NSAIDs - General Flashcards
What is the father of steroidal anti-inflammatory drugs (SAIDs)?
Prednisone
How are NSAIDs classified?
Most are characterized by a specific family denoted by the drugs’ chemical structure.
What is most commonly true when comparing the potency of one NSAID to another?
No one NSAID is more potent than another.
What chemical is the precursor to inflammatory mediators discussed in this section and what pathway leads to each inflammatory mediator?
Arachadonic Acid (AA)
AA –> COX-1 and CPX-2 –> Prostaglandins
AA –> LO enzyme –> Leukotrienes and Bradykinin
What is the mechanism of action of NSAIDs?
Blocks COX-1 and COX-2 pathways inhibiting production of prostaglandins.
What is the mechanism of action of leukotriene receptor antagonists?
Prevent inflammation by preventing leukotrienes from binding to their receptors.
What is the mechanism of action of steroids with regard to inhibiting inflammation?
Inhibit formation of arachadonic acid thereby inhibiting production of prostaglandins and leukotrienes.
Describe the pathophysiology of an “allergy” to NSAIDs.
Some people make excess leukotrienes and bradykinin in response to NSAIDs. Overproduction of bradykinin induces angioedema.
What two medications most commonly induce angioedema?
NSAIDs and ACEIs
What do all proponic acid NSAIDs have in their name and list some examples?
“pro” –> Femoprofen, flurbiprofen, ibuprofen
List 5 indications for the administration of NSAIDs.
Arthritic diseases (osteo, rheumatoid, etc.), gouty arthritis, headache, pain, chemotherapy (maybe)
What are the “three As” of NSAIDs’ mechanism of action?
Anti-inflammatory
Antipyretic
Analgesic
T/F Excessive NSAID use can cause hypothermia.
F - NSAIDs never reduce temperature below normal
What is the primary inflammatory mediator associated with pain?
Prostaglandins.
What is true about the ability of different NSAIDs to inhibit COX-1 and COX-2 activity?
Different NSAIDs will inhibit COX-1 and COX-2 in differing grades.
What is the effect of a small dose (40mg) of aspirin?
Irreversibly inhibit the COX enzyme of a platelet for the life of the platelet –> leads to anticoagulation.
As opposed to aspirin, what is true about the anticoagulation properties of all other NSAIDs?
They are reversible platelet inhibitors.
Where are COX-1 and COX-2 enzymes primarily found?
COX-1 in the gut
COX-2 in the periphery
Which COX enzyme is more commonly inhibited by NSAIDs and what is the clinical implication?
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.
What is the benefit of blocking leukotriene receptors with a leukotriene antagoist?
Leukotrienes mediate allergic and inflammatory reactions with a lot of pulmonary effects.
List two leukotriene receptor antagonists used as PO medications in the management of asthma.
Montelukast and Zafirlukast
List 7 cautions in the administration of NSAIDs?
Renal disease, CHF, Masked febrile reactions, highly plasma protein bound, avoid alcohol, asthma, monitor guaiac stools (occult fecal blood test)
Describe how NSAIDs affect the renal system.
PGs maintain patency of the afferent arteriole. NSAIDs constrict the afferent arteriole and reduce GFR –> causes an increase in serum creatinine.
What are the three most common causes of fever?
Infection, cancer, pregnancy
Why is masking a fever with NSAIDs problematic?
We must find the reason they are febrile and treat it rather than simply masking the symptoms.
Describe how NSAIDs affect patients that consume alcohol.
Alcohol is acidic and a gastric irritant, worsening the GI effects of NSAIDs
Describe how NSAIDs affect asthmatics.
Asthmatics produce more leukotrienes which makes them more likely to be allergic to NSAIDs.
What is the effect of NSAIDs being highly plasma protein bound?
NSAIDs will interact with other highly plasma protein bound drugs, such as warfarin.
