8 - March 13, 2013.docx

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Laboratory Medicine and Pathobiology
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CARDIAC IMMUNOPATHOLOGY Type I hypersensitivity – Leads to cascae of degranulation of efector cells –release of primary mediators – causes smooth muscle contraction – activation of complement, kinins – severe anaphalyctic reaction can cause significant acute distress to someone, due to bronchial constriction and edeme when endothelial vessels become leaky Heart – primary Not a big player with the heart – but leaky blood vessels affected significantly in heart Systemic anaphyalxix – often medical emergency Type 2 – player in cardiac immunopathology Directed against self-antigens – cascade of changes including – recruitment of inflammatory cells, inflammation, tissue injury Special form of type 2 hypersensitivity – involved with rheumatic heart disease – cross-reacting antibodies – develops antibodies against bacteria that cross react with self-antigens – lead to tissue damage in organs that express the self antigens Antibody reaction against bacteria – good – but due to structure of antibody that develops – antibody reacts against self antigens in tissues Type 2 – Antibody-mediated transplant rejection = graft vascular disease Lupus – usually type 3 Pericardiotomy syndrome – pericardioum is covering of the heart; otomy means cut in two; - antibody reaction that develops when tissues of the heart are cut into Post periocardiotomy syndrome – congenital heart disease – open heart surgey to correct the disease – metal wires that surgeons put in – in order to do many of the more complicated congenital surgeries, split the sternum, open the chest to expose the heart, repair, hen wire the sternum together using wire Child had developed fever, pericarditis (inflammation of the heart covering – felt as chest pain) Inflammation of the pleura (lining of chest and lungs) – occurs around two to four weeks after the surgery – Immune system is reacting to antigens that are normally hidden from the immune system within the tissues – but with the disruption of the tissue by surgery or trauma or heart attack, those normally hidden antigens are exposed and antibody readctions can develop against those Post pericardiotomy syndrome – Pericardium was expanded due to fluid, not the enlarged heart – leakage of fluid from vessels surrounding heart – fluid under pressure, accumulated in the sack to prevent heart from pumping properly – cause of death – heart disease repair was fine, but accumulation of fluid that lead to tamponade (pressure as result of accumulated fluid prevented heart from expanding and conracting properly) – if sack isn’t severe, there can be ongoing mild and moderate inflammation – lead to scarring (fibrosis) – both the covering of the heart – Pathogenesis – development of self-antigens Type 4- cytotoxic or cellular mediated immune injury – primary type of immunologic reaction that occurs with cellular rejection of solid organs – Rheumatic fever – occurs after infection with specific bacteria – usual source of bacterial infection is throat – infection most common in throat, tonsillitis or pharyngitis – Rheumatic fever is mult-system but the heart takes the blunt of the pathology In the US – decline in the development of rheumatic fever in people in Less virulent or disease-causing strains compared to before But primarily, due to use of step A antibiotics Mini-epidemics in various places – Can get strep bacteria, small percentage get the disease – but very common bacteria, so still high number of potential people develop the disease Hypersensitivity reaction type 2 – only certain serotypes of the group A streptococci are associated with this – rheumatic fever develops week and a half – first child gets sore throat, takes a week and a half – for the rheumatic disease to develop – group A strep – components of bacteria that have the same antigenic determinants that certain proteins that are present in the heart of mammals – some similarity with antigens in brain and joint tissues and skin – but primarily the heart that has the most Tropoyosin and myosin – responsible for heart contracting Rheuamatic fever – bacteria itself responsible for Latent period fits with the immune response explanation Bacteria into the back of throat – bacteria grow and cause local tissue damage and inflammatory reaction – get sore throat – some bacteria get into lympathic drainage that drains into lymph nodes – gets into lymph node and incites immune reaction there, B cell reaction – antibodies discharged from LN – get into blood stream – aimed at attacking bacteria in throat – they circulate through body – attack heart cell proteins because of matching antigen determinants shared between bacteria and heart – pericardium, myocardium, endocardium (pancarditis – all inflammation of the heart – all layers can be affected) Manifestations – major ones Carditis Subcutaneous noduels – painful bumps on skin Marginatum – rash Syndenham chorea – involvmenet of central nervous system in the brain – uncontrolled movement of arms and legs Minor manifestations – arthraligia is joint pain without swelling Jones criteria – some of these manifestations can occur without the patient having rheumatic fever – identification of minimal criteria that must be met for treatment – strep A infection – strict criteria because the patient needs to be protected from strep A fever for the entire lifetime In rheumatic fever, nearly all deaths due to involvmenet of heart First phase called acute phase – additional attacks Chronic – repeated recurrent attacks Pathology – non supportive = no pus is formed, so neutrophils not component of this injury initially, so no pus-filled inflammatory areas which would be expected if bacteria is causing the issue Inflammatory foci especially evident in the myocarditis Pathogenesis – initial antibody reaction to group A strep M protein Antibodies produced corss react with antigens present in other cells – type 2 reaction where antibody mediated injury to the cell Pericarditisi image Pericardium usuall shiny But inflammation, etc coats the heart so rough-looking Aschoff body – focus of inflammation – has wavy pink stuff in background (fibrin), includes lymphocytes, plasma cels, Aschoff yocytes and macropahges Rheumatic endocarditis – acute inflammation affecting the valves – development of endocarditis – inflammation affecting valve tissue (third layer) Endocarditis is the reason why primary cause for chronic rheumatic heart disease Blood flow is turbulent – called murmur Myocardium – pumping portion – severly affected by inflammation – it can fail, so heart failure Can be significant disturbances in rythum of heart – can be fatal Possibility of developing tamponade – leaky blood vessels – of the three percent of people that get rheumatic fever – develop severe heart disease so jeopardize the lungs – less severe damage, but focus on cardiac valves Recurrent episodes of acute and recurrent damage to structure (esp valves) – response of body distorts valve so they no longer work properly – so chronic disease develops Stenosis = narrowing Tricuspid valve – mostly on the left side Normal heart – blood from atrium – blood ventricle which is main pumping – Valve tissue is transparent – thin – delicate looking Mitral valve with disease – left atrium at top; thick looking firm tissue – chorade endonae instead of being fine structs, they are thickened, they have fused, leaflet tissue is thickened – valves do not work properly – do not open or close properly – severe cases like this, fatal – Mitral stenosis – Stenosis – blood backs up in heart and lungs – do not flap On the right side, opening between the leaflets of the valve – normally the opening should the whole circumference, but here, significantly narrower, leaflets do not bend Example of artificial valve – problems 1 – disc breaks or the struts break Aortic valve – valve distorted and thickened RHEUNMATIC FEVER IMPORTANT DISEASE _____________- LUPUS Cardiovascular disease an important complication of lupus Kidney disease also important READ THE OUTLINE SLE Some examples of multi-system involvement of lupus Pericarditis – inflammation of outer layer of heart – there can be mild carditis – different from rheumatic fever affecting the heart – lymphocytic inflammation – lymphocytes that are in
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