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Anti-Inflammatory Drugs Flashcards

(60 cards)

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0
Q

What mediators mediate swelling/increased vascular permeability?

A

Histamine
Peptido leukotrienes (LTC4, LTD4, LTE4)
Kinins

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1
Q

What mediators facilitate redness?

A

Histamine, PGE2, PGI2, Kinins

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2
Q

What mediators mediate pain (cause pain or reduce threshold)?

A

PGE
PGI
LTB4
Kinins

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3
Q

What mediators are chemotactic, directing migration of neutrophils?

A

LTB4

neutrophils etc

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4
Q

What mediators are chemotactic, directing migration of eosinophils?

A

Peptido leukotrienes

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5
Q

What mediators induce fever?

A

PGE

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6
Q

Mediators of bronchoconstriction

A

Histamine, peptido leukotrienes, kinins, PGD2

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7
Q

Mediators of hypotension

A

Kinins, histamine

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8
Q

Histamine causes…

A

redness, heat, swelling, bronchoconstriction

NOT chemotaxis

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9
Q

PGE2 and PGI2 cause…

A

Vasodilation, increased vascular permeability, cause pain

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10
Q

PGD2 causes

A

bronchoconstriction

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11
Q

Thromboxane causes

A

bronchoconstriction

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12
Q

TXA2 causes

A

Platelet aggregation and vasoconstriction

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13
Q

PGI2 effect

A

opposes platelet aggregation and causes vasodilation (opposite of TXA2)

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14
Q

LTB4 role

A

chemotactic for PMNs

reduces pain threshold

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15
Q

Peptido leukotrienes cause

A

bronchoconstriction, increased vascular permeability, chemotaxis of eosinophils

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16
Q

Kinin (bradykinin and kallidinin) effects

A

Everything
Strong vasodilator –> hypotension
BUT not a strong chemotactic agent

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17
Q

Histamine:

Synthesis, metabolism

A

Synthesized from L-histidine decarboxylase present in mast cells and basophils
Widely distributed enzymes for metabolism, metabolites have little to no pharm activity

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18
Q

Bio role of histamine. What happens with:
Oral
Intracutaneous
IV

A

Oral: nothing, metabolized and inactivated
Intracutaneous: redness within seconds, flare - diffuse red beyond point of application, edema/wheel formation
IV: vasodilation -> dec BP, tachy, bronchoconstriction, flushing of face, HA, wheal and flare, mucus secretion, gastric acid secretion

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19
Q

Histamine receptors and their effect:

H1

A

Bronchoconstriction, contraction of GI smooth muscle, inc cap permeability, pruritis, pain, release of catecholamines from adrenal medulla

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20
Q

H2 receptor effects

A

Most important: gastric acid secretion
Inhibition of IgE-mediated basophil histamine release (neg feedback)
Inhibits T cell mediated cytotoxicity
Suppresses Th2 cells and cytokines

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21
Q

H3 and H4 effects

A

H3: on nerve terminals
H4: on eosinophils, DC, T cells, neutrophils
Both: histamine regulates activity of these cells

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22
Q

The allergy-type effects we normally associate with histamine are usually associated with which receptor?

A

H1
H2 to a much lesser extent
H1/H2 combo can -> cardiac effects: inc HR, inc force of contraction, arrhythmias, slows AV conduction

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23
Q

First generation histamine examples
MOA
Notable/unique effects

A

Deiphenhydramine, Chlorpheniramine
Block H1
Sedation, drying of secretions (anticholinergic due to some homology to muscarinic receptors), GI issues: n/v/d/c

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24
Compare sedation in Diphenhydramine vs Chlorpheniramine
Less sedation with Chlorpheniramine, most suitable for daytime use
25
Difference in second generation antihistamines?
Minimal anticholinergic properties, don't cause sedation or drying of secretions. SG does not reach CNS. FG does.
26
Second Generation Antihistamine examples (3)
Cetirizine, Fexofenadine, Loratidine | Zyrtec, Allegra, Claritin respectively
27
How do we go from phospholipids in cell membrane to Prostanoids and Leukotrienes?
Membrane phospholipid cleaved by PLA2 -> arachidonic acid - Cyclooxygenase COX -> Prostanoids (PG and TX) - Lipoxygenase LOX -> leukotrienes
28
What does COX do? | Difference between COX 1&2?
Key enzyme for 2 steps from AA -> PGH2 (precursor of other PG & TX) COX1: constitutively expressed in most cells inc platelets - Protects gastric mucosa COX2: Inducible (but constit in brain and kidney), not in platelets - Most important isozyme for PG and TX production in inflammation
29
Degradation of COX products
Short lived - Spontaneous hydrolysis or enzymatic degradation - Uptake by cells for enzym deg
30
How do COX products exert their effects?
Bind cell membrane receptors
31
What is the importance of thromboxanes and prostaglandins in the cardiovascular system?
Balance of the two regulates platelet aggregation
32
Which PG is most potent in causing fever?
PGE | IL-1 -> PG -> fever
33
PGs causing the most vasodilation | Also -> increased vascular permeability
PGEs and PGI2
34
Which PGs cause pain? Which lower the pain threshold?
Cause: PGEs | Lower threshold/sensitize receptors: PGEs and PGI2
35
What are the 3 effects of NSAIDs?
Analgesic, anti-pyretic, anti-inflammatory
36
How do NSAIDs exhibit their effects?
Inhibit COX
37
What is the most potent NSAID? Side effects?
Indomethacin | Severe frontal headache & blood disorders
38
Name traditional NSAIDs (7)
Ibuprofen, Naproxen, Ketorolac, Ketoprofen (related to ibuprofen), Indomethacin, Sulindac, Piroxicam PINK KIS
39
Why isn't acetaminophen an NSAID? How does it work? OD injures what organ?
Not anti-inflammatory Inhibits COX effectively in the brain but NOT at sites of inflammation Liver (kidney over years)
40
What effect do NSAIDs have on labor?
Prolongs gestation. PGs are thought to play a role in initiating labor
41
Why do selective COX2 inhibitors theoretically pose a cardiovascular risk?
Reduce prostacyclin production -> less inhibition of platelet aggregation -> thrombotic events Less of a problem with COX1/2 inhibitors because they also reduce TX production -> less platelet aggregation
42
What is FLAP?
5-Lipoxygenase activating protein, takes 5-lipoxygenase to the membrane to act on AA -> 5-HPETE -> production of leukotrienes
43
Where are leukotrienes generated for the most part?
Leukocytes
44
What do HETEs do?
Chemokinetic (random) and chemotactic for WBCs
45
What does LTB4 do?
Most important: Chemotaxis of WBCs Leukocyte adhesion, inc ROS Reduction of pain threshold
46
What are the peptidoleukotrienes? What is another name for them? What receptor do they interact with?
LTC4, LTD4, LTE4 Cysteinyl leukotrienes Interact with Cys LTR1
47
What do peptidoleukotrienes cause?
Most important: bronchoconstriction via Cys LTR1
48
Which leukotrienes play a role in asthma?
LTC4 & LTD4
49
Which LT is found in synovial fluid of RA and gout patients?
LTB4 | ??Chemotaxis of WBCs -> proteases -> damage???
50
What are LT inhibitors used for?
Asthma
51
Which drug inhibits enzyme 5-lipoxygenase, preventing synthesis of LTB4 and peptide-leukotrienes?
Zileuton
52
Notable side effects/interactions of Zileuton?
CYP450 metabolism monitor for hepatic toxicity Modestly effective for chronic asthma maintenance treatment
53
What are the 2 leukotriene receptor antagonists? What are they used for?
Zafirlukast and Montelukast. | Asthma
54
Zafirlukast note
Inhibits one of the CYP450s, could cause drug interactions
55
Montelukast note
Prescribed more than Zafirlukast due to ease of use: QD No administration restrictions based on meal times
56
Where are kinins synthesized? They are mediators of ____
Extracellularly: blood or interstitial fluid | Inflammatory activities: redness, swelling, heat, pain
57
What is the effect of removing the terminal arginine from bradykinin and kallidin? What enzyme does this?
Less active via the B2 receptor, more effective via the B1 receptor Kininase I
58
B1 receptor kinin activities
Important: induced after trauma Chronic inflammatory effects Involved with cytokine production and long term effects Hypotension and pain
59
Kinin B2 receptor activities
IMPORTANT: potent vasodilators --> hypotension Inc capillary perm -> edema Algesic Contract gut and airway smooth muscle Release catecholamines from adrenal medulla Release PGs

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