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Pmcol 343 > 3.10 COX + NSAIDs > Flashcards

3.10 COX + NSAIDs Flashcards

1
Q

Prostaglandins act on…

A

GCPRs

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2
Q

How do prostaglandins act in the stomach?

A

Protect it via:
1. Reduce HCl
2. Increase mucous and HCO3-

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3
Q

How do prostaglandins act in the uterus?

A

Cause contraction

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4
Q

How do prostaglandins affect the kidney?

A

Regulate blood flow (vasoconstriction and dilation)

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5
Q

What are the 2 common side effects of prostaglandins?

A
  1. Fever
  2. Inflammation
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6
Q

What is misoprostol?

A

Synthetic PGE1

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7
Q

What are the uses of misoprostol in pregnancy/birth?

A
  1. Induce labour by causing uterine contractions
  2. Treat bleeding post-partum (constriction)
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8
Q

How does misoprostol treat NSAID-induced ulcers?

A
  1. +EP1/2 to increase HCO3-
  2. +EP4 to increase mucous
  3. +EP2/3 to decrease histamines
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9
Q

What are the side effects of misoprostol?

A

Diarrhea, PPIs are better anyway

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10
Q

What is the mechanism of action for glucocorticoids?

A

+lipocortin to -phospholipase A

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11
Q

Why are glucocorticoids only used to treat chronic inflammation?

A

Big swath of side effects:
- Cushing’s (fat and hairy)
- Acne
- Muscle wasting –> glucose
- Impaired healing, immunosuppression
- Ulcers, hypokalemia

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12
Q

What are the 3 core actions of NSAIDs?

A
  1. Analgesic (anti-pain)
  2. Anti-pyretic (anti-fever)
  3. Anti-inflammatory (ex. arthritis)
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13
Q

What is the MOA of NSAIDs?

A

Inhibit COX = -prostaglandin synthesis, acts at the site of origin and inhibits pain perception + fever

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14
Q

What are the adverse effects of NSAIDs?

A
  1. +Ulcers
  2. -Platelets
  3. -Uterus motility
  4. -Renal blood flow
  5. +Blood pressure (hypertension)
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15
Q

How can chronic NSAIDs cause hypertension (theoretically)?

A

Stop PGE1 synthesis in kidney (-vasodilation) or change TXA2/PGI2 synthesis (-vasodilation)

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16
Q

How does ASA (aspirin) act as an anti-inflammatory?

A

Reduces adhesion and migration of immune cells to the site

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17
Q

How does ASA act as an anti-pyretic?

A

Reduces PGE2 release in hypothalamus, reduces high temperatures without lowering normal temperatures

18
Q

How is ASA anti-platelet?

A

Blocks TXA2 synthesis by platelets, cannot aggregate with each other

19
Q

Why is ASA effective at low doses?

A

Platelets have no nucleus, so they can’t remake COX after its been inhibited. This is enough at low doses to -TXA2 without -other PGs in other cells

20
Q

How is ASA effective on heart attacks?

A

Stop clot formation because platelets can’t aggregate

21
Q

Why can’t ASA be given to those with ulcers?

A

Limiting COX reduces prostaglandins, which reduces the protective effects (-HCl, +HCO3- & mucous) on the stomach, exacerbating ulcers

22
Q

In Canada, what is the use of ASA involving heart attacks?

A

Secondary prevention, not primary. Those with a history of stroke and artery disease

23
Q

Why is ASA the only NSAID used as an antiplatelet drug?

A

The only one that binds irreversibly so it can be used in low doses, other NSAIDs would require high doses

24
Q

Diclofenac is like ___ because of its ___

A

ASA, side effects (extensive)

25
Q

Why choose ibuprofen over ASA?

A

More potent (lower dose) for higher analgesia, lessens chances of GI bleed

26
Q

What is ibuprofen?

A

Non-selective NSAID

27
Q

What is naproxen?

A

Non-selective NSAID

28
Q

Another word for NSAID is…?

A

COX inhibitor

29
Q

What is indomethacin?

A

Non-selective NSAID

30
Q

Indomethacin inhibits COX and…?

A

Phospholipase A2

31
Q

Which COX isoform is inhibited to cause anti-platelet action?

A

COX-1

32
Q

Which COX isoform’s inhibition is involved in gastric irritation?

A

COX-1

33
Q

Why aren’t there COX2 inhibitors if they limit the gastric irritation of other NSAIDs?

A

Increased risk of stroke and heart attack, not worth it

34
Q

How do COX2 inhibitors increase stroke/MI?

A

COX2 converts AA to PGI2, which decreases platelet activation. Inhibiting it but leaving COX1 actively making TXA2 causes platelets to accumulate and create clots

35
Q

How is celecoxib different from rofecoxib?

A

Less selective than rofecoxib, so less concern about CV effects with the lessened GI effects

36
Q

What is acetaminophen?

A

Not an NSAID, just analgesia and anti-pyretic OTC drug

37
Q

Can acetaminophen be given to patients with ulcers/bleeds?

A

Yes, it has little effect on COX1 or COX2

38
Q

Which COX isoform does acetaminophen act on?

A

COX3 - temperature decrease

39
Q

When is acetaminophen preferred to ibuprofen?

A
  1. Patients with ulcers
  2. ASA allergy
  3. Fever in children
40
Q

What treats acetaminophen overdose?

A

N-acetylcysteine

Pmcol 343 (8 decks)

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