Chronic Inflammation, Immunological Basis of Granuloma PDF

Types of acute inflammation, Chronic inflammation Prepared by Ass. Prof. Dr. Rasha M. El-Sawi  Learning Objectives Enumerate Different types of acute inflammation Supuurative: – localized :abscess, furuncle,carbuncle – Diffuse :cel...

Types of acute inflammation, Chronic inflammation Prepared by Ass. Prof. Dr. Rasha M. El-Sawi  Learning Objectives Enumerate Different types of acute inflammation Supuurative: – localized :abscess, furuncle,carbuncle – Diffuse :cellulitis Non-suppurative inflammation – catarrhal, – Serous – Fibrinous – Serofibrinous – Pseudomembranous – Necrotizing – Allergic – Haemorrheagic Each we will discuss :definition ,causes ,morphology Chronic inflammation :definition ,mechanism ,types ,morphology Granuloma ,Definition ,types ,mechanism  types of acute inflammation Acute inflammation Suppurative Non suppurative (Pus) (No Pus)  Suppurative inflammation Definition: It in an acute inflammation characterized by pus formation. Cause: Pyogenic organism (staphylococci, strepococci, gonococci & E. Coli….)  Suppurative inflammation Abscess Localized Furncle Suppurative Carbuncle inflammation Diffuse Cellulitis  Suppurative inflammation Diffuse suppurative Localized suppurative  Suppurative inflammation 1-Abscess Definition: A localized suppurative inflammation characterized by formation of a cavity containing pus. Cause: Staphylococci which secrete coagulase enzyme that converts fibrinogen into fibrin and localize inflammation. Site: Any organ in the body e.g. subcutaneous tissue, breast and brain. Suppurative inflammation 1-Abscess  Pathogenesis & pathological picture: a- Pyogenic bacteria & toxins cause central area of necrosis. b- Necrosis surrounded by acute inflammatory cells mainly polymorphs and dilated congested blood vessels. So, abscess is now formed of 2 zones, central necrosis and peripheral acute inflammation which sometimes called pyogenic membrane. c- Larger numbers of leucocytes are attracted by chemotactic substances to the inflamed area. d- Many PNL die and transformed to pus cells that secrete liquefying enzymes to liquefy the necrotic tissue which is at first separated from the surrounding tissue and is known as slough, then necrotic tissues become completely liquefied. So, abscess now is formed of 3 zones (central necrosis- mid zone of pus & peripheral zone of acute inflammation (pyogenic membrane).  Pyogenic bacteria & toxins 2-surrounded by acute inflammatory cells mainly polymorphs and 1-central area dilated congested blood vessels of necrosis. 3- Larger numbers of leucocytes are attracted by chemotactic substances to the inflamed area. Many PNL------- die ----- 3 zones pus cells (liquefying enzymes) to liquefy the necrotic tissue Acute inflammation  Pathogenesis & pathological picture: e- Abscess enlarge by further necrosis & liquefaction. f- Osmotic pressure inside abscess increases due to digestion and liquefaction of necrotic material which split larger particles to smaller ones. So fluid is absorbed from the surrounding tissue, increasing tension inside the abscess cavity causing throbbing pain. CHARACTERS OF PUS: 1-Thick & creamy 2-Alkaline 3-Yellow (due to bacterial pigments and hemosiderin). 4-Odorless (may be offensive if the cause is E.coli). 5-Do not clot on standing (fibrinogen is destructed by proteolytic enzymes)  Composition of pus 1-The causative bacteria & their toxins 2-Necrotic tissue. 3-Inflammatory fluid exudate 4-Inflammatory cellular exudates with dead polymorphs i.e. pus cells.  Fate of the abscess: The pus is not absorbed rapidly by the body. So, once pus is formed, it should be evacuated. This is followed by healing of the abscess by granulation tissue. If the pus is not evacuated, the abscess becomes chronic i.e. pus become thick and pyogenic membrane gradually change to granulation tissue.  Complications of abscess 2-Spread of 3- 1-Chronic Complication abscess infection: s of healing: (chronicity). If the pus is not Bacteremia, Ulcer evacuated, the abscess becomes chronic Fistula. i.e. pus become Septicemia thick and pyogenic Sinus membrane gradually change Pyemia. to granulation Keloid tissue.  Complication of healing a-Ulcer: Persistent loss of continuity of surface epithelium  Complication of healing c-Fistula: A tract of infected granulation tissue between the abscess cavity and a hollow organ or between b-Sinus: A blind ended two hollow organs tract formed of infected granulation tissue between abscess cavity and the skin surface  Complication of healing -Keloid: large scar projecting on the surface and covered by thin stretched epidermis. It is due to overdone repair.  Complications of abscess 2-Spread of 3- 1-Chronic Complication abscess infection: s of healing: (chronicity). If the pus is not Bacteremia, Ulcer evacuated, the abscess becomes chronic Fistula. i.e. pus become Septicemia thick and pyogenic Sinus membrane gradually change Pyemia. to granulation Keloid tissue.  Pyogenic membrane of an abscess is formed of : a) Central area of necrosis b) Area of liquefaction c) Peripheral zone of acute inflammation d) Fibrosis  Pyogenic membrane of an abscess is formed of : a)Central area of necrosis b)Area of liquefaction c) Peripheral zone of acute inflammation d)Fibrosis  Sinus is : a) A tract between the abscess cavity and a hollow organ b) A blind ended tract between abscess cavity and the skin surface c) A tract between two hollow organs d) A large scar projecting on the surface  Sinus is : a) A tract between the abscess cavity and a hollow organ b) A blind ended tract between abscess cavity and the skin surface c) A tract between two hollow organs d) A large scar projecting on the surface  Suppurative inflammation 2-Furuncle (boil) Small abscess in relation to hair follicle or sebaceous gland Caused by staphylococcus aureus. Site: face, neck and axilla.  Suppurative inflammation 3- Carbuncle Definition: It is a localized suppurative inflammation characterized by multiple communicating deep abscesses, open on the surface by multiple sinuses. swollen cluster of boils with multiple ‘pus’ heads that form a connected area of infection under the skin. Site: Thick skin (back of neck, scalp, buttocks) because superficial fascia is normally divided into compartments by dense fibrous septa. Cause: staphylococci, mainly in diabetic patients. Suppurative inflammation 3- Carbuncle  Suppurative inflammation Abscess Localized Furncle Suppurative Carbuncle inflammation Diffuse Cellulitis  B. Diffuse suppurative inflammation (cellulitis) Definition: It is an acute diffuse suppurative inflammation. Site: loose subcutaneous tissue e.g. areolar tissue of orbit, scrotum and pelvis. The skin over the area of cellulites is hot, red, oedematous and shiny. Cause: streptococcus haemolyticus which secrete streptokinase, hyaluronidase & fibrinolysin, dissolve the ground substance and prevent fibrin network formation. So, allow spread of infection. Cellulitis differs from abscess in: - Pus is thin and slowly formed. - Increased necrosis (slough) - increase RBC’s Content - Rapid spread.  Aspect Abscess Cellulitis Localized collection of pus within a Diffuse infection and inflammation of Definition tissue cavity. the skin and subcutaneous tissues. Often caused by bacteria like Cause Commonly caused by Streptococcus Staphylococcus aureus. Clinical Well-defined, fluctuant swelling with Diffuse redness, swelling, warmth, Appearance redness and tenderness. and pain, without a distinct mass. No discrete pus collection (thin, Yes, pus is present within the abscess Pus Formation slowly formed); inflammation cavity. spreads diffusely. Clear and localized with a fibrous Border Poorly defined and diffuse margins. capsule. Diffuse and may be associated with Pain Localized and often throbbing. tenderness in the area. Systemic May include fever if infection is severe Often presents with fever, chills, and Symptoms or spreading. malaise. Requires drainage of pus (incision Managed with antibiotics and Treatment and drainage) and antibiotics. addressing the underlying infection. Can spread to nearby tissues or May progress to abscess formation Complications cause systemic infections like sepsis. or cause necrotizing fasciitis.  types of acute inflammation Acute inflammation Suppurative Non suppurative (Pus) (No Pus)  II – Non – suppurative inflammation (NOof According to feature Pus) exudates 1- Catarrhal 2- Fibrinous 3- Serous 4- Seroffibrinous 5- Membranous 6- Necrotizing 7- Allergic 8- Hemorrhagic  1-catarrhal inflammation It is a mild acute non suppurative inflammation of mucous membranes characterized by exudates rich in mucin. Sites: Mucosa of G.I.T., upper respiratory system and urinary system, e.g. rhinitis (common cold)  2-SEROUS INFLAMMATION Acute non suppurative inflammation characterized by an exudate rich in serous fluid (watery fluid) Examples: 1- Burn blisters 2- Inflammation of serous membranes (pleura, pericardium & peritoneum).  3-fibrinous inflammation It is an acute non suppurative, inflammation characterized by exudates rich in fibrin. Sites: 1- Serous membranes (pleura, pericardium & peritoneum) 2- Alveoli of the lung (lobar pneumonia).  4- Serofibrinous inflammation Definition: it is an acute non suppurative inflammation characterized by an exudate rich in serous fluid and fibrin. Examples: serous membranes. Gross: visceral and parietal layers are thick, opaque, grey – white, rough with loss of lusterless. Then increased serous fluid ( = effusion). Separation of the two layers from each other show shaggy bread and butter appearance.  4- Serofibrinous inflammation Microscopic examination: Serosal cells are swollen at first then become necrosed and desquamate (ulceration). Other cells appear degenerated and swollen Subserosal tissue: show dilated, congested blood vessels, acute inflammatory cells and oedema. Cavity: exudates rich in fibrin network together with inflammatory cells collect in the cavity. Then clear yellow serous fluid accumulate (effusion) N.B. serofibrinous inflammation Start dry (when fibrin is more) then become wet (when fluid is more) Fate : A- Resolution (if fibrin is destroyed & fluid is absorbed) B-Organization causing fibrous adhesion (if fibrin is not removed). Serofibrinous pericarditis  5-Membranous (pseudomembranous) inflammation. Definition: it is a severe type of acute non suppurative inflammation characterized by formation of a pseudomembrane over the inflamed area. Examples: Diphtheria and bacillary dysentery  Pathogenesis: 1-The causative organism is localized in the mucosa and does not pass to the circulation. It secretes exototin leading to severe necrosis of the mucosa. 2-The blood vessels become dilated and congested outpouring Inflammatory exudate rich in fibrin and polymorphs. 3- Fibrin network mixed with the necrotic tissue, polymorphs and the organism form a pseudomembrane on the surface. Gross: The membrane is thick, dirty, adherent, when removed bleeding & ulcers then reformed again Microscopic examination : Membrane is formed of: 1- bacteria and toxins 2-necrotic tissue. 3-fibrin network. 4-acute inflammatory Cells. * subepithelial connective tissue: show dilated congested blood vessels with oedema and acute inflammatory cells. Complications: Toxins circulate in blood causing toxaemia  6-Hemorrahgic It is an acute non suppurative inflammation characterized by exudates rich in RBCs due to destruction of the capillary walls. Examples. Typhus, small pox and plague.  7- necrotizing inflammation Definition: It is an acute non suppurative inflammation characterized by marked tissue necrosis Examples: Vincent angina and cancrum oris.  8-Allergic inflammation occur when the body is sensitive to a certain antigen. So, a specific antibody is formed Ag-Ab reaction can cause inflammation excess amount of inflammatory exudate (odema) rich in eosinophils) – e.g. eczema (allergic dermatitis), – allergic rhinitis.  II – Non – suppurative inflammation (NOof According to feature Pus) exudates 1- Catarrhal 2- Fibrinous 3- Serous 4- Seroffibrinous 5- Membranous 6- Necrotizing 7- Allergic 8- Hemorrhagic  Chch Site 1-catarrhal exudates rich in mucin. mucous membranes mild inflammation 2-fibrinous exudates rich in fibrin. 1-serous membranes (pleura, inflammation pericardium & peritoneum) 2- Alveoli of the lung 3-SEROUS exudate rich in serous fluid (i.e. serous membranes INFLAMMATION watery fluid) Burns blisters 4- Serofibrinous exudate rich in serous fluid and serous membranes shaggy bread and butter inflammation fibrin. appearance. 5-Membranous exudate rich in fibrin and polymorphs Diphtheria and bacillary Severe (pseudomembranous) formation of a pseudomembrane over dysentery pseudomembrane Fibrin inflammation the inflamed area. network mixed with the necrotic tissue, polymorphs and the organism 6-Haemorrhagic exudates rich in RBCs due to destruction small pox inflammation. of the capillary walls. 7- necrotizing by marked tissue necrosis cancrum oris inflammation 8-Allergic inflammation necrosis, excess amount of inflammatory eczema (allergic antigen-antibody reaction exudate (odema) rich in eosinophils (hypersensitivity reaction dermatitis), allergic rhinitis.  Burn blisters is an example of : a) catarrhal inflammation b) serous inflammation c) fibrinous inflammation d) serofibrinous inflammation e)Pseudomembranous inflammation  Burn blisters is an example of : a) catarrhal inflammation b) Serous inflammation c) fibrinous inflammation d) serofibrinous inflammation e)Pseudomembranous inflammation  Diphteria is an example of : a) catarrhal inflammation b) serous inflammation c) fibrinous inflammation d) Serofibrinous inflammation e)Pseudomembranous inflammation  Diphteria is an example of : a) catarrhal inflammation b) serous inflammation c) fibrinous inflammation d) serofibrinous inflammation e)Pseudomembranous inflammation  CHRONIC INFLAMMATION It is a slow, long-term inflammation lasting for prolonged periods of several months to years. It is characterized by the simultaneous tissue destruction and attempts of healing  Or chronic After repeated from the start acute attacks due to low After acute virulent inflammation organism which fail to cure  Mechanism of chronic inflammation 1-Persistent infections: By certain microorganisms of low toxicity and evoke an immune reaction called delayed type hypersensitivity e.g. tubercle bacilli.  Mechanism of chronic inflammation 2- Prolonged exposure to potentially toxic agents, either exogenous or endogenous: Exogenous: as prolonged exposure to silica particles which causes inflammatory lung disease (silicosis) Endogenous: as atherosclerosis 3- Autoimmunity: autoantigens evoke immune reaction that results in chronic tissue damage and inflammation  Chronic inflammation is characterized by (differ form acute inflammation by): Mild or prolonged irritant Minimal tissue destruction Blood vessels show endarteritis obliterans (EAO) (= thick wall & narrow lumen). Scantly fluid exudates. Cells of chronic inflammation present around the blood vessels (perivascular) or diffuse, which are lymphocytes , eosinophils, plasma cells, macrophages, fibroblasts and foreign body giant cells (large cells, abundant cytoplasm & multiple nuclei). They engulf foreign body and are formed by fusion of several macrophages or repeated division of nucleus of macrophages without division of cytoplasm.  Characteristics of chronic inflammation is an infiltration by mononuclear cells (macrophages) and lymphocytes. It also involves proliferation the of fibroblasts instead of exudates. As a result, the risk of scarring and deformity usually is considered greater than in acute inflammation. Macrophage  so the Morphological Features Minimal tissue destruction Blood vessels show endarteritis obliterans (EAO) (= thick wall & narrow lumen). Scantly fluid exudates.  Types of chronic inflammation: 1-Specific: It is chronic inflammation caused by specific organism which produces characteristic histologic appearance. In many types of chronic specific inflammation, the chronic inflammatory cells may form tumour like mass called granuloma as in TB and bilhariziasis. 2-Non specific: It is chronic inflammation caused by different types of organism which do not produce characteristic histologic appearance.  Major functions of different types of inflammatory cells Cell Type Major Functions Neutrophils First line of defense against bacteria; not found in normal tissues; end cells Eosinophils Can kill worms; cause damage, allergy inflammation Monocytes/ Key cells of chronic, adaptive inflammation; synthesize dozens of macrophages mediators; bactericidal; long-lived Platelets Upkeep of normal endothelium; key roles in blood clotting, hemostasis, thrombosis; source of preformed mediators Mast Related but not identical cells; loaded with histamine, can cells/basophils produce many cytokines. Triggers of acute inflammation. T lymphocytes T-cell immune responses; secrete cytokines; kill cells B lymphocytes B-cell immune responses; produce antibodies; become plasma cells NK cells Cell killing not dependent on the immune response Dendritic cells Antigen presentation Endothelium Mediates exchanges of fluid and cells between blood and tissues Fibroblasts Produce matrix; can modulate to myofibroblasts  Now compare between acute inflammation and chronic inflammation  Acute Chronic infammation inflammation causes Severe irritant. After acute inflammation which fail to cure. Or chronic from the start due to low virulent organism Onset Sudden gradual Duration Short Prolonged -Vascular Present Slight or absent phenomena Fluid exudate Abundant scanty Cardinal signs of Present Slight or absent inflammation Toxemia Acute type Chronic type -Cells Mainly Neutrophil. Lymphocytes Histiocytes appear later on plasma cells, esinophils giant cells, fibroblast. Blood vessels Thin walled, dilated and endarteritis obliterans congested.  A 52-year-old diabetic patient develops a tender, fluctuant swelling on the nape of his neck. Examination reveals multiple sinuses draining pus. Histology confirms the presence of interconnected abscesses surrounded by granulation tissue. What is the most likely diagnosis? a) Furuncle b) Carbuncle c) Sinus d) Fistula  A 52-year-old diabetic patient develops a tender, fluctuant swelling on the nape of his neck. Examination reveals multiple sinuses draining pus. Histology confirms the presence of interconnected abscesses surrounded by granulation tissue. What is the most likely diagnosis? a) Furuncle b) Carbuncle c) Sinus d) Fistula  Suppurative inflammation Abscess Localized Furncle Suppurative Carbuncle inflammation Diffuse Cellulitis  II – Non – suppurative inflammation (NOof According to feature Pus) exudates 1- Catarrhal 2- Fibrinous 3- Serous 4- Seroffibrinous 5- Membranous 6- Necrotizing 7- Allergic 8- Hemorrhagic  Short essay questions 1) Classify suppurative inflammation with examples. 2) Enumerate complications of an abscess. 3) List 4 differences between abscess & cellulitis. 4) Enumerate 4 types of non-suppurative inflammation with examples 5) List 4 differences between acute & chronic inflammation