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Pharmacology Section B > NSAIDs Pathway > Flashcards

NSAIDs Pathway Flashcards

1
Q

When injury occurs, what is the pathway that is activated?

A

Phospholipase A2

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2
Q

Activation of phospholipase A2 catalyzes hydrolysis of…

A

Arachidonic acid from phospholipids in the cell membrane

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3
Q

What do NSAIDs do to this pathway?

A

Inhibit cyclooxygenase enzymes

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4
Q

NSAIDs
- inhibit cyclooxygenase

A

Inhibits prostaglandins (PGs) synthesis with both beneficial and unwanted effects

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5
Q

Cyclooxygenase enzyme

A

Converts Arachidonic acid to prostaglandins (PGs) and thromboxane A2

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6
Q

Prostacyclin (PGI)

A

Released from vascular endothelial cells to prevent platelet aggregation

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7
Q

Thromboxane A2

A

Stimulates platelet aggregation when blood vessels are injured

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8
Q

Other PGs

A

PGE1
PGE2
PGE2a

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9
Q

Other PGs are involved in

A

Pain
Inflammation
Fever
GI cytoprotection
Vasodilation
Maintain renal blood flow

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10
Q

NSAIDs inhibit cyclooxygenase (COX) pathway
- increasing what?

A

Lipoxygenase pathway

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11
Q

NSAIDs inhibit cyclooyxgenase
- increasing lipoxygenase pathway

A

Those with respiratory disease become more susceptible to bronchospasm

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12
Q

5-lipoxygenase enzyme

A

Converts arachidonic acid to leukotrienes

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13
Q

Leukotrienes

A

Mediate allergy-induced bronchoconstriction

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14
Q

Where are leukotrienes produced?

A

Mainly in inflammatory cells (mast cells, basophils, eosinophils, macrophages and polmorphonuclear leukocytes)

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15
Q

What blocks 5-lipoxygenase

A

Zileuton- anti-asthmatic agen

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16
Q

What blocks leukotriene receptors

A

Montelukast (singulair) and zafirlukast
- controlling the symptoms of asthma and bronchoconstriction

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17
Q

COX-1

A

Expressed in the stomach to produce PGs

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18
Q

COX-1
- PGs produce?

A

Cyotprotectin in the GI tract by inhibiting gastric acid secretions
Increasing bicarbonate release
Promoting mucus secretion

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19
Q

NSAIDs inhibit what?

A

Both COX-1 and COX-2 enzymes

20
Q

Non-selective NSAIDs
- inhibitation of COX-1

A

GI side effects
bleeding
Gastric ulcers

21
Q

COX-2 inhibitors

A

Spare COX-1 induced synthesis of PGs, preserving the integrity of the lining of the GI tract

22
Q

MOA of NSAIDs

A

Blockade of prostaglandin synthesis via inhibition of the enzyme cyclooygenase (COX)

23
Q

Nonselective COX-1 and COX-2 inhibitors

A

Acetylsalicyclic acid (asprin)
Ibuprofen
Naproxen

24
Q

NSAIDs properties

A

Antipyretic
Analgesic
Anti-inflammatory

25
Q

Aspirin (acetylsalicylic acid)

A

Covalently binds and irreversibly inhibits COX-1 and COX-2 enzymes of the platelets (prevents platelet aggregation)

26
Q

Single dose of aspirin will..

A

Inhibit platelet COX for 8-11 days (life of the platelet)

27
Q

Adverse effects and contraindications of Aspirin

A

High doses cause salicylism (tinnitus, vertigo, hearing loss)
Contraindicated in children and teenagers with chickenpox and influenza

28
Q

Adverse effects and contraindications
- Chickenpox and influenza

A

Tied to Reye’s disease, which is a potentially fatal disease accompanied by liver damage and encephalopathy

29
Q

When should patients stop taking aspirin?

A

One week prior to surgery or dental procedures d/t tendency of aspirin increasing clotting time and cause excessive bleeding

30
Q

When taking Aspirin what do you avoid?

A

Taking it during pregnancy and breast-feeding

31
Q

Non-selective COX inhibitors

A

Ibuprofen (Motrin-OTC, Advil-OTC)
Naproxen (aleve-OTC, Naprosyn)- longer half-life
Ketorolac

32
Q

Ketorolac

A

Moderate to severe pain and limited to 5 day treatment
Increased incidence of peptic ulcers

33
Q

Ketorolac
- Do not use with who?

A

Patients with renal impariement

34
Q

Celecoxib (celebrex)

A

Less GI bleeding/irritation

35
Q

Celecoxib
- Contraindications

A

Patients allergic to sulfonamides
Avoid in patients with Renal, CV, and cerebrovascular disease (increased risk of heart attack and stroke)

36
Q

Celecoxib inhibits

A

CYP2D6 resulting in severe drug interactions

37
Q

Acetaminophen MOA

A

Unclear

38
Q

Acetaminophen effects

A

Analgesic and antipyretic

39
Q

Acetaminophen is a weak

A

COX-1 and COX-2 inhibitor in peripheral tissues

40
Q

Not an NSAIDs

A

Acetaminophen bc it lacks anti-inflammatory or anti-platelet effects

41
Q

Clinical uses of acetaminophen

A

Mild to moderate pain (HA, myalgia, postpartum pain)

42
Q

Acetaminophen is preferred for what?

A

During pregnancy and breastfeeding

43
Q

Where is acetaminophen metabolized

A

Liver

44
Q

What is generated?

A

minor toxic metabolite that is conjugated to glutathione in the liver and excreted in the kidney

45
Q

Acetaminophen
- Overdose or standard dose patients with liver impairment

A

Toxic metabolite accumulates and induces liver damage
Hepatic renal tubular necrosis may occur

46
Q

How to treat overdose of acetaminophen

A

Use n-acetylcysteine within 8 hours of overdose bc it binds to the toxic metabolite and counteracts acetaminophen toxicity

47
Q

Acetaminophen

A

Tylenol

Pharmacology Section B (6 decks)

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