NSAIDs - General

Question 1

What is the father of steroidal anti-inflammatory drugs (SAIDs)?

Answer 1

Prednisone

Question 2

How are NSAIDs classified?

Answer 2

Most are characterized by a specific family denoted by the drugs’ chemical structure.

Question 3

What is most commonly true when comparing the potency of one NSAID to another?

Answer 3

No one NSAID is more potent than another.

Question 4

What chemical is the precursor to inflammatory mediators discussed in this section and what pathway leads to each inflammatory mediator?

Answer 4

Arachadonic Acid (AA)
AA –> COX-1 and CPX-2 –> Prostaglandins
AA –> LO enzyme –> Leukotrienes and Bradykinin

Question 5

What is the mechanism of action of NSAIDs?

Answer 5

Blocks COX-1 and COX-2 pathways inhibiting production of prostaglandins.

Question 6

What is the mechanism of action of leukotriene receptor antagonists?

Answer 6

Prevent inflammation by preventing leukotrienes from binding to their receptors.

Question 7

What is the mechanism of action of steroids with regard to inhibiting inflammation?

Answer 7

Inhibit formation of arachadonic acid thereby inhibiting production of prostaglandins and leukotrienes.

Question 8

Describe the pathophysiology of an “allergy” to NSAIDs.

Answer 8

Some people make excess leukotrienes and bradykinin in response to NSAIDs. Overproduction of bradykinin induces angioedema.

Question 9

What two medications most commonly induce angioedema?

Answer 9

NSAIDs and ACEIs

Question 10

What do all proponic acid NSAIDs have in their name and list some examples?

Answer 10

“pro” –> Femoprofen, flurbiprofen, ibuprofen

Question 11

List 5 indications for the administration of NSAIDs.

Answer 11

Arthritic diseases (osteo, rheumatoid, etc.), gouty arthritis, headache, pain, chemotherapy (maybe)

Question 12

What are the “three As” of NSAIDs’ mechanism of action?

Answer 12

Anti-inflammatory
Antipyretic
Analgesic

Question 13

T/F Excessive NSAID use can cause hypothermia.

Answer 13

F - NSAIDs never reduce temperature below normal

Question 14

What is the primary inflammatory mediator associated with pain?

Answer 14

Prostaglandins.

Question 15

What is true about the ability of different NSAIDs to inhibit COX-1 and COX-2 activity?

Answer 15

Different NSAIDs will inhibit COX-1 and COX-2 in differing grades.

Question 16

What is the effect of a small dose (40mg) of aspirin?

Answer 16

Irreversibly inhibit the COX enzyme of a platelet for the life of the platelet –> leads to anticoagulation.

Question 17

As opposed to aspirin, what is true about the anticoagulation properties of all other NSAIDs?

Answer 17

They are reversible platelet inhibitors.

Question 18

Where are COX-1 and COX-2 enzymes primarily found?

Answer 18

COX-1 in the gut

COX-2 in the periphery

Question 19

Which COX enzyme is more commonly inhibited by NSAIDs and what is the clinical implication?

Answer 19

Most NSAIDs cannot differentiate between inhibition of COX-1 and COX-2. Inhibition of COX-1 reduces mucus production in the gut and increases the risk of peptic ulcers.

Question 20

What is the benefit of blocking leukotriene receptors with a leukotriene antagoist?

Answer 20

Leukotrienes mediate allergic and inflammatory reactions with a lot of pulmonary effects.

Question 21

List two leukotriene receptor antagonists used as PO medications in the management of asthma.

Answer 21

Montelukast and Zafirlukast

Question 22

List 7 cautions in the administration of NSAIDs?

Answer 22

Renal disease, CHF, Masked febrile reactions, highly plasma protein bound, avoid alcohol, asthma, monitor guaiac stools (occult fecal blood test)

Question 23

Describe how NSAIDs affect the renal system.

Answer 23

PGs maintain patency of the afferent arteriole. NSAIDs constrict the afferent arteriole and reduce GFR –> causes an increase in serum creatinine.

Question 24

What are the three most common causes of fever?

Answer 24

Infection, cancer, pregnancy

Question 25

Why is masking a fever with NSAIDs problematic?

Answer 25

We must find the reason they are febrile and treat it rather than simply masking the symptoms.

Question 26

Describe how NSAIDs affect patients that consume alcohol.

Answer 26

Alcohol is acidic and a gastric irritant, worsening the GI effects of NSAIDs

Question 27

Describe how NSAIDs affect asthmatics.

Answer 27

Asthmatics produce more leukotrienes which makes them more likely to be allergic to NSAIDs.

Question 28

What is the effect of NSAIDs being highly plasma protein bound?

Answer 28

NSAIDs will interact with other highly plasma protein bound drugs, such as warfarin.