Musculoskeletal System Pharmacology (NSAIDs, RA) πŸ’Š Flashcards

1
Q

What are examples of NSAIDs?

A

Aspirin, ibuprofen, naproxen, diclofenac, celecoxib, etoricoxib

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2
Q

How do NSAIDs help to reduce inflammation?

A

They inhibit COX-1 or COX-2 enzymes which convert arachidonic acid into prostanoids

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3
Q

Which two of the NSAIDs are the most selective for COX-2?

A

Celecoxib, etoricoxib

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4
Q

What are the gastrointestinal adverse effects associated with NSAIDs?

A

Dyspepsia, nausea, peptic ulceration, bleeding and perforation, exacerbation of IBD

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5
Q

Why are NSAIDs contraindicated in CKD and heart failure?

A

There is a greater reliance on prostaglandins for vasodilation of afferent arteriole and renal perfusion

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6
Q

Why do COX-2 selective NSAIDs have a higher CVD risk compared to COX-1 selective?

A

COX-2 inhibits the synthesis of PGI2 which is generally protective for the CVS, doesn’t inhibit TXA2 which is generally bad for CVS

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7
Q

What is NSAID protein binding like?

A

Highly protein bound

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8
Q

What is the name and function of the enzyme methotrexate inhibits?

A

Dihydrofolate reductase: essential for synthesis of purines and pyrimidines

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9
Q

How often is the dosing for methotrexate?

A

Taken weekly

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10
Q

What feature of methotrexate should be considered when prescribing to females of reproductive age?

A

Highly teratogenic and abortifacient

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11
Q

What are ADRs associated with sulfasalazine?

A

Myelosupression, hepatitis, rash, N+V

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12
Q

Is sulfasalazine safe to use in pregnancy?

A

Yes, it is safe to use in pregnancy

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13
Q

What type of drug is rituximab?

A

A monoclonal antibody that depletes B-lymphocytes

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14
Q

Reactivation of what infection is a risk with TNF inhibitor drugs?

A

Tuberculosis reactivation

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15
Q

What are two examples of TNF inhibitors?

A

Infliximab, adalimumab

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16
Q

How does hydroxychloroquine work?

A

Increases the pH inside macrophage lysosomes

17
Q

What are two examples of anticholinesterases?

A

Neostigmine and pyridostigmine

18
Q

What can be a consequence of over treatment with an acetylcholinesterase inhibitor?

A

Cholinergic crisis