Vascular & Cellular Changes Produced By Chemical Mediators Causing Inflammation

Vascular & Cellular Changes Produced By Chemical Mediators Causing Inflammation

Inflammation is a vascularised response to injury, mostly an immune response to infectious organisms, trauma, surgery, chemicals and extreme heat and cold. The suffix "itis" e.g. appendicitis characterises inflammation, therefore appendicitis is inflammation of the appendix. 

Acute inflammation Symptoms

Includes vascular and cellular phases including:

1. Redness due to hyperemia (increased blood flow)
2. Heat due to hyperemia
3. Swelling due to increased capillary permeability and filtration
4. Pain due to inflammatory chemicals (bradykinin) and fluid pressure on nerves or nerve injury.

The purpose of inflammation is to decrease the spread of pathogens giving the body an increased chance of removing them and damaged tissue debris and to repair the tissue damage. 

The sequence of acute inflammation

1. Change in vascular calibre and blood flow
2. Change in vascular blood flow
3. Cellular response from leucocytes/White Blood Cells (WBC)
4. Formation of exudate
5. The involvement of the lymphatic system

The Vascular Response in 10 Simple Steps 

1. Increased constriction of arterioles
2. Relaxation of pre-capillary sphincters
3. Vasodilation causes heat and redness
4. Gaps in endothelial cells allow water, salts and small molecules to flow out of the interstitium when the hydrostatic pressure at the arterial end is greater than colloid osmotic pressure. 
5. Fluid fills in from the venous end.
6. The increased amount of fluid increases the dilution of the toxin
7. Decreased blood flow due to increased interstitial fluid
8. Exudate contains proteins e.g. fibrinogen which converts to fibrin which is involved in blood clotting and defensive antibodies and complement proteins
9. Localised spread of toxins and phagocytosis
10. Odema reduces

Lymph drainage

Exudate drained from tissues by lymphatic capillaries Lymph pumps suck exudate from tissues via peristaltic movements through widened endothelial cellular gaps.

White blood cells involved in a cellular response 

How Do I remember this next step?

Never Let Monkeys Eat Bananas 

(most common) Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils (least common).

1. Inflammation causes increased WBC count to the site, 
2. Increased WBC count causes increased Fibrinogen chemical signals, 
3. WBCs marginate on endothelial walls and pavement on the inner lining. 
4. Rouleux causes an increase of red blood cells, 
5. An increase in RBCs causes a decrease in blood flow. 
6. WBCs leave via diapedis and enter the interstitium and then emigrate to the injured site and act as phagocytes. 
7. Neutrophils, monocytes and eosinophils leave first, 
8. Monocytes convert to macrophages
9. Neutrophils and Macrophages both secrete mediators

Mediators are vasoactive chemicals, for example, histamine. Mediators are released by mast cells, platelets, basophils and bradykinin. They are all responsible for dilation of arterioles and precapillary sphincters.

Chemotactic factors are secreted by cells to increase cells to the injury site.

Growth factors help repair the tissue damage.

Pain-producing factors such as Bradykinin are prostaglandins which are produced by arachidonic acid formed from membrane phospholipids.

Cells of acute inflammation

Polymorphonuclear neutrophils - phagocytic and secrete cytokines

Eosinophils - similar to neutrophils but longer living e.g. asthma

Basophils - roles in allergic reactions including hayfever

Macrophages - Monocytes similar to neutrophils

Exudate - includes interstitial fluid, WBCs and plasma proteins. 

Local signs of acute inflammation

• Pain
• Redness
• Heat
• Swelling 

Systemic signs of acute inflammation

• Malaise
• Increased WBC count
• Fever
• Increased acute phase reactants

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