Musculoskeletal, Skin, and Connective Tissue Pharmacology Flashcards
1
Q
acetaminophen–mechanism
A
- reversibly inhibits cyclooxgenase
- mostly in CNS
- inactivated peripherally
2
Q
acetaminophen–use
A
- antipyretic
- analgesic
- NOT anti-inflammatory
- used instead of aspirin to avoid Reye syndrome in children with a viral infection
3
Q
acetaminophen–toxicity
A
- overdose produces hepatic necrosis
- acetaminophen metabolic (NAPQI) depletes glutathione and forms toxic tissue byproducts in liver
4
Q
acetaminophen–antidote
A
- N-acetylcysteine
- regenerates glutathione
5
Q
aspirin–mechanism
A
- NSAID that irreversibly inhibits cyclooxygenase (COX-1 and COX-2) by covalent acetylation –> dec synthesis of TXA2 and prostaglandins
- inc bleeding time
- no effect on PT, PTT
- effect lasts until new platelets are produced
6
Q
aspirin–use
A
- low dose (<300 mg/day): dec platelet aggregation
- intermediate dose (300-2400 mg/day): antipyretic and analgesic
- high dose (2400-4000 mg/day): anti-inflammatory
7
Q
aspirin–toxicity
A
- gastric ulceration
- tinnitus (CN VIII)
- chronic use can lead to:
- acute renal failure
- interstitial nephritis
- GI bleeding
- causes respiratory alkalosis early, but transitions to mixed metabolic acidosis respiratory alkalosis
8
Q
what are children at risk for if have a viral infection that is treated with aspirin?
A
Reye syndrome
9
Q
celecoxib–mechanism
A
- reversibly inhibits specifically the cyclooxogenase (COX) isoform 2 which is found in inflammatory cells and vascular endothelium and mediates inflammation and pain
- spares COX 1
10
Q
what are the benefits of using celecoxib over other NSAIDs?
A
- spares COX-1 which helps maintain gastric mucosa
- so does not have the corrosive effects of other NSAIDs on the GI lining
- spares platelet function as TXA2 production is dependent on COX-1
11
Q
celecoxib–use
A
- rheumatoid arthritis
- osteoarthritis
12
Q
celecoxib–toxicity
A
- inc risk of thrombosis
- sulfa allergy
13
Q
name the NSAIDs
A
- ibuprofen
- naproxen
- indomethacin
- ketorolac
- diclofenac
- meloxican
- piroxican
14
Q
NSAIDs–mechanism
A
- reversibly inhibit cyclooxygenase (both COX 1 and 2)
- blocks prostaglandin synthesis
15
Q
NSAIDs–use
A
- antipyretic
- analgesic
- anti-inflammatory
- indomethacin is used to close a patent ductus arteriosis
16
Q
NSAIDs–toxicity
A
- interstitial nephritis
- gastric ulcer–prostaglandins protect gastric mucosa
- renal ischemia–prostaglandins vasodilate afferent arteriole
17
Q
leflunomide–mechanism
A
- reversibly inhibits dihydroorotate dehydrogenase, preventing pyrimidine synthesis
- suppresses T cell proliferation
18
Q
leflunomide–use
A
- rheumatoid arthritis
- psoriatic arthritis
19
Q
leflunomide–toxicity
A
- diarrhea
- HTN
- hepatotoxicity
- teratogenicity
20
Q
name the bisphosphonates
A
- alendronate
- ibandronate
- risedronate
- zoledronate
21
Q
bisphosphonates–mechanism
A
- pyrophosphate analogs
- bind hydroxyapatite in bone
- inhibits osteoclast activity
22
Q
bisphosphonates–use
A
- osteoporosis
- hypercalcemia
- Paget dz of the bone
- metastatic bone dz
- osteogenesis imperfecta
23
Q
bisphosphonates–toxicity
A
- esophagitis
- if taken orally, patients are advised to take with water and remain upright for 30 minutes
- osteonecrosis of jaw
- atypical stress fractures
24
Q
teriparatide–mechanism
A
- recombinant PTH analog given subcutaneously daily
- inc osteoblastic activity
25
teriparatide--use
* osteoporosis
* causes inc bone growth compared to antiresorptive therapies
* ie. bisphosphonates
26
teriparatide--toxicity
* transient hypercalcemia
27
name the chronic gout drugs (preventive)
* allopurinol
* febuxostat
* pegloticase
* probenecid
28
name the acute gout drugs
* NSAIDs
* glucocorticoids
* colchicine
29
allopurinol--mechanism
* competitive inhibitor of xanthine oxidase
* decrease conversion of hypoxanthine and xanthine to urate
* increase concentrations of azathioprine and 6 MP
* both normally metabolized by xanthine oxidase
30
other uses for allopurinol besides gout
* used in lymphoma and leukemia to prevent tumor lysis--associated urate nephropathy
31
febuxostat--mechanism
* inhibits xanthine oxidase
32
pegloticase--mechanism
* recombinant uricase that catalyzes metabolism of uric acid to allantoin ( a more water soluble product )
33
probenecid--mechanism
* inhibits reabsorption of uric acid in the proximal convoluted tubule
* also inhibits secretion of penicillin
* can precipitate uric acid calculi
34
name the NSAIDs used for gout
* naproxen
* indomethacin
35
what type of NSAID should not be used for acute gout and why?
* salicylates
* all but the highest doses depress uric acid clearance
* even high doses (5-6 g/day) have only minor uricosuric acitvity
36
glucocorticoids--mechanism for use in acute gout
* oral
* intra-articular
* parenteral
37
colchicine--mechanism
* binds and stabilizes tubulin to inhibit microtubule polymerization
* impairs neutrophil chemotaxis and degranulation
38
colchicine--use
acute and prophylactic use for gout
39
colchicine--toxicity
GI side effects
40
name 2 TNF alpha inhibitors
* etanercept
* infliximab, adalimumab
41
what do TNF alpha inhibitors predispose a patient to and why?
* all TNF alpha inhibitors predispose to infection, including reactivation of latent TB
* b/c TNF is important in granuloma formation and stabilization
42
etanercept--mechanism
* fusion protein--receptor for TNF alpha + IgG1 Fc
* produced by recombinant DNA
* "Etaner**cept** is a TNF decoy re**cept**or"
43
etanercept--use
* rheumatoid arthritis
* psoriasis
* ankylosing spodylitis
44
infliximab, adalimumab--mechanism
* anti TNF alpha monoclonal antibody
45
infliximab, adalimumab--use
* inflammatory bowel disease
* rheumatoid arthritis
* ankylosing spondylitis
* psoriasis
46
rasburicase--mechanism
* recombinant uricase that catalyzes metabolism of uric acid to allantoin
47
rasburicase--use
* prevention and treatment of tumor lysis syndrome
