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NSAIDs Flashcards

1
Q

Prostaglandins are synthesized by what type of cells?

A

Endothelial cells

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2
Q

Anti-platelet effects are exerted through inhibition of which type of COX?

A

COX-1

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3
Q

High levels of prostaglandin (PGE2) inhibit platelet aggregation. T or F

A

True. However low levels of PGE2 enhance platelet aggregation along with thromboxane

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4
Q

What are the actions of prostaglandin (PGE2)?

A
  • Vasodilation
  • Increase GFR through vasodilation
  • Inflammation, Pain, Fever
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5
Q

Low dose aspirin preferentially inhibit which COX?

A

COX-1

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6
Q

NSAIDs are very effective for which type of pain?

A

Dull, throbbing pain

Not very good for acute pain

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7
Q

What are the main prostanoids involved in nociceptor sensitization?

A

Prostaglandin E2 and Prostacyclin (PGI2)

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8
Q

Why do we think NSAIDs also have a central site of action?

A

When administered intrathecally, ASA exerts equianalgesic effect as when administered systematically –> Strong evidence for spinal cord site of action exerted by ASA and other NSAIDs

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9
Q

Explain the physiological process of fever.

A

Exogenous pyrogen (bacterial toxins) and cytokines stimulate endothelial cells in the hypothalamus to make PGE2. PGE2 increases the hypothalamic temperature set point resulting in fever.

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10
Q

How does NSAIDs have antipyretic effect?

A

It inhibits PGE2 production, changing the hypothalamic temp. set point back to normal.

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11
Q

Why were COX-2 selective NSAIDs designed?

A

To target pain and inflammation without significantly affecting COX-1 mediated homeostatic mechanisms such as GI protection

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12
Q

Explain the physiological process of gout.

A

Gout is caused by excessive levels of uric acid in the blood which forms monosodium urate crystals and collects around the joints, tendons, and tissues causing inflammation and pain.

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13
Q

In gout, urate crystals are phagocytosed by ________ which then release _________.

A

Synoviocytes, Prostaglandin

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14
Q

NSAIDs MOA in gout

A

Inhibit urate crystal phagocytosis by inhibiting migration of leukocytes to the area and inhibiting prostaglandin production.

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15
Q

Which drug can cause more uric acid build up, worsening gout?

A

Low dose aspirin

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16
Q

What is the onset of action of Indomethacin?

A

2-4 hours

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17
Q

How long does it take for swelling to decrease after starting indomethacin for gout?

A

3-5 days

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18
Q

Distribution characteristic of NSAID

A

Highly protein bound

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19
Q

Excretion of NSAID

A

excreted by glomerular filtration or tubular secretion

20
Q

What is the evidence for COX-2 selective NSAID and increase in CV risk?

A

Currently chances of CV events are the same as non-selective in subjects without prior diagnosis of CV disease

21
Q

NSAID does not increase the risk of A-fib. T or F

A

False. Same risk in selective and non-selective

22
Q

Low dose ASA MOA

A

preferential blockade of thromboxane A2 production causing decrease platelet aggregation and vasodilation

23
Q

List the risk factors for GI ulcer

A
  • History of ulcer and ulcer complications
  • Over age of 60
  • High dose NSAID
  • Multiple NSAID use
  • Long-acting NSAID use
  • Concomitant anticoagulants
  • Heart disease
24
Q

What are the long-acting NSAIDs?

A

Piroxicam, Ketorolac, SR formulations

25
Q

Which 2 NSAIDs are associated with the lowest risk of GI ulceration?

A

ibuprofen and celecoxib

26
Q

All NSAIDs inhibit platelet aggregation to some extent. T or F

A

True

27
Q

What are the effects of NSAIDs on renal?

A

Salt and water retention; edema; hyperkalemia, worsening renal function and nephrotoxicity

28
Q

In the kidney, prostaglandin mediates _____ arteriole vaso____.

A

Afferent arteriole vasodilation

29
Q

In the kidney, angiotensin II mediates _____ arteriole vaso_____.

A

Efferent arteriole vasoconstriction

30
Q

If you have high CV risk, which NSAIDs can you use?

A

Naproxen if low GI risk or add PPI/misoprostol if moderate

31
Q

If you have high GI risk but low CV risk, what NSAID should you take?

A

Avoid NSAID

If must take, celecoxib + PPI

32
Q

When should you recommend a PPI or misoprostol?

A

To patients with moderate risk = 1-2 factors:

age, high dose NSAID, previous ulcer, use of ASA or antiplatelet drug

33
Q

What is the dose per kg that can cause ASA toxicity?

A

200mg/kg

34
Q

What are symptoms of salicylism?

A

Vomiting, tinnitus, decrease hearing, vertigo (reversible)

35
Q

What can be used to treat ASA toxicity?

A

Activated charcoal, gastric lavage

36
Q

Which proposed MOA of APAP can explain why it is not associated with inhibition of platelet aggregation?

A

APAP is a reducing agent that changes COX to its inactive form in cells with low oxidant status. Platelets have high oxidant status so APAP does not work there.

37
Q

Peroxide concentrations are high in the brain so that’s why APAP works there. T or F

A

False, APAP works in the brain because it has low peroxides. Peroxides block APAP actions.

38
Q

Naloxone injected intrathecally can reverse the antinociceptive effects of acetaminophen. (T or F)

A

Partly true. It can reverse it if APAP was injected into the brain and spine at the same time. But not if given to the spine alone.

39
Q

95% of APAP metabolites are produced these 2 pathways.

A

Glucuronidation and sulfation

40
Q

Which CYP enzymes are involved in APAP metabolism?

A

CYP3A4 and CYP2E1

41
Q

Hepatotoxicity from APAP overdose can show up after ____ hours.

A

24-36

42
Q

What drug can you use to treat APAP toxicity?

A

Acetylcysteine - a glutathione substitute

43
Q

What is an important drug interaction of APAP?

A

Warfarin - enhances anticoagulation

44
Q

TRPV1

A

Transient receptor potential vanilloid 1 = activating this receptor in PAG in rats resulted in antinociception

45
Q

Which 2 descending pain inhibitory pathways is it theorized that APAP is involved in?

A

Serotonergic descending pain inhibitory pathway originating in the periaqueductal gray and descending endogenous opioid pathways

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