Airway conditions

Frage	Antworten
Asthma definition	Chronic inflammatory disorder of the airway characterised by hypersensitivity to triggers, which can be fully reversed
Asthma cells	o Mast cells o Eosinophils o T lymphocytes o Macrophages o Neutrophils o Epithelial cells o Goblet cells o Smooth muscle cells
Asthma mediators	Histamine Interleukins Prostaglandins Leukotrienes Nitric acid
Triggers of asthma	Allergens Irritants
Tissue results of asthma	♣ Bronchial smooth muscle spasm ♣ Oedema formation ♣ Thick mucous production ♣ Thickening of airway wall ♣ Further hyper-responsiveness of airway ♣ Neuropeptide release ♣ Mediators + immune cells lead to cell damage and further airway obstruction
Persistent asthma attacks lead to airway remodelling leading to:	Smooth muscle hypertrophy and hyperplasia Epithelial injury Mucus gland hyperplasia Deposition of collagen
Asthma vs COPD	- COPD not fully reversible - COPD progressive - Inflammation caused by irritation of lungs caused by noxious gas inhalation
COPD risk factors	o Smoking – active and passive o Occupational exposure o Air pollution o Genetics
Emphysema definition	Abnormal, permanent enlargement of gas exchange airways accompanied by destruction of the alveoli walls and associated capillary network
Emphysema pathophysiology	o Inhaled oxidants induces inflammation o Inflammation over time causes alveolar destruction and loss of compliance o Loss of surface area and capillaries causes V/Q inequality o Expiration becomes difficult due to stiffening of alveoli o Air trapping causes barrel chest o Significant energy put into breathing
Chronic obstructive bronchitis definition	Hyper-excretion of mucous and chronic productive cough for at least three months of the year for two consecutive years
Chronic obstructive bronchitis pathophysiology	Irritants cause airway inflammation Chronical infiltration by neutrophils, macrophages, lymphocytes Continuous inflammation causes oedema Mucous glands and goblet cells increase in size and number Thick mucous secreted Airway defence mechanisms compromised ♣ Increase pulmonary infections ♣ Bronchospasm and a productive cough Starts with bronchi and progresses to bronchioles Progressive narrowing causing expiratory airway obstruction
Acute Respiratory Distress Syndrome (ARDS)	An acute diffuse, inflammatory lung injury, leading to increased pulmonary vascular permeability, increased lung weight, and loss of aerated lung tissue with hypoxemia and bilateral radiographic opacities, associated with increased venous admixture, increased physiological dead space and decreased lung compliance
ARDS causes	Most common: Sepsis, Multi-trauma o Pneumonia o Burns o Aspiration o Pancreatitis o Blood transfusions o Drug overdose o DIC
ARDS pathophysiology	Inflammation damages alveoli and capillaries Severe pulmonary oedema and hypoxaemia follow Damage can be direct or indirect: Sepsis, Aspiration of vomit Fluids, proteins and white blood cells lead into the interstitial space Inter-pleural shunting occurs Epithelial cell damage due to inflammation causes platelet aggregation and thrombus formation
ARDS clinical manifestation	o Occurs within 24 hours of initial insult o Severe dyspnoea o Rapid shallow breathing (air hunger) o Inspiratory crackles o Decreased compliance Hypoxaemia unresponsive to O2 therapy (don’t come across this too much in the prehospital setting)
Pneumonia	Infection of lower respiratory tract caused by bacteria, viruses, fungi, protozoa or parasites
Risk factors of pneumonia	o Old age o Immunosuppressed individuals o Underlying disease o Alcoholism o ALCO o Smoking o Malnutrition o Immobilisation
Pneumonia pathophysiology	o Aspiration of oropharyngeal secretions o Inhalation of microorganisms o Bacteria infiltrate lungs via blood o Large concentrations of pathogens overwhelm the alveolar macrophages o Immune mediator release causing damage to bronchial mucous membranes and alveoli and associated capillaries
Clinical manifestations of pneumonia	o Usually preceded by an URTI o Fever o Chills o Productive cough o Malaise o Pleural pain o Dyspnoea o Haemoptysis o Inspiratory crackles
Tuberculosis	o Mycobacterium tuberculosis o Airborne droplets o Lodge in upper lung lobes o Multiplying bacteria causes inflammation o Infiltrate lymphocytes o Macrophages and neutrophils form tubercules
Clinical manifestations of TB	o Weight loss o Lethargy o Loss of appetite o Chest pain o Low grade fever o Purulent cough o Night sweats o Anxiety o Dyspnoea o Haemoptysis
Chest infections, acute bronchitis	o Infection of the bronchi o Self limiting o Usually viral o Purulent sputum may occur
Chest infections, influenza	o Different strains -> antigenic drift o Triggers immune response ♣ Mediators ♣ Airway oedema ♣ Excess mucous production o Incubation period of 72 hours
Types of hypoxia - lack of oxygen at tissue level	♣ Hypoxic hypoxia ♣ Ischaemic hypoxia ♣ Anaemic hypoxia ♣ Histotoxic hypoxia – cyanide poisoning
Tidal volume	The lung volume representing the normal volume of air displaced between normal inhalation and exhalation when extra effort is not applied. 500mL
Vital capacity	The maximum amount of air a person can expel from the lungs after a maximum inhalation 3-5L
Expiratory reserve volume	The maximal volume of air that can be exhaled from the end-expiratory position 0.7-1.1L
Inspiratory reserve volume	The maximal volume that can be inhaled from the end-inspiratory level 2-3L
Total lung capacity	The volume in the lungs at maximal inflation, the sum of VC and RV. 4-6L
Causes of hypoventilation	Brain Spinal cord injuries Nerves - polyneuritis Myasthenia gravis Muscular dystrophy Diaphragm - obesity, distention Fractured ribs, flail chest Upper/lower airway obstruction

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	Erstellt von Amelia Tuffley vor etwa 6 Jahre