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PHARMACOLOGY II > NSAIDS > Flashcards

NSAIDS Flashcards

(85 cards)

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1
Q

Physiological response of the body to tissue injury and infection

A

Inflammation

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2
Q

Four cardinal signs of inflammation

A

Calor - heat
Dolor - pain
Rubor - redness
Tumor - swelling

Hot si calor, Nasaktan si Dolor, RR

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3
Q

Mediate responses

A

Vascular diameter (vasodilation) and Vascular permeability

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4
Q

Explain what happens during vascular diameter (vasodilation)

A

Increased blood flow resulting in rubor (reddening) and calor (heating)

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5
Q

Explain what happens during vascular permeability

A

Increased permeability resulting to slow leakage of fluid resulting in swelling (edema)

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6
Q

Leukocytes arrive to site of injury and phagocytize the pathogens releasing _________

A

Soluble mediators: cytokine, leukotriene, prostaglandins

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7
Q

Inflammation can be ____ and ____

A

Acute and Chronic

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8
Q

Acute inflammation occurs _______

A

In response to tissue injury

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9
Q

Chronic inflammation

A

Leads to progressive destruction

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10
Q

Two systems involved in acute inflammatory response

A

Clotting systems and Kinin systems

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11
Q

Explain clotting system (acute inflam response)

A

Fibrin produces clots to stop spread of infection through the blood

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12
Q

Explain kinin system (acute inflam response)

A

Produces bradykinin which results to vasodilation and permeability

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13
Q

During acute inflammation, what dominates the landscape?

A

Non-protein based soluble factors (eicosanoids, bioamines)

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14
Q

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

A

Eicosanoids

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15
Q

Chronic inflammation results from what?

A

Continuous exposure to offending element

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16
Q

T or F: Pathogen persistence causes continuous activation of T-cells and cancers

A

True

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17
Q

In chronic inflammation, the following are activated and accumulated

A

Macrophages, Lymphocytes, Fibroblast

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18
Q

T or F: In chronic inflammation, cytokines, chemokines, growth factors are the primary factors

A

True

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19
Q

Give the 2 treatment strategies

A
  1. Relief of symptoms - NSAIDs
  2. Maintain function and slowing of tissue-damaging process - DMARDs
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20
Q

Phospholipids are converted into ____ by the enzyme ____

A

Into arachidonic acid by phospholipase

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21
Q

What are given to remove the enzyme phospholipase, inhibiting arachidonic acid production?

A

Corticosteroids

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22
Q

Arachidonic acid is converted into ____ by the enzyme ____

A

Into leukotrienes by lipoxygenase

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23
Q

What are given to prevent conversion of AA to Leukotrienes?

A

Lipoxygenase inhibitors

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24
Q

Responsible for an increase in vascular permeability and constriction of smooth muscles (e.g., bronchial airways)

A

Leukotrienes C, D, E

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25
Functions for phagocytic attraction or activation by engulfing pathogens, hence, releasing chemicals responsible for inflammation
Leukotriene B
26
What is given to prevent the phagocytic action of Leukotriene B?
Colchicine
27
What are given to inhibit binding of leukotrienes to their receptors?
Receptor Antagonists (e.g., Montelukast)
28
AA can also be converted to ___, ___, and ___ by the enzyme ____
Into prostaglandin, prostacyclin, thromboxane by cyclooxygenase
29
Cyclooxygenase may be inhibited by ___ and ___?
NSAIDs and Aspirin
30
T or F: Prostaglandins inhibit platelet aggregation
False, prostacyclins
31
From what family are AA?
Eicosanoids
32
Most abundant eicosanoid precursor
AA
33
T or F: Linolenic acid (Omega 3) is converted to Linoleic acid (Omega 6) to form AA
False, Linoleic acid (Omega 6) --> Linolenic acid (Omega 3) --> AA
34
Straight-chain derivatives of eicosanoids
Leukotrienes
35
Cyclic derivatives of eicosanoids
PG, PC, TX
36
Condition common in newborn infants where the opening between aorta and pulmonary artery dose not close resulting to mixing of oxygenated and deoxygenated blood
Patent Ductus Arteriosus
37
To prevent Patent Ductus Arteriosus, we inhibit ___
Production of Prostaglandins
38
T or F: All NSAIDs inhibit PG synthesis
True
39
Enzyme responsible for prostaglandin synthesis
Cyclooxygenase
40
Two forms of COX
COX 1 - constitutive COX 2 - inducible
41
Generates prostanoids for "housekeeping" functions
COX 1
42
Main source of prostanoids responsible for inflammation and cancer
COX 2
43
T or F: NSAIDs are for pain but ironically causes headache as side effect
True
44
Irreversibly inhibits platelet COX and the only NSAID to bind irreversibly
Aspirin
45
T or F: Aspirin is still used as anti-inflammatory
False, rarely used
46
Decreases incidence of transient ischemic attacks, unstable angina, coronary artery thrombosis with MI, and thrombosis after coronary bypass grafting
Aspirin
47
Contraindication of Aspirin
Patients with hemophilia and those at risk for GI bleeding
48
Anti-inflammatory drugs to do not inhibit platelet aggregation
Nonacetylated salicylates
49
T or F: Nonacetylated salicylates are preferred when COX inhibition is undesirable
True
50
COX-2 Selective Inhibitors at usual doses have ____ impact on platelet aggregation
No impact
51
Do COX-2 inhibitors offer cardioprotective effects?
No
52
Benzenesulfonamide COX-2 inhibitor for the treatment of OA, RA, JRA, AS
Celecoxib
53
Inflammation of big joints such as knees and elbows
Osteoarthritis (OA)
54
Inflammation of small joints such as palms of the hand, feet
Rheumatoid Arthritis (RA)
55
Arthritis in children that causes joint swelling and stiffness
Juvenile Rheumatoid Arthritis (JRA)
56
Arthritis that causes inflammation in joints and ligaments of the spine, causing stiffness
Ankylosing spondylitis (AS)
57
Racemic acetic acid derivative COX-2 inhibitor
Etodolac
58
Uses of Etodolac
Treatment of OA, RA, JRA
59
Enolcarboxamide COX-2 inhibitor
Meloxicam
60
Indication of Meloxicam
Treatment of OA, RA, JRA
61
Indole derivative and a potent non-selective COX inhibitor
Indomethacin
62
T or F: Indomethacin does not inhibit phospholipase A and C
False, it inhibits
63
Indomethacin are used less than common NSAIDs, why?
Due to toxicity
64
Indications of Indomethacin
Treatment of OA, RA, AS
65
Adverse effects of Indomethacin
Depression, epilepsy, parkinsonism
66
Propionic acid derivative that non-selectively inhibits COX and inhibits lipoxygenase
Ketoprofen
67
Indications of Ketoprofen
Treatment of OA and RA
68
Ketoprofen ADRs
Thrombocytopenia, Agranulocytosis, Cholestatic hepatitis
69
Only nonacid NSAID which is a ketone prodrug
Nabumetone
70
Nabumetone resembles what drug in its structure?
Naproxen
71
Indication of Nabumetone
Treatment of OA and RA
72
Nabumetone ADR
Diarrhea, Dyspepsia, Abdominal pain
73
Enolcarboxamide derivative that is a non-selective COX inhibitor that also inhibits lymphocyte function
Piroxicam
74
Indication of Piroxicam
Treatment of OA and RA
75
Piroxicam ADR
Peptic ulcer
76
Sulfoxide nonselective prodrug whose active metabolite is a non-selective COX inhibitor
Sulindac
77
Indications of Sulindac
OA, RA, AS, acute gouty arthritis
78
Drug that can be used to inhibit development of colon, breast, and prostate cancer
Sulindac
79
Sulindac ADR
Thrombocytopenia, Agranulocytosis, Nephrotic syndrome
80
Phenylacetic acid derivative
Dicloflenac
81
Difluorophenyl derivative of salicylic acid
Diflunisal
82
Propionic acid derivative
Flurbiprofen, Oxaprozin
83
Simple phenylpropionic acid derivative
Ibuprofen
84
Naphthyl-propionic acid derivative
Naproxen
85
Pyrrole alkanoic acid derivative
Tolmetin

PHARMACOLOGY II (4 decks)

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