Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

PHA6126 Pharmacology 2 Lecture > Nonsteroidal Anti- inflammatory Drugs > Flashcards

Nonsteroidal Anti- inflammatory Drugs Flashcards

1
Q

physiological response to tissue injury and infection

A

inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

T/F: Inflammation is synonymous to infection

A

False

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

may pertain to pain (dolor), heat (calor), redness (rubor), and swelling (tumor)

A

inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Immediate response of inflammation

A
  1. vascular diameter (vasodilation)
  2. vascular permeability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

increases blood flow to the area of injury, resulting in the heating and reddening of the tissue

A

vascular diameter (vasodilation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

allows leakage of fluid from the BV into the damaged tissue, resulting in swelling (edema)

A

vascular permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

after a few hours, leukocytes arrive at the site of injury to phagocytize the invading pathogens and release soluble mediators, particularly ____________________, ______________________, ______________________

A

cytokines, prostaglandins, leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

types of inflammation

A
  1. acute
  2. chronic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

inflammation caused by response to tissue injury

A

acute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

inflammation that can lead to progressive tissue destruction (seen in autoimmunity and certain cancers)

A

chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

T/F: NSAIDs are particularly used for chronic inflammation

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

six phase leukocyte inflammatory response

A

P0: ligand-membrane receptor interaction (other stimuli)
P1: mobilization of cell Ca2+
P2: degranulation (release of mediators)
P3: activation of phospholipase
P4: oxidative burst
P5: transcription and translation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

initial response to inflammation which causes an increase in Ca2+

A

mobilization of cell Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

stored mediators

A

histamine, various proteases, chemoattractants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

increased availability of arachidonic acid due to its activation

A

activation of phospholipase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

activation of phospholipase leads to

A
  1. eicosanoid synthesis
  2. synthesis of platelet activating factor (PAF)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

ROS prodduction

A

oxidative burst

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

production and release of cytokines

A

transcription and translation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

T/F: Non-protein-based soluble factors (eicosanoids, bioamines) dominate the landscape during chronic inflammation

A

False: acute inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

a peptide that induces vasodilation and enhanced vascular permeability, produced by the kinin system

A

bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

fibrin strands form clots, limiting the spread of infection into the blood

A

clotting systems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

following tissue damage, different plasma proteins are activated including the clotting and kinin systems

A

acute inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

results from continuous exposure to the offending element

A

chronic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

accumulation & activation of macrophages, lymphocytes, and fibroblasts is the hallmark of what type of inflammation

A

chronic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

[chronic inflammation]

due to ______________________, autoimmune diseases in which self-antigens continuously activate T cells and cancers

A

pathogen persistence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

goals of inflammation tx in px

A
  1. relief of symptoms
  2. maintenance of function, slowing or arrest of tissue-damaging processes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

provides relief of symptoms

A

NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

maintenance of function, slowing or arrest of tissue-damaging processes

A

DMARDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

inhibit phospholipids, thereby inhibiting arachidonic acid synthesis

A

corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

T/F: inhibition of arachidonic acid would lead to the inhibition of lipoxygenase and cyclooxygenase

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

inhibits COX

A

NSAID, ASA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

inhibit lipoxygenase

A

lipoxygenase inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

inhibit leukotrienes

A

receptor antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

inhibit inflammation caused by leukotrienes

A

colchicine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

COX synthesizes

A

prostaglandins, thromboxane, prostacyclin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

T/F: leukocyte modulation caused by thromboxane would relieve inflammation

A

False: lead to inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

other name for arachidonic acid (AA)

A

5,8,11,14-eicosatetraenoic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

most abundant eicosanoid precursor

A

AA (5,8,11,14-eicosatetraenoic acid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

essential FA that is converted to linolenic acid after conversion to AA

A

linoleic acid (omega-6-fatty acid)

40
Q

T/F: some leukotriene antagonists (e.g., montelukast) are also indicated for asthma

41
Q

examples of prostaglandin antagonists

A

corticosteroids and NSAIDs

42
Q

major effects of PG synthesis inhibition

A
  1. analgesia
  2. antipyresis
  3. anti-inflammatory
  4. anti-thrombic
  5. closure of ductus arteriosus
43
Q

normal constituent needed for body homeostasis (stomach, intestine, kidney, platelet)

44
Q

inducible arachidonic acid that leads to inflammatory site (macrophages, synoviocytes, endothelial cells)

45
Q

a relatively new normal constituent that is specific to the CNS, heart (aorta)

46
Q

blocks mRNA expression leading to the inhibition of COX-2 synthesis from AA

A

glucocorticoids

47
Q

dose of aspirin for anti-platelet activity

A

low-dose (less than or equal to 325 mg)

48
Q

dose of aspirin for anti-inflammatory activity

A

high-dose (greater than 325 mg)

49
Q

generates prostanoids for housekeeping functions (e.g., gastric epithelial cytoprotection)

50
Q

major source of prostanoids in inflammation and cancer

51
Q

T/F: All NSAIDs inhibit PG synthesis

52
Q

enzyme responsible for PG synthesis

53
Q

COX form that is released in normal body hemostasis

54
Q

COX form released only when there is inflammation

55
Q

irreversibly inhibits platelet COX resulting to an antiplatelet effect that lasts for 8-10 days

56
Q

rarely used as anti-inflammatory med and reviewed only in terms of its antiplatelet activity

57
Q

decreases incidence of transient ischemic attacks, unstable angina, coronary artery thrombosis w/MI, and thrombosis after CABG

A

clinical use of aspirin

58
Q

gastric upset (intolerance), gastric and duodenal ulcers

A

adr of aspirin

59
Q

T/F: hepatotoxicity, asthma, rashes, GI bleeding, and renal toxicity rarely occur at anti-thrombotic doses of aspirin

60
Q

aspirin is contraindicated for px with

A

hemophilia

61
Q

nonacetylated salicylates

A

MgCl salicylate, Na salicylate, and salicyl salicylate

62
Q

all are effective anti-inflamm drugs and do not inhibit platelet aggregation

A

nonacetylated salicylates

63
Q

preferable when COX inhibition is undesirable (e.g., in px w/asthma, those w/bleeding tendencies, and those w/renal dysfunction)

A

nonacetylated salicylates

64
Q

inhibit PG synthesis w/o affecting action of the constitutively active COX-1 isozyme

A

COX-2 selective inhibitors

65
Q

at usual doses, have no impact on platelet aggregation which is mediated by TXA2 produced by COX-1

A

COX-2 selective inhibitors

66
Q

T/F: COX-2 selective inhibitors offers cardioprotective effects of traditional non-selective NSAIDs.

A

False: no cardioprotective effect

67
Q

a benzenesulfonamide that is 10-20 times more selective for COX-2 than COX-1

68
Q

indicated for tx of OA, RA, JRA, and ankylosing spondylitis (AS)

69
Q

at 400 mg/d, shows efficacy for adjunct therapy for improving schizophrenic symptoms

70
Q

racemic acetic acid derivative whose MOA is relatively COX-2 selective

71
Q

indicated for tx of OA, RA, and JRA w/recommended dosage of 300 mg bid-tid or 500 mg bid initially, then 600 mg/d

72
Q

an enolcarboxamide related to piroxicam and a relatively selective COX-2 inhibitor at 7.5 mg/d

73
Q

inhibits synthesis of TXA2 even at subtherapeutic doses, but its TXA2 blockade does not result in decreased in vivo platelet function

74
Q

indicated for OA, RA, and JRA px with dosage of 7.5-15 mg/d

75
Q

nonselective COX inhibitors

A
  1. diclofenac
  2. diflunisal
  3. flurbiprofen
  4. ibuprofen
  5. naproxen
  6. oxaprozin
  7. tolmetin
  8. indomethacin
  9. ketoprofen
  10. nabumetone
  11. piroxicam
  12. sulindac
76
Q

phenylactIC adic derivative

A

dIClofenac

77
Q

DIFLUorophenyl derivative of SA

A

DIFLUnisal

78
Q

PROpionic acid derivative

A

flurbiPROfen

79
Q

simple phenylpropionic acid derivative

80
Q

NAPthyl-propionic acid derivative

81
Q

another propionic acid derivative

82
Q

pyrrole alkanoic acid derivative

83
Q

indole derivative and potent nonselective COX-i that may also inhibit phospholipase A and C, reduce neutrophil migration, decrease T-cell & B-cell proliferation

A

Indomethacin

84
Q

propionic acid derivative that inhibits both COX (nonselective) and lipoxygenase

A

Ketoprofen

85
Q

only nonadic NSAID that resembles naproxen

A

Nabumetone

86
Q

enolcarboxamide derivative and nonselective COX-i that at high conc. inhibits polymorphonuclear leukocyte migration, decrease O2 radical production, and inhibit lymphocyte function

87
Q

SULfoxide nonselective prodrug

88
Q

T/F: Selective COX-2 inhibitors increase incidence of edema, HTN, and possibly MI

89
Q

T/F: All newer NSAIDs are analgesic, anti-inflammatory, and antipyretic to varying degrees

90
Q

T/F: All including COX-2 selective agents and nonacetylated salicylates inhibit platelet aggregation

A

False: except for COX-2 selective agents and nonacetylated salicylates

91
Q

NSAIDs can be associated with GI ulcers and bleeding, and are all ________________________

A

gastric irritants

92
Q

All NSAIDs are about equally efficacious except for __________________ and ______________

A

tolmetin (ineffective for gout) and aspirin (less effective for AS)

93
Q

side effects that limit the use of ketorolac

A

GI and renal side effects

94
Q

best for px w/renal insufficiency

A

nonacetylated salicylates

95
Q

associated with more liver function test abnormalities than other NSAIDs

A

diclofenac and sulindac

96
Q

relatively expensive selective COX-2 inhibitor but is probably safest for px at high risk for GI bleeding (but may increase risk of CV toxicity)

PHA6126 Pharmacology 2 Lecture (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions