Nsaids - Part 1 - Cox Enzyme Functions (Msq Drill 177)

1. Eventually the prostaglandins form different tissue isomerase that play multiple roles in various tissues in the body. True or false?

True

False

2. Patients on NSAIDS are at risk for analagesic nephropathy. True or false?

True

False

3. Are prostaglandins also produced from arachidonic acid?

Yes

No

4. If one therefore blocks COX 1, the gastric mucosa will:

Have an overwhelming supply of secretions

Have no secretions and will thus erode

5. If you give a patient a COX inhibitor with bother COX 1 and 2 effect, this will slow down or eliminate macrophage taxis. Will this lead to increased or decreased inflammation?

Increased inflammation

Decreased inflammation

6. Therefore a patient can develop Acute renal failure due to NSAIDS. True or false?

True

False

7. COX 1 initiates the process that eventually leads to the production of ___________ which is responsible for platelet aggregation.

Thromboxane A2

Thromboxane B2

Prostaglandin I2

Prostaglanding E2

8. Decreased renal afferent flow will lead to:

Hyperperfusion of the kidneys

Hypoperfusion of the kidneys

9. Taking an NSAID will reduce perfusion into the kidneys. The kidneys respond by raising or lowering blood pressure?

Raising blood pressure

Lowering blood pressure

10. Arachidonic acid is released from ______ .

Leukotriennes

Phospholipids

Prostaglandin

Cyclooxygenase

Our cell membrane plays a role in the production of arachidonic acid.

Explanation

Our cell membrane plays a role in the production of arachidonic acid.

11. Since prostaglandins can be manipulated by COX 1 and COX 2 to form various tissue isomerases. Which COX enzyme is responsible for maintaining the mucosa, facilitating cytoprotective secretions and increasing secretions?

COX 1

COX 2

12. If all I wanted was an antipyretic effect from an NSAID then I would choose:

A COX 1 inhibitor

A COX 2 inhibitor

antipyretics - drugs that reduce fever

Explanation

antipyretics - drugs that reduce fever

13. If you increased the dose of the COX inhibitor will the inflammation be even more reduced?

Yes

No

14. Which COX enzyme increases fever and also increases my sense of pain?

COX 1

COX 2

COX 2 increased fever and also increases nocicpetion.

Explanation

COX 2 increased fever and also increases nocicpetion.

15. Do COX enzymes cause vasodilation or vasoconstriction?

Vasodilation

Vasoconstriction

16. Are leukotrienes produced directly from phospholipids or from arachidonic acid?

Leukotrienes are produced directly from phospholipase

Leuknotrienes are produced from arachidonic acid

17. So, Aspirin has an effect on COX 1 or COX 2?

Cox 1

Cox 2

18. If you block COX enzymes by taking NSAIDs you increase or decrease leukotrienne formation?

Increase

Decrease

19. What do NSAIDS cause, an increase or decrease in pottasium?

Pottassium gain

Pottassium loss

20. Do both COX enzymes affect microphage chemotaxis?

Yes

No

21. One COX enzyme causes platelet aggregation whilst the other inhibits platelet aggregation. Which COX enzyme inhibits platelet aggregation?

COX 1

COX 2

22. In general, COX enzymes perform the following functions on the kidney:

Increase perfusion

Maintain hydrostatic pressure

Sodium secretion

Control renin

Aldosterone and potassium retention

Submit

23. If you give a patient an NSAID, they will excrete more or less sodium?

More sodium

Less sodium

COX enzyme generally facilitate sodium excretion and potassium retention.

Explanation

COX enzyme generally facilitate sodium excretion and potassium retention.

24. If COX enzymes cause vasodilation, what happens to renal afferent flow when a patient takes an NSAID?

Increased renal afferent flow

Decreased renal afferent flow

25. A physician is considering administering an NSAID to a woman in labor. Will this lead to a quicker delivery or an inhibition of the labor?

Quicker delivery

Inhibited labor

26. What enzyme facilitates the release of arachidonoc acid from phospholipase?

Phospholipase A

Phospholipase B

Phospholipase C

27. What product of arachidonic acid plays a role in pulmonary inflammation and bronchconstriction and therefore has a role in the asthma?

COX 1

COX 2

Prostaglandin 1

Leukotrienne

Thromboxane

28. Eventually patients on NSAIDs will have lower potassium levela and renal tubular _____ .

Acidosis

Alkalosis

29. COX 2 facilitates the production of ________ which is responsible for inhibiting platelet aggregation.

Thromboxane B2

Prostaglandin E2

Prostaglandin I2

30. Which COX enzyme causes vasodilation and thus increased perfusion to the kidneys?

COX 1

COX 2

Both COX 1 and COX 2

31. What eznymes facilitates the prduction prostaglandins from arachidonic acid?

COX 1

COX 2

Phospholipase B

Submit

32. When a patient has an ulcer, their body probably uses COX _____ in the process of wound healing.

COX 1

COX 2

33. What classes of antihypertensive medication should not be used concurrently with NSAIDS

Diuretics

Beta blockers

Angiotensin convertine enzyme inhibitors (ACEIs)

Angiotensin II receptor blockers (ARBs)

Submit

34. Thus, increased leukotrienne formation will result in the following symptoms.

Pulmonary inflammation

Bronchospasms in those who are sensitive

Anaphylactoid

Bronchoconstriction

anaphylactoid - resembling anaphylaxix

Explanation

anaphylactoid - resembling anaphylaxix

Submit

35.
We have established that COX 2 causes platelet aggregation or thrombosis. IF you gave a patient Aspirin, will this thrombotic risk be decreased?

Yes

No

Nsaids - Part 1 - Cox Enzyme Functions (Msq Drill 177)

1. Eventually the prostaglandins form different tissue isomerase that play multiple roles in various tissues in the body. True or false?

2.

What first name or nickname would you like us to use?

2. Patients on NSAIDS are at risk for analagesic nephropathy. True or false?

3. Are prostaglandins also produced from arachidonic acid?

4. If one therefore blocks COX 1, the gastric mucosa will:

5. If you give a patient a COX inhibitor with bother COX 1 and 2 effect, this will slow down or eliminate macrophage taxis. Will this lead to increased or decreased inflammation?

6. Therefore a patient can develop Acute renal failure due to NSAIDS. True or false?

7. COX 1 initiates the process that eventually leads to the production of ___________ which is responsible for platelet aggregation.

8. Decreased renal afferent flow will lead to:

9. Taking an NSAID will reduce perfusion into the kidneys. The kidneys respond by raising or lowering blood pressure?

10. Arachidonic acid is released from ______ .

11. Since prostaglandins can be manipulated by COX 1 and COX 2 to form various tissue isomerases. Which COX enzyme is responsible for maintaining the mucosa, facilitating cytoprotective secretions and increasing secretions?

12. If all I wanted was an antipyretic effect from an NSAID then I would choose:

13. If you increased the dose of the COX inhibitor will the inflammation be even more reduced?

14. Which COX enzyme increases fever and also increases my sense of pain?

15. Do COX enzymes cause vasodilation or vasoconstriction?

16. Are leukotrienes produced directly from phospholipids or from arachidonic acid?

17. So, Aspirin has an effect on COX 1 or COX 2?

18. If you block COX enzymes by taking NSAIDs you increase or decrease leukotrienne formation?

19. What do NSAIDS cause, an increase or decrease in pottasium?

20. Do both COX enzymes affect microphage chemotaxis?

21. One COX enzyme causes platelet aggregation whilst the other inhibits platelet aggregation. Which COX enzyme inhibits platelet aggregation?

22. In general, COX enzymes perform the following functions on the kidney:

23. If you give a patient an NSAID, they will excrete more or less sodium?

24. If COX enzymes cause vasodilation, what happens to renal afferent flow when a patient takes an NSAID?

25. A physician is considering administering an NSAID to a woman in labor. Will this lead to a quicker delivery or an inhibition of the labor?

26. What enzyme facilitates the release of arachidonoc acid from phospholipase?

27. What product of arachidonic acid plays a role in pulmonary inflammation and bronchconstriction and therefore has a role in the asthma?

28. Eventually patients on NSAIDs will have lower potassium levela and renal tubular _____ .

29. COX 2 facilitates the production of ________ which is responsible for inhibiting platelet aggregation.

30. Which COX enzyme causes vasodilation and thus increased perfusion to the kidneys?

31. What eznymes facilitates the prduction prostaglandins from arachidonic acid?

32. When a patient has an ulcer, their body probably uses COX _____ in the process of wound healing.

33. What classes of antihypertensive medication should not be used concurrently with NSAIDS

34. Thus, increased leukotrienne formation will result in the following symptoms.

35. We have established that COX 2 causes platelet aggregation or thrombosis. IF you gave a patient Aspirin, will this thrombotic risk be decreased?

35.
We have established that COX 2 causes platelet aggregation or thrombosis. IF you gave a patient Aspirin, will this thrombotic risk be decreased?