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

Nonsteroidal Anti- inflammatory Drugs Flashcards

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1
Q

physiological response to tissue injury and infection

A

inflammation

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2
Q

T/F: Inflammation is synonymous to infection

A

False

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3
Q

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

A

inflammation

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4
Q

Immediate response of inflammation

A
  1. vascular diameter (vasodilation)
  2. 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 BV into the damaged tissue, resulting in swelling (edema)

A

vascular permeability

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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

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8
Q

types of inflammation

A
  1. acute
  2. chronic
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9
Q

inflammation caused by response to tissue injury

A

acute

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10
Q

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

A

chronic

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11
Q

T/F: NSAIDs are particularly used for chronic inflammation

A

True

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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

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13
Q

initial response to inflammation which causes an increase in Ca2+

A

mobilization of cell Ca2+

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14
Q

stored mediators

A

histamine, various proteases, chemoattractants

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15
Q

increased availability of arachidonic acid due to its activation

A

activation of phospholipase

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16
Q

activation of phospholipase leads to

A
  1. eicosanoid synthesis
  2. synthesis of platelet activating factor (PAF)
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17
Q

ROS prodduction

A

oxidative burst

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18
Q

production and release of cytokines

A

transcription and translation

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19
Q

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

A

False: acute inflammation

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20
Q

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

A

bradykinin

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21
Q

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

A

clotting systems

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22
Q

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

A

acute inflammatory response

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23
Q

results from continuous exposure to the offending element

A

chronic inflammation

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24
Q

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

A

chronic inflammation

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25
[chronic inflammation] due to ______________________, autoimmune diseases in which self-antigens continuously activate T cells and cancers
pathogen persistence
26
goals of inflammation tx in px
1. relief of symptoms 2. maintenance of function, slowing or arrest of tissue-damaging processes
27
provides relief of symptoms
NSAIDs
28
maintenance of function, slowing or arrest of tissue-damaging processes
DMARDs
29
inhibit phospholipids, thereby inhibiting arachidonic acid synthesis
corticosteroids
30
T/F: inhibition of arachidonic acid would lead to the inhibition of lipoxygenase and cyclooxygenase
True
31
inhibits COX
NSAID, ASA
32
inhibit lipoxygenase
lipoxygenase inhibitors
33
inhibit leukotrienes
receptor antagonists
34
inhibit inflammation caused by leukotrienes
colchicine
35
COX synthesizes
prostaglandins, thromboxane, prostacyclin
36
T/F: leukocyte modulation caused by thromboxane would relieve inflammation
False: lead to inflammation
37
other name for arachidonic acid (AA)
5,8,11,14-eicosatetraenoic acid
38
most abundant eicosanoid precursor
AA (5,8,11,14-eicosatetraenoic acid)
39
essential FA that is converted to linolenic acid after conversion to AA
linoleic acid (omega-6-fatty acid)
40
T/F: some leukotriene antagonists (e.g., montelukast) are also indicated for asthma
True
41
examples of prostaglandin antagonists
corticosteroids and NSAIDs
42
major effects of PG synthesis inhibition
1. analgesia 2. antipyresis 3. anti-inflammatory 4. anti-thrombic 5. closure of ductus arteriosus
43
normal constituent needed for body homeostasis (stomach, intestine, kidney, platelet)
COX-1
44
inducible arachidonic acid that leads to inflammatory site (macrophages, synoviocytes, endothelial cells)
COX-2
45
a relatively new normal constituent that is specific to the CNS, heart (aorta)
COX-3
46
blocks mRNA expression leading to the inhibition of COX-2 synthesis from AA
glucocorticoids
47
dose of aspirin for anti-platelet activity
low-dose (less than or equal to 325 mg)
48
dose of aspirin for anti-inflammatory activity
high-dose (greater than 325 mg)
49
generates prostanoids for housekeeping functions (e.g., gastric epithelial cytoprotection)
COX-1
50
major source of prostanoids in inflammation and cancer
COX-2
51
T/F: All NSAIDs inhibit PG synthesis
True
52
enzyme responsible for PG synthesis
COX
53
COX form that is released in normal body hemostasis
COX-1
54
COX form released only when there is inflammation
COX-2
55
irreversibly inhibits platelet COX resulting to an antiplatelet effect that lasts for 8-10 days
aspirin
56
rarely used as anti-inflammatory med and reviewed only in terms of its antiplatelet activity
aspirin
57
decreases incidence of transient ischemic attacks, unstable angina, coronary artery thrombosis w/MI, and thrombosis after CABG
clinical use of aspirin
58
gastric upset (intolerance), gastric and duodenal ulcers
adr of aspirin
59
T/F: hepatotoxicity, asthma, rashes, GI bleeding, and renal toxicity rarely occur at anti-thrombotic doses of aspirin
True
60
aspirin is contraindicated for px with
hemophilia
61
nonacetylated salicylates
MgCl salicylate, Na salicylate, and salicyl salicylate
62
all are effective anti-inflamm drugs and do not inhibit platelet aggregation
nonacetylated salicylates
63
preferable when COX inhibition is undesirable (e.g., in px w/asthma, those w/bleeding tendencies, and those w/renal dysfunction)
nonacetylated salicylates
64
inhibit PG synthesis w/o affecting action of the constitutively active COX-1 isozyme
COX-2 selective inhibitors
65
at usual doses, have no impact on platelet aggregation which is mediated by TXA2 produced by COX-1
COX-2 selective inhibitors
66
T/F: COX-2 selective inhibitors offers cardioprotective effects of traditional non-selective NSAIDs.
False: no cardioprotective effect
67
a benzenesulfonamide that is 10-20 times more selective for COX-2 than COX-1
celecoxib
68
indicated for tx of OA, RA, JRA, and ankylosing spondylitis (AS)
celecoxib
69
at 400 mg/d, shows efficacy for adjunct therapy for improving schizophrenic symptoms
celecoxib
70
racemic acetic acid derivative whose MOA is relatively COX-2 selective
etodolac
71
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
etodolac
72
an enolcarboxamide related to piroxicam and a relatively selective COX-2 inhibitor at 7.5 mg/d
meloxicam
73
inhibits synthesis of TXA2 even at subtherapeutic doses, but its TXA2 blockade does not result in decreased in vivo platelet function
meloxicam
74
indicated for OA, RA, and JRA px with dosage of 7.5-15 mg/d
meloxicam
75
nonselective COX inhibitors
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
phenylactIC adic derivative
dIClofenac
77
DIFLUorophenyl derivative of SA
DIFLUnisal
78
PROpionic acid derivative
flurbiPROfen
79
simple phenylpropionic acid derivative
ibuprofen
80
NAPthyl-propionic acid derivative
NAProxen
81
another propionic acid derivative
Oxaprozin
82
pyrrole alkanoic acid derivative
Tolmetin
83
indole derivative and potent nonselective COX-i that may also inhibit phospholipase A and C, reduce neutrophil migration, decrease T-cell & B-cell proliferation
Indomethacin
84
propionic acid derivative that inhibits both COX (nonselective) and lipoxygenase
Ketoprofen
85
only nonadic NSAID that resembles naproxen
Nabumetone
86
enolcarboxamide derivative and nonselective COX-i that at high conc. inhibits polymorphonuclear leukocyte migration, decrease O2 radical production, and inhibit lymphocyte function
Piroxicam
87
SULfoxide nonselective prodrug
SULindac
88
T/F: Selective COX-2 inhibitors increase incidence of edema, HTN, and possibly MI
True
89
T/F: All newer NSAIDs are analgesic, anti-inflammatory, and antipyretic to varying degrees
True
90
T/F: All including COX-2 selective agents and nonacetylated salicylates inhibit platelet aggregation
False: except for COX-2 selective agents and nonacetylated salicylates
91
NSAIDs can be associated with GI ulcers and bleeding, and are all ________________________
gastric irritants
92
All NSAIDs are about equally efficacious except for __________________ and ______________
tolmetin (ineffective for gout) and aspirin (less effective for AS)
93
side effects that limit the use of ketorolac
GI and renal side effects
94
best for px w/renal insufficiency
nonacetylated salicylates
95
associated with more liver function test abnormalities than other NSAIDs
diclofenac and sulindac
96
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)
celecoxib

PHA6126 Pharmacology 2 Lecture (10 decks)

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