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Flashcards in Inflammation, Immunology and Stress Deck (127)
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1

 

Define Mediators

 

 

-facilitators which orchestrate the body's responses

-low molecular weight proteins which are secreted by one cell for the purpose of altering either its own functions or those of other cells

- act as messangers

-activated with the onset of injury, invasion and/or stress

 

2

What are the three main mediator categories?

cytokines, lymphokines, and monokines

3

 

Where are cytokines released from and what are some examples?

 

 

- released from granulocytes (neutrophils, basophils, and eosinophils)

- histamine, serotonin, heparin, chemotactic factors, tumour necrosis factor, interleukins, and leukotrienes

 

4

 

Where are lymphokines released and what are some examples?

 

 

-released from lymphocytes (b-cells and t-cells)

- tumour necrosis factor, interleukins, interferons, and chemotactic factors

 

5

 

Where are monokines released and what are some examples?

 

 

-released from monocytes and macrophages

- interleukins, tumour necrosis factor, interferons, and chemotactic factors

 

6

 

What are the common characteristics of mediators?

 

 

- regulate the amplitude and duration of inflammation, immune, and stress responses

- initiate their actions by binding to specific surface receptors on the target cell which then leads to a change in RNA and protein synthesis which alters it's behaviour

- act on nearby cells of many types

- multiple physiological actions on the target cell, but can also have functional redundancy with other cells

- act as growth factors of cell division

 

7

 

What are mediators dependent on?

 

 

-local concentration

- type of cell

-other cell regulators to which the target cell is being exposed to at the same time

 

8

 

What are some cell-derived sources of mediators?

 

 

-tissue macrophages

-tissue mast cells

-platelets

-leukocytes (neutrophils, eosinophils, basophils, and monocytes)

-damaged cells and/or endotoxins

 

9

 

Within the cell, where are mediators generated?

 

 

cellular lipids

intra-cytoplasmic granules

 

10

 

How does injury/invasion affect the cell and what is generated by this process?

 

 

-causes disruption of the phospholipid bi-layer of the cell wall

-phospholipid metabolism geneartes the arachidonic acid cascade which leads to either the cyclooxygenase and lipoxygenase pathways

 

11

 

What are some examples of cells containing granules?

 

 

-mast cells

-macrophages

-platelets

-vascular endothelial cells

-granulocytes (neutrophils, eosinophils, basophils)

 

12

 

Why is degranulation important in the inflammatory response?

 

 

-degranulation (releasing granules into the tissue and vascular space)

-a key factor for releasing or making mediators available to initiate, promote, or control the inflammation response

 

13

 

Plasma derived mediators

 

 

-normally circulate in the plasma in an inactive form

-primarily includes components of the three plasma protein systems: coagulation, kinin, and complement system

-triggered by the Hageman Factor and complement components

 

14

What is meant by activation of a cascade?

-a series of reactions which occur in a sequential manner -responding in a cascade manner ensures a more sustained inflammation response

15

 

What are the main physiological actions of the three plasma protein systems?

 

 

-vascular changes of vasodilation and increased permeability

-cellular activation, such as chemotaxis

-clot formation

-chemical stimulation of nerve endings (pain)

-destruction of foreign cells and debris (cytolysis)

 

16

 

Hageman Factor

 

 

-activates all three plasma protein systems

-activated by several substances, including damaged cell and leukocyte products, exposed collagen, damaged endothelial cells, plasmin, and endotoxin.

-stimulates the coagulation system through activation of the intrinsic pathway

-stimulates complement system through activation of C3

-stimulates kinin system through activation of pre-kallikrein

 

17

 

What are the four main functions of the complement system?

 

 

-vasodilation, stimulated by anaphylatoxins

-chemotaxis, especially for phagocytes

-opsonization (tagging, coating, binding) of substances to enhance phagocytosis, components are opsonin

-direct lysis of target cells due to the activity of membrane attack complexes (MACs)

 

18

 

What activates the complement system and what are the two pathways?

 

 

-activated by hageman factor, antigen-antibody complexes, substances released from bacteria, such as endotoxin, and components of other plasma protein systems

-the classical pathway is activated by antibodies bound to specific antigens which activate C1

- the alternate pathway is acticvated by non-specific triggers, such as substances released from damaged cells and/or bacteria

 

19

 

C3

 

 

-split into two fragments C3a and C3b by either classical or alternative pathways

-causes the release of C5a or C5b fragments from C5

 

20

 

vasodilation

 

 

-due to anaphylatoxins, C3a and C5a

-induces mast cell degranulation, releasing mediators, such as histamine, which cause vasodilation and increased vascular permeability

-important to enhance the inflammation response

-increases nutrient delivery (oxygen, glucose, amino acids) and cellular access (neutrophils, monocytes, fibroblasts and platelets)

 

21

chemotactants

C3a, C5a, and C567 attract neutrophils and monocytes/macrophages to the site for phagocytosis

22

 

opsonization

 

 

-enhances phagocytosis

-bind or coat the target cell which tags the cell for destruction by phagocytosis

 

23

 

cytolysis

 

 

-due to the formation and activity of MACs which destroy target cells, especially bacteria

-disrupt the outer membrane o the cell by drilling holes into the membrane, causing an influx of water and substances into the cell, destroying it

 

24

 

Kinin system

 

 

-role not fully identified -produces bradykinin (an important mediator in the inflammatory response)

-also activates the complement and coagulation systems

 

25

Bradykinin

-three main actions include vascular changes (vasodilation and increased permeability), stimulation of peripheral nerve endings to cause pain, and probably neutrophil chemotactant

26

 

Clotting system

 

-activating factors usually circulate in an inactive form and require a stimulus to be activated

 -intrinsic and extrinsic pathways, both converge into a common pathway to form a clot

- when vascular injury occurs the subendothelial structures are exposed to flowing blood. platelets adhere to the injured vessel site and to each other to form a hemostatic plug. Platelets are attracted to injured vessel walls which then cause platelets to change in shape from disks to spiny spheres, thus exposing surface receptors. vonWillebrand factor acts in bridging platelets to the injured vessel wall by binding to platelet receptors and the exposed collagen of the vessel. The platelet plug is formed.

 

27

 

What are the steps involved in hemostasis?

 

 

-platelet adherence and aggregation, forming a platelet plug

-activation of the intrinsic and extrinsic coagulation pathways

-conversion of fibrinogen to fibrin to form a stable clot

-fibrinolysis

 

28

 

Intrinsic pathway

 

 

-activated by circulating Hageman factor with damaged endothelial surface or any type of abnormal surface within the vascular system

-converges to form the common, final pathway when activated by factor X

 

29

 

Extrinsic pathways

 

 

-activated by factor III (tissue thromboplastin) released from damaged tissues or endothelium, when blood is exposed to tissue/cell debris

-converges to form the common, final pathway when activated by factor X

 

30

 

Final Clotting Pathway

 

 

-both intrinsic and extrinsic pathways converge resulting in the thrombin

-induced formation of a stable fibrin clot.

-factor X, calcium, factor V and platelets combine to form prothrombin activator complex (PAC) which converts prothrombin into thrombin.

-thrombin converts fibrinogen into fibrin and also acts with activated factor XIII to stabilize the fibrin clot