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Pharm Exam 4 > Acetaminophen and NSAIDs > Flashcards

Acetaminophen and NSAIDs Flashcards

1
Q

Takes Arachidonic Acid out of the phospholipid membrane.

A

Phospholipase A2

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2
Q

Converts AA to Prostaglandins

A

Cyclooxygenase

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3
Q

COX1 makes:

A

Prostaglandin E2
Thromboxane
Prostacycline

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4
Q

What does PGE2 control?

A

Renal perfusion/GFR

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5
Q

What does Prostacycline control?

A

Gastric acid secretion

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6
Q

COX 2 makes prostaglandins that control what?

A

Pain, inflammation, and fever.

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7
Q

COX 2 makes __________ prostaglandins

A

pro-inflammatory

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8
Q

What do NSAIDs inhibit?

A

COX pathways.

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9
Q

These are anti-pyretic, analgesic, and anti-inflammatory.

A

NSAIDs

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10
Q

Act by inhibiting cyclooxygenase enzymes, causing decreased prostaglandin synthesis.

A

NSAIDs.

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11
Q

Prevent AA from binding to COX so that no prostaglandins are made.

A

NSAIDs

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12
Q

4 types of NSAIDs

A

Aspirin
Ibuprofen
Naproxen
Indomethacin

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13
Q

Aspirin is AKA

A

Acetylsalicyclic acid

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14
Q

NSAIDs that are propionic acids

A

Ibuprofen

Naproxen

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15
Q

Motrin and Advil are:

A

Ibuprofen

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16
Q

Aleve is:

A

Naproxen

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17
Q

Used for fever, mild-to-moderate pain, dental pain, headache, and it has the lowest risk of GI bleeding.

A

Ibuprofen (Motrin and Advil)

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18
Q

NSAID that’s an acetic acid derivative.

A

Indomethacin

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19
Q

Why does the heart make prostaglandins?

A

To keep the vessels supplying the heart open, so more blood can get to the heart.

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20
Q

How do NSAIDs affect the heart?

A

Fewer prostaglandins are made, so less blood travels through the heart.

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21
Q

Action of PGE2 on nociceptive nerve endings.

A

PGE2 sensitizes nociceptive nerve endings to painful stimuli.

Primes nociceptors to sense pain.

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22
Q

How do NSAIDs cause analgesia?

A

They prevent PGE2 from being made, so nociceptors are not primed to sense pain.

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23
Q

T/F: No single NSAID has superior analgesic efficacy over another.

A

TRUE

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24
Q

Pyresis

A

Fever

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25
Q

Pyrogen definition

A

Fever promoting agent

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26
Q

How does PGE2 cause fever in people?

A

It increases the set point for the thermoregulatory center in the brain, and body temperature doesn’t get regulated until it’s pretty high.

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27
Q

How do NSAIDs lower temperature in patients with a fever?

A

They decrease the amount of PGE2 made, so that it cannot reset the hypothalamic thermoregulatory center “set point.”

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28
Q

An inducible isoform that is induced by pro-inflammatory stimuli in migratory cells and inflamed tissues.

A

COX-2

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29
Q

Analgesic doses of NSAIDs are ____ and have a ______.

A

small; ceiling.

30
Q

Anti-inflammatory doses of NSAIDs are ______ and don’t have a _______.

A

high; ceiling.

31
Q

Do NSAIDs have high or low first pass metabolism?

A

Low

32
Q

NSAIDs are weak _____ that are rapidly absorbed in the acidic environment of the stomach.

A

acids.

33
Q

Why do NSAIDs slow the clearance of drugs in the kidney?

A

Bc they inhibit PGE2, thus slowing renal perfusion rate.

34
Q

How do COX1 and COX2 increase GFR in the kidney?

A

By making prostaglandins, which vasodilate the arteries, and increase the amount of blood going to the kidney.

35
Q

Role of PGE2 in the GI mucosa.

A

Gastric protection:

Mucus secretion
Bicarbonate secretion
Increased mucosal blood flow.

36
Q

What does inhibition of COX-1 by NSAIDs do in the GI?

A

Peptic ulcers

GI bleeding

37
Q

Which COX is found in the GI?

A

COX 1

38
Q

Role of PGE2 in the kidney.

A

1) Arteriolar dilation to increase GFR/Renal Perfusion.

2) Increases Na and water excretion.

39
Q

Which COX are found in the kidney?

A

COX 1 and COX 2

40
Q

What does inhibition of Cyclooxygenase by NSAIDs cause in the kidney?

A

1) Na and Water retention.
2) Hypertension
3) Hemodynamic acute kidney injury.

41
Q

Which cyclooxygenases are found in the heart?

A

COX 1 and COX 2

42
Q

What does PGI2 (Prostacyclin) by COX 2 do in the heart?

A

1) Vasodilation of heart arteries

2) Inhibits platelet aggregation

43
Q

What does Thromboxane A2 by COX-1 do in the heart?

A

1) Causes platelet aggregation

2) Vasoconstriction

44
Q

What happens if COX 1 and 2 are inhibited in the heart?

A

Stroke and MI

45
Q

Role of PGE2 in the stomach.

A

Inhibits gastric acid secretion.

46
Q

Role of PGI2 in the stomach.

A

Causes mucus and bicarbonate secretion.

47
Q

What do NSAIDs inhibit in the stomach?

A

PGE2 and PGI2 by inhibiting COX-1 activity.

48
Q

NSAIDs ______ stomach acid secretion and ________ mucus production, thus ________ the adverse effects and toxicities in the GI.

A

increase; decrease, increasing

49
Q

Which prostaglandin is found in the heart?

A

PGI2

50
Q

Which cyclooxygenase makes PGI2 in the heart?

A

COX-2

51
Q

PGI2 is called what?

A

Prostacyclin

52
Q

COX __ makes _____ in the heart.

A

2; PGI2

53
Q

T/F: Cardiovascular toxicity with NSAIDs is due to inhibition of cardioprotective PGI2, which is generated by COX-2.

A

TRUE

54
Q

NSAID that selectively inhibits COX-2

A

Celecoxib

55
Q

T/F: NSAIDs are contraindicated in pregnancy.

A

True

56
Q

_______ is preferred if analgesic or antipyretic effects are needed during pregnancy.

A

Acetaminophen (Tylenol)

57
Q

Why should NSAIDs be avoided in the third trimester?

A

Can cause premature closure of the ductus arteriosus.

58
Q

These NSAIDs have important cardiovascular effects that include increased risk for MI, stroke, heart failure, and hypertension.

A

Celecoxib (COX-2 inhibitor)

59
Q

These cyclooxygenase inhibitors are preferred bc they have fewer symptomatic gastric and duodenal ulcers and a decrease in GI symptoms.

A

COX-2 Inhibitors

60
Q

COX-2 selective inhibitor.

A

Celecoxib

61
Q

This COX inhibitor has a lower incidence of gastroduodenal ulcers compared to nonselective NSAIDs.

A

Celecoxib

62
Q

Higher doses of this drug are clearly associated with an increased cardiovascular risk.

A

Celecoxib

63
Q

T/F: In patients taking routine NSAIDs for 10 days or fewer to alleviate pain, most patients are not at any increased risk of developing adverse CV, GI, renal, or respiratory adverse effects.

A

True

64
Q

This NSAID is used as an anti-platelet.

A

Aspirin

65
Q

Common doses of aspirin

A

81-325 mg once a day

66
Q

Which cyclooxygenase does Aspirin inhibit?

A

COX-1

67
Q

Platelets make this cyclooxygenase.

A

COX-1

68
Q

Aspirin irreversibly inhibits COX-___, preventing ____ synthesis.

This antiplatelet effect lasts 8-10 days (the life of the platelet).

A

1; TXA2

69
Q

How does Aspirin inhibit COX-1?

A

By acetylating it.

70
Q

This NSAID is prescribed as secondary prevention of heart attack and stroke.

A

Aspirin

71
Q

This NSAID is for fever and pain, but not anti-inflammatory.

A

Acetaminophen (Tylenol)

72
Q

Acetaminophen MOA

A

Centrally acting:

1) It raises the pain threshold.
2) It inhibits endogenous pyrogens of the heat-regulating centers in the brain.

Pharm Exam 4 (9 decks)

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