Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the main products of the COX path?

A

prostaglandins, thromboxanes, prostacyclin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do NSAIDs affect the COX path?

A

target COX which converts AA to eicosanoids (?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the main product of the lipoxygenase pathway?

A

leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

lipoxygenase path (leukotrienes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A
  • montelukast
  • leukotriene antagonist
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
What is the mechanism of action of NSAIDs for treating fever?
inhibit of prostaglandin E2 biosynthesis in the preoptic region of the hypothalamus
26
adverse effects of all NSAIDs?
- 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
How do NSAIDs cause hypertension?
- thromboxane causes vasoconstriction - decrease renal blood flow due to inhibition of prostaglandins --> retain Na+ --> increase BP
28
What is the anti-inflammatory mechanism of ASA? In high doses, wat is it used to treat?
- MOA: inhibit both COX isoforms; also interfere with adhesion and migration of granulocytes, leukocytes, and macrophages to site of inflammation - use: rheumatoid arthritis
29
What is the antipyretic mechanism of ASA?
- reduce prostaglandin release in hypothalamus - vasodilation and sweating (autonomic effect)
30
What is the analgesic mechanism of ASA?
peripheral action at site of injury (and maybe CNS)
31
What is the antiplatelet mechanism of ASA? What is the use of ASA's antiplatelet effect? Under which condition should you avoid using ASA?
- 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
Why do we use low does of ASA?
high dose may overcome beneficial antiplatelet effect by stopping prostacyclin synthesis --> increase chance of vasoconstriction
33
adverse effects of ASA?
- gastric irritation and bleeding - salicylism - renal and hepatic damage
34
how does ASA cause gastric irritation and bleeding?
inhibit production of prostaglandins --> inhibit mucus secretion
35
What are some symptoms of ASA caused by salicylism?
vomiting, tinnitus, deafness, vertigo
36
How do ASAs cause renal/hepatic damage?
inhibit prostaglandin which is important in regulating renal blood flow
37
List the following for diclofenac: - drug class/MOA - use/pharmacological properties - effects in comparison with ASA - commercial name
- class/MOA: non-selective COX inhibitor (NSAID) - use: analgesic, anti-inflammatory, antipyretic - adverse effects not much better than ASA - commercial name: voltarin
38
List the following for ibuprofen: - drug class/MOA - use/pharmacological properties - effects in comparison with ASA - commercial name
- 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
List the following for naproxen: - drug class/MOA - use/pharmacological properties
- class: non-selective COX inhibitor (NSAID) - use: osteoarthritis (also analgesic, antipyretic, anti-inflammatory
40
pharmacological properties of COX II inhibitors? compare with COX I.
- analgesic, anti-inflammatory, antipyretic - NOT anti-platelet (do not inhibit COX I) - less gastric irritation (do not inhibit COX I)
41
List the following for celecoxib: - drug class/MOA - selectivity - use - effects in comparison with ASA - adverse effects - commercial name
- 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
What are the prostaglandin receptors? What is each responsible for?
- EP1 = potentiation of responses to painful stimulus - EP2 and EP4 = vasodilation/bronchoconstriction - EP3 = gastric mucus secretion
43
List the following for grapirant: - drug class/MOA - use
- class/MOA: EP4 (prostaglandin receptor) antagonist (NSAID) - use: treat pain and inflammation in vet medicine
44
List the following for acetaminophen: - MOA - pharmacological properties - use - adverse effects - commercial name
- 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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions