Q: What are the 2 most important opsonins? A: The Fc fragment of IgG C3bi Q: What are the 3 processes in phagocytosis? A: Recognition and attachment Engulfment Killing/degradation Q: True or false? NADH oxidase helps produce H2O2 (peroxide)? A: False. NADPH oxidase helps produce H2O2 (peroxide). Q: What are the 4 main features of the role of lymphatics in inflammation? A: * Increased drainage to keep up with exudation * Remove most exuded fluid * Facilitate immune response to foreign antigens (presents antigens to lymph nodes) * Provides possible route for microbial spread Q: Name 5 advantages of acute inflammation. A: * Dilutes irritant * Delivers important proteins like antibodies and complement * Delivers leucocytes * Fibrinous exudate can localise infection * Protein and glucose provide nutrients for tissue cells that aren't inflamed Q: Name 2 disadvantages of acute inflammation. A: * Loss of organ function (eg. brain - swelling, with possible coning, lungs - decrease in possible respiratory gas exchange, larynx - difficulty of maintaining airway) * Stasis in inflamed microvasculature can lead to ischaemia, and eventually to necrosis and infarction of ischaemic tissue Q: What are the 5 cardinal signs of inflammation? A: * redness (rubor) * heat (calor) * swelling (tumour) * pain (dolor) * loss of function (functio laesa) Q: What are the 4 major components in inflammation? A: * vascular response * swelling and exudation * phagocytosis * role of lymphatics Q: What are the 4 steps in leucocyte exudation? A: * Margination and rolling * Adhesion * Emigration/transmigration from the vessels * Chemotaxis Q: What cell types dominates the early (under 24 hours) inflammatory response? A: Neutrophils Q: What cell types dominates the later (24 - 48 hours) inflammatory response? A: Macrophages/monocytes Q: Name 8 different types of exudate A: * Fibrinous * Catarrhal (inflammation and mucous hypersecretion on mucosal surface) * Mucous * Serous * Purulent * Pseudomembranous (necrotic epithelial cells combined with fibrin and inflammatory cells, as with diphtheria) * Ulcerative (with circumscribed loss of epithelial lining) * Haemorrhagic (with necrosis and substantial loss of vessel wall) Q: What are the systemic effects of IL-1 and TNF-alpha? A: * Fever * Anorexia * Neutrphila * Hepatic protein synthesis * Septic shock Q: How do anaphylotoxins, C3a, C4a and C5a, act to increase vascular permeability and vasodilation? A: By releasing histamine from mast cells. Q: True or false? C3b and C3bi aid leucocyte adhesion, chemotaxis, and activation. A: False. C3b and C3bi are opsonins promoting phagocytosis. C5a aids leucocyte adhesion, chemotaxis, and activation. Q: What does the kinin system ultimately result in the release of? A: Bradykinin. Q: What effects does bradykinin have? A: Increased vascular permeability Contraction of smooth mm Vasodilation Pain Q: True or False? Fibrinopeptides cause increased leucocyte adhesion and fibroblast proliferation. A: False. Fibrinopeptides cause increased vascular permeability and chemotaxis. Thrombin (or Factorial) causes increased leucocyte adhesion and fibroblast proliferation. Q: Who am I? I am a multifunctional protease. I cleave C3 to produce C3 fragments. I degrade fibrin. I can activate Hageman factor, which can trigger multiple cascades, amplifying the response. A: I am plasmin. Q: True or false? The fibrinolysis system produces plasmin? A: True. Q: What is the source of histamine and serotonin? A: Mast cells and platelets. Q: What are the 3 possible outcomes of acute inflammation? A: Recovery (with or without residual damage) Acute complications Progression to chronicity Q: What conditions must be true for resolution (no residual damage) to occur after acute inflammation? A: Tissue architecture must not have been destroyed by necrosis. Exudate must have been effectively removed. The organ or tissue must have the capacity to regenerate. Q: If resolution does not occur after acute inflammation, how does recovery take place? A: Organisation of the exudate and repair via granulation tissue, leading to fibrosis/scarring. Q: What are some of the acute complications of acute inflammation? A: Suppuration and/or ulceration, as a consequence of necrosis, caused by bacterial products, O2 metabolites and lysosomal enzymes (or ischaemia). Q: What are the causes of tissue damage from inflammation? A: * Harmful effects of irritant, e.g. direct tissue injury (trauma, burns, etc) and bacterial products (endotoxins, invasins). * Ischaemia due to local swelling, stasis or thrombosis. * Toxic products of inflammatory cells (collateral damage), e.g. superoxide radicals and lysosomal enzymes. Q: What is the histologic criterion for the diagnosis of acute appendicitis? A: Neutrophilic infiltration of the muscularis. Q: What is chronic inflammation? A: Inflammation of a prolonged duration in which active inflammation, tissue destruction and attempts at repair are all proceeding simultaneously. Q: What are the 3 major histological features of chronic inflammation? A: * Infiltration with mononuclear cells (which include macrophages, lymphocytes and plasma cells) * Tissue destruction (largely induced by the inflammatory cells) * Attempts at healing by connective tissue replacement of damaged tissue (particularly angiogenesis and fibrosis) Q: What is the most prominent cell in chronic inflammation? A: The macrophage. Q: What are the 3 mechanism for macrophage accumulation? A: * Continued recruitment of monocytes from the circulation * Local proliferation after their emigration from the bloodstream * Immobilisation with site by certain cytokines and oxidised lipids Q: What is the predominant cell in granulomatous inflammation? A: Activated macrophages with modified epithelial-like (epithelioid) appearance. Q: What is a granuloma? A: A focal area of granulomatous inflammation consisting of a microscopic aggregation of macrophages that are transformed into epithelium-like cells surrounded by a collar of mononuclear leukocytes, principally lymphocytes and occasionally plasma cells and giant cells (formed by the fusion of epitheliold cells with abundant cytoplasm and multiple nuclei). Q: What is bacteraemia? A: The presence of viable bacteria circulating in the bloodstream. Q: What is septicaemia? A: Systemic disease associated with the presence and persistence of pathogenic microorganisms or their toxins in the blood. Q: What is septic shock? A: A condition of profound haemodynamic and metabolic disturbance characterised by failure of the circulatory system to maintain adequate perfusion of vital organs caused by endotoxin in the blood. Q: What is an abscess? A: A localised collection of pus caused by suppuration buried in tissues, organs or confined spaces. Usually due to an infective process. Q: What is pyaemia? A: The invasion of bloodstream by pyogenic organisms. Q: What is a fistula? A: An abnormal passage or communication, usually between two internal organs or leading from an internal organ to the surface of the body. Q: What is a sinus? A: A notch, depression or cavity on the surface of an organ. Q: What is empyema? A: The accumulation of pus in a cavity of the body, when used without a descriptive qualifier, it refers to thoracic empyema. Q: What is a carbuncle? A: A multilocular adscess resulting from extension of a boil into the subcutaneous tissues. Q: What are some of the reasons a irritant may fail to be removed from the body? A: * Nature of the irritant (resistance to phagocytosis/destruction e.g. inorganic patricles, mycobacteria) * Overwhelming dose of the irritant * Inadequate or inappropriate host response (immunodeficency, autoimmunity) * Nature of host tissue (e.g. bone) Q: What is chronic inflammation? A: An orchestrated cellular and vascular response of prolonged duration in which leucocyte recruitment and activation, as well as tisue destruction and repair occur simultaneously. Q: What are the histological featrues of acute inflammation? A: * Infiltration by mononuclear cells - Macrophages, lymphocytes, plasma cells * Tissue destruction of parenchymal cells and stroma - Proteolytic enzymes * Tissue repair - Deposition of extracellular matrix - Fibroblast accumulation (fibrosis) - Proliferation of small blood vessels (angiogenesis) Q: What are the 4 steps to angiogenesis? A: * Degradation of the basement membrane and ECM * Migration of endothelial cells * Proliferation of endothelial cells * Organisation and maturation of blood vessel Q: What pro- and anti-angiogenic factors regulate angiogenesis? A: * bFGF * VEGF * TGF-beta * PDGF Q: What is the main morphological difference between Langhan's type giant cells and foreign-body type giant cells? A: Langhan's type have peripherally located nuclei whereas foreign-body type have haphazardly located nuclei. Q: What are some of the causes of granulomatous inflammation? A: * Mycobacteria - Tuberulosis, leprosy * Spirochetes and related organisms - Syphilis, cat's scratch * Parasites - Schistosomiasis, leishmania * Fungi - Cyrptococcus * Inorganic dusts - Silicosis - Berrylliosis * Drugs - Allopurinol, Isonaizid * Unknown - Sarcoidosis - Crohn's disease Q: What are the differential diagnoses for acute appendicitis? A: * Mesenteric lymphadenitis * Acute salpingitis * Ectopic pregnancy * Urinary tract infection * Meckel’s diverticulitis * Includes almost every cause of acute abdominal pain, plus some supradiaphragmatic conditions. Q: What is the definition of pneumonia? A: Microbial invasion of lung parenchyma and the associated host response. Q: What are some of the defences the host has against infection of the lungs? A: * Filtration and humidification of inspired air * Epiglotic and cough reflexes * Mucociliary transport * Innate immunity - Polymorphonuclear neutrophils, complement * Humoural immunity - B lymphocytes, immunoglobulins, complement * Cellular immunity - Alveolar macrophages, T lymphocytes, cytokines Q: What are 4 typically cultured organisms in community acquired pneumonia? A: * Strep. pneumoniae (50-90%) * Haemophilus influenzae * Staph. aureus * Legionella pneumophila Q: What are 4 typical organisms in atypical pneumonia? A: * Mycoplasma pneumoniae (70%) * Chlamydia psittaci * Coxiella burnetti (Q fever) * Viral: influenza A and B, adenovirii Q: What are the typical microbiological causes for nosocomial pneumonia? A: * Aerobic Gram negative bacilli (60%) - Klebsiella pneumoniae, E. coli, Serratia sp., Enterobacter sp., Pseudomonas aeruginosa * Staph. aureus * Strep. pneumoniae