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PHARMACOLOGY II > NSAIDS > Flashcards

NSAIDS Flashcards

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
Q

Functions for phagocytic attraction or activation by engulfing pathogens, hence, releasing chemicals responsible for inflammation

A

Leukotriene B

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26
Q

What is given to prevent the phagocytic action of Leukotriene B?

A

Colchicine

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27
Q

What are given to inhibit binding of leukotrienes to their receptors?

A

Receptor Antagonists (e.g., Montelukast)

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28
Q

AA can also be converted to ___, ___, and ___ by the enzyme ____

A

Into prostaglandin, prostacyclin, thromboxane by cyclooxygenase

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29
Q

Cyclooxygenase may be inhibited by ___ and ___?

A

NSAIDs and Aspirin

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30
Q

T or F: Prostaglandins inhibit platelet aggregation

A

False, prostacyclins

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31
Q

From what family are AA?

A

Eicosanoids

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32
Q

Most abundant eicosanoid precursor

A

AA

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33
Q

T or F: Linolenic acid (Omega 3) is converted to Linoleic acid (Omega 6) to form AA

A

False, Linoleic acid (Omega 6) –> Linolenic acid (Omega 3) –> AA

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34
Q

Straight-chain derivatives of eicosanoids

A

Leukotrienes

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35
Q

Cyclic derivatives of eicosanoids

A

PG, PC, TX

36
Q

Condition common in newborn infants where the opening between aorta and pulmonary artery dose not close resulting to mixing of oxygenated and deoxygenated blood

A

Patent Ductus Arteriosus

37
Q

To prevent Patent Ductus Arteriosus, we inhibit ___

A

Production of Prostaglandins

38
Q

T or F: All NSAIDs inhibit PG synthesis

A

True

39
Q

Enzyme responsible for prostaglandin synthesis

A

Cyclooxygenase

40
Q

Two forms of COX

A

COX 1 - constitutive
COX 2 - inducible

41
Q

Generates prostanoids for “housekeeping” functions

A

COX 1

42
Q

Main source of prostanoids responsible for inflammation and cancer

A

COX 2

43
Q

T or F: NSAIDs are for pain but ironically causes headache as side effect

A

True

44
Q

Irreversibly inhibits platelet COX and the only NSAID to bind irreversibly

A

Aspirin

45
Q

T or F: Aspirin is still used as anti-inflammatory

A

False, rarely used

46
Q

Decreases incidence of transient ischemic attacks, unstable angina, coronary artery thrombosis with MI, and thrombosis after coronary bypass grafting

A

Aspirin

47
Q

Contraindication of Aspirin

A

Patients with hemophilia and those at risk for GI bleeding

48
Q

Anti-inflammatory drugs to do not inhibit platelet aggregation

A

Nonacetylated salicylates

49
Q

T or F: Nonacetylated salicylates are preferred when COX inhibition is undesirable

A

True

50
Q

COX-2 Selective Inhibitors at usual doses have ____ impact on platelet aggregation

A

No impact

51
Q

Do COX-2 inhibitors offer cardioprotective effects?

A

No

52
Q

Benzenesulfonamide COX-2 inhibitor for the treatment of OA, RA, JRA, AS

A

Celecoxib

53
Q

Inflammation of big joints such as knees and elbows

A

Osteoarthritis (OA)

54
Q

Inflammation of small joints such as palms of the hand, feet

A

Rheumatoid Arthritis (RA)

55
Q

Arthritis in children that causes joint swelling and stiffness

A

Juvenile Rheumatoid Arthritis (JRA)

56
Q

Arthritis that causes inflammation in joints and ligaments of the spine, causing stiffness

A

Ankylosing spondylitis (AS)

57
Q

Racemic acetic acid derivative COX-2 inhibitor

A

Etodolac

58
Q

Uses of Etodolac

A

Treatment of OA, RA, JRA

59
Q

Enolcarboxamide COX-2 inhibitor

A

Meloxicam

60
Q

Indication of Meloxicam

A

Treatment of OA, RA, JRA

61
Q

Indole derivative and a potent non-selective COX inhibitor

A

Indomethacin

62
Q

T or F: Indomethacin does not inhibit phospholipase A and C

A

False, it inhibits

63
Q

Indomethacin are used less than common NSAIDs, why?

A

Due to toxicity

64
Q

Indications of Indomethacin

A

Treatment of OA, RA, AS

65
Q

Adverse effects of Indomethacin

A

Depression, epilepsy, parkinsonism

66
Q

Propionic acid derivative that non-selectively inhibits COX and inhibits lipoxygenase

A

Ketoprofen

67
Q

Indications of Ketoprofen

A

Treatment of OA and RA

68
Q

Ketoprofen ADRs

A

Thrombocytopenia, Agranulocytosis, Cholestatic hepatitis

69
Q

Only nonacid NSAID which is a ketone prodrug

A

Nabumetone

70
Q

Nabumetone resembles what drug in its structure?

A

Naproxen

71
Q

Indication of Nabumetone

A

Treatment of OA and RA

72
Q

Nabumetone ADR

A

Diarrhea, Dyspepsia, Abdominal pain

73
Q

Enolcarboxamide derivative that is a non-selective COX inhibitor that also inhibits lymphocyte function

A

Piroxicam

74
Q

Indication of Piroxicam

A

Treatment of OA and RA

75
Q

Piroxicam ADR

A

Peptic ulcer

76
Q

Sulfoxide nonselective prodrug whose active metabolite is a non-selective COX inhibitor

A

Sulindac

77
Q

Indications of Sulindac

A

OA, RA, AS, acute gouty arthritis

78
Q

Drug that can be used to inhibit development of colon, breast, and prostate cancer

A

Sulindac

79
Q

Sulindac ADR

A

Thrombocytopenia, Agranulocytosis, Nephrotic syndrome

80
Q

Phenylacetic acid derivative

A

Dicloflenac

81
Q

Difluorophenyl derivative of salicylic acid

A

Diflunisal

82
Q

Propionic acid derivative

A

Flurbiprofen, Oxaprozin

83
Q

Simple phenylpropionic acid derivative

A

Ibuprofen

84
Q

Naphthyl-propionic acid derivative

A

Naproxen

85
Q

Pyrrole alkanoic acid derivative

A

Tolmetin

PHARMACOLOGY II (4 decks)

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