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Main clinical symptoms in lung diseases

Main clinical symptoms in lung diseases. 08.09.2016. Case history. 28 years old male Excercise induced dyspnea for 2 years No connection with daytime, season, meal Dry cough in lying position No chest pain Nonsmoker Physical exam: Stridor. Chest x-ray. Lung function (flow-volume curve).

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Main clinical symptoms in lung diseases

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  1. Main clinical symptoms in lung diseases 08.09.2016.

  2. Case history 28 years old male Excercise induced dyspnea for 2 years No connection with daytime, season, meal Dry cough in lying position No chest pain Nonsmoker Physical exam: Stridor

  3. Chest x-ray

  4. Lung function (flow-volume curve)

  5. Bronchoscopy

  6. CT scan

  7. CT scan

  8. Main points in medical history of pulmonary disorders • Present complaints • Previous lung, heart or kidney, other diseases • Smoking (pack-year) • Previous haemoptysis, infection • Family history (cc, allergy) • Skin symptoms • Travelling • Exposition to dust, gases (asbest) • NSAID (Nonsteroid anti-inflammatory drug), salicylate, anticoagulant therapy • Upper or lower GI (gastrointestinal) disease

  9. Main clinical symptoms What to do? History Physical exam Testing -pulsoxymetry -ECG -Chest X-ray -lung function • cough • haemoptysis • dyspnoe • chest pain

  10. Pulmonary causes of cough Acute (< 8 weeks) Lower airways asthma aspiration (1-3 yrs) inhalation (fire, accident) Infection Pleura and lung diseasesPneumonia Pleurisy Ptx Pulmonary embolism Chronic (> 8 weeks) Lower airways and parenchymal chronic bronchitis, COPD (chronic obstructive pulmonary disease) asthma, RADS (Reactive Airways Dysfunction Syndrome) eosinophilic pulmonary diseases lung tumors Infection ILD/DPLD (syst+lung involv.) (Interstitial lung disease/diffuse parenchymal lung d.) aspiration bronchiectasis cystic fibrosis bronchomalacia rare causes (tracheobronchomegalia, amyloid infiltr, tracheobronchopathia, osteoplastica, polychondritis)

  11. Extrapulmonary causes of cough Acute (< 8 weeks)Chronic (> 8 weeks) Upper airways Upper airways - infectious (common cold) - chronic rhinitis, sinusitis, - allergy pharyngitis, laryngitis - vocal cord dysfunction Cardiac diseases- OSA (obstructive sleep apnoe syndrome) with acute pulmomary GERD congestion Drug (ACE inhibitor: angiotensin converting enzyme) Cardiac diseases - any incl. pulmonary congestion - endocarditis

  12. Urgency in acute cough 7. History of malignant tumor 8. History of heavy smoking (> 20 pack-year) 1. Haemoptysis 2. Severe chest pain 3. Dyspnoea 4. High fever 5. TB - epidemiology - contact with sick person - homelessness - illicit drug user 6. Immunsuppressed states - CVID (common variable immunodeficiency) - AIDS - immunsuppressive therapy Szívbetegség -bármely,kisvérköri pangással - endocarditis

  13. Chronic cough without definite chest X-ray or lung function • Upper airway disease 2. „cough variant asthma” 3. GERD (gastroesophageal reflux disease) 4. Taking ACE inhibitor

  14. Chronic cough in diffuse parenchymatous lung – or autoimmune disease • Due to lung involvement (Sjögren sy, Wegener, systemic sclerosis, Churg-Strauss sy, IIP:idiopathic interstitial pneumonia, sarcoidosis) 2. Due to treatment (methotrexate, cyclophosphamide) • Due to infection in the immunocompromised host End-stage ILD, honeycomb lung

  15. Frequent mistakes in the diagnostic workup • Extensive diagnostics in patients taking ACE inhibitor 2. Trivialisation of cough in smokers without diagnostics • Extrapulmonary causes (E.N.T:ears, nose and throat, cardiac, neurologic) are disregarded • Change of the established sequence of tests without reason (e.g. HRCT before BHR: bronchial hyperresponsiveness testing, PFT: pulmonary function test) • No bronchoscopy though cause not determined • Psycogenic cough diagnosed, tumor overlooked

  16. Clinical algorithm for the dg of acute cough History, physical exam Appropriate dg, hospital admission if necessary Immediate dg necessary ? yes no Infection ? Further dg and therapy Bacteriological? Yes no no Symptomatic therapy, if necessary Drug induced ? (e.g. ACE inhibitor) Discontinue/replace drug yes Improvement within 8 weeks? No further action yes no no Dg according to chronic cough algorithm

  17. Clinical algorithm for the dg of chronic cough History, physical exam Cardiac or neurological cause ? Dg and ther Succes? No further action yes yes no nem X-ray: PA+lateral Cough explained by result Further dg and therapy yes no Lung function test Non-specific provocation pathological ? Normal PFT ? yes yes Cough due to BHR no no Smoking or other hazardous exposure ? Further E.N.T. dg and therapy yes absention success no no

  18. … continued No No further action Normal E.N.T. ? Reflux ? treatment success yes yes yes no no no Is HRCT and bronchos- copy normal ? yes Eosinophilic bronchitis Sputum Eosinophilia ? yes no no Further dg and therapy Further E.N.T. dg and ther In-depth reflux dg: - pH-probe - manometry pathological ? reflux ther yes no chronic idiopathic cough due to increased cough reflex

  19. Potential complications of cough I. RespiratoryCardiovascular Pneumothorax Cardiac dysarhytmias Subcutaneous emphysema Loss of consciousnes Pneumomediastinum Subconjunctival hemorrhage Pneumoperitoneum Laryngeal damage Central nervous Musculosceletal System Intercostal muscle pain Syncope Rupture of m. rectus abdominis Headaches Increase in serum CK Cervical disc. prolapse

  20. Potential complications of cough II. Gastrointestinal Esophageal perforation Other Social embarrassment Depression Urinary incontinence Disruption of surgical wounds Petechiae Purpura

  21. Productive cough • Serous • Mucoid • Purulent • Bloody

  22. Hemoptysis • Hemoptysis is the expectoration (coughing up) of blood or of blood-stained sputum from the bronchi, larynx, trachea, or lungs. • The origin of blood can be identified by observing its color. Bright-red, foamy blood comes from the respiratory tract, whereas dark-red, coffee-coloured blood comes from the gastrointestinal tract.

  23. Etiology of hemoptysis I.

  24. Etiology of hemoptysis II.

  25. Interventions in hemoptysis • bed rest • sedatives • supression of cough • ice on the chest • chest x-ray, CT, bronchoscopy • endotracheal tube • suction • balloon catheter under bronchoscopy • blood transfusion • surgical interventions (pulmonary resection) • catheter embolization of bronchial artery • laser , electrocauter

  26. Dyspnoe • Unpleasent or uncomfortable breathing • Difficulty in breathing, often associated with lung or heart disease and resulting in shortness of breath.

  27. Causes of dyspnea

  28. Time course of dyspnea • Sudden onset:ptx, pulm.embol., asthmatic attack, pulmonary edema, aspiration • Days, weeks, months:pneumonia, tbc (bron-chial spreading), anemia,tumorous occlusion, pleurisies, CHF, obesity • Years: asthma, COPD, ILD, pneumoconiosis, autoimmune diseases with lung involvement

  29. Types of dyspnea • Orthopnea: Discomfort in breathing that is relieved by sitting or standing in an erect position. Inability to breathe except in an upright position • Platypnea (orthodeoxia): accentuation of arterial hypoxemia in the erect position. • Trepopnea: dyspnea that is sensed while lying on one side but not on the other. It results from disease of one lung, one major bronchus, or chronic congestive heart failure. • Exercise-induced dyspnoe

  30. Types of dyspnea Diff.dg. - hyperpnea (increase in VE: minute ventilation):abnormal increase in depth and rate of respiration - hyperventilation (increase in VA: alveolar ventilation)Abnormally fast or deep respiration resulting in the loss of CO2 from the blood, causing a decrease in blood pressure and sometimes fainting. Pulmonary ventilation rate greater than that metabolically necessary for gas exchange, resulting from an increased respiration rate, and/or increased tidal volume. It causes an excessive intake of O2 and elimination of CO2 and may cause hyperoxygenenation. Hypocapnia and respiratory alkalosis then occur, leading to dizziness, faintness, numbness of the fingers / toes, possibly syncope, and psychomotor impairment.

  31. Modified Borg Category Scalefor subjective judgment of shortness of breath • 0 nothing at all • 0.5 very, very slight (just noticeable) • very slight • slight • moderate • somewhat severe • severe • very severe • very, very severe (almost maximal • maximal

  32. Anamnesis • Sudden sharp chest pain on right side • Dyspnea • Physical exam • Hyperresonant percussion right side • No breathing sounds on right side by auscultation

  33. Chest pain • The heart, lung, esophagus, great vessels provide afferent visceral input through the same thoracic autonomic ganglia. • Painful stimuli from thoracic organs can produce discomfort described as pressure, burning, aching, and sometimes sharp pain. • Lung parenchyma and visceral pleura are insensitive to pain • Consider cardiac origin in case of risk factors or exertional symptoms • For anyone with chest pain minimal testing includes pulse oxymetry, ECG, chest-Xray.

  34. Characteristics of chest pain I.

  35. Characteristics of chest pain II.

  36. Characteristics of chest pain III.

  37. Lung cancer 08.09.2016.

  38. Epidemiology Globocan 2012. • Lung cancer is the most frequent malignant disease New cases: 1,82 million/year (13%) Mortality: 1,59 million/year Most frequent cause of death amoung malignant diseases>colon+prostate+breast Europe:~1000 death/day Lung cancer fatality: 1,59/1,82 = 0,87 breast cancer fatality: 0,35 Male/female: 2,4/1

  39. New diseases according to ages • Until 40 years : 1%↓ • 40-49 years: 10%↓ • 50-59 years: ~30% • 60-69 years: ~30% • Above 70 years: 30%↓

  40. Etiologic factors Smoking Athmospheric pollution Ionisation Occupational factors asbestos, radon, etcOther lung diseases tb, COPD, ILDGenetic events

  41. Smoking • 400 chemical materials • 60 carcinogens • Gas and particulate phase • Nitrosamines, aromatic amines, benzopyrene, CO, CO2, aldehids, nicotin, free radicals • Pack-year

  42. Smoking and Lung Cancer • 85-90% of lung cancer patients are smokers • Damages of 10-15 gens have role in the development of lung cancer • 86% of smokers have damages of these gens

  43. Molecular biology of lung cancer • Genetic damages • Deletion • Mutations • Amplifications Tumor suppressor gen injury (p53, RB1) Inhibation of proliferation Repair mechanism Induction of apoptosis Protooncogen abnormalities Autocrine growth factors membran receptors transcription factors

  44. Lung Cancer Mutation Consortium Mutationsfrequency M G Kris ASCO Annual Meeting 2011, June 3–7, Chicago

  45. Histology of lung cancer Non small cell lung cancer Squamous cell carcinoma (30%) Well, or less differentiated, with or without keratinisation Adenocancer (45%) acinar papillary bronchioloalveolar with mucus formation Large cell carcinoma (10%↓) clear cell giant cell

  46. Histology of lung cancer Small cell lung cancer (15%) Oat cell Intermediate cell type Combined type Carcinoid tumor Bronchial gland carcinomas Adenoid cystic carcinoma Mucoepidermoid carcinoma

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