Inflammation part 3

Question 1

Histamine

Answer 1

cell derived

source: mast cells, basophils, platelets
actions: vasodilation, increased vascular permeability, endothelial activaiton

activate in response to injury including trauma, cold, heat, allergic reactions and products of complement called anaphylatoxins.

cause dilation of arterioles and icnreases the permeability of venules. Histamine is considered to be the principal mediator of the immediate transient phase of increased vascular permeability, producing interendothelial gaps in venules, as discussed earlier. Its vasoactive effects are mediated mainly via bidning to receptors, called H1 receptors, on microvascular endothelial cells. The antihistamine drugs that are commonly used to treat some inflammatory reactions, such as allergies, are H1 receptor antagonists that bind to and block the receptor. Histamine also causes contraction of some smooth muscles.

Question 2

serotonin

Answer 2

cell derived

source: platelets
actions: vasoconstriction

Question 3

prostaglandins

Answer 3

cell derived

source: mast cells, leukocytes
actions: vasodilation, pain, fever

produced by mast cells, macrophages, endothelial cells, and many other cell types involved in the pathogenesis of pain and fever in inflammation. They are generated by the actions of two cyclooxygenases, called COX1 and COX2. Cox 1 is produced in response to inflammatory stimuli and is also constitutively expressed in most tissues. In contrast, cox 2 is induced by inflammatory stimuli and thus generates the prostaglandins that are involved in inflammatory reactions, but it is low or absent in most normal tissues

Question 4

leukotrienes

Answer 4

Cell derived

source: mast cells, leukocytes
actions: increased vascular permeability, chemotaxis, leukocyte adhesion and activation

Produced by leukocytes and mast cells. Involved in vascular and smooth muscle reaction and leukocyte recruitment. They are generated by the action of lipoxygenase. LTB4 is a potent chemotactic agentsand activator of neutrophils. LTC4, LTD4, and LTE4 cause intense vasoconstriciton, bronchospasm. (asthma)

Question 5

platelet activating factor

Answer 5

cell derived

source: leukocytes, mast cells
actions: vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidatve burst

phspholipid mediator (acetyl glycerol ether phospocholine). produced by neutrophils, monocytes, basophils, endothelium, platelets, others

action: platelet sitmulation, vasoconstriciton, bronchoconsriction, vasodilation, increased vascular permeability, leukocyte activation (adhesion, chemotaxis, degranulation, oxidatve burst)

generated from mebrane phosopholipids by actions of phospholipase A2

Question 6

reactive oxygen species

Answer 6

cell derived

source: leukocytes
action: killing of microbes, tissue damage

Question 7

nitric oxide

Answer 7

cell derived

source: endothelium, macrophages
actions: vascular smooth muscle releaxating; killing of microbes

Question 8

cytokines (TNF, Il1, IL6)

Answer 8

Cell derived

leukocytes, activated macrophages

chemotaxis, leukocyte activation

Question 9

complement

Answer 9

plasma (produced in liver)

leukocyte chemotaxis and activation, direct target killing (MAC), vasodilation (mast cell stimulation)

Question 10

kinins

Answer 10

plasma (produced in liver)

increased vascular permeability, smooth muscle contraction, vasodilation, pain

bradykinin, vasoactive peptides dervied from plasma proteins kinnogen

it is a vasodilator, increases vascular permeability, bronchial smooth msucle ocntraction, pain.

it is short lived (inactivated by kininases.

Question 11

cyclooxygenase inhibitors

Answer 11

aspirin and other nonsteroidal antiinflammatory drugs (NSAIDS) such as ibuprofen. They inhibit both COX1 and COX2 and thus inhibit prostaglandin synthesis (hence their efficacy in treating pain and fever); aspirin does this by irreversibly acetylating and inactivating cyclooxygenases.

Question 12

lipoxygenase inhibitors

Answer 12

5 lipoxygenase is not affected by NSAIDs, and many new inhibitors of this enzyme pathway have been developed. Pharmacologic agents that inhibit leukotriene production are useful in the treatment of asthma.

Question 13

corticosteroids

Answer 13

broad spectrum antiinflammatory agents taht reduce the transcription of genes encoding COX 2, phosopholipase A2, proinflammatory cytokines (IL1 and TNF), and iNOS.

Question 14

leukotriene receptor antagnoists

Answer 14

blocks leukotriene receptors and prevent the actions of leukotrienes

Question 15

vasodilation (eicosanoid)

Answer 15

prostaglandins PGI2 (rpostcyclin), PGE1, PGE2, PGD2

Question 16

Vasoconstriction (eicosanoid)

Answer 16

Thromboxane A2, leukotrienes C4, D4, E4

Question 17

INcreased vascular permeability (eicosanoid)

Answer 17

Luekotrienes C4, D4, E4

Question 18

chemotaxis, leukocyte adhesion (eicosanoid)

Answer 18

leukotrienes B4, HETE

Question 19

C3a and c5a

Answer 19

increase vascular permeability and cause vasodilation by binding to mast cells and inducing histamine release (anaphylatoxins) thereby increase vascular permeability and cause vasodilation. They are called anaphylatoxins because they have effects similar to those of mast cell mediators that are involve din the reaction called anaphylaxis

Question 20

c5a

Answer 20

chemotactic for neutrophils, monocytes, eosinophils, and basophils. increases adhesivness o fneutrophils to endothelium. Stimualtes synthesis and secretion of arachidonic acid metabolites

Question 21

C3b and Ic3b

Answer 21

opsonization and phagocytosis: binds to microbial surface and promotes phagocytosis.

Question 22

hagman factor

Answer 22

it is a protein syntehsized by the liver

called clotting factor XII (inactive form)

provides additional source of vasoactive mediators

activated by negatively charged surfaces, bacterial LPS, sodium urate crystals and enzymes (trypsin and plasmain)