NSAIDs - General Flashcards

1
Q

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

A

Prednisone

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2
Q

How are NSAIDs classified?

A

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

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3
Q

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

A

No one NSAID is more potent than another.

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4
Q

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

A

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

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5
Q

What is the mechanism of action of NSAIDs?

A

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

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6
Q

What is the mechanism of action of leukotriene receptor antagonists?

A

Prevent inflammation by preventing leukotrienes from binding to their receptors.

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7
Q

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

A

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

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8
Q

Describe the pathophysiology of an “allergy” to NSAIDs.

A

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

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9
Q

What two medications most commonly induce angioedema?

A

NSAIDs and ACEIs

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10
Q

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

A

“pro” –> Femoprofen, flurbiprofen, ibuprofen

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11
Q

List 5 indications for the administration of NSAIDs.

A

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

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12
Q

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

A

Anti-inflammatory
Antipyretic
Analgesic

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13
Q

T/F Excessive NSAID use can cause hypothermia.

A

F - NSAIDs never reduce temperature below normal

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14
Q

What is the primary inflammatory mediator associated with pain?

A

Prostaglandins.

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15
Q

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

A

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

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16
Q

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

A

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

17
Q

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

A

They are reversible platelet inhibitors.

18
Q

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

A

COX-1 in the gut

COX-2 in the periphery

19
Q

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

A

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.

20
Q

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

A

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

21
Q

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

A

Montelukast and Zafirlukast

22
Q

List 7 cautions in the administration of NSAIDs?

A

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

23
Q

Describe how NSAIDs affect the renal system.

A

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

24
Q

What are the three most common causes of fever?

A

Infection, cancer, pregnancy

25
Q

Why is masking a fever with NSAIDs problematic?

A

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

26
Q

Describe how NSAIDs affect patients that consume alcohol.

A

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

27
Q

Describe how NSAIDs affect asthmatics.

A

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

28
Q

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

A

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