen equipotent to in inhibiting central prostaglandin synthesis?

A

ASA

40
Q

What population has acetaminophen shown to have significant opioid sparing effects?

A

In all populations, but especially in the pediatric population

41
Q

What is the optically active enantiomer in Ibuprofen?

A

S

42
Q

Why isn’t ASA typically used in a greater dose than 81mg?

A

Less often used in greater doses due to inferiority to other NSAIDs

43
Q

What two symptoms are often reported with Neurotin?

A

Dizziness and lethargy

44
Q

What drug is usually used in conjunction with Neurotin for a multi-modal approach to pain management?

A

Acetaminophen

Pharm 512 Drugs (16 decks)

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