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Pharmacology > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

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
Q

mechanism by which NSAIDs can cause renal ischemia

A

prostaglandins dilate afferent arteriole

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26
Q

name a COX-2 inhibitor

A

celecoxib

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27
Q

what is celecoxib?

A

COX-2 inhibitor

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28
Q

mechanism COX-2 inhibitor

A

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
Q

clinical use COX-2 inhibitor

A

RA or OA

patients with gastritis or ulcers

30
Q

side effects COX-2 inhibitor (2)

A
  1. increase risk thrombosis

2. sulfa allergy

31
Q

mechanism acetaminophen

A

reversibly inhibits cyclooxygenase (mostly in CNS, inactivated peripherally)

32
Q

clinical use acetaminophen

A

antipyretic, analgesic

33
Q

is acetaminophen anti-inflammatory?

A

NO!!

34
Q

what should you use instead of aspirin to avoid Reye syndrome in kids with viral infection?

A

acetaminophen

35
Q

what happens in acetaminophen overdose

A

hepatic necrosis

36
Q

mechanism by which acetaminophen overdose causes hepatic necrosis

A

acetaminophen metabolite (NAPQI) depletes glutathione and forms toxic tissue adducts in the liver

37
Q

antidote to acetaminophen overdose

A

N-acetylcysteine (regenerates glutathione)

38
Q

what are some bisphosphonates?

A

alendronate, other -dronates

39
Q

mechanism bisphosphenates

A

pyrophosphate analogs –> bind hydroxyapatite in bone, inhibiting osteoclast activity

40
Q

clinical use bisphosphenates

A
  1. osteoporosis
  2. hypercalcemia
  3. Paget disease of bone
41
Q

side effects bisphosphenates (2)

A
  1. corrosive esophagitis

2. osteonecrosis of the jaw

42
Q

what gout drugs are used chronically (preventive)? (3)

A
  1. allopurinol
  2. febuxostat
  3. probenecid
43
Q

what gout drugs are used acutely? (3)

A
  1. NSAIDs
  2. glucocorticoids
  3. colchicine
44
Q

allopurinol mechanism

A

inhibits xanthine oxidase –> decrease conversion of xanthine to uric acid

45
Q

clinical use allopurinol (2)

A
  1. chronic (preventive) gout drug

2. lymphoma and leukemia (prevent tumor lysis-associated urate nephropathy)

46
Q

what drugs does allopurinol increase the concentration of? (2)

A
  1. azathioprine
  2. 6-MP
    - -> both normally metabolized by xanthine oxidase
47
Q

should you give salicylates with allopurinol?

A

NO!!! all but the highest doses depress uric acid clearance

48
Q

mechanism febuxostat

A

inhibits xanthine oxidase

49
Q

clinical use febuxostat

A

chronic gout drug (preventive)

50
Q

mechanism probenecid

A

inhibits reabsorption of uric acid in PCT

51
Q

what happens if you take probenecid with penecillin?

A

inhibits secretion of penicillin in kidney

52
Q

clinical use probenecid

A

chronic gout drug (preventive)

53
Q

which NSAIDs are used as acute gout drugs? (2)

A
  1. naproxen

2. indomethacin

54
Q

clinical use NSAIDs in gout

A

acute gout drugs

55
Q

clinical use glucocorticoids in gout

A

acute gout drugs

56
Q

mechanism colchicine

A

binds and stabilizes tubulin to inhibit microtubule polymerization –> impairs leukocyte chemotaxis and degranulation

57
Q

clinical use colchicine

A

acute and prophylactic use for gout (mainly actue gout drug)

58
Q

side effects colchicine

A

GI

59
Q

side effects TNF-alpha inhibitors

A

predispose to infection (including reactivation of latent TB), since TNF blockade prevents activation of macrophages

60
Q

what is etanercept?

A

TNF-alpha inhibitor

61
Q

what is infliximab?

A

TNF-alpha inhibitor

62
Q

what is adalimumab?

A

TNF-alpha inhibitor

63
Q

name three TNF-alpha inhibitors

A
  1. etanercept
  2. infliximab
  3. adalimumab
64
Q

mechanism etanercept

A

fusion protein (receptor for TNF-alpha and IgG1 Fc) from recombinant DNA

65
Q

mechanism infliximab

A

anti-TNF-alpha monoclonal antibody

66
Q

mechanism adalimumab

A

anti-TNF-alpha monoclonal antibody

67
Q

clinical use etanercept

A

RA, psoriasis, ankylosing spondylitis

68
Q

clinical use infliximab

A

IBD, RA, psoriasis, ankylosing spondylitis

69
Q

clinical use adalimumab

A

IBD, RA, psoriasis, ankylosing spondylitis

Pharmacology (8 decks)

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