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Flashcards in MSK/CT - Pharm Deck (40)
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1
Q

Acetominophen MOA

A

REVERSIBLY inhibits COX, mostly in CNS

Inactivated peripherally

2
Q

Acetominophen use

A

Antipyretic and analgesic, but NOT anti-inflammatory

use in kids with viral illnesses

3
Q

Acetominophen toxicity

A

Zone III hepatic necrosis

NAPQI = toxic, depletes glutathione (regenerate with NAC = antidote)

4
Q

Asprin MOA

A

IRREVERSIBLY inhibits COX-1 and COX-2 via acetylation.

Causes decrease in TXA2 (increase bleeding time via decreased platelet aggregation) and prostaglandins

5
Q

Asprin use:

A
LD = anti-coagulant
MD = antipyretic and analgesic
HD = anti-inflammatory
6
Q

Asprin toxicity:

A
  • Tinitus
  • Gastric ulcers
  • Chronic = GI bleed, ARF, AIN
  • Reyes in kids with viruses
  • Early respiratory alkalosis, then mixed with metabolic acidosis
7
Q

Celecoxib MOA

A

REVERSIBLY inhibit COX-2 - inflammatory cells and endothelium for pain and inflammation [NOT gastric mucosa or platelets]

8
Q

Celecoxib Use

A

RA
OA
NO GI effects

9
Q

Celecoxib toxicity

A

Thrombosis:
Block endothelium VD without blocking platelet aggregation –> pro-coagulant state

sulfa

10
Q

NSAIDs

A

REVERSIBLY inhibit COX 1 and COX 2

11
Q

NSAIDs specific use

A

Indomethacin closes PDA, acute gout attacks, treats DI,

12
Q

NSAID toxicity

A
  • interstitial nephritis
  • gastric ulcers
  • renal ischemia
13
Q

Bisphosphonates:

A

Alendronate, other ___dronates

14
Q

Bisphosphonate mechanism

A

PPi analog: bind hydroxyapatite in bone, and inhibit osteoclast activity

15
Q

Bisphosphonates use

A

OP
Hypercalcemia (from malignancies)
Pagets

16
Q

Bisphosphonates toxicity

A
  • Erosive esophagitis

- Jaw osteonecrosis

17
Q

Teriparatide MOA

A

Recombinant PTH analog: give SubQ daily to INCREASE osteoblast activity

18
Q

Teriparatide use

A

OP: actually causes bone growth, not just stopping resorption like bisphosphonates

19
Q

Teriparatide toxicity

A

Transient hypercalcemia

Risk of osteosarcoma

20
Q

Alloputinol MOA

A

inhibits XO after being converted to alloxanthane:

  • decreases hypoxanthane to xanthate
  • decreases xanthine to uric acid
21
Q

Allopurinol use

A

Gout

22
Q

Allopurinol Toxicity

A

Increases levels of 6-MP and azathioprine because they are metabolized by XO

23
Q

Feboxutat

A

Inhibits XO (like allopurinol)

24
Q

Pegloticase

A

uric acid to allantoin (water soluble)

25
Q

Rasburicase

A

uric acid to allantoin (water soluble)

26
Q

Probenecid MOA

A

Inhibits uric acid reabsorption in PCT

27
Q

Probenecid use

A

Gout

Give with cidofovir to decrease nephrotoxicity

28
Q

Probenecid toxicity

A

prevents penicillin secretion
Uric acid crystals (urate nephropathy)
Sulfa

29
Q

Drugs for chronic gout (prevention)

A
Allopurinol
Feboxustat
Pegloticase
Rasburicase
Probenecid
Colchicine
30
Q

Drugs for acute gout

A

NSAIDs (indomethacin and naproxen)
Glucocorticoids: oral or injections
Colchicine

31
Q

Colchicine MOA

A

Stabilize tubulin inhibiting MT polymerization and thus PMN chemotaxis and degranulation

32
Q

Colchicine AE

A

GI: N/V/D

33
Q

Sialycilates in gout

A

BAD!

inhibit uric acid clearance

34
Q

TNF-a inhibitor AE

A

increase infections and reactivation of TB (needed for granulomas)

35
Q

Etanercept

A

Fusion protein of TNF-a-R and IgG1-Fc

36
Q

Etanercept use

A

RA, psoriasis, ankylosing spondylitis

37
Q

Infliximab

A

anti-TNF-a monoclonal Ab

38
Q

Infliximab use

A

IBD, RA, ankylosing, psoriasis

39
Q

Adalimumab

A

anti-TNF-a monoclonal Ab

40
Q

Adalimumab use

A

IBD, RA, ankylosing, psoriasis