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IHO > Anti-Inflammatory Drugs > Flashcards

Anti-Inflammatory Drugs Flashcards

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
Q

Compare sedation in Diphenhydramine vs Chlorpheniramine

A

Less sedation with Chlorpheniramine, most suitable for daytime use

25
Q

Difference in second generation antihistamines?

A

Minimal anticholinergic properties, don’t cause sedation or drying of secretions.
SG does not reach CNS. FG does.

26
Q

Second Generation Antihistamine examples (3)

A

Cetirizine, Fexofenadine, Loratidine

Zyrtec, Allegra, Claritin respectively

27
Q

How do we go from phospholipids in cell membrane to Prostanoids and Leukotrienes?

A

Membrane phospholipid cleaved by PLA2 -> arachidonic acid

  • Cyclooxygenase COX -> Prostanoids (PG and TX)
  • Lipoxygenase LOX -> leukotrienes
28
Q

What does COX do?

Difference between COX 1&2?

A

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
Q

Degradation of COX products

A

Short lived

  • Spontaneous hydrolysis or enzymatic degradation
  • Uptake by cells for enzym deg
30
Q

How do COX products exert their effects?

A

Bind cell membrane receptors

31
Q

What is the importance of thromboxanes and prostaglandins in the cardiovascular system?

A

Balance of the two regulates platelet aggregation

32
Q

Which PG is most potent in causing fever?

A

PGE

IL-1 -> PG -> fever

33
Q

PGs causing the most vasodilation

Also -> increased vascular permeability

A

PGEs and PGI2

34
Q

Which PGs cause pain? Which lower the pain threshold?

A

Cause: PGEs

Lower threshold/sensitize receptors: PGEs and PGI2

35
Q

What are the 3 effects of NSAIDs?

A

Analgesic, anti-pyretic, anti-inflammatory

36
Q

How do NSAIDs exhibit their effects?

A

Inhibit COX

37
Q

What is the most potent NSAID? Side effects?

A

Indomethacin

Severe frontal headache & blood disorders

38
Q

Name traditional NSAIDs (7)

A

Ibuprofen, Naproxen, Ketorolac, Ketoprofen (related to ibuprofen), Indomethacin, Sulindac, Piroxicam
PINK KIS

39
Q

Why isn’t acetaminophen an NSAID?
How does it work?
OD injures what organ?

A

Not anti-inflammatory
Inhibits COX effectively in the brain but NOT at sites of inflammation
Liver (kidney over years)

40
Q

What effect do NSAIDs have on labor?

A

Prolongs gestation. PGs are thought to play a role in initiating labor

41
Q

Why do selective COX2 inhibitors theoretically pose a cardiovascular risk?

A

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
Q

What is FLAP?

A

5-Lipoxygenase activating protein, takes 5-lipoxygenase to the membrane to act on AA -> 5-HPETE -> production of leukotrienes

43
Q

Where are leukotrienes generated for the most part?

A

Leukocytes

44
Q

What do HETEs do?

A

Chemokinetic (random) and chemotactic for WBCs

45
Q

What does LTB4 do?

A

Most important: Chemotaxis of WBCs
Leukocyte adhesion, inc ROS
Reduction of pain threshold

46
Q

What are the peptidoleukotrienes? What is another name for them? What receptor do they interact with?

A

LTC4, LTD4, LTE4
Cysteinyl leukotrienes
Interact with Cys LTR1

47
Q

What do peptidoleukotrienes cause?

A

Most important: bronchoconstriction via Cys LTR1

48
Q

Which leukotrienes play a role in asthma?

A

LTC4 & LTD4

49
Q

Which LT is found in synovial fluid of RA and gout patients?

A

LTB4

??Chemotaxis of WBCs -> proteases -> damage???

50
Q

What are LT inhibitors used for?

A

Asthma

51
Q

Which drug inhibits enzyme 5-lipoxygenase, preventing synthesis of LTB4 and peptide-leukotrienes?

A

Zileuton

52
Q

Notable side effects/interactions of Zileuton?

A

CYP450 metabolism
monitor for hepatic toxicity
Modestly effective for chronic asthma maintenance treatment

53
Q

What are the 2 leukotriene receptor antagonists? What are they used for?

A

Zafirlukast and Montelukast.

Asthma

54
Q

Zafirlukast note

A

Inhibits one of the CYP450s, could cause drug interactions

55
Q

Montelukast note

A

Prescribed more than Zafirlukast due to ease of use:
QD
No administration restrictions based on meal times

56
Q

Where are kinins synthesized? They are mediators of ____

A

Extracellularly: blood or interstitial fluid

Inflammatory activities: redness, swelling, heat, pain

57
Q

What is the effect of removing the terminal arginine from bradykinin and kallidin? What enzyme does this?

A

Less active via the B2 receptor, more effective via the B1 receptor
Kininase I

58
Q

B1 receptor kinin activities

A

Important: induced after trauma
Chronic inflammatory effects
Involved with cytokine production and long term effects
Hypotension and pain

59
Q

Kinin B2 receptor activities

A

IMPORTANT: potent vasodilators –> hypotension
Inc capillary perm -> edema
Algesic
Contract gut and airway smooth muscle
Release catecholamines from adrenal medulla
Release PGs

IHO (2 decks)

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