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Osha 2a > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is pleural effusion?

A
  • collection of fluid in the pleural cavity
  • can be exudative (high protein) or transudative (low protein)
  • causes lung compression
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2
Q

What are exudative causes of pleural effusion?

A
  • inflammatory: protein leaks out of tissue into pleural space
  • lung cancer
  • pneumonia
  • autoimmune: RA, SLE
  • TB
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3
Q

What are transudative causes of pleural effusion?

A
  • caused by fluid shift into pleural space
  • heart, liver or renal failure
  • hypoalbuminaemia
  • myxoedema
  • ascites
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4
Q

What are the symptoms of pleural effusion?

A
  • breathlessness
  • cough
  • pain and fever
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5
Q

What are the signs of pleural effusion?

A
  • reduced chest wall expansion
  • quiet breath sounds
  • dull percussion
  • mediastinal shift away from affected side
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6
Q

What investigations are done for pleural effusions and what does it show?

A
  • CXR
  • blunting of costophrenic angle
  • fluid in lung fissures
  • meniscus and tracheal/mediastinal deviation
  • ultrasound
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7
Q

What is the treatment of pleural effusion?

A
  • conservative management of cause
  • pleural aspiration
  • chest drain
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8
Q

What are the criteria for pleural infection?

A
  • pH <7.2
  • glucose < 3.3 mmol/L
  • PF LDH > 1000IU/L
  • bacterial growth
  • macroscopic appearance of pus
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9
Q

What is empyema?

A
  • infected pleural effusion
  • improving pneumonia but new/ongoing fever
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10
Q

How is empyema investigated and treated?

A
  • aspiration: pus, acidic pH, low glucose, high LDH
  • chest drain to remove pus and antibiotics
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11
Q

What are the causes of empyema?

A
  • community: S. milleri, S. pneumoniae, S. aureus
  • Hospital: MRSA, enterococcus
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12
Q

What investigations are done for pneumothorax and what do these show?

A
  • erect chest X-ray
  • area between lung tissue and chest wall with no lung markings
  • line demarcating where pneumothorax begins
  • CT can detect smaller pneumothorax
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13
Q

How is pneumothorax managed?

A
  • <2cm rim and no SOB: no treatment, follow up 2-4 weeks
  • > 2cm rim/SOB: aspiration and reassessment
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14
Q

What are risk factors for pneumothorax?

A
  • COPD, asthma, CF, lung cancer
  • Marfan’s, RA
  • ventilation
  • smoking
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15
Q

What is pulmonary hypertension?

A
  • inc resistance and pressure in pulmonary arteries
  • causes strain on RHS of heart
  • back pressure in systemic venous system
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16
Q

What are the 5 groups of causes of pulmonary hypertension?

A
  1. primary/connective tissue disease: SLE
  2. left HF: due to MI, htn
  3. chronic lung disease: COPD
  4. pulmonary vascular disease: PE
  5. misc: e.g. sarcoidosis
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17
Q

What is the presentation of pulmonary hypertension?

A
  • shortness of breath
  • syncope
  • tachycardia
  • raised JVP
  • hepatomegaly
  • peripheral oedema
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18
Q

What investigations are done for pulmonary hypertension?

A
  • ECG change: RV hypertrophy, R axis deviation, RBBB
  • CXR: dilated pulmonary arteries, RV hypertrophy
  • Echo
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19
Q

What is the management of pulmonary hypertension?

A
  • IV prostanoids e.g. epoprostenol
  • endothelin receptor antagonist e.g. macitentan
  • phosphodiesterase-5 inhibitor e.g. sildenafil
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20
Q

What is sarcoidosis?

A
  • granulomatous inflammatory condition
  • nodules of inflammation full of macrophages
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21
Q

What is the epidemiology of sarcoidosis?

A
  • young adulthood or around age 60
  • more frequent in black patients
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22
Q

What are the pulmonary manifestations of sarcoidosis?

A
  • bilateral hilar lymphadenopathy with pulmonary infiltrates and fibrosis
  • dry cough, progressive dyspnoea, chest pain
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23
Q

What are the extra pulmonary presentations of sarcoidosis?

A
  • uveitis, conjunctivitis
  • cirrhosis
  • erythema nodosum
  • fever, fatigue, weight loss
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24
Q

What investigations are done in sarcoidosis?

A
  • CXR and high res CT
  • raised serum ACE and IL-2 receptor
  • hypercalcaemia
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25
Q

What is the gold standard diagnosis of sarcoidosis?

A
  • histology from biopsy
  • bronchoscopy w USS guided biopsy of mediastinal lymph nodes
  • non-caseating granulomas with epithelioid cells
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26
Q

What are the differential diagnoses for sarcoidosis?

A
  • TB
  • lymphoma
  • hypersensitivity pneumonitis
  • HIV
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27
Q

What is the treatment of sarcoidosis?

A
  • no treatment if mild
  • oral steroids and bisphosphonates
  • 2nd line: methotrexate/azathioprine
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28
Q

What is the visceral and parietal pleura?

A
  • visceral: covers the lungs
  • parietal: forms the inner lining of the chest wall
  • pleural space is a potential space filled with a small amount of fluid for lubrication
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29
Q

What is the purpose of the pleura?

A
  • to allow optimal expansion and contraction of the lungs
  • pleural fluid allows gliding without friction of pleura
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30
Q

What is pneumothorax?

A
  • collapse of the lung leading to presence of air in the pleural space
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31
Q

What is the pathophysiology of pneumothorax?

A
  • air entering due to hole in lung/pleura or chest wall injury
  • intrapleural pressure is negative leading to air being sucked in and lung collapse
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32
Q

What are the types of pneumothorax?

A
  • primary spontaneous
  • secondary spontaneous
  • traumatic
  • iatrogenic
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33
Q

What is primary spontaneous pneumothorax?

A
  • no underlying lung disease
  • rupture of apical pleural bleb: air escaping into weakness in pleura
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34
Q

What are the risk factors for primary spontaneous pneumothorax?

A
  • tall, thin, males
  • smokers
  • age 20-40
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35
Q

What are the causes of secondary spontaneous pneumothorax

A
  • known lung disease, 60% due to COPD
  • infection
  • genetic predisposition
  • catamenial pneumothorax
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36
Q

What are the symptoms of pneumothorax?

A
  • acute/sudden
  • breathlessness
  • pleuritic chest pain
  • cough
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37
Q

What are the clinical signs of tension pneumothorax?

A
  • tachypnoea
  • hypoxia
  • unilateral chest wall expansion
  • reduced breath sounds
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38
Q

What is tension pneumothorax?

A
  • ONE WAY valve like mechanism causes air to be drawn into chest cavity during inspiration and trapping air in expiration
  • displaces mediastinium causing dec CO and can lead to cardioresp arrest
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39
Q

What are the examination signs of tension pneumothorax?

A
  • Tracheal deviation away from side of pneumothorax
  • Reduced air entry
  • Increased resonance to percussion
  • Tachycardia
  • Hypotension
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40
Q

What is the management of tension pneumothorax?

A
  • insert large bore cannula into 2nd intercostal space in mid clavicular line
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41
Q

What is haemothorax and how is it managed?

A
  • blood in the pleural cavity with a haemtocrit ratio of > 50%
  • management: drainage
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42
Q

What is hydropneumothorax and what are the causes?

A
  • air and fluid in the pleural space
  • cause: iatrogenic, gas forming organisms, thoracic trauma
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43
Q

What is PaO2?

A

the pressure exerted by oxygen molecules when dissolved in blood plasma

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44
Q

What is type 1 respiratory failure?

A
  • Low PaO2 - less than 8.0
  • normal or low PaCO2
  • normal HCO3
  • V/Q mismatch e.g. pneumonia, PE
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45
Q

What is type 2 respiratory failure?

A
  • Low PaO2
  • High PaCO2
  • normal HCO3 (acute) or high if chronic
  • airway obstruction (COPD) or alveolar hypoventilation
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46
Q

What are the causes of a raised alveolar-arterial gradient?

A
  1. V/Q mismatch
  2. defects in diffusion
  3. shunt (R to L)
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47
Q

What is arterial/alveolar gradient?

A
  • measure of the efficiency of gas transfer
  • normal range: 1-2kPa or 1-3kPa in elderly
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48
Q

What are the responses to hypoxia?

A
  • systemic vasodilation
  • pulmonary vasoconstriction
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49
Q

What are the functions of the lungs?

A
  • Gas exchange
  • Acid-base balance
  • Defence
  • Hormones
  • Heat exchange
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50
Q

What is the FEV1/FVC ratio for an obstructive vs restrictive lung disease?

A
  • obstructive: FEV1/FVC <0.7
  • restrictive: normal ratio but lowered FVC
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51
Q

What is DLCO?

A

diffusion factor of the lung for carbon monoxide

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52
Q

What causes a lowered DLCO?

A
  • thickening of alveolar-capillary membrane
  • reduced lung volumes
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53
Q

What causes a raised DLCO?

A
  • increased capillary blood vol
  • pulmonary haemorrhage
  • L to R shunt
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54
Q

What is COPD?

A
  • Irreversible, long term deterioration in air flow caused by lung damage
  • persistent resp symptoms caused by inflammation
  • exacerbations occur triggered by infection
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55
Q

What is the aetiology of COPD?

A
  • caused by smoking
  • chronic inflammation from exposure to noxious particles or gases
  • Alpha 1 antitrypsin deficiency
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56
Q

What is bronchitis?

A
  • chronic cough with sputum production
  • occurring for at least 3 months in the past 2 consecutive years
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57
Q

What is the pathophysiology of bronchitis?

A
  • inc goblet cells
  • inc production of mucus causing plugs
  • thickening of resp epithelia
  • all leading to narrowing of airways
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58
Q

What is emphysema?

A
  • causes holes in the lung
  • loss of elastic tissue
  • destruction of lung parenchyma
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59
Q

What are the risk factors for COPD?

A
  • smoking
  • air pollution
  • occupational exposure (metal/coal dust)
  • genetic factors
  • biomass fumes (unvented fires)
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60
Q

How does COPD present?

A
  • chronic breathlessness
  • cough
  • sputum
  • wheeze
  • recurrent resp infections
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61
Q

How does COPD affect vasculature?

A
  • hypoxia and vascular injury
  • pulmonary artery intima proliferation and thickening
  • reduction in transfer of oxygen into the body
  • contributes to V/Q mismatch
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62
Q

What are the differential diagnoses for COPD?

A
  • heart failure
  • PE
  • pneumonia
  • lung cancer
  • asthma
  • bronchiectasis
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63
Q

How is COPD investigated?

A
  • spirometry (FEV1/FVC <0.7)
  • CXR or CT thorax
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64
Q

What are the 5 grades on the MRC dyspnoea scale?

A
  1. breathless on strenuous exercise
  2. breathless on walking uphill
  3. breathless slowing walking on flat
  4. stop to catch breath after 100m on flat
  5. unable to leave house
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65
Q

What is the immediate COPD management?

A
  • smoking cessation
  • pneumococcal and flu vaccines
  • SABA (salbutamol) PRN
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66
Q

What is the 1st step in the long term management of COPD?

A
  1. SABA (salbutamol) or SAMA (e.g. ipratropium bromide)
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67
Q

What is the 2nd step in long term COPD management?

A
  1. if non-asthmatic: LABA + LAMA
    if asthmatic: LABA + inhaled corticosteroid
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68
Q

What investigations are done for a COPD exacerbation?

A
  • ABG: low pH and raised CO2: resp acidosis
  • raised HCO3 to balance acidic CO2
  • type 1 or 2 resp failure?
  • CXR and sputum
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69
Q

Which drugs can be used to treat a COPD exacerbation?

A
  • salbutamol (SABA)
  • ipratropium (SAMA)
  • prednisolone
  • mechanical (non-invasive) ventilation aiming for 88-92% O2 sats
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70
Q

What is cystic fibrosis?

A
  • autosomal recessive condition affecting mucus glands
  • caused by genetic mutation of CFTR gene on chromosome 7 coding for chloride channels
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71
Q

What are the symptoms of cystic fibrosis?

A
  • chronic cough
  • thick sputum
  • recurrent resp tract infections
  • steatorrhoea
  • child tastes salty due to conc sweat
  • failure to thrive
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72
Q

What are signs of cystic fibrosis?

A
  • low weight or height
  • nasal polyps
  • clubbing
  • crackles and wheeze on auscultation
  • abdo distention
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73
Q

How is cystic fibrosis diagnosed?

A
  • newborn blood spot testing
  • sweat test (GOLD)
  • genetic testing for CTFR by amniocentesis or chorionic villous sampling
  • faecal elastase
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74
Q

What is the sweat test for cystic fibrosis?

A
  • pilocarpine applied to patch of skin
  • electrodes placed either side
  • current passed causing sweating and sample sent to lab for chloride conc testing
  • > 60mmol/L is diagnostic
75
Q

Which bacteria commonly affect children with cystic fibrosis and how is it prevented?

A
  • S. aureus
  • Pseudomonas aeruginosa
  • prophylactic flucloxacillin taken
76
Q

What is the first sign of cystic fibrosis?

A
  • meconium ileus
  • thick and sticky black stool - obstructs bowel
  • not passing within 24 hrs of birth > abdo distention and vomiting
77
Q

What is the pathophysiology behind cystic fibrosis?

A
  • thick pancreatic and biliary secretions: block ducts > lack of digestive enzymes
  • low volume, thick airway secretions > reduce clearance leading to bacterial colonisation and infection
  • congenital bilateral absence of vas deferens
78
Q

What is the pathology of cystic fibrosis?

A
  • issues with Cl- channel on apical membrane of epithelial cells
  • dec Cl- secretion and inc Na+ absorption leads to reduced water secretion and thickened mucus
79
Q

What is the management of cystic fibrosis?

A
  • chest physio: clear mucus
  • exercise: improve resp function
  • high calorie diet: malabsorption
  • bronchodilators: salbutamol
80
Q

What bacteria causes TB and what type is it?

A
  • mycobacterium tuberculosis
  • acid fast bacillus
  • bright red against blue background in Ziehl-Neelsen
81
Q

Describe the spread and pathology of TB

A
  • inhaling saliva droplets from infected people
  • active or latent when encapsulated by immune system
  • reactivated = secondary TB
  • affects lungs, lymph nodes and skin
82
Q

What are risk factors for TB?

A
  • Known contact with active TB
  • Immigrants from areas of high TB prevalence
  • Immunosuppression
  • Homeless people, drug users or alcoholics
83
Q

What is the presentation of TB?

A
  • Lethargy
  • Fever, night sweats
  • Weight loss
  • erythema nodosum
  • Cough ± haemoptysis
84
Q

What investigations are done for TB?

A
  • Mantoux (tuberculin) test (previous immune response): injecting tuberculin
  • interferon gamma release assay (IGRA) +ve
85
Q

What is seen on CXR of TB?

A
  • Primary: patchy consolidation, pleural effusion, hilar lymphadenopathy
  • Reactivated: patchy or nodular consolidation with cavitation in upper zones
  • Disseminated: “millet seeds” uniformly distributed throughout the lung fields
86
Q

What is the management of latent TB?

A
  • Isoniazid and rifampicin for 3 months
  • Isoniazid for 6 months
87
Q

What is the management of active TB?

A
  • Rifampacin - 6 mo
  • Isoniazid - 6 mo
  • Pyrazinamide - 2 mo
  • Ethambutol - 2 mo
88
Q

What is the public health management of TB?

A
  • test contacts
  • notify public health
  • negative pressure rooms for infected patients to prevent airborne spread
89
Q

What route and form are respiratory drugs delivered in?

A
  • inhaled: dry powders - deep penetration and correct dose
  • nebulisers: aerosol form
90
Q

What are the advantages of inhaled medicines?

A
  • large s.a. and rapid absorption
  • medicine acts directly on lung or enters systemic circulation
  • fewer metabolising enzymes than in blood and liver
  • oral route allows administration of small particles
91
Q

What are the 2 categories of bronchodilators?

A
  • adrenergic (SNS): cause bronchodilation and inhibit histamine release
  • anti-cholinergic (PSNS): block bronchoconstriction
92
Q

How do β 2 adrenoreceptor agonists cause bronchodilation?

A
  • activation of adenyl cyclase > inc in cAMP
  • cAMP activates kinase A which inhibits phosphorylation of myosin and lowers intracellular calcium > relaxation
93
Q

How do anti-cholinergic drugs cause bronchodilation?

A
  • block muscarinic receptors (M1-5) on airway smooth muscle preventing contraction, gland secretion and enhancing neurotransmission
  • ipratropium bromide
94
Q

How are muscarinic receptors activated?

A
  • Ach released from airway neurons and non-neuronal cells
  • binds to M1, M2 and M3 receptors
  • found on airway epithelial, smooth muscle cells and submucosal glands
95
Q

How do glucocorticoids reduce inflammation?

A
  • suppress chemotactic mediators
  • reduced adhesion molecule expression
  • suppress inflammatory gene expression in airway epithelial cells
  • can become resistant (esp neutrophilic asthma)
96
Q

What are the different delivery systems for inhaled drugs?

A
  • pressurised metered-dose inhaler
  • spacer: slow down particles and allow more time for evaporation > more inhaled
  • dry powder inhalers
  • nebulisers
97
Q

What is bronchiectasis?

A
  • obstructive lung disease
  • abnormal dilation of bronchi
  • caused by excessive, persistent inflammation
  • influx of inflammatory cells into airway wall
98
Q

What is the presentation of bronchiectasis?

A
  • chronic cough
  • excess sputum
  • dyspnoea
  • chest pain
  • haemoptysis
99
Q

What are the investigations and management of bronchiectasis?

A
  • sputum sample
  • obstructive spirometry: FEV1:FVC <0.7
  • high res CT: signet ring sign dilated bronchi, cysts
  • mucolytics, β2 agonists
100
Q

What is idiopathic pulmonary fibrosis?

A
  • stiffening due to chronic inflammation
  • excess fibrous connective tissue > permanent scarring, airway thickening
  • unclear cause
101
Q

What is the pathophysiology behind idiopathic pulmonary fibrosis?

A
  • fibroblasts repair damaged tissue
  • migrate to the lungs and become myofibroblasts and deposit collagen in ECM
  • thickens and stiffens lungs so can’t contract/inflate
  • inc interstitial barrier between alveoli and capillary membrane
  • fibroblasts are resistant to apoptosis
102
Q

How does idiopathic pulmonary fibrosis present and what are the complications?

A
  • cough, breathlessness
  • bibasal fine inspiratory crackles
  • clubbing
  • leads to T1 resp failure
103
Q

How is pulmonary fibrosis diagnosed and treated?

A
  • spirometry
  • GOLD: high res CT
  • pirfenidone or nintedanib
104
Q

How does pirfenidone work?

A
  • inhibits TGF β
  • reduces proliferation of fibroblasts and therefore thickening of ECM
105
Q

How does nintedanib work?

A
  • inhibits tyrosine kinase receptors
  • reduces growth and differentiation of fibroblasts
  • platelet derived growth factor, vascular endothelial growth factor
106
Q

What is the epidemiology of lung cancer?

A
  • 3rd most common cancer
  • 2:1 male: female
107
Q

What are the causes of lung cancer?

A
  • cigarette smoking (75%)
  • occupational: asbestos, nickel, arsenic (10%)
  • lung fibrosis
  • passive smoking
108
Q

What are the local symptoms of lung cancer?

A
  • continuous cough for 3+ weeks
  • shortness of breath
  • recurrent chest infections
  • haemoptysis
109
Q

What systemic symptoms can occur from lung cancer?

A
  • weight loss
  • malaise (anaemia)
  • paraneoplastic syndrome
110
Q

What are some types of lung tumours?

A
  • carcinoma
  • benign
  • salivary gland type (bronchus)
  • soft tissue tumours (sarcoma)
  • lymphoma
111
Q

What are the types of non-small cell lung carcinoma?

A
  • adenocarcinoma
  • squamous cell carcinoma
  • large cell carcinoma
  • treatment: resection ± chemoradiotherapy
112
Q

What is small cell lung carcinoma?

A
  • neuroendocrine tumour
  • high grade neoplasm: presents rapidly, worse prognosis
  • associated with cigarette smoking
  • primary treatment is chemotherapy
113
Q

How is lung cancer diagnosed?

A
  • bloods
  • CXR and CT, MRI for staging
  • endobronchial biopsy of tumour/metastatic lymph nodes
114
Q

What are signs of cancer on CXR?

A
  • hilar enlargement
  • peripheral opacity
  • pleural effusion (unilateral)
  • collapse
115
Q

What is mesothelioma and what is the cause?

A
  • affects mesothelial cells of pleura
  • linked to asbestos inhalation
  • latent period of up to 45 years
  • palliative surgery
116
Q

Describe the presentation of asbestosis

A
  • pleural plaques
  • pleural effusion
  • fibrotic lung
  • end-inspiratory crackles
  • clubbing
117
Q

What is pneumonia?

A
  • infection of lung tissue and inflammation
  • causes inflammation and sputum in airways and alveoli
  • community, hospital acquired or aspiration
118
Q

What are the atypical causes of pneumonia and how are they treated?

A
  • Legionella pneumophila
  • Mycoplasma pneumoniae
  • Chlamydophila pneumoniae
  • Chlamydophila psittaci
  • Coxiella burnetti
  • macrolides
119
Q

What is the pathophysiology behind pneumonia?

A
  • alveolar macrophages phagocytose bacteria
  • become overwhelmed and produce proinflammatory response to attract neutrophils
  • results in dead bacteria, neutrophils, tissue fluid & inflammatory proteins = inflammatory exudate or ‘pus’ in the airspaces
  • known as consolidation
120
Q

What are the symptoms of pneumonia?

A
  • fever, rigors
  • cough and shortness of breath
  • pleuritic chest pain
121
Q

What type of sputum indicates what type of bacteria?

A
  • rusty: S. pneumoniae
  • none: Mycoplasma, Chlamydophilia, Legionella
122
Q

What are the signs of pneumonia?

A
  • raised HR and resp rate
  • low BP
  • fever
  • dehydration
123
Q

What chest signs present with pneumonia (of consolidation)?

A
  • bronchial breath sounds: harsh
  • focal coarse crackles + wheeze: air passing through sputum
  • dullness to percussion
124
Q

What investigations are done for pneumonia?

A
  • CXR: showing consolidation
  • FBC, U&Es
  • CRP
  • sputum and blood cultures
  • legionella and pneumococcal urinary antigens
125
Q

What is CURB 65?

A
  • Confusion
  • Urea > 7mmol/L (if in hospital)
  • Resp rate ≥ 30/min
  • Blood pressure <90 systolic or ≤60 diastolic
  • age ≥65
126
Q

How is CURB 65 actioned?

A
  • 0/1 treat at home
  • 2 hospital admission
  • ≥ 3 ICU assessment
127
Q

What is the treatment of pneumonia?

A
  • Score 0-1: oral amoxicillin 500mg or if penicillin allergic then clarithromycin/ doxycycline
  • Score 2: oral amoxicillin + clarithromycin
  • Score 3-5: IV co-amoxiclav + clarithromycin
128
Q

How is pneumonia prevented?

A
  • pneumococcal vaccine: adults 65+, immunocompromised, chronic conditions
  • influenza vaccine
  • smoking cessation
129
Q

What are some signs of complications of pneumonia?

A
  • Delerium
  • Renal impairment: Urea rise
  • Respiratory rate high: inc O2 demand due to lactic acid from anaerobic respiration
  • BP drop
130
Q

What is hypersensitivity pneumonitis?

A
  • type III reaction to environmental allergen
  • causes parenchymal inflammation and destruction
131
Q

Describe type III hypersensitivity pneumonitis

A
  • prior sensitisation
  • IgG antibodies retain immune memory
  • antigen-antibody complexes formed on secondary exposure and aren’t cleared
132
Q

How is hypersensitivity pneumonitis tested for?

A
  • bronchoalveolar lavage: collecting cells from airways during bronchoscopy by washing with fluid
  • collecting + testing fluid
  • raised lymphocytes and mast cells
133
Q

How is hypersensitivity pneumonitis managed?

A
  • remove allergen
  • give oxygen
  • steroids
134
Q

What are some specific examples of types of hypersensitivity pneumonitis?

A
  • Bird-fanciers lung: bird droppings
  • Farmers lung: mouldy spores in hay
  • Mushroom workers’ lung: mushroom antigens
  • Malt workers lung: mould on barley
135
Q

Which drugs can commonly cause ILD?

A
  • nitrofurantoin
  • methotrexate
  • amiodarone
  • bleomycin
136
Q

What are the chemical controls of blood?

A
  • chemoreceptors respond to rising CO2 and lowered O2
  • medulla oblongata, carotid and aortic bodies
137
Q

What are the causes of respiratory failure?

A
  • low oxygen delivery: altitude
  • airway obstruction
  • gas exchange/diffusion limitation: lung fibrosis
  • V/Q mismatch: pneumonia, PE
  • alveolar hypoventilation: emphysema
138
Q

What is occupational lung disease?

A
  • inhaling harmful substances in the workplace
  • may develop in the workplace or aggravate symptoms of a pre-existing condition
139
Q

What are some examples of substances causing occupational lung disease?

A
  • dust: chiselling stone, cutting wood
  • fumes: welding
  • mists: metalworking
  • vapours: paint spraying
140
Q

Describe occupational asthma

A
  • variable latent period
  • deteriorating symptoms throughout the week with an improvement over the weekend
141
Q

What are the causes of occupational asthma?

A
  • wood
  • flour
  • metal
  • working fluids
  • isocyanate paint
142
Q

What is asthma?

A
  • chronic inflammatory condition causing bronchospasm
  • narrowed airways > obstruction of airflow to lungs
  • varies over time
143
Q

What is the presentation of asthma?

A
  • episodic
  • diurnal variability and worse at night
  • dry cough, wheeze, shortness of breath
  • atopic triad: hayfever, eczema, asthma
  • family history
144
Q

What are the causes of asthma?

A
  • environmental: pollen, smoke, dust, mould
  • genetics
  • hygiene hypothesis
145
Q

What is the cause of wheeze?

A
  • narrowing of airways causes laminar flow to become turbulent
146
Q

What is the physiology behind asthma?

A
  • smooth muscle contracts on irritation
  • chronic inflammation leads to scarring and airway remodelling
147
Q

What is the pathophysiology behind asthma?

A
  • dendritic cells present allergens to Th2 cells
  • Th2 cells activated and cytokines released which activates humoral immunity
  • inc in mast cells, eosinophils and IgE production
  • IgE leads to mast cell degranulation
  • release of histamines, leukotrienes and tryptase
148
Q

What is the investigation for asthma?

A
  • spirometry: FEV1/FEV <0.7
  • reversibility: give salbutamol and see if ratio normal (0.8)
  • fractional exhaled nitric oxide: over 50ppb (adults)
149
Q

Which types of drugs are used to relax airway smooth muscle?

A
  • β-2 agonists
  • anti-muscarinics
  • theophyllines
150
Q

Which types of drugs are used to dampen inflammation?

A
  • corticosteroids
  • leukotriene receptor antagonists
  • biologics
  • macrolides
151
Q

What is the management of asthma?

A
  • SABA PRN
  • SABA + ICS
  • SABA + ICS + LABA
  • plus LTRA e.g. monteleukast
152
Q

What is an example of:
1. SABA
2. LABA
3. SAMA
4. LAMA?

A
  1. salbutamol
  2. salmeterol
  3. ipratropium bromide
  4. tiotropium bromide
153
Q

How do leukotriene receptor antagonists work?

A
  • Leukotrienes produced by immune system
  • cause inflammation, bronchoconstriction, mucus secretion
  • antagonists block effects
154
Q

What breaks a breath hold?

A

raised CO2 detected in CSF

155
Q

Where does gas exchange begin?

A
  • in the respiratory bronchioles
  • terminal bronchioles > resp bronchioles > alveolar ducts > sacs
156
Q

What is the name for an area of collapsed lung?

A
  • atelectasis
157
Q

What is the name for an accumulation of air around the heart?

A
  • pneumomediastinum
158
Q

How is the severity of stable COPD assessed?

A
  • FEV1 (% predicted)
    Stage 1: >80% of predicted
    Stage 2: 50-79% of predicted
    Stage 3: 30-49% of predicted
    Stage 4: <30% of predicted
159
Q

What are paraneoplastic symptoms of lung cancer?

A
  • ectopic ACTH > Cushing’s
  • ectopic ADH > SIADH
160
Q

What are blood gas results for metabolic alkalosis (pH, PaCO2, HCO3-)?

A
  • pH: high
  • PaCO2: normal/high
  • HCO3-: high
161
Q

What are blood gas results for respiratory alkalosis (pH, PaCO2, HCO3-)?

A
  • pH: high
  • PaCO2: low
  • HCO3-: normal/low
162
Q

What are blood gas results for respiratory acidosis (pH, PaCO2, HCO3-)?

A
  • pH: low
  • pCO2: high
  • HCO3-: normal
163
Q

What are blood gas results for metabolic acidosis (pH, PaCO2, HCO3-)?

A
  • pH: low
  • pCO2: normal/low
  • HCO3-: low
164
Q

What are blood gas results for respiratory acidosis with metabolic compensation (pH, PaCO2, HCO3-)?

A
  • pH: low/normal
  • pCO2: high
  • HCO3-: high
165
Q

What are blood gas results for respiratory alkalosis with metabolic compensation (pH, PaCO2, HCO3-)?

A
  • pH: high/normal
  • pCO2: low
  • HCO3-: low
166
Q

What is the aetiology of pulmonary vasculitis?

A
  • autoimmune: arthritis, lupus
  • infection: TB, legionnaires
  • drugs
  • COPD, asthma
  • genetic
167
Q

What are the causes of lung abcesses?

A
  • Viridans Strep, anaerobes, Klebsiella pneumoniae (and other gram -ve bacteria)
  • aspiration of gastric contents, alcoholic, poor dental hygiene
168
Q

What is the criteria for diagnosis with hospital acquired pneumonia and who does it affect?

A
  • acquired at least 48hrs after admission
  • elderly
  • ventilator
  • post op
169
Q

What is the presentation of hospital acquired pneumonia?

A
  • new fever
  • purulent secretions
  • new radiological infiltrates
  • new WCC or CRP inc
  • inc O2 requirement
170
Q

Which bacteria cause hospital acquired pneumonia?

A
  • Staph. aureus incl MRSA
  • Pseudomonas aeruginosa
  • Acinetobacter baumanii
  • Klebsiella pneumoniae
171
Q

What is the treatment of hospital acquired pneumonia?

A
  • early onset (≤5 days): metronidazole/co-amoxiclav
  • late onset: anti-pseudomonal: piperacillin-tazobactam
172
Q

What is the presentation of whooping cough?

A
  • catarrhal phase (resp infection symptoms) followed by paroxysmal (whooping cough)
  • coughing spasms with whoop when trying to inspire between bouts
  • mainly in children
173
Q

What viruses commonly cause upper resp tract illnesses?

A
  • rhinoviruses
  • influenza A viruses
  • coronaviruses
  • adenoviruses
  • parainfluenza viruses
  • resp syncytial viruses (children)
174
Q

What are the causes of pharyngitis?

A
  • rhinovirus, adenovirus
  • bacterial: Strep pyogenes: lancefield group A β haemolytic
175
Q

How are respiratory viruses diagnosed?

A
  • multiplex PCR
  • green viral throat swab
176
Q

What is pulmonary vasculitis?

A
  • Wegner’s granulomatosis
  • vasculitis affecting small and medium vessels
  • granulomatosis with polyangitis
177
Q

What are the symptoms of Wegner’s granulomatosis?

A
  • saddle shaped nose
  • ear infection
  • diffuse alveolar haemorrhage > haemoptysis
  • glomerulonephritis > haematuria
178
Q

How is Wegner’s granulomatosis diagnosed and treated?

A
  • cANCA +ve
  • corticosteroids e.g. rituximab
179
Q

What is silicosis?

A
  • SiO2 inhalation
  • cough and exertional SOB
  • calcification of hilar lymph nodes
180
Q

What is tidal volume?

A
  • volume that enters and leaves with each breath
181
Q

What is inspiratory and expiratory reserve volume?

A
  • extra volume that can be inspired/expired above tidal volume
182
Q

What is residual volume?

A

volume remaining after max expiration which can’t be measured by spirometry

183
Q

What lung diseases present with an obstructive FEV1/FVC ratio?

A
  • asthma
  • COPD
  • bronchiectasis
184
Q

What lung diseases present with an restrictive FEV1/FVC ratio?

A
  • Pulmonary fibrosis
  • Asbestosis
  • Sarcoidosis
  • ankylosing spondylitis
  • Neuromuscular disorders

Osha 2a (15 decks)

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