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TT BL and DD Exam1 > DD5 - NSAIDS > Flashcards

DD5 - NSAIDS Flashcards

1
Q

Cox1 and 2.

Which one is constitutively expressed ? Induced?

A

Cox 1: constitutively

Cox2: induced

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2
Q

Effects of Cox 1 on GI tract

A

think protective effects

  • ↓ acid/pepsin secretion
  • ↑ mucous/bicarbonate production
  • ↑ contractions of smooth muscle
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3
Q

Effects of COX1 on platelets

A

[TXA2]

• Pro-aggregatory effect

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4
Q

Effects of COX1 on kidneys

A
  • ↑ Renal blood flow (makes for healthy kidney)

* Promote diuresis

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5
Q

Effects of COX1 on vascular smooth muscle

A

[PGI2, PGE2] - vasodilation

[TXA2] - vasoconstriction

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6
Q

Effects of COX1 on Bone

A

PGE2- Stimulates bone formation and resorption

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7
Q

Effects of COX2 on areas of pain/inflammation

A
  • Enhance edema formation
    • Enhance leukocyte infiltration via vasodilation
    • Potentiation of bradykinin pain-producing activity
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8
Q

Effects of COX2 on hypothalamus/fever

A
  • ↑ Heat generation

* ↓ Heat loss

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9
Q

Effects of COX2 on kidneys

A
  • Renal adaptation to stress via maintenance of RBF

* Present constitutively, but most important in elderly

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10
Q

Effects of COX2 on endothelial cells

A
  • Vasodilation

* Anti-aggregatory platelet effects

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11
Q

Effects of COX2 on uterine smooth muscles

A

[PGE2, PGF2]

• Labor contractions near parturition

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12
Q

Effects of COX2 ductus arteriosus

A

[PGE2]

• Maintenance of patent ductus arteriosus via vasodilatory effects

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13
Q

Prostaglandin effects on:

vascular smooth muscle

A

PGE2 causes vasodilation,

TXA2 causes vasoconstriction

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14
Q

Prostaglandin effects on:

platelets

A

TXA2 pro-aggregatory

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15
Q

Prostaglandin effects on:

GI tract smooth muscle and secretory cells

A

PGE2/PGI2 inhibit HCl secretion, increase mucous secretion, increase SM contraction

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16
Q

Prostaglandin effects on:

kidney cells

A

GE2/PGI2 increase RBF, promotes diuresis

17
Q

Prostaglandin effects on:

uterine cells

A

PGE2/PGF2 induces contractions near parturition

18
Q

Prostaglandin effects on:

inflammatory cells

A

PGE2/PGI2 potentiate pain, edema, fever

19
Q

Side effects:

inhibit cox-1

A

GI ulceration,
prolonged bleeding time,
and acute renal failure

20
Q

Side effects:

inhibit cox-2

A

acute renal failure, thrombotic events (COX-2 selective agents), and prolonged gestation

21
Q

Describe the differences between LTB4 and LTC4/LTD4/LTE4 on inflammatory cell function and pulmonary / vascular smooth muscle.

A

• LTB4: Enhanced chemotaxis of neutrophils, aggregation, and transmigration through the endothelium
○ *critical for immune response

• LTC4/LTD4/LTE4: Increased vascular permeability, bronchoconstriction, vasoconstriction
○ Important role in asthma, psoriasis, and various hypersensitivity processes.

22
Q

4 types of NSAIDS

A

Aspirin
Acetaminophen
tNSAIDs
COX-2 Selective inhibitors (celecoxib)

23
Q

Aspirin Effect on COX-1&2

A

1&2 Irreversible

24
Q

Acetaminophen Effect on COX-1&2

A

CNS Cox2 inhibitor

25
Q

tNSAIDs Effect on COX-1&2

A

1&2 Reversible

26
Q

COX-2 selective inhibitors

(celecoxib) Effect on COX-1&2

A

2 Reversible

27
Q

Aspirin therapeutic uses

A

AG, AP, AI, AT

*only one that is AT

28
Q

Acetaminophen

A

AG, AP

*only one that is not AI

29
Q

tNSAIDs

A

AG, AP,AI

30
Q

Celecoxib (cox2 selective inhibitor)

A

Ag, AP, AI

31
Q

Which one, COX1 or 2 is Pro thrombic?

A

Cox1 - likes to clot - good for you usually

32
Q

Which one, COX1 or 2 is Anti thrombic?

A

Cox2

33
Q

Aspirin at low or high doses is antithrombotic? why?

A

low:
aspirin (ASA) concentrates in the hepatic portal vein → concentration differential between endothelial surface and platelets → selective inhibitory effect on platelet COX1 and endothelial COX2 → preferential inhib effect on Cox1 → block the pro-clotting COX1 = antithrombotic effect

34
Q

Aspirin and acetominophen are metabolized via which phase I or II?

A

Phase 2

TT BL and DD Exam1 (23 decks)

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