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I3 Exam 1 > Lipid Mediators of Inflammation (O'Brien) > Flashcards

Lipid Mediators of Inflammation (O'Brien) Flashcards

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1
Q

What do cells synthesize and release after inflammation activations?

A

pro-inflammatory eicosanoids (prostaglandins, leukotrienes, histamine, bradykinin)

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2
Q

What do prostaglandins do within the body? How does it present on the outside?

A

Induce dilation and increase permeability of blood vessels at affected sites (resulting in local accumulation of blood, plasma, and fluid) –> results in redness, heat, sweating

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3
Q

Histamine and leukotrienes induce…

A

leukocyte infiltration into affected site

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4
Q

Describe the general arachindonic acid pathway

A

stimulus –> phospholipase A2 releases –> phospholipids –> arachidonic acid from lipid bilayer–> 2 pathways: lipoxygenages (LOX) and cyclooxygenases (COX)

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5
Q

EPA and arachidonic acid are metabolized into what kind of eicosanoids, respectively?

A

Omega 3 and omega 6

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6
Q

T or F: different eicosanoids have different biological effects?

A

True

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7
Q

What is the general function of eicosanoids?

A

bind and activate specific receptors (often G-protein coupled) in cell membrane and trigger cell activity related to inflammation

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8
Q

What do leukotrienes do?

A

stimulate bronchoconstriction

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9
Q

PGI2 induces…

A

vasodilation and inhibits platelet aggregation

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10
Q

Thromboxanes stimulate…

A

platelet aggregation, clot formation, and thrombosis

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11
Q

Which are more potent: omega 3 or omega 6 eicosanoids?

A

omega 6, because they compete for same receptor

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12
Q

What does intake of omega-3 fatty acid from fish oil do (mechanism)?

A
  • Inhibits delta6-desaturase via competitive inhibition, which would normally take linoleic acid omega 6 from diet to arachidonic acid omega 6
  • compete with arachidonic acid for COX and LOX, inhibiting synthesis of omega 6 and 3 from arachidonic acid
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13
Q

What are 2 major enzymes in prostanoid synthesis and how are they expressed?

A

Cox-1 and Cox-2 or PGH2 synthase; expressed in cell specific manner

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14
Q

What are the 3 major prostanoids?

A

PGE2, TXA2, PGI2

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15
Q

What does PGE2 do, what is it made from, is it pro/anti-inflammatory, what does it protect against?

A

-increase body temp, made from COX-2, pro-inflammatory, protective against peptic ulcers

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16
Q

What is TXA2 involved in, where is it synthesized and from what, and what does it do?

A

Platelet aggregation, made from platelet COX-1, vasoconstricton/bronchoconstriction

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17
Q

What synthesizes PGI2, what does it do?

A

Vascular endothelium; inhibits platelet aggregations (counteracting TXA2) via vasodilation and relaxing smooth muscle

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18
Q

What are leukotrienes (LTs) generated by? What is one specific one?

A

lipoxygenases, specifically 5-LOX

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19
Q

Products of 5-LOX play roles in … by increasing…

A

inflammation, asthma, CV disease, anaphylactic shock…increases neutrophil infiltration, bronchoconstriction, vascular permeability

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20
Q

LTA4 and LTB4 are converted to lipoxins LXA4 and LXB4 which are…and play a role in…

A

anti-inflammatory; play a role in resolution of inflammation

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21
Q

What can generate epilipoxins which are similar to the action of LXA4 and LXB4?

A

aspirin

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22
Q

Resolution is an ACTIVE biological process that requires decreased synthesis of….and synthesis of…

A

decreased synthesis of prostaglandins and leukotrienes and synthesis of anti-inflammation and pro-resolving lipid mediators

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23
Q

What does “lipid mediator class switching” refer to? What is responsible for it?

A

Resolution of acute inflammation: at high concentrations, PGD2 and PGE2 stimulate up-regulation of 15-LOX to induce lipid mediator class switching in neutrophils, mucosal epithelial cells, and fibroblasts to synthesize pro-resolution molecules (lipoxins, resolvins, protectins, and maresins)

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24
Q

Aspirin is unique in its ability to…

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A

increase pro-resolution molecules

25
Acetylated COX2 can use arachidonic acid, EPA, and DHA to produce...
intermediates that are the precursors for synthesis of a series of pro-resolving molecules
26
COX-1 and COX-2: which is constitutively expressed and which is expression induces by stress, growth factors, cytokines, inflammatory mediators?
COX1 - constitutively
27
Inhibition of COX1 leads to...
GI-related side effects (PGs inhibit acid secretion from parietal cells)
28
COX2 is a major source of ___ at sites of inflammation (cancer)
prostanoids
29
What does COX1 do?
synthesizes prostanoids for "housekeeping" functions (gastric protection, kidney function, blood clotting)
30
What is a drug that only inhibits COX2?
Celecoxib
31
What drugs inhibits both COX1 and COX2?
Aspirin, Ibuprofen, naproxen
32
NASAIDs are ____ competitive inhibitors of ___ and _____. Except ____ is an ______ inhibitor.
reversible, COX1 and COX2, aspirin is irreversible
33
What is the major biological effect of NSAIDs?
inhibition of prostagladin synthesis
34
What are the therapeutic effects of NSAIDs at low doses?
analgesia; antipyretic (lower fever)
35
What are the therapeutic effects of NSAIDs at high doses?
anti-inflammatory
36
What are the GI adverse effects of NSAIDs? Why do they occur?
Pain, nausea, diarrhea, gastric ulcers, etc. due to inhibition of PGs that are gastroprotective
37
What are the renal adverse effects of NSAIDs? Why do they occur?
- renal insufficiency, failure, hyperkalemia proteinuria, decreased effectiveness of anti-hypertensive meds - analgesic nephropathy --> slowly progressive renal failure because decreased PGE2 means less renal blood flow
38
All NSAIDs except aspirin have black box warnings for...
thrombotic events
39
What increases the risk of thrombotic events with NSAIDs?
- can occur short-term | - increased risk with time on drugs, people who have heart disease
40
Why do thrombotic events occur with NSAIDs?
inhibition of PGI2 in vessel endothelium, which inhibits platelet aggregation and induces vasodilation
41
Name main 3 functions of aspirin
analgesis, antipyretic at low doeses, anti-inflammatory (irreversible inhib of COX1 and 2)
42
How is aspirin cardioprotective?
decreased platelet aggregation at low doses because TXA2 synthesis is prevented
43
How is aspirin metabolized? Is it always irreversible?
metabolized into acetate and salicylate, which is a competitive, reversible inhibitor
44
How is aspirin secreted?
proximal tubule and glomerular filtration
45
What are the renal effects of aspirin? Low vs high doses?
- analgesic nephropathy --> decreased renal perfusion - low doses: decrease urate excretion; high plasma urate - high doses: induce uricosuria; low plasma urate
46
People hypersensitive to aspirin are provoked by ____ doses
low
47
Aspirin/Salicylate poisoning causes what? Therapeutic vs toxic doses?
- tinnitus | - Acid/base balance problems
48
Aspirin/Salicylate poisoning at therapeutic levels do what to acid/base balance?
respiratory alkalosis followed by renal compensation and increased excretion of bicarb, NA, and K
49
Aspirin/Salicylate poisoning at toxic levels do what to acid/base balance?
respiratory and metabolic acidosis due to increased lactic acid due to uncoupling of ox phos and mitochon toxicity
50
Co-admin of ibuprofen with aspirin causes what toxicity?
increased cardioprotection and anti-inflammatory effects
51
What is the half life of naproxen?
14 hours! - long!
52
Celecoxib (celebrex) should be avoided in patients prone to...
cardiovascular or cerebrovascular disease
53
Does acetaminophen have strong anti-inflammatory activity?
no!
54
What pathways are saturated with acetaminophen toxicity?
glucuronidation and sulfation
55
Induction of CYP___ increases risk of acetaminophen toxicity. Results in what type of toxicity?
CYP2E1; hepatotoxicity
56
What is given for acetaminophen overdose?
N-acetylcystein (Mucomyst)
57
Indomethacin is used for... and what are the toxicities?
closure of patent ductus; toxicity: GI effects, panceatitis, thrombocytopenia, aplastic anemia
58
Sulindac is a prodrug. What is it used for?
anti-cancer
59
Piroxicam should be given how many times a day? What percentage of patients get side effects>
once a day due to 50 hour half life; 20% patients

I3 Exam 1 (1 decks)

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