NSAIDS Exam 4 Flashcards

1
Q

What are NSAIDS commonly used for?

A

temporary management of pain

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2
Q

What 3 things we use NSAIDS for?

A

Anti-pyretic, analgesic and anti-inflammatory

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3
Q

What is the MOA for NSAIDs

A

Depress eicosanoids action, inhibiting action of prostaglandins and thromboxane

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4
Q

NSAIDS inhibit?

A

COX-1 and COX-2

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5
Q

Two pathways of Arachidonic Acid?

A

Leukotrienes

Eicosanoids

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6
Q

What enzyme creates leukotrienes?

A

5-lipoxygenase

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7
Q

What enzyme creates PGs?

A

Cyclooxygenase

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8
Q

Both NSAIDs and glucocorticoids inhibit?

A

COX-2

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9
Q

Where is COX-1 found?

A

in all cells especially stomach “housekeeper”

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10
Q

Where is COX-2 found?

A

in all inflammatory cells, kidney, lungs

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11
Q

COX-1 is a major product of what?

A

thromboxane

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12
Q

Aspirin works on what pathway?

A

COX-1, COX-2, and Lipoxygenase

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13
Q

MOA of corticosteroids?

A
  1. increase Lipocortin, inhibiting PLA

2. Block expression of inflammatory genes

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14
Q

MOA of Leukotriene inhibitors?

A

block leukotriene activity

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15
Q

MOA of 5-ASA?

A

inhibits COX-1, COX-2, lipoxygenase.

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16
Q

MOA of Zileuton (Zyflo CR)

A

inhibits lipoxygenase

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17
Q

MOA of Zafirulask (Accolate) and Montelukast (Singulair)?

A

block LT receptors

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18
Q

Used to treat asthma and seasonal allergies

A

Zafirlukast and montelukast

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19
Q

Used to treat IBD

A

5-ASA

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20
Q

What is unique about aspirin?

A

irreversibly inhibits

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21
Q

NSAIDs blocking the Cox pathway could cause what?

A

shunting to LT synthesis

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22
Q

What dose does NSAIDs inhibit COX?

A

low doses 200mg

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23
Q

What dose dose NSAIDs produce anti-inflammatory effects?

A

larger doses (600-800mg)

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24
Q

T/F Aspirin is less potent than NSAIDs?

A

True

25
Q

At what dose does Aspirin reduce platelet aggregation?

A

<100mg

26
Q

What dose does aspirin provide analgesic and antipyretic effects?

A

up to > 200mg

27
Q

What dose does aspirin provide anti-inflammatory effects>

A

> 800mg (risk of gastric intolerance)

28
Q

How does NSAIDs provide anti-inflammatory effects @ high doses?

A

blocks ATP-binding site on IkK to prevent it from phosphorylating IkB and activating NFkB

29
Q

DOC for antipyresis?

A

Acetominophen

30
Q

DOC for analgesia?

A

Acetaminophen

31
Q

DOC for primary dysmenorrhea?

A

Ibuprofen

32
Q

DOC for inhibiting parturition?

A

Indomethacin

33
Q

DOC for preventing GI polyps and cancer?

A

Daily aspirin for > 10 yrs

34
Q

DOC for inflammation?

A

ALL NSAIDs work equally

35
Q

What diseases are NSAIDs used for?

A

osteoarthritis, Rheumatoid arthritis, ankylosing spondylitis, muscle soreness and joint pain

36
Q

SDE of Aspirin?

A

Tinnitus

37
Q

What can interfere with aspirin anti-platelet effects?

A

NSAIDs such as ibuprofen

38
Q

What dose is needed for anti-inflammatory effects in arthritis?

A

150-300mg/L

39
Q

What drug carries a risk for MI?

A

Diclofenac (Voltaren)

Coxib drugs

40
Q

SDE of Indomethacin?

A

CNS side effect esp. in elderly

41
Q

What drug doesn’t interfere with anti-platelet effect of aspirin?

A

Celecoxib (COX-2 inhibitors)

42
Q

Used to treat arthritis, dysmennorhea, post surgical pain

A

Celecoxib

43
Q

ADR of aspirin?

A

hypersensitivity: rhinoconjunctitivs, angioedema, uricaria

44
Q

ADR of NSAIDs

A
Increased Bp
Nephrotoxicity
GI ulceration and bleeding
CNS reaction
NSAIDS C/I in preggo/lactation
45
Q

Which NSAIDs can be used in pregnancy and lactation?

A

Acetaminophen

46
Q

What is the biggest worry of taking Acetaminophen?

A

hepatic toxicity

47
Q

What causes acetaminophen toxicity?

A

NAPQI (N-acetyl- benzoquinoneimine)

48
Q

What is the antidote for acetaminophen toxicity?

A

N-acetylcysteine

49
Q

T/F Gout is a metabolic disease

A

True

50
Q

Gout drug used to stop formation of urate?

A

Allopurinal

51
Q

What does Allopurinal inhibit?

A

Xanthine Oxidase

52
Q

Why does acute attacks appear after allopurinal?

A

due to urate shunting into the tissues

53
Q

What is a alternative to Allopurinal?

A

Febuxostat

54
Q

MOA of Colchicine?

A

binds tubulin preventing polymerization. Inhibits leukocyte migration

55
Q

SDE of Colchicine?

A

diarrhea, abdominal pain, alopecia, neutropenia

56
Q

MOA of Uricase?

A

breaks down uric acid after formation

57
Q

Uricase is a ?

A

enzyme

58
Q

Compared to aspirin, Celeboxib has no effect on what?

A

platelet aggregation and GI problems

59
Q

What is contributed to nasal polyps in adults and adult asthma?

A

Aspirin