Cytopathology-5 DR. MAHA AL-SEDIK
Definition: Local defense and protective response against cell injury or irritation or Local vascular and cellular reaction, against an irritant.
Causes: • Living: • Bacteria, • Fungi, • Virus, • Parasite or their toxins. • Non-Living: • Chemical burn • Irradiation • Mechanical trauma • Thermal injury
Inflammation is designated by adding the suffix (itis) to the end of the name of the inflamed organ or tissue e.g. cellulitis, nephritis, urethritis and glossitis.
Q- Is inflammation beneficialor not ? • You have to understand that inflammation is a protective response. • Its goals are: • • Eliminate the initial cause of cell injury. • • Remove necrotic cells and tissue. • • Initiate the process of repair . • Inflammation may be harmful as in hypersensitivity, rheumatoid arthritis, anaphylactic reaction and atherosclerosis.
Main Types of Inflammation Acute: Rapid onset and of shorter duration. Subacute: Slower onset with longer duration than acute. Chronic: Slowest onset with longer duration.
Cardinal signs of inflammation (Macroscopic signs): 1)Redness. 2)Hotness. 3)Swelling. 4)Pain and tenderness. 5)Loss of function.
1. Acute inflammation Definition: A rapid and transient response to injury or irritant Signs (macroscopic signs): The same cardinal signs but with rapid onset and of shorter duration. Changes in inflammation: 1. Local vascular change. 2. Formation of inflammatory exudate.
Inflammatory response: (microscopic signs) First: Local vascular changes: 1. Initial temporary vasoconstriction for few seconds. 2. Active vasodilatation of arterioles and capillaries (by chemical mediators: Histamine) and passive dilatation of venules. 3. Increase in capillary permeability (fluid exudate to the extravascular tissue) thus concentration of blood cells, slowing of blood flow (stasis). 3. the margination of leukocytes.
Active vasodilatation of arterioles and capillaries (and passive dilatation of venules.
Second: Formation of inflammatory exudates: • Infiltration of the various fluid and plasma proteins outside the blood vessels into the surrounding tissue without injury of the blood vessels. • This is due to the increased capillary permeability caused by the high osmotic pressure of the surroundings.
Leukocytes seem to leave the smallest blood vessels by inserting pseudopodia into the interendothelial junctions and sliding through the wall by amoeboid movement. • The early stages are marked by the predominance of polymorphs especially neutrophils migration, particularly when the inflammation is caused by pyogenic cocci.
Acute inflammatory exudates • Composition: • Fluid: contains plasma proteins, immunoglobulin and salts. • Fibrin: high molecular weight filamentous insoluble protein. • Inflammatory cells: Neutrophil, macrophage and lymphocyte.
Functions of inflammatory exudates: • Dilute the invading microorganism and its toxins. • Bring antibodies through the plasma to the inflamed area. • Bring leukocytes that engulf the invading microorganisms. • Bring fibrinogen through the plasma, which is converted, to fibrin mesh, helping in trapping the microorganism and localize the infection.
Cells of inflammatory response •Phagocytic cells –macrophages –PNL (particularly neutrophils) –Eosinophil –Basophil •Non-phagocytic cells –Lymphocytes –Plasma cells
Neutrophil Eosinophil Basophil Lymphocyte Monocyte Plasma cell
SO • Stages of Acute Inflammation • Transient Vasoconstriction • Persistent Vasodilatation and Stasis • Increased Permeability of Vessel Walls • Fluid Exudate and Formation of Edema • Cellular Exudate (Neutrophil Emigration & Accumulation) • Resolution or progression
Types of acute inflammation (based on type of exudates): 1- Catarrhal inflammation. 2- Serous inflammation. 3- Fibrinous inflammation. 4- Hemorrhagic inflammation. 5- Gangrenous inflammation. 6- Purulent inflammation.