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Pulmonary defense
The document summarizes the pulmonary defense system. It describes the protective mechanisms in the nose, throat, cough reflex, mucociliary clearance, surfactants, immune cells and proteins that work together to defend the lungs from infection. These defenses are able to keep the lungs free of infection under normal conditions. Pulmonary function tests objectively measure lung function and are used to diagnose respiratory diseases.
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Pulmonary defense
- 1. Pulmonary Defense Dr. ManuMohan K
- 2. Introduction •Lungs are dailyexposed to 10,000 liters of air which contain noxious particles, infectious agents, etc •Respiratory system must recognise and eliminate unwanted elements in inspired air to keep pulmonary structures free of infection.
- 3. •The fact thatthe normal respiratory tract is free of infection is a testimony to the efficiency of a defense system •Elements of defense system spread through out the respiratory tract
- 4. Nose and oropharynx •Formidablebarrier •Nasal hair exclude large particles •Sneezing and blowing •Rhinorrhoea •Mucociliary clearance •Air conditioning
- 5. Nose and oropharynx (contd.) •Nasalsecretion •Oral cavity – tongue movements •Secretory IgA in saliva
- 6. Cough •Most important protectivereflex as well as most common symptom of respiratory diseases. •Provoked by number of stimuli •Afferent – myelinated irritant nerve endings, intravascular nonmyelinated J receptors, via C fibers and myelinated fibers
- 7. Cough (contd.) •Center -medulla 5 HT receptors •Efferent – nerve supply to larynx, ribcage and diaphragm
- 8. Cough (contd.) •Phases •Inspiration •Compression ofintrathoracic gas against closed glottis •Explosive expulsion as glottis opens •Relaxation of airways
- 9. Cough (contd) •Result •Expectoration offoreign debris and mucus from the larger airways due to extremely high local turbulence by the reflex •Chronic bronchitis – 50% clearance is contributed by cough
- 10. Cough (contd) Cough reflexis inhibited by •physiological – swallowing •central action – codeine •blocking the afferent signal – local anesthetics
- 11. Mucociliary clearance • Inhealthy subjects cough ineffective in removing inhaled small particles • Mucociliary clearance almost entirely responsible for tracheobronchial cleanliness • Complex interaction between cilia and mucus
- 12. Mucociliary clearance • 200cilia per one bronchial epithelial cell. • Cilia composed of contractile protein tubulin arranged as nine outer and one central micro tubular pairs • Outer microtubule has a pair of dyneine arms • Mucus forms a raft on top of cilia which sweeps in the cephalad direction. • Cilia carry about 10 grams with out slowing • Cilia beats @ 12-14 times per second
- 13. Ultra structure ofcilia
- 14. Mucociliary clearance Test forciliary motility •Saccharin test •Cine bronchography •Imaging technique
- 15. Mucociliary clearance • Mucussecreted by goblet cells and submucosal glands of the first several bronchial generations • Secretions controlled by neuropeptides like substance P, Vasoactive intestinal peptide, bombesin, vagal stimulation - acetylcholine.
- 16. Mucus Physical function •To trapand clear particles •Dilute noxious influences •Lubricate airway •Humidify inspired air
- 17. Mucociliary clearance • Theviscoelastic or rheological properties of mucus determined probably by concentration of different type of mucins • External factors influencing mucociliary clearance – direct ciliary damage • cigarette smoke, pollutants, local and general anaesthetics, bacterial and viral products, eosinophil products in asthma, etc
- 18. Primary Ciliary Dyskinesia • Autosomalrecessive • Ciliary dynein may be defective • Male infertility • Situs inversus • Result in repeated sinusitis and respiratory infection and severe bronchiectasis
- 19. Surfactants •Complex surface activematerial lining the alveolar surface •Reduces surface tension and prevent lungs from collapsing •Simple and elegant way of alveolar clearance •At end expiration surface tension decrease and the surface film moves from the alveoli towards bronchioles
- 20. Surfactants •4 types –sp-A, sp-B, sp-C, sp-D •Functions •On alveolar macrophages –Chemotaxis, enhancement of phagocytosis and killing of microorganisms
- 21. Surfactant proteins •SP- Amost abundant •Closely resemble complement c1q •Enhances alveolar macrophage phagocytosis of microorganisms like staph aureus, pneumocystis carinii •SP- D share same effect •Inhibit endotoxin stimulated release of interleukin-1, IL-6, TNF
- 22. Surfactant •Can be damagedby noxious stimuli •Alteration of surfactant quantitatively and qualitatively in ARDS •Loss of lung function and gas exchange •Susceptibility of injured lung to bacterial colonization and infection •Surfactant replacement therapy
- 23. Protective Proteins of Lung Antibacterial surfactantproteins ( A & D), immunoglobulin ( IgA), defensin, lactoferrin, lysozyme, complement Antiproteinases alpha 1 proteinase inhibitor, alpha 1 antichymotrypsin, alpha 2 macroglobulin
- 24. Immunoglobulins •IgA abundant •IgG andIgM in small quantities •Produced by B lymphocytes and plasma cells often associated with bronchial epithelial cells •IgA deficiency associated with local defects in immunity to bacterial infections
- 25. Complement proteins •Alveolar macrophagesecrete c3a, c3b and c5a •C3 deficiency – recurrent infections •Enhances removal of bacteria by macrophages and other phagocytes
- 26. Antiproteinases •High molecular (alpha 1 antiproteinase, alpha 2 macroglobulin) •Low molecular (secretory leukoproteinase inhibitor and elafin) •Protect local tissue against damage that would occur due to release of proteinases by inflammatory cells
- 27. Alveolar macrophages •Derived fromblood borne monocytes •Patrol the alveolar lining •Live for several weeks
- 28. Functions • Primary hostdefense - phagocytosis • Inflammatory response: – Initiation • Generation of neutrophil chemokines ( IL-8) • Generation of monocyte chemokines (MIP-12) • Generation of agents that activate endothelial cells (IL-1, TNF alpha) – Amplification • stimulate bone marrow generation of leucocytes ( IL-1, TNF alpha, IL-3) – Resolution • scavenging of necrotic and apoptotic cell debris
- 29. Functions • Repair andfibrosis • Remodeling: elastase, collagenase • Scar formation: IL-1, PDGF, FGF • Immune response • Antigen presentation • Anti tumour effect – Lysis of tumor cells by TNF alpha and nitric oxide dependent mechanisms
- 30. Pulmonary marginated pool ofneutrophils • Circulating pool • Marginated pool • Dynamic equilibrium • Exercise and epinephrine • Vascular bed of the lung and spleen • Neutrophils loitering in pulmonary microvasculature- local immunity
- 31. Defense mechanism inthe alveolar spaces
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- 35. PFT •Objectively measure theability of lungs to ventilate and carry out gas exchange
- 36. Components • Tests ofairway function • Tests of pulmonary volume • Tests of gas exchange • Tests of respiratory muscle function • Tests of ventilatory control mechanism • Tests of exercise performance
- 37. Indications • Establishing orexcluding a respiratory cause of dyspnea • Diagnosis of obstructive airway disease • Localize site of obstruction • Prognostic purpose • Evaluation of pulmonary involvement in systemic diseases or side effect of drugs like amiodarone • Preoperative evaluation • Epidemiological observations • Evaluation of exercise performance
- 38. Principle •Measure either displaced volumeor air velocity •All volumes are expressed at BTPS (body temperature ambient barometric pressure and saturation)
- 39. Tests of AirwayFunction • Peak expiratory flow • Most widely used • Measure maximum expiratory flow rate over the first 10 milliseconds of an expiration • Effort dependent • Reduced in airway obstruction and expiratory muscle weakness
- 40. Forced expiratory volume • Integratedflow over first second of expiration • Normal 70 – 80% • Airway obstruction • FeV1 reduced more than forced vital capacity so that FeV1/FVC is reduced below 70% • Restrictive • Both FeV1 and FVC are reduced proportionately, so that the FeV1/FVC is normal.
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- 42. Flow volume loopin severe airway obstruction
- 43. Flow loop inrestrictive lung disease
- 44. Maximum midexpiratory flow rate(MMEFR) •FeF(25-75%) is the average expiratory flow during middle half of the forced vital capacity •More variable than FeV1 •Sensitive index of small airway function
- 45. Flow volume loop •Isalso useful for localizing the site of obstruction •Whether intrathoracic or extrathoracic •Whether fixed or variable
- 46. Flow volume loopin extrathoracic obstruction
- 47. Flow volume loopin variable intrathoracic obstruction
- 48. Flow volume loopin fixed airway obstruction
- 50. Test of LungVolume • Measurement of lung volumes provides valuable and functional information. • Total lung capacity and residual volume measurement require indirect methods such as gas dilution technique or plethysmography
- 52. • Airway diseaseincrease residual volume, the RV/TLC % is increased. • Parenchymal diseases produce a restrictive ventilatory defect reducing total lung capacity and vital capacity with RV unaffected.
- 53. Respiratory muscle function •Peak inspiratoryand Peak expiratory maximal mouth pressure by sucking at and breathing out respectively against the shutter of pressure transducer device
- 54. Diffusing capacity •Carbon monoxidegas transfer •Mixture of helium and carbon monoxide 0.03% •The change in the concentration of gases are measured by automated equipment. • DLCo reduced in ILD,Pneumonia
- 55. Exercise test • Measureintegrated cardiorespiratory functions • 6 or 12 minute walk test • Plotting heart rate and minute ventilation against o2 uptake with estimation of respiratory quotient– cycle ergometer or tread mill.
- 56. •Arterial blood gasmeasurement •Noninvasive oxymetry
Editor's Notes
- #56 Normal response is linear Increase in heart rate and an increase in minute ventilation initially increasing the tidal volume and later by increasing the rate.