Inflammation & Repair

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1 Inflammation & Repair By Dr. Maha M. Abu-Hashim Spring 2016

2 Inflammation Definition:- It is local reaction of living tissue to injurious agents. It is the vascular response to injury. Aim of inflammation is to localize and get rid of the injurious agent. Inflammation may be acute or chronic. The suffix itis is added to the base word to state the condition e.g tonsil/tonsilitis. Appendix/appendicitis. Page 2

3 Acute inflammation.objectives 1. Definition 2. List 4 cardinal signs of acute inflammation and the reason for each. 3. Describe the vascular and cellular events of acute inflammation (Pathogenesis). 4. List the cells of the inflammatory process and their activity. 5. Define exudate, transudate, and pus. 6. Define the following, fibrinous, serous, suppurative and catarrhal inflammation, abscess, and cellulitis. Page 3

4 Acute inflammation It is a type of inflammation characterized by. 1. Sudden onset 2. Short duration 3. Caused by strong irritant 4. Exudative in nature 5. Followed by repair Page 4

5 Cardinal Signs of acute inflammation 1- Redness 2- Heat 3- Swelling 4- Pain 5- Loss of function Redness Hotness Swelling Pain Loss of function Page 5

6 Acute inflammation Vascular changes Initial (seconds-5 min.) arteriolar vasoconstriction. After that there s precapillary arteriolar vasodilatation resulting in greater blood flow to the area. This lasts as long as the acute inflammation persists (redness and hotness) Also, there s increased vascular permeability (exudate &swelling) Page 6

7 Exudate and transudate Definitions:- 1- Exudate.. It is a protein rich fluid that occurs in acute inflammation due to increased vascular permeability. 2- Transudate It is a protein poor fluid that occurs due to increased vascular hydrostatic pressure. Page 7 Exudate -Due to increased vascular permeability. - Rich in protein esp. fibrin( aspect is turbed) - Coagulates on standing. - High specific gravity more than 1018). - Contains inflammatory cells. Transudate - Due to increased hydrostatic pressure. - Low protein content. (aspect is clear) - Does not. - Low specific gravity less than 1018). - No( few) inflammatory cells

8 Acute inflammation Cellular events 1. After vasodilatation, leukocytes (especially polymorphes) move from the vessel into the interstitial tissue (emigration). 2. Neutrophils (polymorphes are the first cells to emigrate in acute inflammation followed by macrophage. Page 8

9 . Page 9

10 Cellular events Vascular and cellular events 1- Emigration 2- Chemotaxis - It is the directional movement of leucocytes towards the irritant within the area of inflammation. Page 10

11 Cellular events Vascular and cellular events 1- Emigration 2- Chemotaxis 3- Phagocytosis It is the ingestion and destruction of particulate material (tissue debris, living or dead bacteria and other foreign cells) by phagocytic cells mainly neutrophils and monocytesmacrophages. Phagocytosis is facilitated by opsonization which is the coating of particulate material by substances that immobilize the particles to the surface of the phagocytes. Page 11

12 Phagocytosis Page 12

13 Vascular and cellular changes in acute inflammation 1- Vaso-constriction. 2- Vasodilataion. 3- Increased vascular permeability. 4- Formation of fluid exudate (characters and differences between it and transudate). 5- Emigration of leukocytes (neutrophils first them macrophages). 6- Chemotaxis. 7- Phagocytosis (after opsonization). 8- Bacterial destruction. Page 13

14 Types of acute inflammation According to the presence or absence of pus, acute inflammation is either suppurative or non-suppurative - Suppurative (purulent) - Severe acute inflammation with pus formation - It is caused by pyogenic bacteria e.g. staph.aureus, strept. Pyogenes, E.coli..etc. Pus is a semi fluid, formed of dead and living neutrophils, micro-organism, necrotic tissue and fluid exudate Page 14

15 Types of suppurative inflammation Localized 1.abscess 2. boil (fruncle) and 3.carbuncle 1 Abscess:- * A localized suppurative inflammation characterized by the formation of an irregular cavity containing pus. Page 15

16 Types of suppurative inflammation 2- Boil Small abscess related to hair follicles, sweat or sebaceous glands. 3-Carbuncle Multiple communicating suppurative foci in the subcutaneous tissue opening to the surface by multiple sinuses. It is common in diabetic patients Diffuse suppurative inflammation = Cellulitis Boil Carbuncle Cellulitis Page 16

17 Non suppurative inflammation Types 1- Serous and serofibrinous inflammation 2- Catarrhal inflammation e.g common cold 3- Pseudomembranous inflammation e.g diphtheria & bacillary dysentry. 4- Hemorrhagic inflammation.vascular damage and hemorrhage 5- Necrotizing inflammation. Excess tissue necrosis 6- Allergic inflammation. From Antigen/Antibody reaction Page 17

18 Non-suppurative inflammation 1- Serous inflammation Excess watery fluid exudate. Occurs in burns and some viral infections where (blisters) are formed. Page 18

19 Non-suppurative inflammation 2- Serofibrionous inflammation. Exudation of serous fluid rich in fibrinogen. 3- Catarrhal inflammation Mild acute inflammation of the mucous membranes with excess mucin secretion. 4- Pseudomembranous inflammation Acute inflammation characterized by formation of pseudomembrane formed of fibrin, desquamated epithelium and inflammatory cells. 2 Page 19 4

20 Outcomes (Fate) of Acute Inflammation 1-Resolution..complete restoration of normal tissues 2-Abscess (via liquefactive necrosis) 3-Scar (sometimes occurs even if pathogen is eliminated) 4-Persistent inflammation (chronic inflammation) due to a failure to completely eliminate the pathological insult (injury) Page 20

21 Chronic inflammation & Repair. Objectives 1. Discuss chronic inflammation including definition, how it arises, its cells, and histology. 2. Distinguish granulomatous inflammation as to causes and morphology. 3. Define labile, stable and permanent cells relative to healing. Give tissue examples. 4. Describe the process of wound healing by first intension and second intension. 5. Describe systemic and local influences that may modify the quality of the repair process. Define the following, ulcer, fistula, and sinus. Page 21

22 Chronic inflammation A type of inflammation characterized by 1. Gradual onset 2. Long duration 3. Caused by mild irritant 4. Proliferative in nature (excess cells) 5. Associated with repair - Chronic inflammatory cells include..lymphocytes, plasma cells and macrophages - Chronic inflammation may be specific or non specific Page 22

23 Chronic specific inflammation. Granuloma Definition - It is a type of chronic specific inflammation in which the histiocytes play a predominant role. - It starts as small granules then fuse to form a grossly, tumorlike mass Page 23

24 Types of granulomas 1- Infective - Bacterial.. Tuberculosis, syphilis,leprosy - Fungal histoplasma, Candida. - Viral lymphogranuloma inguinal. - Parasitic. Bilharziasis. - Suppurative granuloma.actinomycosis 2- Non infective - Foreign body..around surgical stitches. - Allergic..Rheumatic fever. 3- Of unknown cause - Sarcoidosis Page 24

25 Page 25 Tuberculous granuloma

26 Acute and Chronic inflammation Acute -Sudden onset -Short duration -Severe irritant - Vascular phenomena - Exudative - Polymorphs &macrophages -Followed by repair Chronic -Gradual onset -Long duration -Mild irritant -End arteritis obliterans -Proliferative -Lymphocytes, plasma cells & macrophages. -Associated with repair Page 26

27 Repair, Regeneration, and Fibrosis Repair means Replacement of damaged tissue by a healthy new one. It occurs when body defense and treatment overcomes the irritant Regeneration: (generate, to bring to life). Replacement of injured cells by cells of the same type, sometimes with no trace of injury. - This occurs when the connective tissue infrastructure remains intact. - The surviving parenchymal cells must have the capacity to regenerate. Page 27

28 Repair, Regeneration, and Fibrosis According to their proliferative potential, cells of the body are Three types.. 1-Labile- These are continuously dividing cells throughout life to replace the damaged cells. - Examples are epidermis of the skin, and hemopoietic cells of the bone marrow 2-Stable cells which do not proliferate under normal conditions but only when there is need. They include hepatocytes, renal tubular cells, glandular cells, and mesenchymal cells e.g smooth muscle, osteoblasts, cartilage cells, 3-Permanent cells that do not proliferate in the post natal life. Permanent cells are found in the central nervous system and heart. Once they are destroyed, they cannot regenerate. Page 28

29 Healing by fibrosis Fibrosis It is replacement of the damaged tissue by granulation tissue which matures to fibrous tissue. It occurs if the connective tissue infrastructure is destroyed or if the cells of the tissue can not divide. Granulation tissue:- It is a transitory tissue formed of capillaries and fibroblasts. Page 29

30 Wound Healing Wound healing can occur by one of two ways according to the type of wound 1- Primary intention: the usual case with a surgical wound, in which there is a clean (sterile) wound with minimal tissue destruction, well-apposed edges, and therefore, there s minimal scar formation. 2-Secondary intention: when wound is infected, with excessive tissue destruction, edges cannot be apposed, (e.g., following wound infection), then the wound slowly fills with granulation tissue from the bottom up. A large scar usually results. Page 30

31 Primary intension Secondary intension Granulation tissue - Clean surgical wound. - Minimal tissue loss - Sterilization, no infection - Well opposed edges - Rapid healing with minimal complications - Gaping wound. - Excess tissue loss - Infected with tissue debris - Not well opposed edges - Slow healing with many complications Page 31

32 Factors that influence wound healing 1.Type, size, and location of the wound 2.Vascular supply 3.Infection - delays wound healing and leads to more granulation tissue and scarring 4.Movement - wounds over joints do not heal well due to traction 5.Radiation - ionizing radiation is bad, UV is good Page 32

33 Factors that influence wound healing 6.Overall nutrition: vitamin and protein deficiencies lead to poor wound healing, especially vitamin C, which is involved in collagen synthesis,also zink and calcium are important. 7.Age: younger is definitely better! 8.Hormones - corticosteroids drastically impair wound healing, because of their profound effect on inflammatory cells Page 33

34 Complications of wound healing I. Defective formation of granulation tissue and fibrous tissue. 1- Wound dehiscence failure of the wound to heal. 2- Decreased cellular proliferation, this can lead to formation of ulcer, sinus, or fistula. a- Ulcer = discontinuity of the surface epithelium of the skin or mucous membrane. b- Sinus = A blind ended tract opening on the surface. c- Fistula = A tract joining two hollow organs. 3- Weak scar.incisional hernia. Page 34

35 Complications of wound healing Wound dehiscence Oral ulcer Sinus Page 35 Oral maxillary fistula

36 Complications of wound healing II. Excessive Formation of granulation tissue & scarring 1- Proud flesh Excessive formation of granulation tissue above the surface of the wound. - This prevents epithelialization of the surface. - Surgical removal or cautery is required for complete healing of the wound 2-Keloids (hypertrophy scars) - Are the result of over-exuberant production of scar tissue, which is primarily composed of type III collagen - Surgical removal is usually followed by recurrence Page 36

37 Complcations of wound healing Keloid Page 37

38 Page 38 Thank U

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