Inflammation and Wound Healing (1c)

Question 1

Definition of inflammation

Answer 1

Response of body tissue to immune reactions, injury, or ischemic damage
Acute and Chronic

Question 2

Acute inflammation overview

Answer 2

8-10 days from onset to healing
Immediate response by tissue, an innate component of immune response, aimed at removing harmful stressors and minimizing tissue damage

Question 3

5 cardinal signs of inflammation

Answer 3

Redness 
Heat
Swelling
Pain
LOF

Question 4

Endothelial cells in inflammation

Answer 4

Produce antiplatelet and antithrombotic agents, vasodilators and constrictors.
Provide selectively permeable barrier
Regulate leukocyte extravasation
Synthesize and release inflammatory mediators
Produce growth factors which aid in angiogensis and ECM synthesis
CSF (colony stimulating factors) for producing non RBCs

Question 5

Platelets

Answer 5

Initial cessation of bleeding
Release 300+chemical mediators
Affect endothelial function such as increasing vascular permeability, altering chemotactic, adhesive and proteolytic functions

Question 6

Neutrophil

Answer 6

A leukocyte involved in phagocytosis which arrives in first 90 minutes.
Surface receptors are involved in their activation.
Ingest bacteria and dead tissue

Question 7

Monocytes/macrophages

Answer 7

Monocytes are larger WBCs than neutrophils, and become macrophages with inflammatory stimuli.
Both ingest microbes/dead tissue (monophages much more than neutrophils)
Both produce postaglandins, leukotriens, platelet activating factor, cytokines and growth factors.
They can surround and wall off material than can’t be digested

Question 8

Eosinophils

Answer 8

Large role in allergic reactions, and contain a protein toxic to parasitic worms too big to be phagocytized

Question 9

Basophils/Mast cells

Answer 9

Release histamine when bound to IgE

Poons notes just say heparin

Question 10

Vascular stage of inflammation

Answer 10

Vasodilation and increased permeability is a result of chemical mediators (histamine and nitric oxide) which allows protein rich fluid (exudate) into extravascular spaces. This results in increased concentration of RBCs, leukocytes, platelets, and clotting factors.
This allows initiation of clotting processes, dilution of offending agent, and limits systemic spread

Question 11

Vascular stage of inflammation continued

Answer 11

The loss of plasma proteins reduces intracap osmotic pressure causing the edema, pain and impaired function.

Question 12

How is the increased permeability in the vascular stage created?

Answer 12

Binding of chemical mediators (histamine, bradkinin, leukotrines) cause contraction of endothelial cells and separation of intercellular junctions

Question 13

Cellular stage of inflammation

Answer 13

Mast cells are first to react by releasing chemical mediators immediately
Mast cells and macrophages already positioned

Question 14

Cell stage leukocyte response (after initial mast cell/macrophage response)

Answer 14

• Margination and adhesion to endothelium
• Transmigration across endothelium
• Chemotaxis
• Activation and phagocytosis

Question 15

Margination and adhesion (step one in leukocyte cell response)

Answer 15

Margination - chemical mediators cause leukocytes to slow and adhere to endothelium, and move along it periphery of blood vessels
Adhesion - cytokines released to tightly bind leukocytes.

Question 16

Transmigration (step 2 in leukocyte cell response)

Answer 16

Adhesion of leukocytes and chemical mediators cause endothelial cells to shrink and open gaps, this allows leukocytes to extend pseudopodia between endothelial cells and transmigrate into ECM

Question 17

Chemotaxis (step 3 in cell leukocyte response)

Answer 17

Chemokines (small proteins directing leukocytes) bacterial and cell debris cause purposeful and energy-directed movement of leukocytes to desired areas

Question 18

Activation (part of step 4 in cell leukocyte response)

Answer 18

Specific receptors activate monocytes/neutrophils and macrophages. Activated by bacteria and or cell debris

Question 19

Phagocytosis (other part of step 4 in cell leukocyte response)

Answer 19

Agent is engulfed by pseudopod and trapped in cytoplasmic vesicle, which may merge with lysosomes that help kill and digest insulting agent.
*This can produce ROS as byproduct

Question 20

Plasma derived mediators (3)

from liver

Answer 20

Acute-phase proteins
Factor XII
Complement proteins

Question 21

Cell derived mediators (2)

Answer 21

Preformed and newly synthesized

Question 22

Acute phase proteins (from plasma derived mediators)

Answer 22

Fever and inflammation

Question 23

Factor XII (from plasma derived mediators)

Answer 23

Clotting/fibrinolytic system
Kinin system (bradykinin)

Question 24

Compliment proteins (from plasma derived mediators)

Answer 24

Activation of complement system

Question 25

Preformed mediators (from cell derived mediators)

Answer 25

Mast cells (release histamine)
Platelets (serotonin)
Neutrophils/macrophages (lysosomal enzymes)

Question 26

Newly synthesized (cell derived mediators)

Answer 26

Leukocytes (prostaglandin/ leukotriens/PAF)
Leukocytes/macrophages (NO and oxygen derived free radicals)
Macrophages/leukocytes/endothelial cells)