Chronic Obstructive Pulmonary Disease (COPD) & Valvular Heart Disease PDF

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) “heterogenous lung condition characterized by chronic resp symptoms due to airway and/or alveoli abnormalities that cause persistent, progressive, airflow obstruction” Diagnostic criteria Presence of non-fully reversible airflow limitation FEV1/FVC 2 mode...

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) “heterogenous lung condition characterized by chronic resp symptoms due to airway and/or alveoli abnormalities that cause persistent, progressive, airflow obstruction” Diagnostic criteria Presence of non-fully reversible airflow limitation FEV1/FVC 2 moderate exacerbations / >1 leading to hosptializaiton = LABA & LAMA VALVULAR HEART DISEASE Causes & Risk factors Aortic stenosis Senile calcification Bicuspid valve Rheumatic heart disease Aortic insufficneicy Infective endocarditis Aortic root dilation Marfan’s syndrome Ascending aortic dissection Pulmonary stenosis Congenital Can be carcinoid syndrome or Rheumatic fever Pulmonary insufficneicy Iatrogenic Infective endocarditis Rheumatic heart disease Carcinoid syndrome Can be congenital Clinical classification By valve and then either stenosis or insufficiency Tricuspid stenosis Rheuatmic heart disease Carcinoid syndrome Infective endocarditis Triscupid insufficneicy RV dilation Rheuatmic heart disease Infective endocarditis Carcinoid syndrome Ebstein anomaly Mitral stenosis Rheuatmic heart disease Left atrial myxoma Mucopoly saccharidosis Mitral insufficneicy Infective endocarditis MI Rheumatic heart disease pMVP Connective tissue disorders Aortic stenosis Exertional angina Syncope Dyspnoea Mitral stenosis Exertional dyspnoea & angina are less common Rarely haemoptysis Pink forth sputum = HF Murmur timing Aortic stenosis = between S1 & S2 (short) Aortic insufficneicy = During S2 Pulmonary stenosis = between S1 & S2 (short) Pulmonary insufficiency = During S2 Tricuspid stenosis = after S2 Tricuspid insufficneicy = Between S1 & S2 (long) Mitral stenosis = After S2 Mitral insufficneicy = between S1 & S2 (long) Aortic regurgitation May be asymptomatic for decades Severe = angina, dyspnoea & features of HF Associated signs ( Cool dudes quickly try mullets) Corrigan's sign = bounding carotid pulse De Musset’s sign = nodding of head in with heart beating Quincke’s sign = capillary pulsations Traube’s sign = systolic & diastolic sounds heard over femoral arteries Muller’s sign = uvula pulsation Rheumatic heart disease Most important cause of acquired heart disease in young adult sin resource limited countries Pulmonary stenosis Exertional dyspnoea & signs of right HF Mitral valve prolapse 75% of patients only mild/no mitral regurgitation Ventricular arrhytmias (low risk) Mitral regurgitation Mild is often asymptomatic When severe symptoms are similar to HF Pulmonary regurgitation Usually asymptomatic Clinical manifestation only evident with onset of RV dysfunction RV enlargement may lead to ventricular arrhytmias Tricuspid regurgitation Asymptomatic and diagnosed solely by echocardiogram Highly complaint so haemodynamic consequences only seen in severe TR Tricuspid stenosis Uncommon and rarely exists in isolation Chronic manifests as venous congestion due to hindrance of blood flow in RA ASTHMA & ALLERGIC DISORDERS Immunopathogenesis of asthma Large airway inflammation = submucosal Small airway inflammation = outside airway smooth muscle Multiple inflammatory cells involved Eosinophils Neutrophils CD4 T cells Mast cells Airway remodelling in asthma Smooth muscle & epithelial changes Goblet cell hyperplasia Angiogenesis Fibroblast accumulation Reticular basement membrane thickening Asthma phenotypes Th2 high phenotype = early onset allergic Early onset Mild – severe Allergic symptoms Thicken subepithelial basement membrane Specific IgE, Th2 cytokines Steroid responsive (Th2 targeted) Th2 high phenotype = late onset eosinophilic Adult onset Often severe Sinusitis & less allergic Steroid refractory eosinophilia Interleukin 5 Responsive to antibody modifiers ( Il5 & cysteinyl leukotriene steroid refractory Th2 low phenotype = neutrophilic Adult onset Low FEV1 = more air trapping Sputum neutrophilia, Th17 pathways & IL-8 Possibly response to macrolide antibiotics Treatment of asthma Omalizumab Binds to Fc portion of Ige & forms soluble immune complexes Decrease IgE = decreased airway eosinophil, mat cells, basophils and T&B cells Inconsistent effects on airway hyperresponsiveness Mepolizumab Reduces sputum & blood eosinophils = reduces asthma exacerbation Eosinophil count >0.15 = 52% reduction Eosinophil count >0.5 = 70% reduction Benralizumab Anti-IL5Ralpha antibody = binds to IL5Ralpha on eosinophils & basophils Completely supressed blood eosinophil and reduced airway eosinophil by 90% Reduces asthma exacerbations & symptoms Improves FEV1 Allows decrease/withdrawal of oral steroids Dupilumab Anti-Il4 receptor alpha antibody Blocks signalling of IL4 & IL13 Fewer exacerbations Improved FEV1 and quality of life Most improve seen in patients with T2 biomarkers Tezepelumab Anti-TSLP antibody (thymic stromal lymphopoietin) Interferes with upstream in inflammatory cascade Reduced asthma exacerbation Improves lung function & asthma control