1. Pathophysiology
For
Pharmacy students

2. A-Non-suppurative inflammation (no pus formation):
1- Serous inflammation: → contain protein in exudates
→ Little amount of cellular content → Very clear watery fluid
→Example: Burns there is abundant protein-rich fluid exudate with a relatively low cellular content. Examples include inflammation of the serous cavities, such as peritonitis, and inflammation of a synovial joint, acute synovitis.
2- Sero-fibrinous inflammation
 Fluid accumulates in serous sac. (Cavity)
 Fibrins are precipitated on the outer surface of visceral layer and inner surface of parietal layer of pleura
 Serous layers appear opaque and rough
 Example : pleurisy (inflammation of the pleural cavity)

3. 3- Catarrhal inflammation:
Mild acute inflammation of mucus membrane characterized by excess mucus secretion due to vasodilatation and increase in blood flow.
Example: common cold
1st: red, hot, swollen and dry mucus membrane
Then increase in watery mucoid discharge.
Later it becomes thickened yellowish.
4- Membranous inflammation
Severe Inflammation. Characterized by formation of pseudo-membrane on affected mucosal surface. Example: Diphtheria and bacillary dysentery
5- Allergic inflammation:
Occur due to Ag- Ab reaction: Characterized by: Outpouring of large amount of inflammatory Exudate.
Eosinophils and Basophiles Present in tissue and blood Esinophelia and Basophelia
 Examples: 
 Eczema, Urticaria  Allergic rhinitis
 Bronchial asthma
 Sites of inflammation:
 Skin, Bronchi, Mucus membrane of upper respiratory tract.
6- Hemorrhagic inflammation
 Sever acute inflammation characterized by destruction of blood vessels wall which lead to escape of large numbers of RBCS to the site of inflammation.
 Example:  Haemolytic streptococcal infection

7. Chronic Inflammation Chronic inflammation may:
(a) follow acute inflammation if the causal agent is not removed
(b) Be “primary” i.e. there is no pre-existing acute stage.
Common causes of primary chronic inflammation include:
(a) Persistent infections e.g. tuberculosis where the organisms are resistant to neutrophil attack.
(b) Foreign material e.g. silicates, asbestos.
(c) Auto-immune diseases e.g. auto-immune thyroiditis.
(d) Conditions of unknown aetiology e.g. Crohn's disease.

8. What do neutrophils do Phagocytosis?
Contact, Recognition, Internalisation.
4-Phayocytosis :
it is defensive mechanism against bacteria & foreign substances where macrophage ingest bacteria

10. SYSTEMIC EFFECTS OF ACUTE INFLAMMATION
Fever
‘Endogenous pyrogens’ produced: IL1 and TNFa
IL1 - prostaglandins in hypothalamus hence aspirin etc. reduce fever
Leukocytosis
IL1 and TNFa produce an accelerated release from marrow
Macrophages, T lymphocytes produce colony- stimulating factors
Bacterial infections - neutrophils, lymphocytes
Clinically useful

11. ACUTE INFLAMMATION: RESOLUTION.
What may happen after the development of acute inflammation?
1) Complete resolution.
2) Continued acute inflammation with chronic inflammation.
3) Chronic inflammation and fibrous repair, probably with tissue regeneration.
4) Death.