Inflammation ( part 4) l General pathology revision for dental student

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acute non-suppurative Inflammation ; Catarrhal , serous,  pseudomembranous, allergic, hemorrhagic inflammation (describing histopathology of each disease) l General pathology revision for dental student

II- Acute non- suppurative inflammation

• Increase RBCs : hemorrhagic inflammation
• Increase fluid exudate : serous / serofibrinous / Catarrhal
• Increase necrosis : Necrotizing - membranous - Allergic

 

Catarrhal inflammation

Definition :

• Mild acute inflammation of ! M.M characterized by increase mucous secretion.

Sites :

• M.M of R.T or GIT. ! best known example is ! common cold = coryza = Catarrhal rhinitis.

N/E : 

• Mucus membrane is :edematous , congested , swollen and red & covered epithelium : 1^st serous fluid then mucoserous then mucus.

M/E:

•   Mucosal cells appear swollen due to mucous accumulation (mucoid degeneration) & may rupture or desquamate. 
•   Superficial parts of sub-epithelial tissue show hyperemia, inflammatory edema and mild neutrophil infiltration.

 

Fate :

1. inflammation subsides & regeneration occur.
2. 2ry infection e pyogenic bacteria (exudate becomes muco-purulent).
3. chronic inflammation may lead metaplasia of surface epithelium & fibrosis of underlying tissue.

Membranous (pseudomembranous) inflammation 

 

Def :

• Characterized by formation of membrane formed of fibrin, desquamated epith & inflamed Connective tissues.

Cause :

• Bacteria w have a low invasive capacity but grow on ! surface of mucous membrane & produce exotoxins as :   

1. Diphtheria 
2. Shigella (causing bacillary dysentry).

Site

• mucous membrane (M.M).

Pathogenesis:-

1. Bacteria stick to the surface of the mucous membrane and releases exotoxin.
2. The exotoxin produces superficial necrosis and acute inflammation of underlying tissue.
3. As the exudate passes to the surface the fibrinogen in it clots & encloses the necrotic epithelium in fibrin network to form the pseudo membrane
4. the pseudo membrane contains also the causal bacteria, neutrophils &erythrocytes (RBCs)
5. Neutrophils accumulate at junction of living & dead tissue.
6. Their digestive enzymes detach the membrane leaving a raw surface
7. Toxemia is evident (as exotoxin is absorbed in the blood stream). 

N/E :

• Early, mucous membrane is red with grayish yellow patches of necrosis. Next, patches coalesce to form diffuse slightly elevated membrane which is first adherent to underlying structures (due to rich fibrin content). If removed by force, it leaves a raw bleeding surface & it reforms again. Lymphadenitis of draining lymph nodes. 

M/E :

1. Epithelium : replaced by pseudomembrane which contain :

• fibrin network intangling in its meshes [ necrotic tissue , organism , inflammation cells ]
• necrotic tissue.
• organism
• inflammation cells.

2. Sub-epithelium :  

• The pseudomembrane: is formed of necrotic mucosal cells , bacteria, acute inflammatory cells & excess fibrin. sub epithelial tissue shows features of acute inflammation; hyperemia, inflammatory edema, excess fibrin & acute inflammatory cells specially neutrophils and erythrocytes

Fate:   

1. Re-epithelialization                 
2. Loss of mucosal glands & fibrosis.

Serous inflammation

 

Def :

• Acute inflammation characterized by formation of increase fluid exudate rich in fibrinogen
• Acute inflammation characterized by increase watery fluid exudate.

 

Cause :

•  It occurs more severe injuries & greater vascular permeability allows passage of fibrinogen  molecules.

Site :

1. inflammation in serous sacs (pleura, pericardium & peritoneum).
2. lung alveoli (lobar pneumonia).
3. Skin as in herpes simplex & burn where watery vesicles are seen.
4. Serofibrinous inflammation

Pathology :

N/E:

• Parietal & visceral layers become red, opaque, rough & thickened.
• Fine gray granules = fibrin are seen on both internal surfaces.
• Serous fluid collects in the cavity
• According to proportion of serous fluid & fibrin.

1. If ++ fibrin deposition è is of dry type.
2. If ++ serous fluid collects in sac,è !wet type.

M/E :

• Serosa of  visceral & parietal layers are swollen or desquamated è bare surfaces.
• fluid exudate rich in fibrinogen from the bare surfaces è changes to fibrin network on both  visceral & parietal layers entangling acute inflammatory  Cells 
• subserosa shows è hyperemia, edema & fibrin network enclosing the inflammatory Cellss.

Fate : 

• repair by organization.

Hemorrhagic inflammation

 

Def :

• Acute inflammation characterized by vascular damage è hemorrhage

Cause :

• Severe injuries sufficient to cause vascular damage.
• Causative bacteria : Small pox, meningococci , strept. hemolyticus & Rickettsia.

Necrotizing inflammation

Def 

acute inflammation characterized by extensive tissue necrosis 

Example 

• Vincent’s angina and cancrum oris in the mouth 
• Infective gangrene in the lungs

ALLERGIC inflammation

definition : 

• A type of inflammation in which the inflammatory reaction results antigen / antibody reaction

 

Course of acute inflammation depends on:

1. type of tissue inflamed
2. amount of tissue destroyed (w depends on the nature & severity of the irritant).

Fate of acute inflammation

Resolution :

•  complete restoration of tissues to (N) normal after acute inflammation.
• conditions that favor resolution are :

1. Minimal or no cell death.
2. Rapid removal of inflammatory exudate. e.g. Lobar pneumonia.

Healing by fibrosis. After tissue destruction:

•  In tissues that can not regenerate.
•  abundant fibrin or necrosis

Progression to chronic inflammation

spread :  death.