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22 Cards in this Set

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ENDOTHELIAL CELLS


Monolayer lining the vascular system for homeostasis and circulatory function

EC HETEROGENEITY


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

EC CIRCULATORY FUNCTION

EDRF eg NO


EDCF eg endothelin peptides, angiotensin II, thromboxane 2


Inhibit platelet aggregation


Have anticoagulant heparin-like molecules


Produce t-PA for fibrinolysis

EC HOMEOSTASIS


Regulate vascular smooth muscle


Electrical continuity via ion channel activation to relax SM


Angio- and vasculogenesis via VEGF and MMPs

EC IMMUNE REPSONSE


Leucocyte rolling, adhesion, arrest and transendothelial migration


EC MHCII expression by INFy


Activated in immune regulation and autoimmunity

ARTERIAL PULMONARY HTN


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

APH AND ECs


EC functional mutation = SM proliferation


ECs sense increased flow and hypoxia leading to more constrictive and proliferative signalling to muscle cells

PHTN TREATMENT - ENDOTHELIN


Pathway involved pre-pro-ET converting to pro-ET to cause vasoconstriction and proliferations


Drugs are endothelin receptor anatagonists

PHTN TREATMENT - NO-cGMP

L-arginine conversion to L-citrulline causes vasodilation and antiproliferation


Drugs are phosphodiesterase 5 inhibitors and guanylate cyclate stimulators

PHTN TREATMENT - PGI2


Arachidonic acid to PGI2 causes vasodilation and antiproliferation


Drugs are Prostacyclin Receptor Agonists

OTHER TYPES OF PHTN

PH with LHD


PH with lung disease or hypoxaemia


Heritable - due to BMPRII muts leads to sporadic PAH

VASCULAR ENOTHELIUM - ROLE


Vasomotor tone


Cell/nutrient trafficking


Maintain blood fluidity, inflammation and coagulation balance


Cell adhesion and growth

ROLE OF NO


SM relaxation


Prevent leucocyte adhesions


Inhibit platelet aggregation/adhesion


Anti-inflammatory

CASUES OF ENDOTHELIAL DYSFUNCTION


Lifestyle, age and obesity


Systemic conditions


Local factors eg blood flow


Inflammation


DYSFUNTION = ATHEROMA/ATHEROSCLEROSIS

VASCULITIDES - DEFINITON


Vessel wall inflammation


Immune mediated or pauci-immune


Primary or secondary; secondary have known associations eg RA


VASCULITIDES - CAUSES

Infection eg meningococcus, aspergillus etc


Irradiation


Immune complexes and autoantibodies


Complement activation or deficiency (complement clears complexes via C3b)

PAUCI-IMMUNE VASCULITIS


No immune complexes or autoantibodies


Immune response directed at inflammatory cells

ANCA

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

VASCULITIDES - CLASSIFICATION


Necrotising - polyarteritis nodosa


Non-necrotising - Buerger's


Leukocytoclastic - HSP


Granulomatous - wegener's, GCA


Eosinophilic - churg-strauss

WEGENER'S


ANCA positive


Granulomatous with polyangitis


Small and medium vessels


Causes necrotising inflammation of resp tract, systemic necrotising vasculitis and renal disease

VASCULITIS - CLINICAL FEATURES


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

PRESENTATION OF ANCA VASCULITIDES

Alveolar haemorrhage


Haematuira


Purpura


Red eye


Mononeuritis multiplex