General Pathology PDF Sinai University

Dr. Mohammed Abdellah General Pathology sinaiuniversity.ne t  Inflammation By the end of lecture:you should be able to: -Define inflammation and recognize its clinical manifestations -Understand the major differences among acute and chronic inflammation -Explain vascular events...

Dr. Mohammed Abdellah General Pathology sinaiuniversity.ne t  Inflammation By the end of lecture:you should be able to: -Define inflammation and recognize its clinical manifestations -Understand the major differences among acute and chronic inflammation -Explain vascular events in acute inflammation and describe their underlying - mechanisms and resultant morphology. -Explain the cellular events in acute inflammation and describe its morphology. -Define exudate and understand its composition -Identify function of the exudate in acute inflammation. -Identify local signs of inflammation -List different types of acute inflammation -Differentiate between the major subtypes of acute inflammation -Enumerate subtypes of each of the major acute inflammatory subtypes -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 Aetiology (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. acids, 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: 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 o 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. 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:  : Schematic illustration of pathogenesis of increased vascular permeability in acute inflammation  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. 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. McDonald RE, Avery DR, Dean JA. Dentistry for the child and adolescent. 11th edition, Hardcover ISBN: 9780323287456 St Louis, Missouri: Mosby, Inc; 2021. -Nikhil M. Textbook of pediatric dentistry, 2nd edition , Jaypee, London; 2019. -Proffit WR, Fields HW, Sarver D M. Contemporary orthodontic, 6th edition, Mosby, Elsevier; 2018 - Arathi Rao. Principle and practice of pedodontics, 3rd edition , Jaypee; 2012. -Ghoname NA.Clinical evaluation of open- face fixed space maintainers. Egyptian Orthod J 2008; 34: - Ghoname NA. Clinical efficiency of two different types of bonded space maintainers. Egyptian Dent J 2013; 59:2773- 2780. - Ghoname NA. Clinical evaluation of chairside band and loop space maintainers Egyptian Orthod J 2013; 43; 1-14. - Heasman P. Restorative dentistry pediatric dentistry and orthodontics London New York Oxford Philadelphia, 3rd edition; 2013.  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. Leucocytosis: 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 haemolyticus 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.  Types of 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) Furunclc. (c) Carbuncle. - Diffuse: e.g. Cellulitis, suppurative appendicitis, suppurative peritonitis.. etc.  Types of 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 communi-cating 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. carbuncle  Types of acute inflammation 2. Diffuse suppurative inflammation: Cellulitis: Definition: Acute diffuse suppurative inflammation. Cause: Streptococcus haemolyticus 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.  Complications of suppurative inflammation: 1. Lymphatic spread of infection causes lymphangitis and lymphadenitis. 2. Blood spread of bacteria and its toxins causes bacteraemia, septicaemia or toxaemia. 3. Septic thrombophlebitis causes pyaemia. 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 toxiaemia.  Types of acute inflammation 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  Types of acute inflammation II. ACUTE NON-SUPPURATIVE INFLAMMATION 3. Serofibrinous inflammation: Definition: acute inflammation characterized by excess fluid exudates rich in fibrinogen. Examples: it affects serous membranes (pleura, pericardium, periton) 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  Types of acute inflammation II. ACUTE NON-SUPPURATIVE INFLAMMATION 6. Haemorrhagic 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 Thanks