Nsaids - Part 2 (Msq Drill 176)

1. Would you give an NSAID to a patient that has a history of ASA induced bronchospasm?

Yes

No

2. Analegesic nephropathy can also occur due to NSAID administration. True or false?

True

False

3. Therefore Aspirin inhibits platelet function for the life of the platelet. True or false?

True

False

4. Inhibiting COX 1 leads to edema because of increased ADH. Inhibiting COX 2 also leads to edema. Is the mechanism exactly the same?

Yes, ADH is involved in both mechanisms

No, sodium retention causes edema in COX 2 inhibition

5. Are elderly patients at a higher risk of GI erosion from NSAIDS?

Yes

No

6. What should you watch for with tylenol?

Hepatotoxicity

Nephrotoxocity

7. Can ASA contribute to Salicylism?

Yes

No

8. How does Aspirin prevent clotting?

It reversibly acetylates COX

It irreversibly aceylates COX

9. Can you get headaches from taking NSAIDS?

Yes

No

10. In addition to edema, inhibiting COX 2 will also affect fluid and electrolyte balance. True or false?

True

False

11. Do platelets have a nuclei?

Yes

No

12. If you give a low dose of Aspirin (which will be hereto referred to as ASA) is this more selective for COX 1 or COX 2?

Low dose ASA selective for COX 1

Low dose ASA selective for COX 2

13. Aspirin is a platelet inhibitor. True or false?

True

False

14. Does ADH upregulation lead to fluid retention or fluid excretion

Fluid retention

Fluid excretion

15. Can ASA induce bronchospasm?

Yes

No

16. The following drugs are all COX 2 drugs. Which drug is COX 2 specific?

Celexocib ( celebrex)

Meloxicam (mobic)

Nabemutone (Relafen)

Edotolac (lodine)

17. If a pateint has a GI risk which COX will you opt for. You will either give the COX inhibitor at the normal dose or with a PPI if you use a classic dose?

COX 1

COX 2

18. What method is better for administering COX inhibitors?

High doses for the shortest amount of time

Low doses for the shortest amount of time

Low doses over a long time

19. A child taking ASA is at risk for:

Steven Johnson's syndrome

Reye's syndrome

Chronic fatigue syndrome

Fibromyalgia

20. Do platelets make new COX after Aspirin has IRREVERSIBLY reversed their COX?

Yes, it is a continuous process

No, they cannot make new COX because they have no nuclei.

21. Which patients are at risk for complications if they take NSAIDs?

A patient with hypertension

A patient who is 20 years old and has bursitis, and is dehydrated and diabetic

A patient with CHF

A patient with impaired kidney function

An old patient

HARDD - Htn, aged, renal impairement, dehydrated/diuresed. diabetic.)

Explanation

HARDD - Htn, aged, renal impairement, dehydrated/diuresed. diabetic.)

Submit

22. Whereas misoprostol 9cytotec) is a prostaglandin analog, ____________ is a proton pump inhibitor.

Lasix (furosemide)

Protonix (pantoprazole)

Zantac (ranitidine)

drugs ending in prazole. Zantac is a histamine H2 receptor agonist not a PPI.

Explanation

drugs ending in prazole. Zantac is a histamine H2 receptor agonist not a PPI.

23. Acetaminophen has a HUGE anti-inflammatory effect. True or false?

True

False

It has minimal anti-inflammatory effect.

Explanation

It has minimal anti-inflammatory effect.

24. COX 1 or COX 2?

increased GI erosion
Decreased renal perfusion
decreased platelet aggregation

COX 1

COX 2

25. Does tylenol have minimal or severe GI effects?

Minimal GI effects

Severe GI effects

26. What is the acetominophen toxic intermediate that is capable of necrotizing hepatocytes?

Organophosphate

NAPQ 1

3-methylindole

27. What is the specific antidote for acetaminophen?

Atropine

Vitamin K

Benadryl

Acetylcysteine

AKA mucomyst

Explanation

AKA mucomyst

28. Do you see decreased renal perfusion with COX 1 or COX 2 or both?

COX 1 only

COX 2 only

Both COX 1 and COX 2

29. What is the hallmark of salicylism?

Blindness

Weight gain

Bleeding

Tinnutis

30. When renal perfusion is decreased, is ADH secretion upregulated or downregulated?

ADH secretion is upregulated

ADH secretion is downregulated

31. Celexocib (celebrex) should not be administered to a patient with ______ allergy.

Sulfonamide

Shell fish

Pottasium

Peanut

32. Would you give a patient presenting with acute gout acetaminophen?

Yes, it will reduce the pain

No, it is not useful for acute gout

33. What is salisylism?

Toxic overdose of ibuprofen

Toxic effects of overdosage with acetylsalicylic acid only

Toxic effects of overdosage with salicylic salts

34. Therefore giving a patient a COX 1 inhibitor, will decrease renal perfusion, increase ADH secretion and thus lead to which symptoms?

Edema

Polyuria

Hypertension

Hypotension

Submit

35. Ibuprofen, naproxen and ketorolax(toradol) are all non specific COX inhibitors. Of these three drugs which has has the MOST COX 1 selectivity and thus has the greatest rsik of GI erosion?

Ibuprofen

Naproxen

Ketorolac (toradol)

36. Macrophage chemotaxis is mediated by COX enzymes. If you give a patient low dose ASA, does this also block the mediatory effect of COX 2 on macrophages?

Yes

No

37. Giving low dose ASA may contribute to ASA resistance. True or false?

True

False

38. Since ketorolac (toradol) has the greatest risk of GI erosion it should only be administered for ___ days.

1

2

3

4

5

39. If you inhibit COX _____ you decrease renal perfusion via EFFERENT constriction.

1

2

This can lead to ARB and elevated BP as covered in part 1 of this quiz. This is worse when combined with ACEI-ARBs.

Explanation

This can lead to ARB and elevated BP as covered in part 1 of this quiz. This is worse when combined with ACEI-ARBs.

40. ASA: salicylic acid or acetylsalicylic acid?

Salicylic acid

Acetylsalicylic acid

same compound but it is acetylated in ASA.

Explanation

same compound but it is acetylated in ASA.

41. Tinnutis is the hallmark of salicylism. What other symptoms can be present? check all that apply.

Hyperpyrexia

Sweating

Hyperventilation

Metabolic acidosis with respiratory alkalosis

Metabolic alkalosis with respiratory acidosis

hyperpyexia - abnormally high fever.
"Alive until dead."

Explanation

hyperpyexia - abnormally high fever.
"Alive until dead."

Submit

42. Taking misoprostol (cytotec) whilst taking an NSAID can prevent toxicity. What class does misoprostol belong to?

Proton pump inhibitor

Prostaglandin inhibitor

Diuretic

Anti hypertensive

43. Which of the following increases the risk of GI erosion?

Duplicating and NSAID dose

Taking NSAIDS when you have a prior history of GI or cardiovascular disease

Taking an NSAID concurrently with an SSRI

Taking an NSAID for arthritis

Taking NSAIDS with steroids

Submit

44. What is often the FIRST symptom of NSAID toxicity?

Mild GI bleed

Chronic GI bleed

Life threatening GI bleed

Most people are asymptomatic initially

Explanation

Most people are asymptomatic initially

45. It is better to take a low dose antiacid with an NSAID. True or false?

True, a low dose antiacid will decrease the risk of GI erosion

False, concurrent low dose antacid intake with an NSAID puts you at risk for GI erosion

46. Which of the following is a CNS manifestation that you might observe in a patient with systemic lupus eythmatosus who is also taking NSAIDS?

Psychosis

Septic meningitis

Avascular necrosis

Aseptic meningitis

Subdural hematoma

47.
Which of the following are classes of drugs or drugs that NSAIDS seem to interfere with?

Lithium - cause decreased elimjination

Diuretics

Antihypertensives

All antipsychotics

Submit

48. Which of the following drugs are non selective COX acting drugs?

Ibuprofen

Naproxen

Ketorolax (toradol)

ASA

Meloxicam (mobic)

Submit

49. What can you take to try and prevent GI erosion is you going to take an NSAID?

An ASA every morning.

Misoprostol (cytotec)

Omeprazole (prilosec)

Lasix (furosemide)

Submit

50. Which of the following should never take an NSAID?

Creatine clearance >60

Creatine clearance >30

Allergy to ASA

GI injury

At risk for thrombosis

Nsaids - Part 2 (Msq Drill 176)

1. Would you give an NSAID to a patient that has a history of ASA induced bronchospasm?

2.

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

2. Analegesic nephropathy can also occur due to NSAID administration. True or false?

3. Therefore Aspirin inhibits platelet function for the life of the platelet. True or false?

4. Inhibiting COX 1 leads to edema because of increased ADH. Inhibiting COX 2 also leads to edema. Is the mechanism exactly the same?

5. Are elderly patients at a higher risk of GI erosion from NSAIDS?

6. What should you watch for with tylenol?

7. Can ASA contribute to Salicylism?

8. How does Aspirin prevent clotting?

9. Can you get headaches from taking NSAIDS?

10. In addition to edema, inhibiting COX 2 will also affect fluid and electrolyte balance. True or false?

11. Do platelets have a nuclei?

12. If you give a low dose of Aspirin (which will be hereto referred to as ASA) is this more selective for COX 1 or COX 2?

13. Aspirin is a platelet inhibitor. True or false?

14. Does ADH upregulation lead to fluid retention or fluid excretion

15. Can ASA induce bronchospasm?

16. The following drugs are all COX 2 drugs. Which drug is COX 2 specific?

17. If a pateint has a GI risk which COX will you opt for. You will either give the COX inhibitor at the normal dose or with a PPI if you use a classic dose?

18. What method is better for administering COX inhibitors?

19. A child taking ASA is at risk for:

20. Do platelets make new COX after Aspirin has IRREVERSIBLY reversed their COX?

21. Which patients are at risk for complications if they take NSAIDs?

22. Whereas misoprostol 9cytotec) is a prostaglandin analog, ____________ is a proton pump inhibitor.

23. Acetaminophen has a HUGE anti-inflammatory effect. True or false?

24. COX 1 or COX 2?increased GI erosionDecreased renal perfusiondecreased platelet aggregation

25. Does tylenol have minimal or severe GI effects?

26. What is the acetominophen toxic intermediate that is capable of necrotizing hepatocytes?

27. What is the specific antidote for acetaminophen?

28. Do you see decreased renal perfusion with COX 1 or COX 2 or both?

29. What is the hallmark of salicylism?

30. When renal perfusion is decreased, is ADH secretion upregulated or downregulated?

31. Celexocib (celebrex) should not be administered to a patient with ______ allergy.

32. Would you give a patient presenting with acute gout acetaminophen?

33. What is salisylism?

34. Therefore giving a patient a COX 1 inhibitor, will decrease renal perfusion, increase ADH secretion and thus lead to which symptoms?

35. Ibuprofen, naproxen and ketorolax(toradol) are all non specific COX inhibitors. Of these three drugs which has has the MOST COX 1 selectivity and thus has the greatest rsik of GI erosion?

36. Macrophage chemotaxis is mediated by COX enzymes. If you give a patient low dose ASA, does this also block the mediatory effect of COX 2 on macrophages?

37. Giving low dose ASA may contribute to ASA resistance. True or false?

38. Since ketorolac (toradol) has the greatest risk of GI erosion it should only be administered for ___ days.

39. If you inhibit COX _____ you decrease renal perfusion via EFFERENT constriction.

40. ASA: salicylic acid or acetylsalicylic acid?

41. Tinnutis is the hallmark of salicylism. What other symptoms can be present? check all that apply.

42. Taking misoprostol (cytotec) whilst taking an NSAID can prevent toxicity. What class does misoprostol belong to?

43. Which of the following increases the risk of GI erosion?

44. What is often the FIRST symptom of NSAID toxicity?

45. It is better to take a low dose antiacid with an NSAID. True or false?

46. Which of the following is a CNS manifestation that you might observe in a patient with systemic lupus eythmatosus who is also taking NSAIDS?

47. Which of the following are classes of drugs or drugs that NSAIDS seem to interfere with?

48. Which of the following drugs are non selective COX acting drugs?

49. What can you take to try and prevent GI erosion is you going to take an NSAID?

50. Which of the following should never take an NSAID?

24. COX 1 or COX 2?

increased GI erosion
Decreased renal perfusion
decreased platelet aggregation

47.
Which of the following are classes of drugs or drugs that NSAIDS seem to interfere with?