BMS 151 Inflammation Lecture Notes PDF

BMS151 Lecture 1 Inflammation FACULTY of MEDICINE S p r i n g 2 0 2 5 FOUNDATIONS OF PATHOLOGY DR. MOHAMED MAHMOUD DR. ROFANDA BAKEER  By the end of lectures; you should be able to: 1. Causes of cell injury (Causes of Disea...

BMS151 Lecture 1 Inflammation FACULTY of MEDICINE S p r i n g 2 0 2 5 FOUNDATIONS OF PATHOLOGY DR. MOHAMED MAHMOUD DR. ROFANDA BAKEER  By the end of lectures; you should be able to: 1. Causes of cell injury (Causes of Disease). 2. Define inflammation and identify its types. 3. Understand the major differences between acute and chronic inflammation 4. Understand vascular events in acute inflammation and describe their underlying mechanisms and resultant morphology. 5. Understand cellular events in acute inflammation and describe its morphology. 6. Define exudate and understand its composition 7. Identify function of the exudate in acute inflammation. 8. Identify local signs of inflammation 9. Identify types of acute inflammation 10. Differentiate between subtypes of acute inflammation 11. Enumerate subtypes of each of the major acute inflammatory subtypes 12. Demonstrate examples for each of these subtypes and highlight its features  Introduction to Pathology Pathology is the science that concern about the study of the disease (its cause, nature and effects on tissues). It includes the following: 1. Definition and Etiology (the causes of the disease). 2. Pathogenesis: The mechanism of the development of the disease. 3. Pathological picture: Which include: Gross picture: The naked-eye changes in the tissue. Microscopic picture: Changes seen by the microscope 4. Fate: The end results of the disease whether healing, complications or death.  Causes of cell injury (Causes of Disease): 1. Living Irritants: Bacteria and their toxins, viruses, parasites and fungi. 2. Non Living Irritants: Include:  Physical irritants: e.g. excess heat, excess cold and radiation.  Chemical irritants: e.g. acides, alkalis, poisons.  Mechanical irritants: e.g. trauma, friction. 3. Hypoxia (Decrease in Oxygen supply) as in anemia. 4. Ischemia (Decrease in blood supply): as in arterial occlusion. 5. Immunological reactions. 6. Nutritional disturbances. 7. Genetic disorders.  INFLAMMATION Definition: Biological and protective reaction of living tissue to an irritant. It may be acute or chronic. Causes: all causes of cell injury, mainly living irritants (see before). NB: The suffix "itis" to the name of the organ to denote its inflammation  ACUTE INFLAMMATION *It has usually rapid onset and short duration. The acute inflammatory reaction consists of: I. Local tissue damage: The central cells are killed i.e. necrosis. The surrounding cells are less severely injured i.e. degeneration II. Local vascular reactions: 1. Transient vasoconstriction; direct vascular smooth muscle response to injurious stimulus (transient, few seconds or minutes) 2. Vasodilatation: (effect of chemical substances as histamine from mast cells, serotonin from platelets and bradykinin and kallikrein from damaged cells); leading to increased blood input and hydrostatic pressure; slowing of circulation..  ACUTE INFLAMMATION 3. Increased vascular permeability: the effect of inflammatory mediator (histamine, bradykinin and leukotrienes) predominantly in venules. Increased vascular permeability accompanies vasodilatation and this leads to formation of protein-rich exudate (increased osmotic pressure) and tissue edema. 4. Formation of inflammatory fluid exudates: Formation of inflammatory fluid exudate and vascular leakage: due to: -Increased capillary permeability. -Increased intravascular hydrostatic pressure. -Increased extravascular osmotic pressure. -Increased fluidity of the ground substance.  ACUTE INFLAMMATION Function of inflammatory fluid exudates: a. Dilute the irritant with its toxins b. Bring antibodies from blood c. Its fibrinogen coagulates into fibrin and: Localize the irritant Forms network for phagocytic cells and repair cells to move on d. Bring nutrition to the cells and remove the waste products. *Fate of fluid exudates: drained by the dilated lymphatics: ACUTE INFLAMMATION The drained exudate may carry bacteria and their toxins to lymphatics causing lymphangitis then to the draining lymph nodes causing acute lymphadenitis→The nodes become enlarged. The exudate may carry bacteria and their toxins to the blood stream causing toxaemia, bacteraemia or septicaemia.  Schematic illustration of pathogenesis of increased vascular permeability in acute inflammation Schematic illustration of pathogenesis of increased vascular permeability in acute inflammation 5. The inflammatory cellular exudates: a. Margination and pavementing of leucocytes b. Emigration of polymorphs and monocytes c. Diapedesis of red cells d. Chemotaxis: the unidirectional movement of the polymorphs and macrophages towards the irritant. As they move on the fibrin threads. -Chemotactic substances: bacterial products, complement fractions as C3a and C5a, lymphokines, prostaglandin E1, lectins leukotriene B4 and chemokines as IL-8. e. Phagocytosis: ingestion and destruction of the bacteria and necrotic tissue by the phagocytic cells, which are: polymorphs= neutrophils Macrophages= derived from blood monocytes and tissue histiocytes. Sequence of changes in the exudation of leucocytes: A- Normal axial flow of blood with central column of cells and peripheral zone of cell-free plasma. B- Margination and pavementing of neutrophils with narrow plasmatic zone. C- Adhesion of neutrophils to endothelial cells within the intercellular junctions. D- Emigration of neutrophils and diapedesis with damaged basement membrane.  Chemical mediators of acute inflammation 1-Plasma factors : The kinin system (bradykinin) The complement system (C5a & C3a) The coagulation and fibrinolytic systems 2- Factors released form tissue cells: Vasoactive amines as histamine & serotonin Arachidonic acid metabolites as prostaglandins and leukotrienes Lysosomal components Lymphokines and monokines. Effects and functions of chemical mediators: Increased vascular permeability. Vasodilation and chemotaxis.  ACUTE INFLAMMATION The course & fate of acute inflammation: 1. Resolution: complete restoration of normal condition 2. Regression and healing 3. Progression and spread: when the bacteria overcome the defense mechanism. 4. Chronicity. The general changes in acute inflammation: 1. Leukocytosis : increase in blood leucocytes above 10.000/mm3 2. Fever 3. High erythrocyte sedimentation rate (ESR) The cardinal signs & symptoms of acute inflammation: 1. Hotness 2. Redness 3. Swelling 4. Pain &tenderness 5. Loss of function  Types of acute inflammation I. Suppurative inflammation. II. Non suppurative inflammation. I. ACUTE SUPPURATIVE INFLAMMATION (Pyogenic or Septic) Definition: Severe acute inflammation characterized by pus formation. Causes: Pyogenic microorganisms as staphylococcus aureus, streptococcus hemolyticus and others. Pathogenesis of Pus Formation:  Pyogenic microorganisms cause marked tissue necrosis and attract polymorphonuclear leucocytes.  Many leucocytes are killed and are called pus cells.  The dead leucocytes release proteolytic enzymes which cause rapid liquefaction of the necrotic tissue and the fibrin threads.  The resulting fluid material mix with the other products of the inflammatory process (fluid and cellular exudate) → forming the pus.  Acute Inflammation  Composition of Pus:  1- Bacteria: living and dead and their toxins. 2- Liquefied necrotic tissue. 3- Inflammatory cellular exudates. 4- Inflammatory fluid exudate. Types of suppurative inflammation: - Localized: (a) Abscess. (b) Furuncle. (c) Carbuncle. - Diffuse: e.g. Cellulitis, suppurative appendicitis, suppurative peritonitis.. etc. acute inflammation  Acute inflammation 1. Localized suppurative inflammation: A. Abscess: Definition: A localized suppurative Inflammation resulting in the formation of an irregular cavity containing pus. Commonly caused by staphylococcus aureus that produce coagulase enzyme that helps fibrin formation and localization. B. Boil: Definition: small abscess related to hair follicles or sebaceous gland C. Carbuncle: Definition: A localized suppuration forming multiple communicating suppurative foci in the skin and subcutaneous fat discharging pus through several openings. Cause: Staphylococcus aureus. More common in diabetes mellitus. Sites: back of the neck, scalp and buttocks. Acute lung abscess Appendicitis Localized suppurative inflammation; Abscess  Acute inflammation 2. Diffuse suppurative inflammation: Cellulitis: Definition: Acute diffuse suppurative inflammation. Cause: Streptococcus hemolyticus which produces two enzymes: (1) Fibrinolysin (streptokinase): Dissolves fibrin. (2) Hyaluronidase (spreading factor): Dissolves hyaluronic acid of ground substance helping spread of bacteria and its toxins. Sites: Loose connective tissue as subcutaneous tissue, thc orbit, pelvis, scrotum and wall of the appendix. Cellulitis Complications of suppurative inflammation: 1. Lymphatic spread of infection causes lymphangitis and lymphadenitis. 2. Blood spread of bacteria and its toxins causes bacteraemia, septicemia or toxemia. 3. Septic thrombophlebitis causes pyemia. 4. Inadequate drainage and treatment changes the abscess to a chronic one. 5. Complications of healing in the form of chronic ulcer,sinus , fistula and keloid 6. Putrefaction and gangrene.  N.B.;  TOXAEMIA: bacterial toxins circulating in the blood. Some toxic manifestations: fever, rigors, headache, weakness, acute heart failure, anemia, septic shock…….  BACTERAEMIA: transient presence of some bacteria in blood without toxic manifestations.  SEPTICAEMIA: circulation and multiplication of large numbers of virulent bacteria and their toxins in the blood. It is highly fatal condition.  PYAEMIA: circulation of septic emboli in the blood with their arrest in different organs resulting in multiple small abscesses. It is highly fatal condition, associated usually with septicemia and severe toxemia. II. ACUTE NON-SUPPURATIVE INFLAMMATION 1. Catarrhal inflammation: Definition: mild acute non-suppurative inflammation of mucous membranes characterized by excess mucous secretion. Examples: rhinitis, bronchitis, appendicitis,…. 2. Membranous=Pseudomembranous inflammation: Definition: severe acute non-suppurative inflammation of mucous membranes characterized by formation of pseudomembrane Examples: Diphtheria and bacillary dysentery  II. ACUTE NON-SUPPURATIVE INFLAMMATION 3. Sero-fibrinous inflammation: Definition: acute inflammation characterized by excess fluid exudates rich in fibrinogen. Examples: it affects serous membranes (pleura, pericardium, peritonium) 4. Fibrinous inflammation: Definition: characterized by exudates with excess fibrin Examples: lobar pneumonia 5. Serous inflammation: Definition: characterized by excess serous exudate Examples: burn, herpes simples  II. ACUTE NON-SUPPURATIVE INFLAMMATION 6. Hemorrhagic inflammation: Definition: characterized by exudates rich in red blood cells due to vascular damage Examples: small pox 7. Necrotizing inflammation: Definition: characterized by marked tissue necrosis Examples: cancrum oris 8. Allergic inflammation: Definition: due to antigen-antibody reactions Examples: allergic rhinitis Pseudomembranous inflammation; Diphtheria Fibrinous pericarditis Gangrenous inflammation Thanks