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Pharmacology > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

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1
Q

what does the lipoxygenase pathway yield?

A

leukotrienes

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2
Q

action of LTB4

A

neutrophil chemotaxis

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3
Q

action of LTC4, LTD4, and LTE4

A

increase bronchial tone

increase vascular permeability

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4
Q

action PGI2 (4)

A

decrease platelet aggregation
decrease vascular tone (vasodilation)
decrease bronchial tone
decrease uterine tone

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5
Q

action PGE2, PGF2alpha (2)

A

increase uterine tone

decrease bronchial tone

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6
Q

action TXA2 (3)

A

increase platelet aggregation
increase vascular tone
increase bronchial tone

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7
Q

mechanism aspirin

A

irreversibly inhibits COX-1 and COX-2 by acetylation –> decrease synthesis TXA2 and prostaglandins

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8
Q

effect of aspirin on bleeding time, PT, and PTT

A

increase bleeding time (until new platelets produced – 7 days)
NO EFFECT on PT or PTT

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9
Q

clinical use aspirin at low dose

A

decrease platelet aggregation

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10
Q

clinical use aspirin at intermediate dose

A

antipyretic and analgesic

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11
Q

clinical use aspirin at high dose

A

anti-inflammatory

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12
Q

side effects aspirin

A
  1. gastric ulcers
  2. tinnitus (CN VIII)
  3. acute renal failure, interstitial nephritis (chronic use)
  4. upper GI bleeding (chronic use)
  5. hyperventilation –> respiratory alkalosis (stimulates respiratory centers)
  6. Reye syndrome in children with virus
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13
Q

what happens if you use aspirin in children who have a viral illness?

A

Reye syndrome

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14
Q

what effect does aspirin have on pH

A

respiratory alkalosis (causes hyperventilation)

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15
Q

name some NSAIDs! (5)

A
  1. ibuprofen
  2. naproxen
  3. indomethacin
  4. ketorolac
  5. diclofenac
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16
Q

drug class ibuprofen

A

NSAID

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17
Q

drug class naproxen

A

NSAID

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18
Q

drug class indomethacin

A

NSAID

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19
Q

drug class ketorolac

A

NSAID

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20
Q

drug class diclofenac

A

NSAID

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21
Q

mechanism NSAIDs

A

reversibly inhibit cyclooxygenase (both COX-1 and COX-2) –> block prostaglandin synthesis

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22
Q

clinical use NSAIDs

A

antipyretic, analgesic, anti-inflammatory

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23
Q

what drug do you use to close a PDA?

A

indomethacin

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24
Q

side effects NSAIDs

A
  1. interstitial nephritis
  2. gastric ulcer (PGs protect gastric mucosa)
  3. renal ischemia
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25
mechanism by which NSAIDs can cause renal ischemia
prostaglandins dilate afferent arteriole
26
name a COX-2 inhibitor
celecoxib
27
what is celecoxib?
COX-2 inhibitor
28
mechanism COX-2 inhibitor
reversibly inhibit COX-2 (found in inflammatory cells and vascular endothelium - -> spares COX-1 --> maintains gastric mucosa - -> spares COX-1 --> spares platelet function (TXA2 production depends on COX-1)
29
clinical use COX-2 inhibitor
RA or OA | patients with gastritis or ulcers
30
side effects COX-2 inhibitor (2)
1. increase risk thrombosis | 2. sulfa allergy
31
mechanism acetaminophen
reversibly inhibits cyclooxygenase (mostly in CNS, inactivated peripherally)
32
clinical use acetaminophen
antipyretic, analgesic
33
is acetaminophen anti-inflammatory?
NO!!
34
what should you use instead of aspirin to avoid Reye syndrome in kids with viral infection?
acetaminophen
35
what happens in acetaminophen overdose
hepatic necrosis
36
mechanism by which acetaminophen overdose causes hepatic necrosis
acetaminophen metabolite (NAPQI) depletes glutathione and forms toxic tissue adducts in the liver
37
antidote to acetaminophen overdose
N-acetylcysteine (regenerates glutathione)
38
what are some bisphosphonates?
alendronate, other -dronates
39
mechanism bisphosphenates
pyrophosphate analogs --> bind hydroxyapatite in bone, inhibiting osteoclast activity
40
clinical use bisphosphenates
1. osteoporosis 2. hypercalcemia 3. Paget disease of bone
41
side effects bisphosphenates (2)
1. corrosive esophagitis | 2. osteonecrosis of the jaw
42
what gout drugs are used chronically (preventive)? (3)
1. allopurinol 2. febuxostat 3. probenecid
43
what gout drugs are used acutely? (3)
1. NSAIDs 2. glucocorticoids 3. colchicine
44
allopurinol mechanism
inhibits xanthine oxidase --> decrease conversion of xanthine to uric acid
45
clinical use allopurinol (2)
1. chronic (preventive) gout drug | 2. lymphoma and leukemia (prevent tumor lysis-associated urate nephropathy)
46
what drugs does allopurinol increase the concentration of? (2)
1. azathioprine 2. 6-MP - -> both normally metabolized by xanthine oxidase
47
should you give salicylates with allopurinol?
NO!!! all but the highest doses depress uric acid clearance
48
mechanism febuxostat
inhibits xanthine oxidase
49
clinical use febuxostat
chronic gout drug (preventive)
50
mechanism probenecid
inhibits reabsorption of uric acid in PCT
51
what happens if you take probenecid with penecillin?
inhibits secretion of penicillin in kidney
52
clinical use probenecid
chronic gout drug (preventive)
53
which NSAIDs are used as acute gout drugs? (2)
1. naproxen | 2. indomethacin
54
clinical use NSAIDs in gout
acute gout drugs
55
clinical use glucocorticoids in gout
acute gout drugs
56
mechanism colchicine
binds and stabilizes tubulin to inhibit microtubule polymerization --> impairs leukocyte chemotaxis and degranulation
57
clinical use colchicine
acute and prophylactic use for gout (mainly actue gout drug)
58
side effects colchicine
GI
59
side effects TNF-alpha inhibitors
predispose to infection (including reactivation of latent TB), since TNF blockade prevents activation of macrophages
60
what is etanercept?
TNF-alpha inhibitor
61
what is infliximab?
TNF-alpha inhibitor
62
what is adalimumab?
TNF-alpha inhibitor
63
name three TNF-alpha inhibitors
1. etanercept 2. infliximab 3. adalimumab
64
mechanism etanercept
fusion protein (receptor for TNF-alpha and IgG1 Fc) from recombinant DNA
65
mechanism infliximab
anti-TNF-alpha monoclonal antibody
66
mechanism adalimumab
anti-TNF-alpha monoclonal antibody
67
clinical use etanercept
RA, psoriasis, ankylosing spondylitis
68
clinical use infliximab
IBD, RA, psoriasis, ankylosing spondylitis
69
clinical use adalimumab
IBD, RA, psoriasis, ankylosing spondylitis

Pharmacology (8 decks)

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