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Pharmacology > Block 2: Inflammation and Eicosanoids > Flashcards

Block 2: Inflammation and Eicosanoids Flashcards

0
Q

Histamine: source, physiological response, mechanism

A

source: mast cells and basophils
response: vasodilation, increased vascular permeability, pain
mechanism: activation of GPCRs

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1
Q

Bradykinin: what is it, source, physiological response, mechanism

A

type: vasoactive peptide
source: endothelial cells
response: vasodilation, increased microvessel permeability, pain
mechanism: activation of GPCRs

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2
Q

Elevated CRP is associated with what?

A

increased risk of diabetes, hypertension, and cardiovascular disease

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3
Q

Cytokines: two pro-inflammatory examples, how they cause fever

A

IL-1, TNF-alpha
Increased expression of cyclooxygenase in hypothalamus -> increased formation of PGE2 which acts via cAMP to reset temperature set-point in hypothalamus -> increase body temp.

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5
Q

Prostaglandin: what is it, physiological response, mechanism

A

pro-inflammatory lipid mediator

response: vasodilation/vasoconstriction, pain, fever, platelet aggregation
mechanism: activation of specific GPCRs

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5
Q

Glucocorticoids: what they are, source, physiological response, mechanism

A

anti-inflammatory lipid mediators that inhibit arachidonic acid release

source: adrenal cortex
response: decrease expression of COX-2 and inhibits phospholipase-A2 (enzyme that cleaves phospholipid and releases arachidonic acid)
mechanism: activation of nuclear receptors

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6
Q

Leukotrienes: what is it, source, physiological response, mechanism

A

pro-inflammatory lipid mediator

response: increased vascular permeability, chemoattractant for neutrophils, bronchoconstriction
mechanism: activation of GPCRs

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7
Q

NSAIDs: mechanism

A

inhibition of cyclooxygenase, reduces production of inflammatory prostanoids

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8
Q

zafirlukast and zileuton: what each of them are, theapeutic use

A

zafirlukasat: competitve antagonist of leukotriene receptors
zileuton: inhibits 5-lipoxygenase and thus the synthesis of leukotrienes
use: prophylaxis and chronic treatment of asthma

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9
Q

TNF inhibitors (2)

A

etanercept, infliximab

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10
Q

etanercept and infliximab

A

TNF inhibitors

etanercept: receptor analog
infliximab: monoclonal antibody

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11
Q

precursor of eicosanoids

A

arachidonic acid

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12
Q

what enzyme synthesizes leukotrienes and from what precursor?

A

5-lipoxygenase from arachidonic acid

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14
Q

prophylaxis and chronic treatment of asthma (2)

A

zileuton and zafirlukast

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15
Q

Complement system: source, physiological response, mechanism

A

source: synthesized by liver, circulate in blood
physiological response: chemotaxis, release of mediators from neutrophils, increase vascular permeability
mechanism: complement complexes cause osmotic lysis, activation of GPCRs

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16
Q

Cytokines: physiological response, mechanism

A

physiological response:
TNF-alpha: fever, sepsis
IL-1: fever, fibroblast and lymphocyte proliferation
mechanism:
1. increase cyclooxygenase and lipoxygenase
2. increase adhesion molecule expression
3. induce collagenase (fibrosis)

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17
Q

function of phospholipase A2

A

hydrolyzes phospholipids to release arachidonic acid

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18
Q

function of cyclooxygenase

A

converts free arachidonic acid to PGH2 which is transformed enzymatically to prostacyclin, thromboxane, PGE2, PGF2

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19
Q

difference between COX-1 and COX-2

A

COX-1 is constitutive and expresed in all tissues

COX-2 is inducible and is more commonly seen in inflammation

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20
Q

function of 5-lipoxygenase

A

synthesize leukotrienes from arachidonic acid

21
Q

types of drugs that inhibit phospholipase A2

A

glucocorticoids

22
Q

type of drug that inhibit COX-1 and COX-2

23
Q

type of drug that decrease expression only of COX-2

A

glucocorticoids

24
Q

inhibitors of lipoxygenase

A

zileuton and zafirlukast

25
Q

physiological response of leukotrienes

A

bronchoconstriction, increase vascular permeability, chemotaxis

26
Q

inhibits 5-lipoxygenase

27
Q

leukotriene receptor antagonist

A

zafirlukast

28
Q

Eicosanoids related to pain in periphery

A

PGE2 and PGI2

29
Q

what eicosanoid is important in fever?

30
Q

what second messager molecule is important in fever?

31
Q

what eicosanoid is responsible for platelet aggregation and what is the mechanism? include appropriate receptor

A

thromboxane
mechanism: activation of phospholipase A2 –> release of arachidonic acid –> converted to thromboxane by COX-1 –> stimulates TP receptors that couple to increase in calcium

32
Q

does thromboxane cause vasocontstriction or vasodilation?

A

vasoconstriction

33
Q

what eicosanoid is responsible for inhibiting platelet aggregation and what is the mechanism? include appropriate receptor

A

prostacyclin (PGI2)
mechanism: activation of phospholipase A2 –> release of arachidonic acid –> converted to prostacycling by COX-1 and COX-2 –> stimulates IP receptor that couples to cAMP

34
Q

does prostacyclin cause vasoconstriction or vasodilation?

A

vasodilation

35
Q

what is the cellular source of prostacyclin?

A

endothelial cells

36
Q

what prostaglandins cause vasodilation of cardiovascular/vascular smooth muscle?

A

PGE2, PGI2

37
Q

which prostaglandin is a potent vasoconstrictor?

A

thromboxane

38
Q

circulating vasoconstrictor autocoid

A

angiotensin II

39
Q

what prostaglandin maintains patency of ducrus arteriosus?

40
Q

what prostaglandins increase renal blood flow via vasodilation?

A

PGE2 and PGI2

41
Q

which COX enzye is important in GI and how?

A

COX-1, synthesize cytoprotective prostaglandins that inhibit gastric acid secretion, stimulates release of mucus, increase gastric mucosal blood flow

42
Q

why are therapeutic uses of prostaglandins limited?

A

adverse effects and short half-life

43
Q

dinoprostone: analog of what, therapeutic uses, second messengers, adverse effects

A

PGE2 analog
uses: cervical ripening and termination of early pregnancy
second messengers: calcium, cAMP
adverse effects: GI-related, fever

44
Q

what is the only PGE2 analog?

A

dinoprostone

45
Q

misoprostone: analog of what, therapeutic use, second messenger, adverse effects

A

PGE1 analog
use: prevention of ulcers caused by NSAIDs
second messenger: cAMP
adverse effects: contraindicated in pregnancy

46
Q

analogs of PGE1

A

misoprostol, alprostadil

47
Q

alprostadil: analog of what, therapeutic uses, second messenger

A

PGE1 analog
uses: impotence, maintenance of patent ductus arteriosus
second messenger: cAMP

48
Q

epoprostenol: analog of what, therapeutic use, mechanism (include appropriate receptor and second messenger)

A

PGI2 analog

use: primary pulmonary hypertension
mechanism: acts at PGI2 or IP receptor to cause a cAMP-mediated dilation of pulmonary artery vascular smooth muscle

Pharmacology (6 decks)

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