Respiratory 2.45-2.52

Question 1

KCO significance?

Answer 1

Means drops if lung itself is affected e.g. COPD; but if extrapulmonary then TLCO decreases but KCO normal or even SUPERNORMAL to compensate

Question 2

TLCO and KCO in obesity ie extrapulmonary restriction?

Answer 2

TLCO decreased, KCO increased/normal

Question 3

Burden of occupational lung disease?

Answer 3

Causes 15% COPD/asthma, 2% lung cancer, 80% EAA; plus mesothelioma, infection, pneumoconiosis

Question 4

Fibrogenic and non-fibrogenic occupational lung disease?

Answer 4

Silicosis, CWP and asbestosis all fibrogenic; non-fibrogenic includes siderosis (Fe) and baritosis (barium)

Question 5

Silicosis?

Answer 5

Silica dust. Need unnatural forces to get small enough particules ie sandblasting, masonry, mining/quarrying. Much smaller lethal exposure than CWP. Restrictive pattern; dense fibrosis. Nodules are bifringent and sparkling. Get classic silicosis, acute silicosis, COPD, cancer, (TB) i.e. increases everything.

Question 6

Early and late appearance of silicosis?

Answer 6

1. Early = diffuse, well-defined nodules on CXR. Predominately upper lobe. May see calcification. On CT, may see hilar and mediastinal l’dopathy, lymph node calcifciation. (DD sarcoid, Tb, diffuse malignancy);
2. Late.See multiple solid masses in upper zone; usually symmetrical/bilateral, graduallly migrating towards the hilum.

Question 7

CWP?

Answer 7

Fibrogenic pneumoconiosis; coal deposition. Same appearance as silicosis i.e. simple gives nodular upper zone shadowing, progressive massive fibrosis gives multiple large opacities (predominately upper/middle zones). See dust accumulation around terminal bronchioles on histology.

Question 8

Causes of high TLCO?

Answer 8

Polycythaemia, asthma (may be normal), exercise (increased pulmonary blood volume), pulmonary haemorrhage

Question 9

Pleural thickening?

Answer 9

aka benign diffuse pleural thickening. Can occur in silicosis/Tb/radiation/chronic
pneumonia/empyema but will be unilateral; bilateral in asbestos. SOB, restriction. Fibres cause inflammation, leading to chronic pleural effusions and fibrosis (thickening). 15-20 years latency . Irreversible but usually not progressive. DD inc. mesothelioma. Need regular screening

Question 10

Asbestosis?

Answer 10

Diffuse interstitial fibrosis; parenchymal (separate to pleural disease). Basal! Rare for fibrosis. Get severe SOB, increased risk of lung cancer. Hear fine end inspiratory crackles. Get restrictive deficit, TLC and VC down. Ratio preserved. Diffusion impaired (TLCO/KCO) so get hypoxaemia. Can get cor pulmonale eventually.

Question 11

Diagnosing asbestosis?

Answer 11

Imaging or histology consistent with it, evidence of causation (occupational history, markers of exposure (pleural plaques, recovery of asbestos bodies), exclusion of alternative possibilities HRCT better than CXR.. Most will have concurrent pleural plaques.

Question 12

Key differential for asbestosis?

Answer 12

IPF. Occupational history, pleural plaques; clubbing less common in asbestosis. Important for treatment. Remember not all asbestos lung disease is asbestosis!

Question 13

Malignant mesothelioma?

Answer 13

Long latency (40 years), breathlessness, pain, sweats, weight loss and anorexia. Death in 18 months. Pleura “enroaches” onto lung; may see reduction in lung volume so mediastinum shifts towards lesion. Predilection for direct invasion and metastasis.

Question 14

Diagnosing mesothelioma?

Answer 14

CXR and CT for suspicion; confirm with aspiration[thoracentesis] for malignant cells/tissue biopsy [thoracoscopy]. DD HF, Tb.

Question 15

How many years is generally needed for CWP?

Answer 15

~20. Silicosis is fewer (remember graph)

Question 16

Findings that point towards EAA?

Answer 16

BAL with lymphocytosis, compatible CXR and HRCT, IgG to farmer’s lung-type microbes etc., histology, compatible history or evidence of exposure from Ab, decreased TLCO, positive challenge test

Question 17

BAL in EAA?

Answer 17

Negative findings are useful to rule out EAA; positive (i.e. alveolar lymphocytosis) is useful but may also be found in asymptomatic people (false positives)

Question 18

Treating EAA?

Answer 18

Reduce exposure, give steroids; stopping immediately usually not the best thing to do!

Question 19

What are Light’s criteria?

Answer 19

1. Pleural fluid protein divided by serum protein >0.5
2. Pleural LDH / serum LDH >0.6
3. Pleural LDH >2/3 ULN for serum LDH.
   Pleural fluid is an exudate if one or more are met.

Question 20

How does mineral dust cause lung disease?

Answer 20

Particles become lodged, are taken up by macrophages, which are activated and released cytokines etc. As silica etc. is indigestible, macrophage dies, particle is taken up by another and process is perperuated.

Question 21

Two types of occupational asthma?

Answer 21

1. Sensitiser-induced OA (90%). Latency period between first exposure and immunological response (allergy); IgE mediated (so must be reaction to protein?)
2. Irritant-induced OA = RADS (reactive airway dysfunction syndrome). Occurs a few hours after exposed to high concentration of irritant; acutely dangerous but may have chronic sequelae (i.e. lifelong asthma)

Question 22

IgE in occupational asthma?

Answer 22

Total IgE raised indicates atopy and therefore predilection; can look for specific IgE to allergen but may get false negatives.

Question 23

Use of methylcholine challenge?

Answer 23

Take baseline FEV1; inhale increasing doses of potent bronchoconstrictor; get PD20 (dose needed to reduce FEV1 by 20%. If very low, indicates airway hyper-responsiveness (hallmark of asthma).

Question 24

Why are OA symptoms often worse after work?

Answer 24

Get late response after ~12 hours; must observe for this when testing for OA. Same as with allergy (early is mast cell degranulation following specific IgE cross-linking; late is mast cell mediated and recruits lymphocytes/eosinophils to site; takes 8-12 hours).

Question 25

Causative agents for OA?

Answer 25

1. HMW allergens (flour, dander, enzymes). Proteins, make specific IgE and get type 1 HS response. Natural counterparts. 2. LMW agents (CHEMICALS) e.g. isocyanates, epoxy resins. Small and very reactive; react with proteins to give novel allergens but are not themselves allergens; may be no specific IgE (hence FNs). No natural counterparts.

Question 26

Features of OA?

Answer 26

Onset often in one year of new work, have latent phase of asymptomatic exposure, get evening/night-time symptoms (delayed response), worse when working and BETTER AT WEEKENDS/HOLIDAYS, worse with heavier exposure/no protection, associated nasal/eye symptoms, other workers likely to be affected?

Question 27

Sputum eosinophils in OA?

Answer 27

Induce fresh sputum with hypertonic saline; associated with inhalation challenge testing (PD20). Levels of eosinophilic airway inflammation. Suppressed by cigarette smoking. More associated with HMW than LMW.

Question 28

Risk factors for OA?

Answer 28

Atopy increases risk of OA in HMW agents; smoking increases risk of sensitisation to flour, seafood, isocyanatesm platinum salts, coffee and castor bean. Atopy also means develop sensitisation to HMW (IgE forming) FASTER

Question 29

Most common causes of OA in UK?

Answer 29

Isocyanates (e.g. paint-spraying), flour/grain, latex, cleaning products.

Question 30

Preventing OA?

Answer 30

1. Limiting exposure (ventilation, RPE, reallocation) 2. Pre-employment screening not effective unless history of sensitisation to certain Ag 3. Health surveillance could be key in identifying early

Question 31

Prognosis OA?

Answer 31

Loss of income, 1/3 achieve symptomatic recovery; likely to worsen if remain exposed. 1/3 unemployed <6 years after diagnosis

Question 32

Post-OA?

Answer 32

Once becomes established, can get symptoms triggered by "normal" asthma factors like cold/exercise etc. Means can miss "better on weekends"!

Question 33

Serial PEFs/spirometry in OA?

Answer 33

Done when at work and when away; may show variable AW obstruction (hallmark of asthma) and possible relationship between symptoms/PFTs/work. Assessment may be difficult as can exaggerate or underplay.

Question 34

Serial methycholine measurements?

Answer 34

Should show sequential improvement away from work and rapid deterioration when return

Question 35

Chronic bronchitis pathophysiology?

Answer 35

Chronic/recurrent excessive mucus secretion in the bronchial tree; caused by smoke irritation so should improve when stops smoking. Caused by mucous gland hypertrophy and increased number of goblet cells.

Question 36

Emphysema pathophysiology?

Answer 36

Increase in size of air spaces distal to terminal bronchioles accompanied by destruction of their walls without obvious fibrosis; causes obstruction because airways collapse with distal air trapping so FEV1 drops.

Question 37

Indications for LTOT in COPD?

Answer 37

1. Pa02 <7.3 when stable 2. Pa02 <8 and one of: - > secondary polycythaemia - > nocturnal hypoxaemia - > peripheral oedema - > pulmonary HTN

Question 38

Diagnosing chronic bronchitis?

Answer 38

Symptom based; presence of cough productive of sputum on most days for at least 3 months of 2 successive years.

Question 39

Three causes of airway obstruction (in small airways)?

Answer 39

1. Emphysema (loss of elastic recoil leaves alveoli prone to collapse on expiration) 2. Airway inflammation (airway wall thickens, due to smoke); get squamous cell metaplasia and fibrosis. 3. Mucus secretions accumulating and obstructing lumen

Question 40

What is minute volume and why is it helpful?

Answer 40

Volume of gas inhaled and exhaled in one minute/ inversely proportional with PaC02 (hypoventilation)

Question 41

"Cause" of T2 RF?

Answer 41

Hypoventilation, increased deadspace ventilation (areas that are not exchanging) and some V/Q mismatching. T2 RF is synonymous with ventilatory failure (ventilation is adequate in T1)

Question 42

Nocturnal hypoventilation characterised by?

Answer 42

Increased PaCO2, reduced PaO2.

Question 43

Causes of hypoventilation/resp. insufficiency?

Answer 43

Muscle disease, chest wall abnormality, COPD, central and obstructive sleep apnoea, spinal injury, diaphragm paralysis

Question 44

Respiratory function tests for hypoventilation?

Answer 44

1. FVC/SNIP/MIP/MEP (assess insp/exp. function); do not actually assess hypoventilation. Useful prognostically. 2. Overnight O2/CO2 monitoring 3. ABG (urgency of treatment). Invasive. 4. Venous bicarb (total CO2) 5. Sleep studies

Question 45

Physical signs of respiratory insufficiency?

Answer 45

Reduced chest expansion, fast RR, weak cough, wean sniff, accessory muscle recruitment at rest. Particularly important for patients with bulbar involvement who cannot perform PFTs

Question 46

Venous bicarb. vs ABG?

Answer 46

ABG may be normal during the day but venous bicarb is "summary" of 24 hours so may be increased in nocturnal hypoventilation. Also easier to obtain.

Question 47

Signs of OSA?

Answer 47

Crowded pharangeal airspace, increased Mallampati score, retrognathia, tonsils, "difficult to intubate", collar size >16.5, nasal obstruction e.g. polyps

Question 48

Deciding on treatment for OSA?

Answer 48

Qualitative decision; based on level of symptoms, severity of OSA (used AHI score). Important because compliance with CPAP is very poor.

Question 49

How does CPAP work in OSA?

Answer 49

Continuous; does not ventilate/cycle; just splints the upper airway open. Newer machines can auto-titrate. Symptoms improve over ~6 months; must be on treatment forever or symptoms will return. Can check compliance.

Question 50

Driving and OSA?

Answer 50

Untreated = 8* risk of RTA; CPAP normalises this. Patient must inform DVLA of diagnosis.

Question 51

DMD and hypoventilation?

Answer 51

Hereditary NM disease causing respiratory failure; X linked, recessive, mean LE 19. 3/4 deaths due to hypercapnic respiratory failure.

Question 52

NIV and hypoventilation?

Answer 52

NIV = BIPAP. Has changed life expectancy. Issues are with timing of NIV, nutrition, quality of life, cough assist, cardiomyopathy etc.

Question 53

Progression from hypoventilation (of any cause)?

Answer 53

Get nocturnal hypoventilation, then continuous hypoventilation, then chronic respiratory failure. Improved survival and QoL with NIV.

Question 54

Why do ventilation symptoms present when asleep?

Answer 54

Lose ventilatory drive and ventilation; not a problem in healthy individuals. Respitatory centre in medulla gets less stimulation from cortex, and is less responsive to chemical (e.g. hypercapnia) and mechanical (chest wall/AW receptors) stimuli. Minute volume falls, PCO2 rises, respiratory muscle activity decreases (particularly in REM).

Question 55

What happens in alveolar hypoventilation?

Answer 55

O2 is not replenished properly and CO2 is not washed out so get T2 RF. (T1 is V/Q problem so CO2 will stay normal as long as ventilation is preserved). Can manifest as acute asphyxia or chronic ventilatory failure.

Question 56

Is all ventilatory failure (T2 RF) lung related?

Answer 56

No; can be anywhere from brain to alveoli (polio, foreign body, tonsils, diffuse airway obstruction, ARDS, pleural tumour/fibrosis, rib fracture, obesity, kyphoscolioisis, trauma, GBS, muscle relaxants, myopathy, CVA).

Question 57

Four main causes of chronic T2 RF (ventilatory failure)?

Answer 57

Obesity, thoracic cage abnormalities, NM disease, obesity-related hypoventilation syndrome.

Question 58

How does NIV work?

Answer 58

Patient inspiring triggers positive pressure, increasing volume inspired. As patient breathes out, machine reduces pressure (not to zero), allowing expiration while keeping small airways open for longer (increased tidal volume).

Question 59

Difference between T2RF and OSA?

Answer 59

T2RF is ventilatory failure; caused by obesity/NM disease/thoracic cage defects etc.; is present all the time (and apparent on ABG) but gets worse during the night purely because ventilatory drive is reduced. OSA is disease that only occurs at night due to collapse of upper airway with loss of pharangeal tone; will have normal function during the day. Treatment for first is BIPAP (as have ventilatory failure), OSA is CPAP.

Question 60

Treating OSA implications for IHD? And CPAP?

Answer 60

Recurrent apnoeas/arousals causes formation of ROS which damage vasculature and promote inflammation; increases HTN/CVA/MI. Also get increased SNS arousal and blood pressure when trying to halt apnoeas. Clear link between OSA and metabolic syndrome, in both directions. CPAP shown to reduce HTN.

Question 61

Actual criteria for OSA diagnosis?

Answer 61

>15 apnoeas or hypopnoeas per hour, each lasting 10 seconds (AHI >15); usually associated with O2 desaturation of >4%. To be regarded as clinically significant, need this alone with daytime sleepiness etc.

Question 62

What is central sleep apnoea?

Answer 62

Relatively uncommon condition where cessation of airflow at nose and mouth is associated with lack of respiratory muscle activity. Assoc. with unstable ventilatory control system; can be caused by brainstem infarcts. May be secondary reflex to OSA (obstructive apnoeas precede central apnoeas), or seen in Cheyne-Stokes.

Question 63

Diagnosing IPF?

Answer 63

Exclude other causes, restrictive pattern, impaired gas exchange, imaging shows bibasal reticular abnormalities, ground-glass shadowing (seen also in hypersensitivity pneumonitis), age >50, >3 months illness, bibasal inspiratory crackles, biopsy/BAL shows no alternative diagnosis, insidious unexplained SOB.

Question 64

HRCT sarcoidosis?

Answer 64

Bilateral hilar l'dopathy, small nodules with beading on fissures, and nodules in bronchovascular pattern.

Question 65

Investigating sarcoid?

Answer 65

CXR, HRCT, then biopsy (trans/endobronchial showing granulomas in 90% BAL shows lymphocytic alveolitis. Can be diagnosed on clinical grounds (BHL key).

Question 66

Histology of sarcoid?

Answer 66

Non-necrotising, (non-caseating) granulomas. May progress to cause fibrosis. BAL shows lymphocytosis. Biopsy shows alveolar wall infiltration.

Question 67

Presentation of HP/EAA?

Answer 67

Cough, SOB, and often systemic features ie fever, weight loss, flu-like due to immune component. Inflammatory reaction to inhalation of allergen (organic or non organic). Pigeon fancier's, farmer's, cheese washer's.

Question 68

O/E EAA?

Answer 68

Crackles, wheeze (as it affects terminal bronchioles) and SQUEAKS (due to bronchiolitis; seen in kids too). Odd for interstitial lung disease, but occurs because it affects the small airways

Question 69

Ideal imaging in EAA?

Answer 69

Expiratory HRCT; get mosaic attenuation with black areas where air is trapped distal to inflamed bronchioles, and white areas where the distal alveoli are inflamed. Also see prominent groundglass shadowing. Late features include honeycombing (with fibrosis). Mid and upper zones!!!!

Question 70

Diagnosing EAA?

Answer 70

History/exposure, +ve antibody response, compatible imaging (HRCT). Biopsy often unnecessary (but would show lymphocytic infiltrate).

Question 71

EAA patho?

Answer 71

In sensitised individuals, inhalation of allergens e.g. avian proteins provokes hypersensitivity reaction. Acutely, alveoli infilitrated with acute inflammatory cells. Chronically, get granuloma formation and obliterative bronchiolitis.

Question 72

PFTs in EAA?

Answer 72

Reversible restrictive pattern, reduced TLCO during acute attacks (acute); chronic sees persistent changes.

Question 73

Where in lung do you see EAA changes?

Answer 73

Upper zone; get consolidation/mottling acutely and chronically get fibrosis/honeycombing.

Question 74

Bloods for EAA?

Answer 74

Positive serum precipitins (IgG against specific Ag); just indicates exposure and sensitisation rather than active disease so get false positives in asymptomatic patients.. Not IgE!

Question 75

Symptoms of EAA?

Answer 75

Within 4-6 hours of exposure, get fever, rigors, myalgia, dry cough, dyspnoea, crackles, wheeze less prominent. Chronically, get increasing SOB, weight loss, type 1 RF and cor pulmonale.

Question 76

Egg-shell calcification of hilar nodes?

Answer 76

Silicosis

Question 77

Causes of high TLCO?

Answer 77

Asthma, polycythaemia, L-R cardiac shunts, exercise.

Question 78

What two parameters are likely to trigger NIV in acute COPD?

Answer 78

Acidaemia and hypercapnia (more likely to be needed in patients at risk of T2RF).

Question 79

Four contraindications to NIV?

Answer 79

Reduced consciousness, facial/upper airway trauma or surgery, pneumothorax, inability to protect the airway e.g. nerve paralysis

Question 80

Other tests in asthma?

Answer 80

FeNo, blood eosinophils, bronchoconstrictor challenge test (airway hyperresponsiveness), allergy testing (skin prick, RAST)

Question 81

Chronic vs acute EAA?

Answer 81

Acute is flu-like, 4-8 hours post exposure, infiltrate on CXR, responds well if removed Ag. Lung volume tests may show volume reduction and impaired gas exchange; CXR may be normal.Chronic is progressive DOB, upper zone fibrosis, restrictive IRREVERSIBLE spirometry).

Question 82

Common features of ILD?

Answer 82

Progressive breathlessness, dry cough, lung crackles. Diffuse infiltrates on CXR. PFTs show restriction, impaired gas diffusion and hypoxaemia with hypocapnia.

Question 83

Which two ILDs have granulomas?

Answer 83

Sarcoidosis, EAA.

Question 84

Lymphocytic alveolitis is characteristic of?

Answer 84

Sarcoidosis, EAA. (Neutrophilic lavage in IPF).

Question 85

Early and late ILD?

Answer 85

Early tends to be inflammatory and responsive to corticosteroids; late tends to be irreversible fibrosis.

Question 86

HRCT in IPF?

Answer 86

Typically shows advanced fibrosis, with extensive reticulation and honeycombing in lower zones; minimal ground glass opacities (inflammation).

Question 87

What is hypersensitivity pneumonitis?

Answer 87

Immunologically mediated lung disease in which a hypersensitivity response occurs in an individual sensitised to a particular inhaled Ag e.g. Farmer's lung. Inhalation provokoes complex immune response, with Ab reaction, IC formation, and complement activation giving alveolitis. Less common in smokers, because of smoke's immunosuppressive effect.

Question 88

Diagnosing OSA?

Answer 88

Epworth score differentiates OSA from snoring; relatives often provide history of snore-apnoea cycle. Sawtooth oximetry supports this; if this is negative or equiovoal can do inpatient assesment with oximetry and video assessment. Full polysomnography rarely needed. >15 apnoeas/hypopnoeas in any hour of sleep = diagnosis.