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PMCOL 343 > NSAID/Lipid Mediators > Flashcards

NSAID/Lipid Mediators Flashcards

1
Q

What are eicosanoids? What are they derived from? When are they converted and how?

A
  • shorter, smaller phospholipid derivatives that act as signaling molecules
  • derived from arachidonic acid (AA)
  • converted during inflammation by PLA2, PLC, diacylglycerol lipase, kinase
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2
Q

What are the 4 AA oxidation pathways and what are their respective products?

A
  • COX path: prostaglandins, thromboxanes, prostacyclin
  • lipoxygenase path: leukotrienes
  • P450 Epoxygenase path: epoxygenases
  • isoprostane path: isoprostanes
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3
Q

What are the main products of the COX path?

A

prostaglandins, thromboxanes, prostacyclin

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4
Q

How do NSAIDs affect the COX path?

A

target COX which converts AA to eicosanoids (?)

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5
Q

which eicosanoid has an important role in the regulation of renal blood flow?

A

prostaglandins

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6
Q

What are the normal physiological functions of prostaglandins?

A
  • prevent peptic ulcers by controlling mucus secretion
  • promote uterine contraction during labor and period
  • regulate inflammation
  • vasodilation at kidney during drop of BP to avoid HR increase from RAAS (i.e. maintain blood supply to kidney)
  • target hypothalamus to promote fever
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7
Q

What are the 2 main isoforms of COX? Describe them. When do they function?

A
  • COX I = constitutive prostaglandin synthesis (always functioning)
  • COX II = inducible prostaglandin synthesis (function during inflammation and pain)
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8
Q

What are the functions of prostacyclin (PGI2) and thromboxane?

A
  • prostacyclin: vasodilation, inhibit platelet aggregation, relax bronchiole smooth muscle
  • thromboxane: vasoconstriction, promote platelet aggregation, constrict bronchiole smooth muscle

(i.e. opposing functions)

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9
Q

What is the main product of the lipoxygenase pathway?

A

leukotrienes

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10
Q

Which path/eicosanoid plays a role in asthma and anaphylactic shock?

A

lipoxygenase path (leukotrienes)

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11
Q

Which drug is used to treat asthma? What is the class/mechanism?

A
  • montelukast
  • leukotriene antagonist
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12
Q

What does generation of platelet activating factors (PAFs) lead to? What is it released by?

A
  • AA synthesis –> more eicosanoids –> inflammation (asthma)
  • released by PLA2
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13
Q

Which drug can antagonize the effects of PAF (in asthma/inflammation)? How does it do this?

A

glucocorticoids inhibit PLA2 by upregulating expression of lipocortin (annexin)

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14
Q

Describe the synthesis pathway of PAF. (consider enzymes involved)

A
  • phosphatidyl choline converted to lyso-PAF by PLA2
  • lyso-PAF converted to PAF by acetyl transferase
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15
Q

What are the 3 phases of the inflammatory response? Which comes first/second/third?

A

1) acute inflammation
2) innate immune response
3) chronic inflammation

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16
Q

What products does acute inflammation release? What are the effects?

A
  • autacoids: histamine, serotonin, bradykinin, prostaglandins, leukotrienes
  • effects: vasodilation, increased vascular permeability, chemotaxis, pain
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17
Q

What mediators does chronic inflammation involve? what chronic condition may these mediators initiate? What is the release of AA facilitated by?

A
  • mediators: IL-1,2,5,6,13 and tumor necrosis factor alpha –> rheumatoid arthritis
  • release of AA (and lysosomal enzymes) mediated by bradykinin, which stimulates PLA2
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18
Q

List the following for misoprostol:
- class of drug
- MOA
- uses

A
  • class: synthetic PGE1
  • MOA: the only prostaglandin-mimicking drug
  • uses: induce labour, treat peptic ulcers
19
Q

Which NSAID induces lipocortin which inhibits PLA2?

A

corticosteroids

20
Q

What are some symptoms of corticosteroid toxicity?

A
  • abnormal fat deposition, hair growth (Cushing’s syndrome)
  • acne, developmental disorder
  • breakdown of protein to glucose
  • muscle wasting
  • impaired wound healing
  • peptic ulcers, hypokalemia
  • immunosuppression
21
Q

What are 3 general pharmacological properties of NSAIDs?

A
  • analgesic
  • antipyretic
  • anti-inflammatory
22
Q

Are NSAIDs used to treat mild to moderate pain or moderate to severe pain?

A

mild to moderate pain

23
Q

What are NSAIDs used to treat?

A
  • mild to moderate pain (headache, myalgia, arthralgia, post-op pain, dysmenorrhea)
  • fever
  • arthritis and other inflammatory diseases
  • gout and hyperuricemia
24
Q

What is the mechanism of action of NSAIDs?

A

inhibit COX –> inhibit synthesis of eicosanoids

25
Q

What is the mechanism of action of NSAIDs for treating fever?

A

inhibit of prostaglandin E2 biosynthesis in the preoptic region of the hypothalamus

26
Q

adverse effects of all NSAIDs?

A
  • GI ulceration and intolerance
  • blockade of platelet aggregation (not COX II selective NSAIDs)
  • inhibit uterine motility
  • inhibit prostaglandin-mediated renal function
  • hypersensitivity reactions
  • hypertension
27
Q

How do NSAIDs cause hypertension?

A
  • thromboxane causes vasoconstriction
  • decrease renal blood flow due to inhibition of prostaglandins –> retain Na+ –> increase BP
28
Q

What is the anti-inflammatory mechanism of ASA? In high doses, wat is it used to treat?

A
  • MOA: inhibit both COX isoforms; also interfere with adhesion and migration of granulocytes, leukocytes, and macrophages to site of inflammation
  • use: rheumatoid arthritis
29
Q

What is the antipyretic mechanism of ASA?

A
  • reduce prostaglandin release in hypothalamus
  • vasodilation and sweating (autonomic effect)
30
Q

What is the analgesic mechanism of ASA?

A

peripheral action at site of injury (and maybe CNS)

31
Q

What is the antiplatelet mechanism of ASA? What is the use of ASA’s antiplatelet effect? Under which condition should you avoid using ASA?

A
  • MOA: inhibit thromboxane A2 –> inhibit platelet aggregation –> thin blood
  • use: reduce risk of myocardial infarction and stroke episodes (via stopping clot formation in coronary vessels)
  • avoid when: hemophilia
32
Q

Why do we use low does of ASA?

A

high dose may overcome beneficial antiplatelet effect by stopping prostacyclin synthesis –> increase chance of vasoconstriction

33
Q

adverse effects of ASA?

A
  • gastric irritation and bleeding
  • salicylism
  • renal and hepatic damage
34
Q

how does ASA cause gastric irritation and bleeding?

A

inhibit production of prostaglandins –> inhibit mucus secretion

35
Q

What are some symptoms of ASA caused by salicylism?

A

vomiting, tinnitus, deafness, vertigo

36
Q

How do ASAs cause renal/hepatic damage?

A

inhibit prostaglandin which is important in regulating renal blood flow

37
Q

List the following for diclofenac:
- drug class/MOA
- use/pharmacological properties
- effects in comparison with ASA
- commercial name

A
  • class/MOA: non-selective COX inhibitor (NSAID)
  • use: analgesic, anti-inflammatory, antipyretic
  • adverse effects not much better than ASA
  • commercial name: voltarin
38
Q

List the following for ibuprofen:
- drug class/MOA
- use/pharmacological properties
- effects in comparison with ASA
- commercial name

A
  • class/MOA: non-selective COX inhibitor (NSAID)
  • use: analgesic, anti-inflammatory, antipyretic
  • analgesic effects at lower dose than ASA (i.e. more potent)
  • commercial name: motrin, advil
39
Q

List the following for naproxen:
- drug class/MOA
- use/pharmacological properties

A
  • class: non-selective COX inhibitor (NSAID)
  • use: osteoarthritis (also analgesic, antipyretic, anti-inflammatory
40
Q

pharmacological properties of COX II inhibitors? compare with COX I.

A
  • analgesic, anti-inflammatory, antipyretic
  • NOT anti-platelet (do not inhibit COX I)
  • less gastric irritation (do not inhibit COX I)
41
Q

List the following for celecoxib:
- drug class/MOA
- selectivity
- use
- effects in comparison with ASA
- adverse effects
- commercial name

A
  • class: COX II inhibitor (NSAID)
  • selectivity: COX II
  • use: rheumatoid arthritis, osteoarthritis
  • ASA comparison: less GI upset
  • adverse effect: hypertension (from altered ratio of thromboxane to prostacyclin
  • commercial name: celebrex
42
Q

What are the prostaglandin receptors? What is each responsible for?

A
  • EP1 = potentiation of responses to painful stimulus
  • EP2 and EP4 = vasodilation/bronchoconstriction
  • EP3 = gastric mucus secretion
43
Q

List the following for grapirant:
- drug class/MOA
- use

A
  • class/MOA: EP4 (prostaglandin receptor) antagonist (NSAID)
  • use: treat pain and inflammation in vet medicine
44
Q

List the following for acetaminophen:
- MOA
- pharmacological properties
- use
- adverse effects
- commercial name

A
  • MOA: effect on COX III in brain (but little effect on COX I and II)
  • pharm properties: analgesic, antipyretic (NOT anti-inflammatory or anti-platelet)
  • use: mild pain, fever in children (less risk of Reye’s syndrome), inadequate alone for arthritis
  • adverse effects: dizziness, excitement, disorientation, hepatic damage, renal damage
  • commercial name: tylenol

PMCOL 343 (27 decks)

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