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22 Cards in this Set
- Front
- Back
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ENDOTHELIAL CELLS |
Monolayer lining the vascular system for homeostasis and circulatory function |
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EC HETEROGENEITY
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Differ from one vascular bed to another or within the same bed for function Vary in capillaries due to selective barrier Continuous with less villi in BBB Fenestrated with more villi in gut |
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EC CIRCULATORY FUNCTION
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EDRF eg NO EDCF eg endothelin peptides, angiotensin II, thromboxane 2 Inhibit platelet aggregation Have anticoagulant heparin-like molecules Produce t-PA for fibrinolysis |
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EC HOMEOSTASIS
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Regulate vascular smooth muscle Electrical continuity via ion channel activation to relax SM Angio- and vasculogenesis via VEGF and MMPs |
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EC IMMUNE REPSONSE |
Leucocyte rolling, adhesion, arrest and transendothelial migration EC MHCII expression by INFy Activated in immune regulation and autoimmunity |
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ARTERIAL PULMONARY HTN
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Loss of arteriolar function; narrowing leads to resistance Narrowing due to increased SM and perivascular fibrosis Deoxygenated blood shunted back to normal circulation and RV failure |
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APH AND ECs
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EC functional mutation = SM proliferation ECs sense increased flow and hypoxia leading to more constrictive and proliferative signalling to muscle cells |
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PHTN TREATMENT - ENDOTHELIN
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Pathway involved pre-pro-ET converting to pro-ET to cause vasoconstriction and proliferations Drugs are endothelin receptor anatagonists |
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PHTN TREATMENT - NO-cGMP
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L-arginine conversion to L-citrulline causes vasodilation and antiproliferation Drugs are phosphodiesterase 5 inhibitors and guanylate cyclate stimulators |
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PHTN TREATMENT - PGI2
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Arachidonic acid to PGI2 causes vasodilation and antiproliferation Drugs are Prostacyclin Receptor Agonists |
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OTHER TYPES OF PHTN
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PH with LHD PH with lung disease or hypoxaemia Heritable - due to BMPRII muts leads to sporadic PAH |
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VASCULAR ENOTHELIUM - ROLE |
Vasomotor tone Cell/nutrient trafficking Maintain blood fluidity, inflammation and coagulation balance Cell adhesion and growth |
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ROLE OF NO
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SM relaxation Prevent leucocyte adhesions Inhibit platelet aggregation/adhesion Anti-inflammatory |
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CASUES OF ENDOTHELIAL DYSFUNCTION
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Lifestyle, age and obesity Systemic conditions Local factors eg blood flow Inflammation DYSFUNTION = ATHEROMA/ATHEROSCLEROSIS |
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VASCULITIDES - DEFINITON |
Vessel wall inflammation Immune mediated or pauci-immune Primary or secondary; secondary have known associations eg RA |
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VASCULITIDES - CAUSES |
Infection eg meningococcus, aspergillus etc Irradiation Immune complexes and autoantibodies Complement activation or deficiency (complement clears complexes via C3b) |
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PAUCI-IMMUNE VASCULITIS
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No immune complexes or autoantibodies Immune response directed at inflammatory cells |
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ANCA
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Anti-neutrophilic Cytoplasmic Antibody Cytoplasmic (PR3) or perinuclear (MPO) Pauci-immune small vessel vasculitides Binds to and activates cytokine-primed neutrophils which express ANCA Ags PR3 and MPO; neutrophils bind to endothelium causing inflammation |
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VASCULITIDES - CLASSIFICATION
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Necrotising - polyarteritis nodosa Non-necrotising - Buerger's Leukocytoclastic - HSP Granulomatous - wegener's, GCA Eosinophilic - churg-strauss |
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WEGENER'S
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ANCA positive Granulomatous with polyangitis Small and medium vessels Causes necrotising inflammation of resp tract, systemic necrotising vasculitis and renal disease |
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VASCULITIS - CLINICAL FEATURES
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Constitutional eg fever and malaise Localised and systemic features Cutaneous, ocular, renal, oral, neuro GI eg ulceration, ischaemia, pancreatitis C/P eg haemopthysis, asthma, nodules, valve disease, arrhythmias Digital ischaemia |
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PRESENTATION OF ANCA VASCULITIDES
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Alveolar haemorrhage Haematuira Purpura Red eye Mononeuritis multiplex |
