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NSAIDs Flashcards

1
Q

a physiological response to tissue injury and infection

A

inflammation

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2
Q

other term for inflammation

A

inflammatory response

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3
Q

T or F: inflammation is not a synonym for infection

A

True

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4
Q

Mediate response to inflammation

A

vascular diameter, vascular permeability

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5
Q

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

A

vascular diameter (vasodilation)

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6
Q

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

A

vascular permeability

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7
Q

when will NSAIDs be used

A

when inflammation is CHRONIC

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8
Q

During chronic inflammation - leukocytes arrive at the site of injury to _________ the invading pathogens and release __________

A

phagocytize; soluble mediators

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9
Q

soluble mediators released during chronic inflamm

A

cytokines, prostaglandins, leukotrienes

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10
Q

response to tissue injury

A

Acute inflamm

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11
Q

leading to progressive tissue destruction, as seen in chronic infections, autoimmunity, and certain cancers

A

Chronic inflamm

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12
Q

T or F: chronic inflamm can lead to autoimmunity and cancers

A

True

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13
Q

Type of inflamm wherein clotting and kinin systems are activated

A

Acute

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14
Q

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

A

Clotting systems

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15
Q

Clotting systems - ________ strands to form clots, limiting the spread of infection into the blood

A

fibrin

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16
Q

Kinin system results in the production of ____________

A

bradykinin

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17
Q

a peptide that induces vasodilation and enhanced vascular permeability

A

bradykinin

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18
Q

dominate the landscape during acute inflammation

A

Non-protein–based soluble factors

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19
Q

represent a diverse family of lipid mediators with fundamental roles in physiology and disease

A

Eicosanoids

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20
Q

results from continuous exposure to the
offending element.

A

Chronic inflammation

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21
Q

Due to _____________, autoimmune diseases in which self-antigens continuously activate T cells, and cancers.

A

pathogen persistence

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22
Q

Hallmark of chronic inflammation

A

the accumulation and activation of macrophages and lymphocytes and fibroblasts

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23
Q

primary factors of chronic inflammation

A

Cytokines, chemokines, growth factors, and secreted/released enzymes, and ROS

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24
Q

The treatment of patients with inflammation involves two primary goals:

A

the relief of symptoms (NSAIDS) and the maintenance of function, slowing or arrest of the tissue-damaging processes is desirable, and
disease-modifying drugs (DMARDs) are necessary.

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25
Q

the most abundant of the eicosanoid precursors

A

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

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26
Q

an essential fatty acid, is converted to linolenic acid, followed by conversion to AA. (omega-6-fatty acid)

A

Linoleic acid

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27
Q

Major Effects of PG Synthesis Inhibition

A
  1. Analgesia
  2. Antipyresis
  3. Anti-inflammatory
  4. Anti-thrombotic
  5. Closure of Ductus Arteriosus
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28
Q

generates prostanoids for “housekeeping” functions such as gastric epithelial cytoprotection

A

COX-1

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29
Q

is the major source of prostanoids in inflammation and cancer.

A

COX-2

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30
Q

All NSAIDs inhibit

A

PG synthesis

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31
Q

Prostaglandin, prostacyclin (PG1) and thromboxane (TXA2) are produced from _____________

A

Arachidonic acid

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32
Q

The enzyme responsible for NSAIDs is ______________ also known as cyclooxygenase or COX

A

prostaglandin synthase

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33
Q

COX in 2 forms:

A

constitutive COX-1 and inducible COX 2

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34
Q

NSAIDs ADR for CNS

A

Headaches, tinnitus, dizziness, and rarely aseptic meningitis.

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35
Q

NSAIDs ADR for Cardiovascular

A

Fluid retention, hypertension, edema, and rarely myocardial infarction and congestive heart failure (CHF).

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36
Q

Gastrointestinal ADR of NSAIDs

A

Abdominal pain, dyspepsia, nausea, vomiting, and rarely ulcers or bleeding

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37
Q

Hematologic ADR of NSAIDs

A

Rare thrombocytopenia, neutropenia, or even aplastic anemia.

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38
Q

Hepatic ADR of NSAIDs

A

Abnormal liver function test results and rare liver failure.

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39
Q

Pulmonary ADR of NSAIDs

40
Q

Skin ADR of NSAIDs

A

Rashes, all types, pruritus

41
Q

Renal ADR of NSAIDs

A

Renal insufficiency, renal failure, hyperkalemia, and proteinuria.

42
Q

Aspirin irreversibly inhibits platelet _________

43
Q

aspirin’s antiplatelet effect lasts ____________ (the life of the platelet)

A

8–10 days

44
Q

T or F: Aspirin is now rarely used as an anti-inflammatory medication

45
Q

decreases the incidence of transient ischemic attacks, unstable angina, coronary artery thrombosis with myocardial infarction, and thrombosis after coronary bypass grafting

46
Q

Aspirin ADR

A

gastric upset (intolerance) and gastric and duodenal ulcers. Hepatotoxicity, asthma, rashes, GI bleeding, and renal toxicity rarely if ever occur at antithrombotic doses

47
Q

Aspirin is contraindicated inpatients with ___________.

A

hemophilia

48
Q

Long-term low-dose aspirin usage in patients with type 2 diabetes increases risk for ___________

A

GI bleeding

49
Q

NONACETYLATED SALICYLATES

A

Magnesium choline salicylate, sodium salicylate, and salicyl salicylate

50
Q

All nonacetylated salicylates are effective anti-inflammatory drugs, and they _______ (inhibit/do not inhibit) platelet aggregation

A

do not inhibit

51
Q

non acetylated salicylates is preferable when COX inhibition is undesirable such as in patients with ________-

A

asthma, bleeding tendencies, renal dysfunction (under close supervision)

52
Q

were developed in an attempt to inhibit prostaglandin synthesis by the COX-2 isozyme induced at sites of inflammation without affecting the action of the constitutively active “housekeeping” COX-1 isozyme found in the GI tract, kidneys, and platelets

A

Cox 2 selective inhibitors

53
Q

COX-2 selective inhibitors, or _______, were developed in an attempt to inhibit ____________ by the COX-2 isozyme induced at sites of inflammation without affecting the action of the constitutively active “housekeeping” COX-1 isozyme found in the GI tract, kidneys, and platelets

A

coxibs; prostaglandin synthesis

54
Q

COX-2 selective inhibitors, or coxibs, were developed in an attempt to inhibit prostaglandin synthesis by the COX-2 isozyme induced at sites of inflammation __________ affecting the action of the constitutively active _____________ found in the ______________

A

without: “housekeeping” COX-1 isozyme; GI tract, kidneys, and platelets

55
Q

COX-2 inhibitors at usual doses have no impact on ___________ which is mediated by ____________ produced by the ________

A

platelet aggregation; thromboxane; COX-1 isozyme

56
Q

have no impact on platelet aggregation, which is mediated by thromboxane produced by the COX-1 isozyme.

A

COX-2 inhibitors at usual doses

57
Q

do not offer the cardioprotective effects of traditional nonselective NSAIDs

A

COX-2 inhibitors

58
Q

a benzenesulfonamide

59
Q

is a selective COX-2 inhibitor, about 10–20 times more selective for COX-2 than COX-1

60
Q

is indicated for the treatment of OA, RA, JRA, and AS

61
Q

Usual dose of Celecoxib

A

100–200 mg bid

62
Q

Celecoxib at _________ has also shown efficacy as an adjunctive therapy for improving __________, most likely due to suspected __________ in the disorder

A

400 mg/d; schizophrenic symptoms; neuroinflammation

63
Q

racemic acetic acid derivative whose mechanism of action has been described as relatively COX-2 selective

64
Q

Etodolac is indicated for the treatment of __________

A

OA, RA, and JRA

65
Q

recommended dosage of etodolac

A

300 mg bid–tid or 500 mg bid initially, then 600 mg/d

66
Q

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

67
Q

T/F: even at subtherapeutic doses, meloxicam’s blockade of thromboxane A2 does not reach levels that result in decreased in vivo platelet function

68
Q

Indications and Dosage of meloxicam

A

OA, RA, and JRA patients. Dosage is 7.5–15 mg/d

69
Q

phenylacetic acid derivative

A

Diclofenac

70
Q

difluorophenyl derivative of salicylic acid

A

Diflunisal

71
Q

propionic acid derivative

A

Flurbiprofen

72
Q

simple phenylpropionic acid derivative

73
Q

a naphthyl-propionic acid derivative

74
Q

another propionic acid derivative NSAID

75
Q

pyrrole alkanoic acid derivative

76
Q

an indole derivative) and a potent nonselective COX inhibitor that may also inhibit phospholipase A and C, reduce neutrophil migration, and decrease T-cell and B-cell proliferation

A

Indomethacin

77
Q

Indomethacin may also inhibit

A

phospholipase A and C, reduce neutrophil migration,

78
Q

Indomethacin may also decrease

A

T-cell and B-cell proliferation

79
Q

T/F: Because of perceived toxicity, indomethacin is used less commonly than other NSAIDs

80
Q

a propionic acid derivative that inhibits both COX (nonselectively) and lipoxygenase.

A

Ketoprofen

81
Q

is the only nonacid NSAID in current use and resembles naproxen in structure

A

Nabumetone

82
Q

an enolcarboxamide derivative is a nonselective COX inhibitor

83
Q

Piroxicam at high concentrations also inhibits _________, decreases
_______, and inhibits __________.

A

polymorphonuclear leukocyte migration; oxygen radical production; lymphocyte function

84
Q

is a sulfoxide nonselective prodrug whose active metabolite is a nonselective COX inhibitor

85
Q

Asprin ____________ (reversibly/irreversibly) acetylates and blocks platelet COX

A

irreversibly

86
Q

T/F: non-COX-selective NSAIDs are reversible inhibitors

87
Q

The selective COX-2 inhibitors (do not affect/affects) platelet function at their usual doses

A

do not affect

88
Q

T/F: The in vivo efficacy of COX-2-selective drugs equals that of the older NSAIDs, while GI safety may not be improved

A

False; may be improved

89
Q

selective COX-2 inhibitors increase the incidence of ____________, ____________ and _________

A

edema, hypertension, and possibly myocardial infarction

90
Q

T/F: all newer NSAIDs are analgesic, anti-inflammatory, and antipyretic, and all including the COX-2–selective agents and the nonacetylated salicylates inhibit platelet aggregation.

A

false; except the COX-2–selective agents and the nonacetylated salicylates

91
Q

T/f: NSAIDs are all gastric irritants and can be associated with GI ulcers and bleeding as well

92
Q

T/F: the newer agents tend to cause less GI irritation than aspirin

93
Q

seems not to be effective for gout, and is less effective than other NSAIDs
(eg,indomethacin) for AS Ankylosing spondylitis

94
Q

T/F: The GI and renal side effects of ketorolac limit its use

95
Q

best for renal insufficiency

A

nonacetylated salicylates

96
Q

__________ and _______are associated with more liver function test abnormalities than other NSAIDs

A

Diclofenac and sulindac

97
Q

___________ is probably safest for patients at high risk for GI bleeding but may have a higher risk of cardiovascular toxicity

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