INFLAMMATION.pptx at Health Tutors' College

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1. BODY RESPONSE TO INJURY/ INFECTION

2. PRESENTERS ASIIMWE Angela ASEA Emmanuel BALUKU Adidas FACILITATORS Dr. Onyai Partrick Mr. Kirumura Jimmy

3. What do you think the patient is presenting with?

4. INFLAMMATION Presenters ASIIMWE Angela ASEA Emmanuel BALUKU Adidas Facilitators Dr. ONYAI Patrick Mr. KIRUMIRA Jimmy

5. Lecture objectives By the end of the lesson, student should be able to; Define inflammation Explain the types of inflammation Outline the causes of inflammation Explain the roles of different inflammatory mediators Describe the pathophysiology of inflammation

6. Mention the investigations for inflammation Manage inflammation List the complications of inflammation

7. Definition Inflammation is the response of living tissues to injury due to any agent. These agents may be; Physical Chemical (concentrated acid) Microbiologic (bacterium, virus)

8. Types of inflammation ACUTE INFLAMMATION Rapid onset Short duration Neutrophils and monocytes vasodilatation Vascular leakage and edema Leukocyte emigration

9. ACUTE INFLAMMATION

10. Acute inflammation

11. Chronic inflammation Onset- insidious Longer duration Lymphocytes, macrophages, plasma cells as inflammatory cells Its not dependent on chemical mediators

12. INJURY RESOLUTION Autoimmune disease Chronic inflammation Acute inflammation Viral infection Chronic irritation Mediators Mediators Mediators

13. Causes of inflammation Exogenous causes: Physical agents Mechanic agents: fractures, sand, etc. Thermal agents: burns, freezing Chemical agents: toxic gases, acids, bases Biological agents: bacteria, viruses, parasites

14. Endogenous causes Circulation disorders: thrombosis, infarction, hemorrhage Enzymes activation – e.g. acute pancreatitis Metabolic products – uric acid, urea Persistent infection like bacteria, fungi, protozoa, viruses Autoimmunity for example in rheumatoid arthritis

15. Chemical mediators of inflammation chemical mediator is any messenger that acts on blood vessels, inflammatory cells or other cells to contribute to an inflammatory response.

16. VASOACTIVE AMINES Histamine Made by mast cells in most tissues, basophils . Binding of antibody to mast cells and basophils . Action Causes vasodilatation, Increases vascular permeability Causes smooth muscle contraction

17. Serotonin Made by platelets, mast cells and basophils and also in CNS When platelets are activated and when mast cells/ basophils degranulate. Action Causes vasoconstriction Increases vascular permeability

18. Bradykinin Made by tissues and blood When blood clots, in trauma and inflammation Action Causes pain Causes of vasodilatation

19. Prostaglandins Made nearly all cells but not stored but made from cell membranes as required. Many different stimuli e.g drugs, toxins, hormones Action Fever Vasodilatation Increases vascular permeability

20. Heparin Made by liver, mast cells, basophils Released when cell degranulate Action Anticoagulant which maintains blood supply to injured tissue and washes away microbes and wastes

21. COMPLEMENT SYSTEM Three pathways: Classical pathway (antibodies) Alternate pathway (microbe LPS) Lectin pathway (sugar on microbes)

22. Important functions of the complement system C3a and C5a (anaphylatoxins) release histamine (mast cells) increased vascular permeability chemotactic for many inflammatory cells Opsonize microorganisms to facilitate phagocytosis

23. Continuation Membrane Attack Complex (MAC) Lysis of pathogens

24. Pathophysiology of inflammation The acute inflammatory response occurs in the following sequence; Increased blood flow Increased tissue fluid formation Migration of leukocytes Increased core temperature Pain Suppuration

25. Increased blood flow Following injury, there is local release of a number of chemical mediators from damaged cell e.g histamine and serotonin. This leads to both arterioles supplying the damage area and the local capillaries dilate, increasing blood flow to the site. Increased blood flow to the area of tissue damage provide more oxygen and nutrient for increased activity

26. Vasodilation

27. This leads to increased temperature and reddening of an inflamed area and contributes to the swelling and edema associated with inflammation. Increased tissue fluid formation This is partly due to increased capillary permeability caused by inflammatory mediators such as serotonin and prostaglandins and partly due to elevated pressure inside the vessel

28. Most of the excess tissues fluid drains away in the lymphatic vessels and takes damaged tissues, dead and dying cells and toxins with it. Proteins also escape into the tissues through the leaky capillary walls. This increases the osmotic pressure of the tissue fluid and draws more fluid out of the blood.

29. Continuation Sometimes tissue edema can be harmful. For instance, swelling around respiratory passage can obstruct breathing and significant swelling often pain. Migration of leukocyte Loss of fluid from the blood thickens it, slowing flow and allowing the normally fast flowing white blood cells to make contact with and adhere to the vessel wall.

30. In acute stages, the most important leukocyte is the neutrophil which adheres to the blood vessel lining, squeezes between the endothelial cells and enters the tissue. Its main function is in phagocytosis of antigen. Phagocyte activity is promoted by raised associated with inflammation.

31. After 24 hours, macrophages become the predominant cell types at the inflamed site and they persist in the tissue if the situation is not resolved leading to chronic inflammation. Macrophage are larger and longer lived than the neutrophils. They phagocytose dead/dying tissue, microbes and other antigenic materials and dead /dying neutrophils.

32. Continuation Chemotaxis This is the chemical attraction of leukocytes including neutrophils and macrophages, to an area of inflammation. These chemo-attractants include; microbial toxins, chemicals released from leukocytes, prostaglandins from damaged cells and complement proteins.

33. Increased core temperature The inflammatory process may be accompanied by a rise in body temperature. Body temperature rises when an endogenous pyrogen (interleukin 1) is released from macrophages and granulocytes in response to microbial toxins or immune complexes.

34. Continuation The interleukin 1 is a chemical mediator that resets the temperature thermostat in the hypothalamus at a higher level causing pyrexia and other symptoms that accompany inflammation. These symptoms include fatigue and loss of appetite. pyrexia increases metabolic rate of cells in the inflamed area.

35. Pain This occurs when local swelling compresses sensory nerve endings. It is exacerbated by chemical mediators of the inflammatory process like bradykinin and prostaglandins that potentiate the sensitivity of the sensory nerve endings to painful stimuli.

36. Suppuration (pus formation) Pus consists of dead phagocytes, dead cells, cell debris, fibrin, inflammatory exudate and living and dead microbes. It is contained within a membrane of new blood capillaries, phagocytes and fibroblasts. The common causative pyogenic microbes are staphyloccus aureus and streptoccus pyogens .

37. Cardinal signs of acute inflammation Heat ( Calor ) Redness ( Rabor ) Swelling (Tumor) Pain (Dolor) +/_Loss of function ( Functio laesa )

38. Investigations Complete blood count X-rays Blood for culture and sensitivity

39. Management of inflammation Inflammation is part of the healing process. Treating the cause is the main form of treatment. Some times reducing inflammation is helpful. Non-steroidal anti-inflammatory drugs can be given like ibuprofen, aspirin

40. Continuation Corticosteroids such as cortisol are also important for conditions like arthitis , allergic reactions, dermatitis.

41. Complications Acute organ insufficiency Abscess formation pyonecrotic cavity Persistence of inflammation and chronicity Fibrosis Cirrhosis Chronic organ insufficiency

42. REFERENCES Khurana I. Essential of medical physiology. Noida , uttar Pradesh, Indian: Elsevier; 2008.215. Bailey and Love, Short Practice of Surgery, 26 th Edition Ross and Wilson. Anatomy and Physiology. 11 th edition