Physiology > STUDY GUIDE > PHCY 4450 Pathophysiology Exam 3 (All)

PHCY 4450 Pathophysiology Exam 3

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 Glomerulonephritis (GN) o Most causes are immunologic  Antigen/antibody  Antibodies reacting with intrinsic antigens (autoimmune)  Antibodies reacting with antigens planted in glomerulus  Cell-mediated  Less common  T cells may have a role in progression of GN  Plays a role in transplant rejection o Circulating Immune Complex Nephritis  Circulating immune complexes become trapped within glomeruli  Glomeruli are not immune targets, but become innocent bystanders to the immune response  Immune complexes become trapped in mesangium  Trapped antibodies interact with leukocyte’s Fc receptors  Mesangial and endothelial cells proliferate Granular staining  Antigens may be either endogenous or exogenous  Endogenous: SLE, tumors  Exogenous: streptococci, Hep B & C, Terponema pallidum, Plasmodium falciparum, tumor antigens  Prognosis  If course is transient, recovery is possible if immune complexes are cleared (e.g. post-streptococcal GN)  If chronic, long term damage results o Continuous “shower” of antibody/antigen complexes  Charge determines location of deposits  Highly Cationic: cross GBM and become Subepithelial  Highly Anionic: may cross endothelial cells but not GBM (may not be nephritogenic at all)  Neutral: may accumulate in mesangium  Large Complexes: usually not nephritogenic because they are cleared by phagocytes and don’t cross into GBM o Anti-GBM antibody induced nephritis (in-situ)  Antibodies against a fixed antigen in the glomerular basement membrane  Antibodies bind along the line of the GBM  Autologous antibodies often cross-react with other basement membranes  Lung alveoli  Antibodies bind to the non-collagenous domain or alpha-3 chain of collagen type IV  5% of GN cases  S&S: severe crescentric glomerular damage and rapid progression o Antigens planted within glomerulus  Certain antigens have an affinity for GBM  Cationic molecules that bind to anionic sites  Antigens  DNA, nucleosomes, nuclear proteins  Large aggregated proteins  Pathogen products  Drugs  These react with other antibodies and complement resulting in inflammation  Granular immunofluorescent staining

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