Respiratory conditions

  • Created by: MazzaW
  • Created on: 03-12-19 14:41


Caused by unnatural forces blasting particles to make them smaller (masonry, sandblasting, ceramics, building sites)

Can lead to silicosis which may lead on to progressive massive fibrosis. Also increases risk of TB, lung cancer and COPD.

Early = small diffuse nodules on CXR

Late = solid mass in upper zone

Biopsy = dense fibrosis with birefringent particles

1 of 16

Coal worker's pneumoconiosis

Causes fibrosis due to dust deposition.

Early = small diffuse nodules on CXR

Late = solid mass in upper zone

Biopsy = fibrosis with dust accumulation in terminal bronchioles

2 of 16

Asbestos-related disease

Asbestosis only refers to fibrosis caused by asbestos- SOB, basal diffuse interstital fibrosis, basal reticular shadowing on CXR, fine end-inspiratory crackles, long latency, relatively uncommon, pleural plaques on CXR, differentiate from IPF by occupational Hx/presence of pleural plaques/presence of clubbing (less common in asbestosis)

Heavy exposure -> lung Ca, asbestosis. Light exposure -> mesothelioma, plaques

Pleural plaques are not a disease or pre-malignant and are asymptomatic. They only indicate previous exposure (with 10yr latency period). Holly leaf appearance on CXR (calcification)

Benign diffuse pleural thickening- SOB and restricted lung expansion due to pleural effusion, rarely progresses once established

Malignant mesothelioma- SOB, chest pain, anorexia, wt loss, sweats, long latency period, will usually see pleural plaques, no cure, death occurs in 12-18 months (palliative care only)

3 of 16

Occupational asthma

Occupational asthma = Sx due to exposure to agent at work, may be sensitiser induced (90%, IgE mediated, allergy to agent) or irritant induced (starts few hrs after exposure to irritant fumes/gas/ vapours at work, long-term Sx from then onwards). Work aggravated asthma = increased Sx at work due to exposure to exercise/dust/cold etc

Features: GETS BETTER AT WEEKENDS/ON HOLIDAY, worsens through week, onset within 1yr of new job, latency period between 1st exposure and onset of Sx, evening/nighttime Sx, nasal/eye Sx, worse with heavier exposure

Ix: good occupational Hx, serial peak flows (at home + work, analyse using OASYS), methacholine challenge test (PD20=20% reduction in FEV1, see if better when off work), allergy testing (skin test, serum IgE), workplace visits, gold standard = direct inhalational challenge test

Prevention: avoid sensitisation (PPE in workplaces), RPE. Rx with asthma Rx/omalizumab

Legal: companies should provide health+safety at work where 'reasonably practicable', employer MUST report to HSE (RIDDOR), employees can refer self/company to HSE, workers can apply for Industrial Injuries Disablement Benefit

4 of 16

Pulmonary hypertension

COPD -> loss of capillary beds -> hypoxia/hypercapnia -> vasoconstriction -> increased aveolar pressure. Arterioles respond with medial hypertrophy.

Pulmonary HTN increased afterload on right ventricle -> RV failure (increased end-diastolic pressure, increased central venous pressure, RV hypertrophy and dilatation)

Hypoxia can also induce polycythaemia so there is increased blood viscosity which further impairs RV function.

5 of 16


Chronic bronchitis + emphysema.

Irreversible obstructive picture on spirometry with increased TLC + residual volume (due to hyperinflation + air trapping). TLCO and KCO are decreased. Steeple shape on flow volume loop

All pts should be offered intensive smoking cessation support + pulmonary rehabilitation. High risk of exacerbations = LABA/LAMA/ICS, salbutamol PRN. Low risk = SABA -> LAMA -> LABA/LAMA. Exacerbations: 30mg prednisolone OD for 5 days, Abx if purulent sputum. Consider mucolytics if chronic productive cough or frequent exacerbations.

At each visit: check inhaler technique, oximetry (refer if <92% at rest or desaturation on exercise), screening for anxiety/depression/other comorbidities. 

Long term O2 therapy indicated if PaO2 <7.3 when stable OR PaO2 <8 when stable + 1 of: secondary polycythaemia, nocturnal hypoxaemia (SaO2 <90% more than 30% of the time), peripheral oedema, pulmonary HTN

6 of 16

COPD exacerbation

Give O2- if T2RF, needs to be maintained between 88-92% (Venturi mask), otherwise can give via nasal cannula/face mask/reservoir mask

Oral steroids- prednisolone 30mg OD for 5 days

Abx if required (purulent sputum etc)

Nebulised bronchodilators

BiPAP if tiring/unable to maintain respiratory effort

7 of 16

Obstructive sleep apnoea

Collapse of upper airway during REM sleep. More common in obesity.

Sx: sleepiness, awaking unrefreshed, poor sleep quality, waking frequently, snoring, partner notices breath holding, resuscitative grunt

Ix: Epworth sleepiness scale, overnight oximetry (shows obstructions), overnight trascutaneous CO2 (O2 obstructions, increase in CO2 and HR), polysomnography (records brain activity, PaO2, HR, RR, arm + leg movements), ABG/bicarbonate

Mgmt: treat underlying cause (wt loss, wean opiates, ENT surgery), CPAP if required

8 of 16


May occur in:

  • obesity
  • thoracic cage abnormalities
  • neuromuscular weakness (resp muscles) e.g. diaphragmatic palsy, MS
  • obstructive sleep apnoea
  • decreased central drive (e.g. opiates)

Decreased TLCO but normal/raised KCO, often have restrictive pattern on spirometry with decreased TLC

Sx of hypercapnia: sleepiness, sleep phenomena, altered conscious level, poor concentration, early morning headaches, twitching (CO2 retention flap)

9 of 16

Non-invasive ventilation


  • DELIVERY: via face mask, CPAP = constant positive pressure during inspiration and expiration, BiPAP = 2 levels of positive pressure (baseline for expiration, greater pressure for inspiration)
  • CLINICAL USE: CPAP for T1RF (hypoxia only- acute pulmonary oedema, upper airway collapse, OSA), BiPAP for T2RF (good at increasing CO2 expiration)
  • MECHANISM OF ACTION: CPAP works by preventing alveolar collapse (splinting airways) but does not ventilate, BiPAP increases airflow in inspiration and prevents airway collapse in expiration to help you take bigger breaths (ventilates)
  • RESPIRATORY MUSCLE USE: still have to use own resp muscles with CPAP, BiPAP more useful in pts with fatiguing resp muscles (reduces workload)

PEEP = can be applied in any ventilator mode, permits use of lower FiO2 while preseving arterial oxygenation. Increases end-expired lung volume and decreases airspace closure at end of expiration. Lower levels limit atelectasis from endotracheal intubation/sedation/ paralysis/supine positioning. Higher levels improve oxygenation in some conditions (pulm oedema, ARDS)

10 of 16

Obesity hypoventilation syndrome

Obesity + chronic respiratory failure

Often co-exists with ither causes of respiratory failure (especially COPD)

Reduced TLCO, normal/raised KCO, reduced TLC with restrictive picture on spirometry

Mgmt: wt loss (1st line), may need CPAP

11 of 16

Interstitial lung disease

Causes: IPF (most common), sarcoidosis, hypersensitivity pneumonitis, pneumoconiosis, connective tissue disease (SSc, RA, SLE), drug-related (nitrofurantois, bleomycin, methotrexate, amiodarone)

Sx: SOB (progressive), dry cough, failure to respond to treatment for other conditions, occupational/hobbies, clubbing, cyanosis, fine inspiratory crackles (often at bases in IPF/asbestosis), decreased chest expransion

Ix: CXR, HRCT (best), restrictive lung function tests, ABG (T1RF), autoAbs (anti-CCP, ANA, Rh factor, anti-Scl-70, dsDNA), rarely get biopsy (may cause exacerbation)

IPF mgmt: supportive if SOB/decreased ET (pulmonary rehabilitation, O2), pirfenidone/nintedanib (halve rate of progression, only if meet strict criteria), transplant (if young and disabled enough), recruit to clinical trials, very poor prognosis (mortality within a few yrs of Dx)

12 of 16


Multisystem granulomatous disease primarily affecting lung. Cause unknown.

Typical CXR finding of bilateral hilar lymphadenopathy (DDx: TB, lymphoma, cancer) - also seen on HRCT (perifissural beading, may also see ILD).

Staging based on CXR findings: 0 (no abnormalities), 1 (lymphadenopathy), 2 (lymphadenopathy + pulmonary infiltration), 3 (just pulmonary infiltration), 4 (fibrosis)

Ix: EBUS (endobronchial USS) - caseating granuloma

Rx: ideally no treatment, steroids if required (symptom control only)

13 of 16

Hypersensitivity pneumonitis

Many types. Occur due to biological proteins (e.g. hay dust, bird faeces) that people develop immune response. Environmental Hx very important (occupation, hobbies, pets)

May present with: cough, SOB, occasionally systemic Sx (wt loss, fever etc - rule out malignancy)

O/E: crackles, wheezes and squeaks

Imaging: patches of black (gas trapping) on HRCT, diffuse haziness on CXR

Dx: usually enough to have appropriate exposure, positive Ab response and clinical/radiological picture

Rx: avoid Ag, steroids if required

14 of 16

Asthma (chronic)

Reversible airway inflammation with increased mucus production.

Features: SOB, wheeze, cough, chest tightness, variable Sx, recurrent episodes, absence of Sx indicating alternative Dx, PMH/FH of atopy, variable spirometry/PEFR

If low chance of asthma- investigate/treat for other causes. If high chances- initiate treatment and objectively assess response (symptom score, spirometry). Poor response to treatment/other Dx unlikely = intermediate chance: test for reversible airway obstruction, PEFR charting, challenge tests, FeNO, blood eosinophils, serum IgE/skin testing, watchful waiting if asymptomatic

Children < 5 cannot do spirometry so watchful waiting/monitored initation of Rx only.

Refer to specialist if: uncertain Dx, possibly occupational, poor response to Rx, severe/life-threatening attack, patient/parental anxiety, red flags (prominent systemic features, unexpected clinical findings, persistent non-variable SOB, chronic sputum production, restrictive spirometry, CXR shadowing, marked eosinophilia, failure to thrive, Sx present from birth, born with perinatal lung problem, excessive vomiting/posseting, nasal polyps, FH of unusual chest disease, severe URTI

15 of 16

Asthma (acute)

Moderate: PEFR 50-75% best/predicted, increased Sx, no features of acute severe asthma

Severe = ANY OF: PEFR 33-50% best/predicted, RR 25+, HR 110+, inabiliy to complete sentences in 1 breath

Life-threatening = ANY OF: PEFR <33% best/predicted, silent chest, exhaustion, altered conscious level, arrhythmia, hypotension, cyanosis, poor respiratory effort, SaO2 <92%, PaO2 <8, normal/raised PaCO2 (4.6-6.0)

Mgmt: admit if severe/life-threatening, ABCDE, high-flow O2 (guided by ABG), CXR (exclude pneumonia + pneumothorax), steroids, nebulised salbutamol + ipratropium, escalate care (inform senior, consider aminophylline and magnesium sulphate), consider ITU if needs ventilatory support/failing to respond to treatment

Follow up by informing GP and referral to respiratory specialist.

16 of 16


No comments have yet been made

Similar Medicine resources:

See all Medicine resources »See all Respiratory resources »