Respiratory System 2 - Presentation PDF

THE RESPIRATORY SYSTEM 2 CHRONIC OBSTRUCTIVE PULMONARY DISEASE CLINICAL TERM CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) REFERS TO EMPHYSEMA AND CHRONIC BRONCHITIS, WHICH ARE ACCOMPANIED BY CHRONIC OR RECURRENT OBSTRUCTION TO AIR FLOW WITHIN THE LUNG THE INCREASE IN SMOKIN...

THE RESPIRATORY SYSTEM 2 CHRONIC OBSTRUCTIVE PULMONARY DISEASE CLINICAL TERM CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) REFERS TO EMPHYSEMA AND CHRONIC BRONCHITIS, WHICH ARE ACCOMPANIED BY CHRONIC OR RECURRENT OBSTRUCTION TO AIR FLOW WITHIN THE LUNG THE INCREASE IN SMOKING AND ENVIRONMENTAL POLLUTION HAS LED TO INCREASE IN COPD CHRONIC BRONCHITIS PERSISTENT COUGH WITH SPUTUM PRODUCTION FOR AT LEAST THREE MONTHS IN AT LEAST TWO CONSECUTIVE YEARS MIDDLE-AGED MEN ESPECIALLY SMOKERS SMOKE PREDISPOSES TO INFECTION BY INTERFERING WITH CILIARY ACTION AND CAUSING DIRECT DAMAGE TO EPITHELIUM 10-25% OF THE URBAN POPULATION DUE TO IRRITATION BY INHALED POLLUTANTS Respiratory System 2016-2017 EMPHYSEMA CONDITION OF THE LUNG CHARACTERISED BY ABNORMAL PERMANENT ENLARGEMENT OF THE AIR SPACES DISTAL TO THE TERMINAL BRONCHIOLE, WITH DESTRUCTION OF THEIR WALLS ELASTASES DESTROY ELASTIN FREE RADICALS FROM SMOKE EMPHYSEMA  EMPHYSEMA PATHOLOGICAL TERM LUNG SHOWS ABNORMAL PERMANENT ENLARGEMENT OF THE AIR SPACES DISTAL TO THE TERMINAL BRONCHIOLES DESTRUCTION OF ALVEOLAR WALLS COMMONER IN MEN, 50-80YRS HEAVY SMOKING 25% OF SMOKERS DEVELOP COPD 85-90% OF PATIENTS WITH COPD HAVE SMOKED AT SOME TIME PATIENTS WITH CHRONIC BRONCHITIS GENETIC SMALL % EMPHYSEMA: PATHOGENESIS  PROTEASES (ELASTASE) OR  ANTIPROTEASES (ANTIELASTASE, ALPHA-1-ANTITRYPSIN)  ELASTIN DESTRUCTION IN ALVEOLAR WALLS  DEVELOPMENT OF EMPHYSEMA IN SMOKERS THERE IS LUNG INFECTION WITH  NEUTROPHILS AND MACROPHAGES, WHICH PRODUCE ELASTASE  LUNG DAMAGE STIMULATED NEUTROPHILS RELEASE OXYGEN FREE RADICALS - CAUSE DAMAGE EMPHYSEMA PROGNOSIS WITH SEVERE EMPHYSEMA, COR PULMONALE (HEART DISEASE SECONDARY TO LUNG DISEASE) AND CONGESTIVE HEART FAILURE DEVELOP DEATH DUE TO HEART FAILURE AND RESPIRATORY FAILURE ASTHMA INCREASED RESPONSIVENESS OF BRONCHIAL TREE TO VARIOUS STIMULI, RESULTING IN PAROXYSMAL CONSTRICTION OF THE BRONCHIAL AIRWAYS TRIGGERED BY EXPOSURE TO AN ALLERGEN BRONCHOSPASM TRIGGERS SEVERE DYSPNOEA AND WHEEZING BETWEEN ATTACKS ASYMPTOMATIC AN UNREMITTING ATTACK, STATUS ASTHMATICUS, MAY PROVE FATAL  ASTHMA LUNGS ARE OVER DISTENDED BRONCHI ARE OCCLUDED BY THICK MUCOUS PLUGS EOSINOPHILS & OEDEMA IN BRONCHIAL WALLS HYPERTROPHY OF BRONCHIAL SMOOTH Acute Asthma  ASTHMA TYPES OF ASTHMA PRECIPITATING MECHANISM FACTORS IMMUNE REACTION ALLERGIC (ATOPIC) SPECIFIC ALLERGENS TYPE I (IGE) OCCUPATIONAL CHEMICALSTYPE I & CELL MEDIATED NONATOPIC RESPIRATORY TRACT UNKNOWN; HYPER INFECTION REACTIVE AIRWAYS HYPER REACTIVE AIRWAYS, WHICH RESPOND TO NON-SPECIFIC IRRITANTS - COLD, EXERCISE AND STRESS ASTHMA IS ASSOCIATED WITH OBESITY ASTHMA IS MORE COMMON IN BOYS THAN GIRLS BUT IN ADULTS, THE RATIO REVERSES ? AIRWAY SIZE ASTHMA ATOPIC OR ALLERGIC ASTHMA COMMONEST TYPE TRIGGERED BY ENVIRONMENTAL ANTIGENS - DUSTS, POLLEN, FOODS, HOUSE DUST MITE FAMILY HISTORY COMMON - ALLERGIC RHINITIS, URTICARIA OR ECZEMA GENETIC PREDISPOSITION POSITIVE SKIN TESTS CLASSIC TYPE I IGE HYPERSENSITIVITY REACTION OCCUPATIONAL ASTHMA AFTER REPEATED EXPOSURE FUMES /GASES - RESINS, PLASTICS /TOLUENE ORGANIC/CHEMICAL DUSTS - WOOD, COTTON, PLATINUM CHEMICALS - FORMALDEHYDE, PENICILLIN  TYPE I: ANAPHYLACTIC HYPERSENSITIVITY E.G. ANAPHYLAXIS, HAY FEVER, ASTHMA EXPOSURE TO ALLERGEN HIGH IGE PRODUCED  ACTIVATES MAST CELLS AND BASOPHILS TO RELEASE GRANULES MAINLY HISTAMINE  CONSTRICTS SMOOTH MUSCLE  VASODILATATION  INCREASED VASCULAR PERMEABILITY  PRIMARY MALIGNANT LUNG TUMOURS EPITHELIAL 90 - 95% NON SMALL CELL CARCINOMA 70-80% SQUAMOUS CELL 25-40% ADENOCARCINOMA 25-40 LARGE CELL 10-15% SMALL CELL CARCINOMA 20-25% OAT CELL CARCINOID – LOW GRADE 1-5% LYMPHOMA US figures BRONCHIAL CARCINOMA INCIDENCE MALE TO FEMALE RATIO IS NOW 2:1 IN US LESS COMMON IN FEMALES IN MALTA, BUT INCREASING PEAK INCIDENCE IN 50S TO 60S INCREASES WITH AGE, COMMON BETWEEN 40 - 70 YEARS FATALITY COMMONEST FATAL PRIMARY TUMOUR IN MEN WORLDWIDE IN WOMEN IT IS SECOND ONLY TO BREAST OR COLON CANCER, EVEN IN MALTA IN MALTA, IN 2013, DEATHS FROM LUNG CANCER WERE 5% OF ALL DEATHS AND 18% OF CANCER DEATHS  BRONCHIAL CARCINOMA STRONGLY ASSOCIATED TO SMOKING, CIGARETTES RELATED TO NUMBER SMOKED 25 CIGARETTES A DAY - 12% RISK OF DYING FROM CANCER RISK DIMINISHES ON STOPPING SMOKING SMOKE CONTAINS HYDROCARBONS (CARCINOGENS) PASSIVE SMOKERS CHROMATES / ASBESTOS / POLLUTION CHEST X-RAY – SQUAMOUS CELL CA CHEST X-RAY AND CT - ADENOCARCINOMA Respiratory System 2016-2017 LUNG TUMOURS SQUAMOUS ARISES IN A MAIN CARCINOMA BRONCHUS FROM SQUAMOUS BRONCHIAL EPITHELIUM, METAPLASTIC FROM RESPIRATORY EPITHELIUM A LARGE FRIABLE MASS, WHICH MAY ULCERATE, PROJECTING INTO LUMEN WITH STENOSIS OF THE BRONCHUS EXTENDS INTO SURROUNDING LUNG MAY ERODE INTO ADJACENT BLOOD VESSELS MAY ALSO ARISE FROM A PERIPHERAL BRONCHUS ADENOCARCINOMA PERIPHERAL TUMOURS ORIGINATE FROM GLANDULAR EPITHELIUM NEUROENDOCRINE CARCINOMA ARISES IN A MAIN BRONCHUS AND ORIGINATES FROM ENDOCRINE CELLS IN EPITHELIUM PRODUCE HORMONES: ACTH (ADRENOCORTICOTROPHIC HORMONE) OR ADH (ANTIDIURETIC HORMONE) OR PTH (PARATHYROID HORMONE) WITH RELEVANT CLINICAL SYNDROMES BRONCHIAL CARCINOMA SPREAD & METASTASES LOCAL : LUNG, HILAR TISSUES, LARGE BLOOD VESSELS, PERICARDIUM, OESOPHAGUS ,PLEURA LYMPHATICS : HILAR FIRST, PARA-TRACHEAL, CERVICAL BLOOD : LIVER, ADRENAL GLANDS, BRAIN, BONE NON METASTATIC SYSTEMIC EFFECTS FINGER CLUBBING, CACHEXIA, NEUROLOGICAL SYNDROMES PARANEOPLASTIC SYNDROMES HORMONE PRODUCTION: ACTH / ADH / PTH SMALL CELL OR SQUAMOUS CELL BRONCHIAL CARCINOMA PROGNOSIS IS GENERALLY POOR SURGICAL RESECTION WHEN PRACTICAL POSSIBLE IN ONLY 20 - 30% OF PATIENTS 30-40% 5YR SURVIVAL AFTER SURGERY SQUAMOUS CARCINOMA AND ADENOCARCINOMA HAVE A BETTER PROGNOSIS  SECONDARY TUMOURS MULTIPLE NODULES ANY TUMOUR BREAST, KIDNEY AND TESTICULAR TUMOURS - COMMON  STUDY GUIDE 1. DEFINE CHRONIC BRONCHITIS AND EMPHYSEMA. 2. DISCUSS THE PATHOGENESIS OF EMPHYSEMA. 3. DISCUSS THE PATHOGENESIS OF ASTHMA. 4. DESCRIBE THE CLASSIFICATION OF MALIGNANT LUNG TUMOURS. 5. DISCUSS THE INCIDENCE, CAUSE AND PROGNOSIS OF PRIMARY LUNG CARCINOMA. 6. DESCRIBE THE SPREAD OF PRIMARY BRONCHIAL CARCINOMA. 7. DISTINGUISH SECONDARY LUNG TUMOURS FROM PRIMARY LUNG TUMOURS.