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Respiratory

Respiratory

by arthur.czokalski@graduates.jcu.edu.au, Apr. 2011

Subjects: respiratory

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163 Cards in this Set

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	Who is at risk of S.pneumoniae LRTI	YOPI young old pregnant immunocompromised
	What different types of symptoms differentiate typicals from atypical pneumonia	Respiratory symptoms typical, opaque, localised consolidation Atypicals exhibit systemic symptoms and diffuse opacity in xrays
	What are the modes of transmission of S.pneumonia	inhalation aspiration (from nasopharyngeal mucus by comatose, sleep, alcohol/drug affected persons) haematogenous spread contiguous extension penetration, trauma, contamination
	describe the pathogenesis of pneumonia	Entry to alveoli tissue injury inflammation fluid accumulation and spread to adjacent alveoli penetration of capillary and bacteraemia, systemic effects sepsis
	What are the virulence factors of S.pneumoniae	a haemolytic capsule facultative anaerobe and can hide in mucous tissues and serous fluid
	What are the principal pathologies of S.pneumoniae	Pneumonia Meningitis Otitis media
	Describe how virulence factors cause lung infection by S.pneumoniae	Adhesins. Lipoteicoic acid Pneumolysin, IgA protease able to destroy immune cells and antibodies Capsule prevents phagocytosis, increases virulence by 100,000 Autolysis: sharing of AB resistance genes
	How does S.pneumoniae develop resistancr	1) b lactamase 2) Rapid mutations in Penicillin Binding Proteins makes it resistant to all penicillins by preventing binding to the cell wall
	How is causitive agent of pneumonia determined	Hx: age, occupation, other risk factors (smoking, immunocompromised) xray (consolidation v diffuse) sputum (but not sensitive)
	How is S.pneumonia distinguished from GAS, GBS	Haemolysis
	What are the classes of beta lactams	penicillins cephalosorins cephamycins carbapenems monobactams
	What is the toxicity effect of macrolides	High concs allow binding to mammalian ribosomes
	What is the problem of Pneumovax 23. What is the solution	Low antigenicity in children under 2yo Use Prevenar 7, covers 80% of strains. The carbohydrate moiety is bound to a carrier protein making it conjugated and greater antigenicity. Prevenar 13 on the way will minimise "vaccine escape" caused by limited subset of serotypes covered by Prevenar 7
	What is the atypical common in children and young adults	Mycoplasma pneumoniae 5-35 yo
	What precautions are taken with pregnant women prior to birth	GBS swab of cervix prior to delivery to prevent infection of neonate (most common)
	Describe a terminal bronchiole	lined with epithelium no cartilage supplies a lobule
	how is a respiratory bronchiole different	Lined with resp epithelium, smoth muscle at the end but lined with alveoli no cartilage
	What are K cells	Neuroendocrine cells Foetal remnant Source of cancer
	Describe a lobule	Contains bronchiole, arteriole Lobular septum contains veins and lymphatic drainage Associated with lymphoid tissue (BALT) and alveolar macrophages
	Describe respiratory bronchiolitis	Marker of smoker, asymptomatic Accumulations of magrophages containing pigment
	What is DAD	Diffuse alveolar damage associated with ARDS: Damage to the whole alveolar septum exudative phase: Congested haemorraged alveoli, damaged endothelium and epithelium causing leakage of fibrin leading to hyaline membrane formation interfering with gas exchange (can be fatal) fibroproliferative phase: type 2 pneumocytes proliferate, organisation after 10 days with fibroblasts - fibrosis and late phase respiratory distress, infiltration of bronchiole lumen with fibroblasts
	What are the patterns of acute lung injury	diffuse alveolar organisation pneumonia
	What are the steps of lung infection	Infection of bronchus, acute inflammatory response causing bronchitis Congestion: vascular engorgement of alveoli containing bacteria Red hepatization: inflammatory respnse involving neutrophils (margination, capillary leakage, epithelial damage, fibrin deposition) Grey hepatization: degradation of RBC's by macrophages Resolution: activation of type 2 pneumocytes, repair and organisarion, coughing up of remaining exudate
	What is found on examination with lobar pneumonia	consolidation throughout the entire lobe (always S.pneumoniae) Pleural rub
	What are the two types of bacterial pneumonia	Bronchial (S.aureus) Lobar (S.pneumoniae)
	What is the course of viral influenza	Necrotising inflammation of the bronciolar epithelium Infiltration by T cells Alveolar inflammation without neutrophils, mainly T cells
	What is the outcome of allergy to aspergilus	Mucoid impaction of the airways by mucoid, eosinophils
	What is the typical infection caused by aspergillis in immunosuppressed	1) Aspergiloma containing eosinophils, giant cells 2) Invasive sspergilosis invading the arterioles, causing ischemia and infarcts
	What fungal infection can arise in immunocompetent lungs	Cryptococcus cryptoccoma
	What is the course of PCP	Infection of interstitium resulting in foamy exudate in the lumens and alveoli without lymphocytes
	What is the type of infection of TB	Inhalation of M.tuberulium, Infiltration by neutrophils but capsule is resistant. Conversion of macrophages to secretory epithelioid cells forming a caseating granuloma which includes necrosis, fibrin and lymphocytes because of type 4 hypersensitivity to tuberculin. Included are Langhan's giant cells which are fused macrophages
	How is secondary TB different to the primary infection	Infects apices, as opposed to mddle. Can be invasive causing TB pneumonia, empyema (of the pleural spaces) and penetration into bloodstream entering any organ (gi, uterus, etc). Miliary TB is extreme outpouring of TB into bloodstream cauding massive widespread infection and death
	What is bronchiectasis	Dilatation of bronchi caused 1) post inflammatory, typically measles pneumonitis in children. Mucocillary escalator is destroyed resulting in mucus pooling and recurring infections. The dilation can be extreme, compressing large areas of alveoli, reducing surface area 2) obstructive eg by a carcinoma causing localised bronchiectasis 3) cystic fibrosis 4) immotile cilia
	What is the cause of lung abcesses	aspirstion post pneumonia secondary causes, mainly bacterial proliferation
	What does the dual blood supply supply in the lung	Bronchial arteries supply bronchioles, pulmonary arteries supply alveoli
	What is bronchial pneumonia	patchy solid foci of consolidation located around the bronchiolar branchings
	What organism commonly forms secondary bacterial pneumonia folowing infuenza A	Staph lobar pneumonia
	What are the stages of infection by pneumonia	Inflammation and infiltration of neutrophils Red hepatisation - extravasation of rbcs into alveolar space grey hepatisation: fibrinisation and grey exudate of broken down neutrophils, rbc's, dead bacteria, cellular debris resolution repair and fibrosis
	How are atypical infections different	interstitium is infected rather than luminal and alveolar epithelium
	Complications of typical bacterial pneumonia	pleural effusion empyema, pyothorax (pus in the pleural cavity) abcess formation respiratory failure bacteraemia, sepsis pulmonary fibrosis bronciectasis
	What are the atypicals	pcp legionella mycoplasma, legionella
	What is the course of aspergillus in an immunocompromised	infects blood vessels causing invasive aspergillitis
	What does pcp look like histologically	crushed ping pong balls
	What is the difference between the look of the lung in cryptococcus v aspergillosis	crypto: areas of solid white consolidation aspergillus: invades blood vessels so large areas of red, necrotic lung
	What is the course of primary TB	Gohn complex (primary focus plus mediastinal node involvement) forms in the mid portion, sub pleural, where epitheloid macrophages congregate and giant cells wall off the granuloma. This is followed by fibrosis and calcification.
	What is unique about the tb granuloma	It is a necrotic granuloma exhibiting caseous necrosis (cheese like)
	Describe miliary TB	Numerous disseminated small lesions, large load of mycopladma in blood disseminating to other organs
	What are the outcomes of TB	fibrosis and calcification of primary focus progressive primary tb disseminating tb, miliary tb
	What are the atypicals	mycoplasma pneumoniae chlamydia legionella viruses (RSV, Influenza A and B, parainfluenza virus, SARS)
	What are bacteria causing acute CAP	S.pneumoniae S.aureus Klebsiella pneumoniae Pseudomonas Moraxella catharralis
	A patient with a severe pneumonia has sputum cultured containing Strep pyogenes. What type of pneumonia is likely	Acute necrotising with abcesses
	In an acute exacerbation of COAD, what antibiotic coverage is needed	H.influenza, M.catarrhalis and Klebsiella are the most common organisms, hence gram -ve coverage is needed for all of them
	What are the complications of pneumonia	Abcesses and necrosis Fibrosis Empyema Bronchiectasis Dissemination (brain, meninges, heart valves & pericardium, joints, kidneys)
	What are the 4 stages of lobar pneumonia	1) congestion (vascular engorgement, few neutrophils, heavy bacterial burden) 2) red hepatization: blood, fibrin and neutrophils filling alveoli of lobe 3) grey hepatization: macrophage reabsorption of RBCs, neutrophils leaving grey fibrinosupprative exudate 4) resolution: enzymatic breakdown of exudate followed by organisation
	What is the level of hospitalisation of CAP	14% hospitalised, 50% of them go to ICU
	What are the sources of pneumonia	community nosocomial ventilator
	What are the classificatioms of pneumonia	typical atypical viruses non infective
	What altered lung mechanics occur in pneumonia	Decreased v/q due to shunting Decreased lung compliance and greater respiratory effort required
	What are the likely organisms causing admission to icu	chlamidia pneumococcus mycoplasma
	What are the issues regarding storage of sputum samples	Not stable if left sitting Easily contaminated by oral bacteria (need low epithelial cells, high leukocytes)
	How is v/q maintained with pneumonia (compensation mechanism)	Vasoconstriction to decrease perfusion in poorly ventilated regions.
	What is the pneumonia severity index	Identifies risk of mortality based on risk factors: drop in blood pressure, tachycardia, age, comorbidity, diastolic hypotension Class 1 no risk of dying (can treat 1 & 2 in community) Class 3 1% admit (diabetics fall in this class) Class 4 10% Class 5 30% ICU
	An asthmatic is treated with 25mg d of prednisolone but develops a prurulent cough, rigors and dyspnoea. What is the likely organism	Pseudomonas
	What bacteria should be considered in nosocomial pneumonia	gram negatives MRSA aspiration of anaerobes, chemical pneumonia
	What are the 4 types of obstructive airway diseases	1) asthma 2) chronic brinchitis 3) emphysema 4) bronciectasis
	What changes occur to airflow and capacity can be detected in obstructive airway disease v restrictive disease using spirometry	OAD: FEV1 decreased, FVC increased, FEV1/FVC decreased RD: FEV1 normal but reduced proportionately to FVC, therefore, FEV1/FVC is normal
	Define a lobule and acinus	A lobule is the structure distal to a terminal bronchiole made up of 3-5 acini and a respiratory bronchiole An acinus is a group of alveoli budding off a respiratory duct, distal to a respiratory bronciole
	Describe the 3 types of emphysema	1) distal acinar: overinflation of acinar alveoli causing a breakdown of walls between them and loss of surface area. Generally caused by upper lung fibrosis, atelectasis and affects pleura causing spontaneous pneumothorax 2) centriacinar: respiratory bronchioles dilated. Caused by cigarettes 3) panacinar: (whole of lobule) both respiratory bronchiole and distal acini are dilated, usually at the bases and results from a1-antitrypsin deficiency
	What is the sequence of tissue destruction caused by cigarette smoke	1) Nicotine and cigarette smoke activates transcription factor NF-kB switching on genes for TNF-a, IL8 which act as chemokines for neutrophils and macrophage to infiltrate alveolar spaces 2) reactive oxidases from cigarette smoke inactivates a1-antitrypsin 3) Neutrophils are now unchecked and destroy alveolar and respiratory bronchiolar elastic tissue 4) macrophages independently secrete elastase and, in greater numbers, further break down alveolar connective tissue 5) oxidant-antioxidant balance shifted with overwhelming of antioxidant molecules (glutathione, superoxide dismutase) leading to protein and DNA damage.
	Define chronic bronchitis	Obstruction of the large airways and small bronchioles with mucin and fibrosis. Hyperplasia of seromucinous glands and goblet cells produces excessive mucus and plugging. There is also hypertrophy/plasia of longitudinal smooth muscle and destruction of respiratory epithelium and metaplasia into squamous epithelium (pre cancerous)
	How is bronchiolitis seen histologically	Macrophages containing smoke carbon etc filling the lumen and thickened walls with smooth muscle and fibrosis
	What is the main cause of pan acinar emphysema	a1-antitrypsin deficiency
	How does hypoxia cause cor pulmonale	Arterioles constrict in response to hypoxia Chronic constriction causes permanent occlusion of lumen by smooth muscle infiltration of intima
	How is asthma differentiated from emphysema histologically	Both have enlarged alveoli but no floating septa in asthma
	What are Curshmann spirals	Casts of epithelium, eosinophils and mucus plugging the bronchioles in asthmatics (can be coughed up)
	How are the walls of asthmatic bronchioles different to chronic bronchitis	More hyperreactive SM, eosinophils and lymphpcytes in asthmatic walls cf mucous glands and goblet cells in chronic bronchitis
	What is IPF	Idiopathic pneumonitis fibrosis, a degenerative restrictive airway disease, starting in the lower lobes and fibrosis & contraction of the septa. Honeycombing (elithelium lined alveolar sized closed spaces) replaces alveoli, bronchiectasis and ground glass pattern of inflammatory areas on ct.
	What connective tissue diseases are asociated with interstitial lung disease	Scleroderma SLE RA
	Describe the pathology of sarcoidosis	Non caseating granulomas with epitheloid Langhan giant cells. No necrosis. Follows the lymphatics and causes enlargement of the mediastinal lymph nodes
	What is the pathology caused by silica inhalation	pneumonconiosis: Conversion of macrophages into epitheloid cells, becoming fibrogenic and formation of collagen nodules within the walls of bronchioles
	What is a feature of the pleura in asbestosis	Pleural plaques on the visceral and parietal pleura
	What is the epidemiology of lung CA	12% of all cancers (most common), 18% deaths from all cancers 99% are carcinomas with 90% 5 year mortality
	What is the relationship between lung CA and smoking	Squamous and small cell carcinoma associated with amount and duration of smoking. Adenocarcinoma generally occurs in non smokers
	What are paraneoplastic syndromes	Endocrine secreting tumours eg adenocarcinoma can secrete ACTH. Squamous cell can secrete PTH
	What are the 4 main types of lung cancers	Adeno. SCC Small or large cell
	What methods are used for obtaining lung tissue samples for diagnosing and staging lung cancers	Sputum cytology Broncoscopy Pleural fluid cytology FNA under CT guidance through the chest wall
	How is lung cancer spread	Local extension: parenchymal, peribronchial, pleural, mediastinal Lymphatic: lymphangitis lymphancomatosa (tumours along the parenchymal lymphatics) Haematogenous: metastases to adrenal glands, brain, liver, bone Transcoelomic: spread into the pleural cavity causing effusion
	How is lung cancer staged	Lung scan Bone scan PET scan
	What is the prognosis of SCLC	Very poor, most die within a year.
	Describe squamous cell carcinoma and histology	smokers, aggressive, spreads centrally from broncii outwards to adjacent lung. Histologically identified by keratin pearls within clusters of squamous cell epithelium. Intercellular bridges present due to desmosomes
	How is squamous dyaplasia identified	Mitotic bodies above the basal layer, ucleu enlarged and abnormal
	How does adenocarcinoma progress differently to SCC	Peripheral to central spread ie forms in peripheral lobule parenchyma
	How is adenocarcinoma identified histologically	Form gland like structures ie surround spaces or form finger like projections
	Describe bronchioalveolar carcinoma	Cancer of the alveolar pneumocytes. Is a cancer in situ. No stromal, vascular or pleural invasion. Forms a lot of mucin and sputum filling alveoli
	Small cell lung cancers - describe	Neuroendocrine carcinoma High mitotic count Early metastatic, particularly to brain Forms central masses that obstruct SVC causing neck congestion
	What are non small cell carcinomas	Large cell carcinoma Adenocarcinoma SCC
	What are LCC	Originates from K cells Neuroendocrine carcinomas Lack markers of SCC (no bridging or keratin), no glands (not adenoma), large cells (not SCC)
	What are carcinoid tumours	Orderly, slow growing neuroendocrine tumours but metastatic. Bleed profusely if resected, highly vascularised
	What is the most important pleural tumour type	Mesothelioma Presents with chest pain, pleural effusion, dyspnoea Dx by pleural biopsy or pleural fluid cytology If nil treatment, death in 10 months Histology: epithelioid or sarcomatoid
	List the 4 obstructive airway diseases, their aetiologies and the predominant tissues affected	1) Chronic bronchitis, smoking, air pollution, trachea and bronchi 2) emphysema, smoking, congenital a1-antitrypsin def: alveoli 3) bronchiectasis, recurrent lung infections, large airways 4) asthma, immunological, small airway inflammation
	A 52 YO patient has been coughing every day for some time. He is a steel worker but claims to have quit smoking 10 years ago. What are his risk factors for COPD	1) persistent cough for 2 months out of 2 years 2) age over 40 3) ex smoker 4) exposure to air pollution (steelworks)
	Why is COPD a major health problem in Australia	1) underdiagnosed 2) under treated 3) 3rd leading burden of disease after IHD and CVA 4) 4th leading cause of death
	What is the best predictor of severity of COPD	FEV1
	What investigations should be performed for suspected COPD	1) spirometry 2) CXR 3) V/Q scan 4) CT
	How can bronchodilators be used to help diagnose COPD	FEV1 not substantially improved in spirometry if COPD (irreversible airway obstruction). If normalised then it's asthma
	When are corticosteroids used with COPD	Severe disease with frequent exacerbations (evidence shows decreased frequency of exacerbations but no improvement in lung function)
	List primary, secondary and tertiary public health strategies for COPD	1) stop smoking and treat nicotine dependence 2) screening by lung function tests, flow spirometry and imaging 3) prevent complications via vaccinations: influenza, pneumococcal, haemophilus
	What is needed for type II respiratory failure in COPD	Positive pressure ventilation
	What are the causes of death in emphysema	1) pulmonary acidosis and coma 2) cor pulmonale due to congestion caused by destruction of blood vessels in emphysematous lung 3) etalectasis caused by pneumothorax
	Explain the mechanism behind why O2 delivery to COPD can be dangerous	If chronic bronchitis then cyanosed (high CO2). Hypercapnic drive adapts and respiraton is driven mainly by chronic hypoxia. If O2 is administeed, drive is lost and patient goes into respiratory arrest.
	What are the complications of COPD	1) cor pulmonale 2) metaplasia (replacement of respiratory epithelium by squamous epithelium -> lung cancer
	What are the main radiological differences between chronic bronchitis and emphysema	1) CB: enlarged heart and hylar vessels 2) emphysema: normal heart and vessels, enlarged chest and lung fields below 6th rib, flat diaphragm and tenting, darkened regions indicating bullae
	What does low and high FEV1/FVC indicate	Low: obstruction (asthma, COPD, bronchiectasis) High: restrictive lung disease, decreased compliance
	Which carcinoma is most common in the upper airways	SCC
	Which carcinomas are most prevalent in the lower airways	SCC and adrnocarcinoma
	What are the ddx of a laryngeal swelling	Epiglottitis (croup) SCC Scarlet fever
	What are the classifications of laryngeal SCCs	Supra or infra or transglottic. Landmark is the ventricle of the larynx
	What is a complication of an ulcer forming within a laryngeal SCC	Perforation and fistula forming between the infraglottal larynx and he oesophagus
	What are the risk factors for developing lung cancers	smoking, pollution, exposure to dusts (silica, asbestos, berylium, coal), COPD
	What features of a carcinoid tumour indicates metastatic disease	Mitotic bodies Necrosis
	What are the distinguishing features of small cell carcinoma	Cells are 2-3 times larger than leukocytes Nuclei mold to one another
	What features of hx indicate carcinoma	Weight loss, cough, pleuric pain, smoking hx, occupation, haemoptysis, dyspnoea, hoarse voice
	What carinoma looks like pneumonia on xray	Bronchioalveolar carcinoma
	What syndrome can arise from small cell carcinoma	paraneoplastic syndrome secreting hormones: ACTH, VIP, PTH
	What are common lung complications secondary to bronchial obstruction by carcinoma	atelectasis infection
	What is a common form of necrosis caused by SCC. What are complications of this lesion	Cavitation, bleeding, aspergillus colonisation pneumothorax if located adjacent to pleura
	What is the TNM staging of lung cancer	tumour size (<>3 cm stages 1 & 2) nodal involvement metastases
	Why is EGFR-TK tested for in lung cancer patients	EGFR positive patients are responsive to treatment by gefitinib targeted therapy
	A mixture of dark and light disseminated tumours occur throughout a lung. What is the pathology?	Metastases, probably arising from melanoma
	Lower zone reticular xrays are typical of	Interstitial lung disease ie the interstitium between the alveoli
	Causes of haemoptysis	PE. Pneumonia, Goodpastures, TB, cancer, bronchiectasis
	What are the main causes of breathlessness	v/q, intra and extrapulmonary shunt, restriction, decreased alveolar permeability
	What infection should be considered for someone with long standing bronchiectasis	pseudomonas
	What are the symptoms of primary lung cancer. How are they caused?	Dyspnoea: large airway obstruction and atelectasis Wheeze: fixed airway obstruction Haemoptysis Pain
	Where is a pancoast tumour normally located and what are the typical signs on examination	1) apex of lung affecting T1 spinal nerve and cervical sympathetic ganglion 2) Horner's syndrome (and/or bovine cough if RLN is compressed)
	What syndrome is manifested by small cell carcinoma and what are the abnormalities	Paraneoplastic syndrome: 1) hyponatremia through dilution and hypervolaemia (SIADH) 2) cushings (ACTH)
	What are the key criteria indicating sepsis	Evidence of an infection Tachypnoea Confusion
	Describe the inflammatory cascade	Cell surface responds to endo or exotoxins releasing NF kB Macrophage activation IL1, 6, TNF Neutrophil recruitment and cytokine storm leads to end organ damage
	Sirs criteria	2 or more of tachycardia, tachypnoea, fever
	What are 4 triggers of Sirs	Infection Inflammatory eg pancreatitis Trauma and burns Ischemia
	What is sepsis	SIRS plus infection
	What is the difference between Sirs and severe sepsis	Sirs plus infection plus organ dysfunction (lactic acidosis, oliguria, systolic hypotension despite adequate hydration)
	What are two pathways for a poor outcome from sepsis	Excessive immune response: Sirs to MOD to irreversible shock Inadequate response: overwhelming by organsm
	Describe ARDS	Inflammatory response Damage to alveolar basement membrane Influx of exudate ie serum, protein
	What are causes of ARDS	Direct lung injury aspiration, near drowning, pulmonary contusion, pneumonia Indirect lung injury from sepsis, shock, pancreatitis, fat emboli (from marrow due to bone trauma) massive transfusion (plasma, whole blood)
	Describe the stages of ards	Exudative phase: Injury to either type 1 pneumocytes (direct: near drowning, gastric inspiration or indirect: sepsis, pancreatitis) exacerbated by neutrophil infiltration, release of reactive oxygen species and elastase by neutrophils and macrophages increased pulmoary capillary permeability (neutrophil arachadonic acid derivatives) exudate infusion, inactivation of surfactant and loss of alveolar function Fibroproliferative phase: type II pneumocyte and fibroblast proliferation, collagen deposition resulting in decreased compliance Resolution
	Describe late stage ards	Type 2 proliferation Collagen deposition ?
	How is ards treated	Correct underlying cause O2 Ttitrated to PO2 Ventilation to avoid over distension (damaged alveoli are stiff due to loss of surfactant and exudate but normal alveoli can be damaged) Prevent nosocomial infection
	How is septic shock treated	Related to cause: vasodilation and decreased contractility treated with vasopressors like metaraminol plus noradrenaline plus inotropes plus fluid resuscitation to maintain renal function
	What are the neurological effects of sepsisWhat is the effect of sepsis on coagulation	Cytokines affect blood brain barrier causing oedema, delerium and coma Critical illness polyneuropathy
	How is pneumonia severity classified	CURB65 Confusion Urea > 7 RR > 7 Bp < 90 sys or 60 dias
	List the viral causes of pneumonia	influenza parainfluenza SARS
	What are the fungal infections causing pneumonia	PCJ Cryptococcus Aspergillus
	complications of pneumonia	sepsis empyaema bronchiectasis fibrosis
	What is the cauae of end stage coma in emphysema	There is no v/q mismatch, therefore respiratory acidosis occurs because of type 2 acidosis
	Define pneumoconiosis	Non neoplastic interstitial lung disease caused by inhaled particles
	List the 3 interstitial lung diseases	Idiopathic pulmonary fibrosis pneumoconiosis non specific interstitial pneumonia
	Which interstitial lung disease is treatable by steroids	non specific interstitial pneumonia
	Name 3 types of atelectasis	restrictive compressive reabsorption
	What is the radiological feature of ARDS	Ground glass
	What are the typical features of aspergillosis	1) Invasive aspergillosis is a diffuse pneumonia in the immunocompromised with invasion of blood vessels causing ischaemic necrosis 2) Aspergilloma in cavities formed by cavitations (eg cavitating necrosis of secondary TB)
	List 5 respiratory causrs of clubbing	Cancer Cystic fibrosis Tuberculosis Empyema Interstitial lung disease (idiopathic pulmonary fibrosis, pneumoconiosis, mesothelioma)
	List 5 respiratory causrs of clubbing	Cancer Cystic fibrosis Tuberculosis Empyema Interstitial lung disease (idiopathic pulmonary fibrosis, pneumoconiosis, mesothelioma)

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