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FA - Musculoskeletal > MS - Pharm (Part 2: Biphosphonates, Gout drugs, & TNF-alpha inhibitors) > Flashcards

MS - Pharm (Part 2: Biphosphonates, Gout drugs, & TNF-alpha inhibitors) Flashcards

Pg. 440-441 in First Aid 2014 Sections include: -Biphosphonates -Gout drugs -TNF-alpha inhibitors

1
Q

What is an example of Bisphosphonates? In what suffix do they usually end?

A

Alendronate, other -dronates

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2
Q

What are the mechanism and effects of Bisphosphonates?

A

Pyrophosphate analogs; Bind hydroxyapatite in bone, inhibiting osteoclast activity

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3
Q

What are 3 clinical uses for Bisphosphonates?

A

(1) Osteoporosis (2) Hypercalcemia (3) Paget disease of bone

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4
Q

What are 2 toxicities of Bisphosphonates?

A

Corrosive esophagitis (patients are advised to take with water and remain upright for 30 minutes), Osteonecrosis of the jaw

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5
Q

What musculoskeletal drug is known for its corrosive esophagitis toxicity? How is this managed/prevented clinically?

A

Biphosphonates; Corrosive esophagitis (patients are advised to take with water and remain upright for 30 minutes)

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6
Q

What are 3 chronic (preventive) gout drugs?

A

(1) Allopurinol (2) Febuxostat (3) Probenecid

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7
Q

What are the mechanism and effect of Allopurinol?

A

Inhibits xanthine oxidase, decreasing conversion of xanthine to uric acid

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8
Q

Besides gout, in what other clinical conditions is Allopurinol used, and why?

A

Also used in lymphoma and leukemia to prevent tumor lysis-associated urate nephropathy

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9
Q

What 2 drug concentrations does Allopurinol affect, and how/why?

A

Increase concentrations of azathioprine and 6-MP (both normally metabolized by xanthine oxidase).

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10
Q

What type of drugs should not be given with Allopurinol, and why?

A

Do not give salicylates; All but the highest doses depress uric acid clearance. Even high doses (5-6 g/day) have only minor uriocosuric activity.

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11
Q

What is the mechanism of Febuxostat? What other drug shares this mechanism?

A

Inhibits xanthine oxidase; Allopurinol

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12
Q

What are the mechanisms of Probenecid?

A

Inhibits reabsorption of uric acid in PCT (also inhibits secretion of penicillin).

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13
Q

What are 3 types of acute gout drugs?

A

(1) NSAIDs (2) Glucocorticoids (3) Colchicine

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14
Q

What are 2 examples of NSAIDs used as acute gout drugs?

A

(1) Naproxen (2) Indomethacin

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15
Q

What are 2 administration routes for glucocorticoids used as acute gout drugs?

A

(1) Oral or (2) Intraarticular

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16
Q

What are the mechanism and effects of Colchicine?

A

Binds and stabilizes tubulin to inhibit microtubule polymerization, impairing leukocyte chemotaxis and degranulation.

17
Q

Is Colchicine valuable as an acute or prophylactic intervention for gout?

A

Acute and prophylactic value

18
Q

What kind of side effects are associated with Colchicine use?

A

GI side effects

19
Q

Draw a diagram showing the major steps in the progression from Purines entering the body to being excreted in the urine. Include and label the steps at which each of the following drugs act: (1) Allopurinol, Febuxostat (2) Diuretics and low-dose salicylates (3) Probenecid and high-dose salicylates.

A

See p. 441 in First Aid 2014 for visual at top right of page

20
Q

What are 2 sources of Purines in the body?

A

(1) Diet (2) Nucleic acids

21
Q

What are the major steps taken by Purines to become plasma uric acid? What roles do Xanthine oxidase play in this context?

A

Purines => Hypoxanthine => Xanthine => Plasma uric acid; Xanthine oxidase catalyzes formation of Xanthine AND Plasma uric acid

22
Q

What INHIBITS tubular absorption versus secretion of uric acid?

A

INHIBITORS OF TUBULAR ABSORPTION: Probenecid and high-dose salicylates; INHIBITORS OF TUBULAR SECRETION: Diuretics and low-dose salicylates

23
Q

To what general condition do all TNF-alpha inhibitors predispose, and why? Give a particular example of this.

A

All TNF-alpha inhibitors predispose to infection, including reactivation of latent TB, since TNF blockade prevents activation of macrophages and destruction of phagocytosed microbes

24
Q

What are 3 examples of TNF-alpha inhibitors?

A

Etanercept, Infliximab, Adalimumab

25
Q

What is the mechanism of Etanercept? How is it made?

A

Fusion protein (receptor for TNF-alpha + IgG1 Fc), produced by recombinant DNA; Think: “etanerCEPT is a TNF decoy reCEPTor”

26
Q

What is the mechanism of Infliximab? What other drug shares this mechanism?

A

Anti-TNF-alpha monoclonal antibody; Adalimumab

27
Q

What are 3 clinical uses for Etanercept?

A

(1) Rheumatoid arthritis (2) Psoriasis (3) Ankylosing spondylitis

28
Q

What are 4 clinical uses for Infliximab, Adalimumab?

A

(1) IBD (2) Rheumatoid arthritis (3) Ankylosing spondylitis (4) Psoriasis

FA - Musculoskeletal (19 decks)

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