Содержание
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The pulmonary database
Dr.A.Solomonov. Pulmonology
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Respiratory symptoms 1
Dyspnea Acute (over a period of hours to days) An acute attack of asthma Acute pulmonary edema Bacterial pneumonia A pneumothorax A pulmonary embolus Dr.A.Solomonov. Pulmonology
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Respiratory symptoms 2
A subacutedyspnea(over days to weeks) Exacerbation of preexisting airways disease (asthma or chronic bronchitis) Infection or a noninfectious inflammatory process (PCP, mycobacterial or fungal pneumonia, eosinophilic or organizing pneumonia and others) Neuromuscular disease (Guillain-Barre syndrome, myasthenia gravis) Pleural effusion Chronic cardiac disease (congestive heart failure) Dr.A.Solomonov. Pulmonology
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Respiratory symptoms 3
A chronic dyspnea (over months to years) Chronic obstructive lung disease Chronic interstitial lung disease Chronic cardiac disease Cough and sputum production Suggeststs airway disease as asthma, chronic bronchitis, or bronchiectasis Dr.A.Solomonov. Pulmonology
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Hemoptysis
Massive hemoptysis- >100 ml/24 h The most common site of bleeding is the airwais Acute or chronic bronchitis & bronchiectasis Bronchogenic carcinoma Blood originating from the parenchyma From a localized source (lung abscess, tuberculosis) From a diffuse diseases (an autoimmune process such as Goodpasture’s syndrome, Wegener’s granulomatosis or lupus) Dr.A.Solomonov. Pulmonology
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Dr.A.Solomonov. Pulmonology
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Dr.A.Solomonov. Pulmonology
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Goodpasturesyndrom
Genetical predisposition Typically affected young male smokers Progressive glomerulonephritis & renal failure Diffuse pulmonary hemorrhage Anti-GBM antibody – against type IV collagen Treatment: plasmaphersis, steroids & cytotoxic agents Dr.A.Solomonov. Pulmonology
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Dr.A.Solomonov. Pulmonology
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Wegener granulomatosis
Gramulomatous inflammation and vasculitis of: Upper airways (rinitis, ulceration, perforation of septum, nose deformity, sinusitis, otitis media) Lung: large, multiple nodules and often cavitated Glomerulonephritis Same times a disseminated vasculitis Anticytoplasmic antibody – c-ANCA Treatment: cyclophosphamide and prednisone Dr.A.Solomonov. Pulmonology
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Dr.A.Solomonov. Pulmonology
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Dr.A.Solomonov. Pulmonology
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Dr.A.Solomonov. Pulmonology
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Hemoptysis 2
Disorders of the pulmonary vasculature Pulmonary embolic disease Mitral stenosis or left hart failure Pulmonary arteriovenous malformations (Osler Rendu Weber Syndrome) Dr.A.Solomonov. Pulmonology
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Dr.A.Solomonov. Pulmonology
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Dr.A.Solomonov. Pulmonology
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Dr.A.Solomonov. Pulmonology
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Respiratory symptoms 4
Chest pain from involvement of the parietal pleura Pleural neoplasm or inflammatory disorders Pneumonia or pulmonary infartion hoarseness (tumor involvement o the left recurrent laryngeal nerve) Dr.A.Solomonov. Pulmonology
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History 1
Cigarette smoking Chronic obstructive lung disease – COPD and lung cancer are the two most important respiratory complications of smoking Occupational exposures Inorganic dust : Silica, silicates (asbestos, talc), hard metal, beryllium. Organic dust : Thermophilic bacteria (e.g. farmer’s lung); animal proteins (e.g. bird fancier’s lung). Dr.A.Solomonov. Pulmonology
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History 2
A history of coexisting systemic disease Systemic rheumatic diseases associated with pleural or parenchymal lung disease Metastatic neoplastic disease in the lung Hematologic malignancies Dr.A.Solomonov. Pulmonology
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Pulmonary complication of connective tissue diseases 1
Rheumatoid arthritis – is common in women, but lung complicationmorefrequntly in men Pleural affusion: small & unilateral exudate Very low glucose
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Pulmonary complication of connective tissue diseases 2
Systemic lupus erythematosus (SLE) Pleural effusions – small and bilateral in 50% of cases High titer of ANF & LE cells Pulmonary fibrosis Organising pneumonia Pulmonary hypertension as result of venous thromboses (lupus anticoagulant) Pulmonary infection Pulmonary haemorrhage Dr.A.Solomonov. Pulmonology
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Pulmonary complication of connective tissue diseases 3
Systemic sclerosis Pulmonary fibrosis (nearly in all patients) Pulmonary arterial hypertension Intimal proliferation of small blood vessels Aspiration pneumonia Dermatomyositis Pulmonary fibrosis Respiratory muscle weakness Dr.A.Solomonov. Pulmonology
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History 2
Risk factors for AIDS Previous treatment Chemotherapy, radiation therapy, or treatment with amiodarone can cause interstitial lung disease Beta-blocking agents causing airflow obstruction Angiotensin converting enzyme inhibitors causing cough Dr.A.Solomonov. Pulmonology
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History 3
Family history of diseases that have a genetic component Cystic fibrosis A1 – antitrypsin deficiency asthma Dr.A.Solomonov. Pulmonology
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Physical examination 1
Inspection Rate and pattern of breathing Asymmetric expansion of the chest and/or deviation of the trachea Endobronchial obstruction of a large airway Unilateral parenchymal or pleural disease (pneumothorax) Unilateral phrenic nerve paralysis Kyphoscoliosis and ankylosingspondilitis Dr.A.Solomonov. Pulmonology
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Physical examination 2
Palpation Fremitus is decreased or absent in pleural effusion or in endobronchial obstruction Fremitus is increased over an area of underlying pulmonary consolidation Percussion Dullness – over the consolidated lung or a pleural effusion Hyperresonant – over the air in the pleural space Dr.A.Solomonov. Pulmonology
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Auscultation
Vesicular breath sounds, in which inspiration is louder and longer than expiration Breath sounds are weaker or absent Endobronchial obstruction Liquid in the pleural space Bronchial breath sounds Over the consolidated lung (a more pronounced expiratory phase) Dr.A.Solomonov. Pulmonology
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Abnormal breath sounds
Crackles (rales) Interstitial lung disease or filling of alveoli by liquid Wheezes (airflow limitation as bronchospasm) Rhonchiis – a low-pitched vibratory sounds created when there is free liquid in the airway lumen Pleural friction rubs Stridor – occurs primarily during inspiration represent flow through a narrowed upper airway Dr.A.Solomonov. Pulmonology
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General physical examination 1
Enlarged lymph nodes Disturbances of mentation in acute carbone dioxide retention and hypoxemia Infected teeth and gums predispose to aspiration pneumonitis and lung abscess Clubbing of digits can be found in: Lung cancer Interstitial lung disease Chronic infections in the thorax, such as bronchiectasis, lung abscess and empyema Dr.A.Solomonov. Pulmonology
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General physical examination 2
A systemic diseases may be associated with pulmonary complications such as systemic lupus erythematosus, scleroderma and rheumatoid arthritis Sarcoidosis can have findings on physical examination Ocular findings (uveitis, conjunctivalgranulomas) Skin findings (erythemanodosum, cutaneousgranulomas) Dr.A.Solomonov. Pulmonology
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Imaging 1
Chest radiography is normal in 10% of patients with parenchymal lung diseases Infiltrates Alveolar Interstitial Nodular pattern Increased radiolucency Localized (cyst or bulla) Generalized (emphysema) Dr.A.Solomonov. Pulmonology
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Dr.A.Solomonov. Pulmonology
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Dr.A.Solomonov. Pulmonology
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Dr.A.Solomonov. Pulmonology
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Dr.A.Solomonov. Pulmonology
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Imaging 2
Computed tomography (CT) of chest (8 to 10 mm slices) with or without contrast material Characterize the density, size and accurate site of lesions Assessing hilar and mediastinal disease High-resolution CT (HRCT)examines (1 – 2 mm slices) The best technique for the diagnosis of bronchiectasis Useful for diffuse lung diseases Helical CT useful for the diagnosis of pulmonary emboli in main or segmental pulmonary arteries Dr.A.Solomonov. Pulmonology
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Imaging 3
Magnetic resonance (MRI) useful for diagnosis Superior sulcus tumor Tumor invasion of Mediastinum Chest wall Diaphragm Venous thromboembolism PET-FDG Gallium scan Dr.A.Solomonov. Pulmonology
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Imaging 4
Ventilation-perfusion lung scanning Performed for evaluation of pulmonary embolism Using intravenously albumin macro aggregates labeled with technetium The distribution of the trapped radioisotope follows the distribution of blood flow Inhaled, radio labeled xenon gas demonstrate the distribution of ventilation Pulmonary angiography Ultrasound Dr.A.Solomonov. Pulmonology
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Physiologic features
The primary functions of the respiratory system To remove CO2 to blood Provide adequate O2 to blood For these functions, there must be adequate Ventilation Circulation of blood through the pulmonary vasculature (perfusion) Movement of gas between alveoli and pulmonary capillaries (diffusion) Contact between alveolar gas and pulmonary capillary blood (ventilation-perfusion matching) Dr.A.Solomonov. Pulmonology
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Disturbance of respiratory function
Disturbances in ventilatory function Restrictive pattern (decrease in lung volumes) Obstructive pattern (decrease in expiratory flow rates) Dissturbances in gas exchsnge Disorders relating to CNS of ventilation Dr.A.Solomonov. Pulmonology
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Table 250-2. commonrespiratory disease by diagnostic caf
Dr.A.Solomonov. Pulmonology
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Disturbances in the pulmonary circulation
Output of the rught ventricle is 5 l/min & mean pulmonary artery pressure is 15 mmHg in a normal adult rest Can be measured via pulmonary arterial Swan-Ganz catheter Mean pulmonary arterial pressure remain stable, even with a three to fourfold increase in cardiac output Dr.A.Solomonov. Pulmonology
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Pulmonary hypertension
Alveolar hypoxia is a very potent stimulus for pulmonary vasoconstriction Chronic obstructive lung disease (COPD) interstitial lung disease (ILD), chest wall disease, and the obesity hypoventilation-sleep apnea syndrome (SAS) Diseases affecting the pulmonary vessels Recurrent pulmonary emboli Primary pulmonary hypertension or scleroderma Dr.A.Solomonov. Pulmonology
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Primary Pulmonary hypertension
Rare Death from right heart failure (2-3 years without treatment) Association with diet pills Familial in 6% of cases (autosomal dominant) 2 female:1 male Dr.A.Solomonov. Pulmonology
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Pulmonary hypertension
Mean PAP At rest > 20 – 25 mmHg Exercise > 30 mmHg Dr.A.Solomonov. Pulmonology
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Pathogenesis
Impaired function of vascular endotelium Increased activity of thromboxan and endotelin Decreased activity of prostacycline and nitric oxide Occlusion of small pulmonary arteries Vasospasm Medial hypertrophy Intimal hyperplasia In situ thrombosis Dr.A.Solomonov. Pulmonology
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Diagnosis
Dyspnea, fatigue, chest pain and syncope Right heart failure Echo or cardaic catheterization Exclusion of other causes Cardiac and lung diseases (lung function tests ABG & CT of lung) Pulmonary embolism History of cocaine inhalation or use of diet pills Liver cirrhosis (liver and spleen scan) Screening for HIV or collagen diseases Blood coagulation tests Dr.A.Solomonov. Pulmonology
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Survival & natural history
The median period of survival after diagnosis was 2.5 years, but patients may survive for lengthy periods with the use of newer means of treatment. Anticoagulants nearly double the 3-year survival rate & patients who respond to calcium-channel blockers have a 5-year survival rate of 95%. The 5-year survival rate among patients who were treated with i.v. prostacyclin was twice that of matched historical control patients. Dr.A.Solomonov. Pulmonology
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Treatment
Vasodilators Calcium channel antagonist Intravenous prostacyclin Nitric oxide (NO) – effects lasted for 2-5 min Aerosoledilloprost Endothelin antagonists Viagra (↑L-argenine – NO precursor) Oxygen and anticoagulation therapy Dr.A.Solomonov. Pulmonology
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Arterial blood gases
Pao2 – partial pressures of O2 in arterial blood Paco2 – partial pressures of CO2 on arterial blood Oxygenated Hg is the primary form in which O2 is transported in blood The small amount of O2 is dissolved in plasma The normal Pao2 in arterial blood is 100 mmHg and O2 saturation is about 97,5% The Po2 in venous blood is 40 mmHg and and O2 saturation is about 75% Dr.A.Solomonov. Pulmonology
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Additional diagnostic evaluation
Pulse oximetry continuously measure O2 saturation – not measure PaCO2 Misleading results in the presence of Increased level of carboxyhemoglobin Increased level of methemoglobin Hyperbilirubinemia Dark skin pigmentation Fingernail polish Poor perfusion Dr.A.Solomonov. Pulmonology
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Dr.A.Solomonov. Pulmonology
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Normal acid – base homeostasis 1
The normal Paco2 in arterial blood is 40 mmHg The normal Pco2 in venous blood is 46 mmHg The Paco2 controlled by the central nervous system and respiratory systems Underexcretion of CO2 produced hypercapnia (usually the result of hypoventilation) Overexcretion causes hypocapnia Primary changes in Paco2 can cause respiratory acidosis (Paco2 > 40 mmHg)or alkalosis (PAco2
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Normal acid – base homeostasis 2
The normal plasma bicarbonate [ HCO3 ⁻] is 24mEq/l Regulated by the kidneys through “reabsorption” of filtered HCO3 ⁻ Excretion of NH4 ⁺ in the urine A primary change in the plasma [HCO3 ⁻] can cause metabolic acidosis or alkalosis Results in compensatory changes in ventilation that blunt the changes in blood pH Dr.A.Solomonov. Pulmonology
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Normal acid – base homeostasis 3
The normal arterial pH is maintained between 7.35 and 7.45 The pH regulated by respiratory (Paco2) and renal [HCO3 ⁻] mechanisms CO2+H2O ↔ H2CO3 ↔ H⁺ + HCO3⁻ Dr.A.Solomonov. Pulmonology
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General types of acid – base disorders
Simple acid-base disorders Metabolic acidosis or alkalosis Respiratory acidosis or alkalosis Since compensation is not complete, the pH is abnormal in simple disturbances Mixed acid-base disturbances Dr.A.Solomonov. Pulmonology
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Metabolic acidosis
“metabolic” means a primery changes in HCO3⁻ Can occur because of An increase in endogenouse acid production (such as lactate and ketoacids) Loss of bicarbonate (as in diarrhea) Accumulation of endogenous acid (as in renal failure) pH is low base excess negative Ventilation is increases that lowers the Pco2 The Paco2 ↓1.25 mmHg for each 1mmol/L ↓ in HCO3⁻ Dr.A.Solomonov. Pulmonology
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Metabolic alkalosis
It is manifested by: An increase in the serum [HCO3⁻] An elevated arterial pH An increase in Paco2 as a result of compensatory alveolar hypoventilation It is often accompanied by hypochloremia and hypokalemia The Paco2 increases 6 mmHg for each 10 mmol/L increase in the [HCO3⁻] above normal Base excess is increased Dr.A.Solomonov. Pulmonology
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Respiratory acidosis 1
Caused by an increase in Pco2 Chronic obstructive pulmonary disease A sedative drug overdose Respiratory muscle fatigue pH is low (acidemia) Increase in bicarbonate (compensation) In acute acidosis – HCO3⁻ - increases 1 mmol/L for every 10 mmHg increase in Paco2 Dr.A.Solomonov. Pulmonology
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Respiratory acidosis 2
In chronic acidosis (> 24 h), renal adaptation occurs and the HCO3 – increases by 4 mmol/L for every 10 mmHg increase in Paco2 The serum HCO3 – usually does not increase above 38 mmol/L pH does not fully return to its normal level of 7.4 A rapid increase in Paco2 may cause anxiety, dyspnea, confusion and coma Chronic hypercapnia results in loss of memory, daytime somnolence and headaches (due to raised intracranial pressure) Dr.A.Solomonov. Pulmonology
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Respiratory alkalosis 1
Alveolar hyperventilation decreases Paco2 and increase pH (alkalemia) It is important to rule out pulmonary embolism Bicarbonate is low (it is unusual to observe a plasma HCO3⁻ 2-6 h) renal compensation is develop→ increased HCO3⁻ excretion (10 mmHg fall in Paco2 causes 5 mmol/L drop in HCO3⁻) Dr.A.Solomonov. Pulmonology
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Respiratory alkalosis 2
There is a negative base excess Acute respiratory alkalosis causes intracellular shifts of Na⁺, K⁺, and reduces free [Ca2⁺] by increasing the protein-bound fraction The effect of respiratory alkalosis is reduced cerebral blood flow Dizziness Mental confusion seizures Dr.A.Solomonov. Pulmonology
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Respiratory acid-base disorders
Dr.A.Solomonov. Pulmonology
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Dr.A.Solomonov. Pulmonology
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