Y3 Resp

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Causes of metabolic acidosis

Causes of metabolic acidosis - either inc acid production/ingestion or decreased acid excretion or GI/renal HCO3 loss A metabolic acidosis would have the following characteristics on an ABG: ↓ pH ↓ HCO3- ↓ BE 1) Inc anion gap: § Lactic acidosis - shock, infection, tissue ischaemia § Urate - renal failure § Ketones - DM, alcohol § Drugs/toxins 2) Normal anion gap - loss of HCO3/ingestion of H+: § Renal tubular acidosis § Diarrhoea § Addison's

Try to think of key clues for the most common diagnoses in the 'weeks to months' causes for SOB

1) • COPD − Remember that COPD is a bracket term encompassing chronic bronchitis and emphysema. − History of chronic bronchitis (a clinical diagnosis, based on the presence of a cough, productive of sputum (~10 mL daily), on most days of 3 months for 2 consecutive years) and permanent, largely irreversible, shortness of breath. − Presence of risk factors suggesting a cause for COPD: − Smoking (usually more than 20 pack years) − Occupational exposure to lung irritants, e.g. in coal miners, tunnel workers − α1-Antitrypsin deficiency (liver failure, family history). − Signs of COPD: − Hyperexpanded chest − Breathing through pursed lips − Reduced air entry/chest expansion − Hyper-resonant percussion note (particularly resonance over the heart and liver). 2) Chronic asthma − History of transient, reversible cough, wheeze and shortness of breath - often worse at night, during exercise, or when exposed to allergens or cold − Presence of associated atopic conditions personally or in family members (eczema, hayfever, allergies, nasal polyps) − Symptoms may be exacerbated by drugs such as non-steroidal antiinflammatory drugs (NSAIDs), aspirin, β-blockers (including those in eye drops used for glaucoma) − Wheeze on auscultation of the lungs. 3) Pulmonary fi brosis − History of exposure to asbestos, silica, or coal (pneumoconioses causing fibrosis), exposure to drugs (e.g. methotrexate) − Signs on examination include: − Clubbing (in usual interstitial pneumonitis) − Reduced air entry/chest expansion − Late inspiratory, fine crackles (often heard throughout the chest rather than just the lung bases as in pulmonary oedema). 4) Heart failure − History of shortness of breath on exertion, orthopnoea (breathless when lying flat), paroxysmal nocturnal dyspnoea (waking up short of breath) − Presence of risk factors suggesting a cause for heart failure: − Ischaemic heart disease (smoking, diabetes mellitus, hypercholesterolaemia, hypertension, South Asian descent, strong family history) − Other atherosclerotic disease (e.g. stroke, transient ischaemic attack (TIA), limb claudication) - Hypertension ( − can cause heart failure by itself, in the absence of ischaemic heart disease) − Valvular disease (e.g. rheumatic fever, endocarditis, Marfan's syndrome) − Cardiomyopathy **Signs on examination include: − Displaced apex beat − Third and fourth heart sounds − Crackles in both lung bases − Raised jugular venous pressure (JVP), hepatomegaly, peripheral oedema (ankles, sacrum). 5) Anaemia − History of bleeding (menorrhagia, melaena, haematochezia) or malnutrition ('tea and toast' diet in elderly, poor diet of homeless). Fatigue as well as shortness of breath on exertion − Signs of peripheral (fingers) or central (tongue) cyanosis. Specific signs such as koilonychia, glossitis, and angular stomatitis (all rare). Checking for conjunctival pallor is routinely done but is unreliable. 6) Bronchiectasis would be suggested by a history of productive cough and recurrent chest infections, or a history of cystic fibrosis. 7) Obesity, kyphoscoliosis, ankylosing spondylitis can be excluded on inspection. 8) Physical deconditioning is a diagnosis of exclusion.

What does COPD encompass? Give some RFs and signs

Presentation of heart failure

What is contraindication for chest drain?

An INR >1.3 is a relative contraindication for chest drain insertion. § A chest drain is a tube inserted into the pleural cavity which creates a one-way valve, allowing movement of air or liquid out of the cavity. § Chest drain insertion is indicated in cases of: o Pleural effusion o Pneumothorax not suitable for conservative management or aspiration o Empyema o Haemothorax o Haemopneumothorax o Chylothorax o In some cases of penetrating chest wall injury in ventilated patients. § Insertion of a chest drain is relatively contraindicated in patients with any of the following: o INR > 1.3 o Platelet count < 75 o Pulmonary bullae o Pleural adhesions § Please note, all of the above represent only RELATIVE contraindications, addressing respiratory compromise in an emergency situation should always be on an individual case basis. § Once patient consent has been obtained and patient imaging assessed, the patient should be positioned in a supine position or at a 45º angle. § The patient's forearm may be positioned behind the patient's head to allow easy access to the axilla. Identify the 5th intercostal space in the midaxillary line. Alternatively, positioning may be determined by ultrasound guidance, British Thoracic Society Guidance 'strongly recommend' use of ultrasound guidance in all cases of fluid within the pleura. § The area should be anaesthetised using local anaesthetic injection (lidocaine, up to 3mg/kg). § The drainage tube should then be inserted using a Seldinger technique. The drain tubing should then be secured using either a straight stitch or with an adhesive dressing. § Positioning can be confirmed by aspiration of fluid from the drainage tubing, by 'swinging' of the fluid within the drain tubing when the patient inspires and on chest x-ray **Complications that may occur and which the patient should be advised of in the process of obtaining consent: § Failure of insertion - the drain may be abutting the apical pleura, in which case it should be pulled back, or may be subcutaneous or in rare cases could enter the abdominal cavity. § In both latter cases, the drain should be removed and re-sited. § Bleeding - around the site of the drain or into the pleural space § Infection § Penetration of the lung § Re-expansion pulmonary oedema **Re-expansion pulmonary oedema may be preceded by the onset of a cough and/or shortness of breath. In the event of concerns regarding re-expansion pulmonary oedema, the chest drain should be clamped and an urgent chest x-ray should be obtained. To avoid re-expansion pulmonary oedema, it is recommended that the drain tubing should be clamped regularly in the event of rapid fluid output i.e. drain output should not exceed 1L of fluid over a short period of time (less than 6 hours). **Removal of the chest drain is dependent upon the indication for insertion: § In cases of fluid drainage from the pleural cavity, the drain should be removed when there has been no output for > 24 hours and imaging shows resolution of the fluid collection. § In cases of pneumothorax, the drain should be removed when it is no longer bubbling spontaneously or when the patient coughs and ideally when imaging shows resolution of the pneumothorax. § Drains inserted in cases of penetrating chest injury should be reviewed by the specialist to confirm an appropriate time for removal.

Man with CURB of 1 how should be managed?

In GP, Oral amoxicillin

What does this show?

pneumonia

Is asthma reversible?

yes

COVID clinical course

§ pathogen - SARS COV2 virus § disease - COVID 19

Describe the timescales of acute and chronic coughs

§Acute - < 3 weeks § Chronic - > 8 weeks

Generate a management plan for pneumonia

● Assess severity using the British Thoracic Society Guidelines o CURB-65 is a simple, validated scoring system o 1 point for each: ▪ Confusion - abbreviated mental test <8 ▪ Urea >7mmol/l ▪ Respiratory rate greater than or equal to 30 ▪ BP < 90 systolic and/or 60 diastolix ▪ Age greater than/equal to 65 o 0 - 1: home treatment if possible o 2: hospital therapy o 3 or more: severe pneumonia - consider ICU 1) Assess using ABC: a) Treat hypoxia (sats <88%) with oxygen, starting at 24-28% if history of COPD/hypercapnia b) Treat hypotension/shock from infection c) Assess for dehydration - give IV fluid support 2) Start empirical antibiotics o Mild: oral amoxicillin (if allergic - use macrolide or tetracycline) o Moderate: IV/oral amoxicillin + clarithromycin o Severe: IV co-amoxiclav + clarithromycin o If penicillin allergic, use cephalosporin instead of co-amoxiclav. o If atypical suspected: a) Legionella pnuemophilia: add levofloxacin + rifampicin b) Chlamydophilia species: add tetracycline c) Pneumocystis jiroveci: high-dose co-trimoxazole o If hospital acquired or neutropenic disorder: IV aminoglycoside e.g. gentamicin + antipseudomonal penicillin e.g. ticarcillin o If aspiration pneumonia: cephalosporin IV + metronidazole IV o Switch to appropriate antibiotic based on sensitivity 3) Supportive treatment o Oxygen o IV fluids o CPAP, BiPAP or ITU care for respiratory failure o Surgical drainage may be needed for lung abscesses and empyema 4) Discharge planning: o If TWO OR MORE features of clinical instability are present (e.g. high temperature >37.5, tachycardia, tachypnoea >24RR, hypotension <90SBP, low oxygen sats <90%, abnormal mental status) there is a high risk of re-admission and mortality 5) Consider other causes if pneumonia is not resolving 6) Prevention o Pneumococcal vaccine o Haemophilus influenzae type B vaccine o These are only usually given to high risk groups (e.g. elderly, splenectomy)

Explain the aetiology/risk factors of COPD

● Bronchial and alveolar damage is caused by environmental toxins (e.g. cigarette smoke, dust, nitrogen dioxide) - due to the innate and adaptive immune response to long term exposure to noxious particles and gases. ● The pathological changes result in increased resistance to airflow in the small conducting airways. ● There is increased compliance of lungs, air trapping and progressive airflow obstruction. ● The airways become obstructed so the lungs don't empty properly leading to trapped air o This is why FVC - the maximum amount of air you can breathe out in one breath - is lower. This reduction is most noticeable in the first second of the breath, hence FEV1, is even lower than FVC. Hence FEV1/FVC ratio is LOW. o Whereas, for air going in to the lungs, the TLC is usually higher due to air trapping. 1) RARE CAUSE: a-1 antitrypsin deficiency Though this is rare, consider it in young patients, who have never smoked, presenting with COPD type symptoms (and may have accompanying symptoms of cirrhosis). Alpha-1 antitrypsin is a protease inhibitor generate by the body to protect against unintended damage by proteases 2) Chronic Bronchitis: o Exposure to irritants and chemicals causes hypertrophy and hyperplasia of the bronchial mucinous glands and the goblet cells of the smaller airways (bronchiolitis - bronchial inflammation). This causes increased mucus production in small and large airways. The excess mucus causes obstruction Furthermore, smoking also makes cilia short and less mobile so the mucus is harder to move to back of throat - hence patients rely on coughing. The airway trapping causes a larger PCO2 in the lungs and decreased PO2. This increased CO2 also makes it harder for CO2 to leave blood and enter alveoli, hence, patients are hypoxic with high CO2 levels. o The mucus plugging can also cause infections 3) Emphysema: o Destruction and enlargement of alveoli due to inflammatory reaction to irritants. Enzymes break down structural proteins like collagen and elastin. o Alveoli permanently enlarge and lose recoil elasticity that keeps small airways open in expiration. o Progressively larger spaces develop called bullae (diameter > 1 cm) o In healthy lungs, during exhalation, air goes through the airways with high velocity hence at low pressure (Bernoulli principle). This lower pressure tends to pull the airway inward but airways full of elastin can withstand the pressure and do not collapse. Elastin holds the airway open allowing air to escape in exhalation. When elastin is lost and airway walls are weak, they collapse inwards during exhalation. The collapsed airway traps a tiny bit of air. o The loss of elastin also makes lungs more compliant during inhalation, hence air fills up in airways but has difficult leaving. o Septa, the alveolar walls, also start to break down and neighbouring alveoli coalesce into larger air spaces reducing the surface area for gas exchange. o The diminished gas exchange and air trapping causes shortness of breath. To counteract this, patient use pursed lip breathing to increase pressure inside the airways preventing them from collapsing. o Excessive energy loss on breathing can lead to weight loss. o The air trapping and hyperinflation over time causes barrel chest (inc A-P diameter), a flattened diaphragm and increased lung field lucency on CXR. ● In these areas of decreased gas exchange, blood vessels undergo vasoconstriction to shunt blood to areas with better exchange but as a large proportion of the lungs are not exchanging efficiently, this leads to increased vascular resistance and hence pulmonary hypertension - this means right side of heart must work harder and can lead to right-sided heart failure (cor pulmonale) **Risk factors: § cigarette smoking § advanced age § genetic factors § white ancestry § occupation § age ((Will see productive cough, wheeze, SOB)

Recognise the presenting symptoms of ARDS

● SOB ● Respiratory distress ● Cough ● Acute onset

Summarise the epidemiology of idiopathic pulmonary fibrosis

● RARE ● 6/100,000 ● More common in MALES (2x) (typically seen in 50-70 y/o)

Lung Volumes and Capacities

● Tidal breathing: amount of inspiration and expiration which meets metabolic demand ● Functional residual capacity: lung volume at end of a tidal breath ● Residual volume: lung volume at end of full expiration ● Key volumes ⇒ Total lung capacity: lung volume when you inspire all the way in and fill lungs up as much as possible ⇒ Vital capacity: how much air is in the confines of what we are able to inspire and expire ⇒ Functional residual capacity: volume of air in lungs when the outwards recoil of rib cage and inward recoil of lungs are in equilibrium ⇒ Inspiratory capacity: how much extra air you can take in on top of FRC

Recognise the signs of Aspergillus lung disease on physical examination

● Tracheal deviation (only with very large aspergillomas) ● Dullness in affected lung ● Reduced breath sounds ● Wheeze (in ABPA) ● Cyanosis (possible in invasive aspergillosis)

Summarise the epidemiology of extrinsic allergic alveolitis

● UNCOMMON ● 2% of occupational lung disease ● 50% of reported cases affect farm workers ● Geographical variation

Summarise the epidemiology of Aspergillus lung disease

● UNCOMMON ● Mainly occurs in the ELDERLY and IMMUNOCOMPROMISED

Summarise the epidemiology of COPD

● VERY COMMON (8% prevalence) ● Presents in middle age or later ● More common in males - this may change because there has been a rise in female smokers

reversible causes of reduced ventilation

e.g. airway obstruction due to reduced consciousness, opiate medication

causes of reduced gas exchange

e.g. pneumothorax, pneumonia, pulmonary oedema, PE

pleural effusion vs pulmonary oedema

effusion= abnormal accumulation of fluid in the pleural space oedema= excess fluid in the lungs

GOAL study

showed that ICS/LABA improved asthma controls at all levels of asthma severity

HRCT bronchiectasis

signet ring sign § Left image = normal CT scan § Right image = bronchiectasis (dilated bronchioles)

Lung cancer with low blood Na and high urine Na. What is most likely cancer?

small cell - produces SIADH (retain water so hyponatraemic in serum and more concentrated urine)

Which antibiotics are commonly given to patients with CAP and HAP pneumonia and why?

**CAP: Amoxicillin and Clarithromycin: Atypical mycoplasma (legionella) **HAP: § Metronidazole: anaerobes- HAP is often caused by gastric aspiration due to ineffective swallow/ post-op

What are key prognostic factors for sarcoidosis?

A significant minority of patients with pulmonary sarcoidosis have a poor prognosis Lung function impairment, fibrosis extent and pulmonary hypertension are key prognostic factors Role of FDG-PET in predicting response to treatment in selected patients, particularly in the context of fibrosis, to be further explored Improve our knowledge on how to prevent and treat severe sarcoidosis

What cells accumulate in sarcoidosis

Accumulation of oligoclonal T cells at sites of granuloma formation suggest antigen-specific cell-mediated immune response Kveim-Siltzbach spleen extract skin tests suggest specific immune response Features resemble other antigen-induced disorders, including chronic beryllium disease, hypersensitivity pneumonitis, and mycobacterialinduced granulomatous disease

Apart from X-ray, what else needed to diagnose sarcoid

Apart from selected scenarios, histology is needed to make a confident diagnosis of sarcoidosis Particularly so if immunosuppressive treatment being considered and/or diagnostic uncertainty (tb, lymphoma, lymphangitis, etc) The decision to move towards bronchoscopic histological confirmation to be reached on discussion with the patient, particularly if observation is being considered

Broad cohort outcomes for sarcoidosis

Stage I: isolated bilateral hilar lymphadenopathy (BHL): good outcome Stage II: pulmonary infiltrates + BHL: progression in one third at 5 years Stage III: pulmonary infiltrates, no BHL: progression in two thirds at 5 years Stage IV: overt fibrotic disease, significant mortality

DDx of cough

**Acute dry cough: § Asthma § Rhinitis/sinusitis with post-nasal drip § Upper respiratory tract infection § Drug-induced **Acute productive cough: § Lower respiratory tract infection § COPD § TB **Chronic dry cough: § Asthma § GORD § Post-nasal drip § Smoking § Lung cancer **Chronic productive cough: § Bronchiectasis § TB § Lung cancer

acute management of pneumonia

**Acute: •Oxygen (+ sit up patient) •IV fluids •IV painkillers •IV antibiotics •CPAP (if required)

Which biological therapy preferred in refractory sarcoidosis

(Infliximab favoured as first choice) REFRACTORY sarcoidosis: • Active and progressive disease despite conventional (non biologics) treatment • Toxicity or lack of tolerability to conventional treatments

Define extrinsic allergic alveolitis

(type of interstitial lung disease) DEFINITION: interstitial inflammatory disease of the distal gas-exchanging parts of the lung caused by inhalation of organic dusts. Also known as hypersensitivity pneumonitis. Many cases are caused by occupational exposure.

Recognise the presenting symptoms and the signs of sarcoidosis

** Asymptomatic in 20-40% 1) General Symptoms o Fever o Malaise o Weight loss o Bilateral parotid swelling o Lymphadenopathy o Hepatosplenomegaly o Hypercalcaemia o Hypercalciuria o Renal stones 2) Pulmonary Symptoms o Breathlessness o Dry cough o Chest discomfort o Minimal clinical signs 3) Musculoskeletal Symptoms o Bone cysts - terminal phalangeal (e.g. dactylitis) o Polyarthralgia o Myopathy 4) Eye Symptoms o Keratoconjunctivitis sicca (inflammation of the conjunctivitis and surrounding tissues due to the eyes being dry) o Glaucoma o Uveitis o Papilloedema 5) Skin Symptoms o Lupus pernio (red-blue infiltrations of the nose, cheeks, ears and terminal phalanges) o Erythema nodosum o Maculopapular eruptions 6) Neurological Symptoms o Lymphocytic meningitis o Space-occupying lesions o Pituitary infiltration o Cerebellar ataxia o Cranial nerve palsies o Peripheral neuropathy o Meningitis 7) Cardiac Symptoms o Arrhythmia o Bundle branch block o Pericarditis o Cardiomyopathy o Congestive cardiac failure

Identify appropriate investigations for asthma

**ACUTE: o Peak flow o Pulse oximetry o ABG - usually shows normal or slightly low PaO2 and low PaCO2 (hyperventilation) - if PaCO2 raised, transfer to HDU for ventilation o CXR - to exclude other diagnoses (e.g. pneumonia, pneumothorax) o FBC - raised WCC if infective exacerbation o CRP o U&Es o Blood and sputum cultures ** CHRONIC: o Peak flow monitoring at least 3 days/week for several weeks - often shows diurnal variation with a dip in the morning (>20% variation) o GOLD STANDARD: Pre- and post-bronchodilator spirometry - shows obstructive defect and usually a >15% improvement in FEV1 following b2-agonist or steroid trial o CXR: hyperinflation o Bloods - check: a) Eosinophilia b) IgE level c) Aspergillus antibody titres o Skin prick tests - helps identify allergens o Aspergillus serology

Features of life-threatening asthma

**CHEST acronym: § Cyanosis - SpO2 <92%, PaO2 <8 kPa § Hypotension § Exhaustion - Poor inspiratory effort, Confusion, Normal PCO2 § Silent chest § Tachy-/Brady- Arrhythmias § normal CO2 is BAD because if hyperventilating they should be getting rid of CO2, if breathing fast but unable to get rid of CO2 shows ventilation is bad and that they're getting tired and worse.

Acute COPD management ludley

**Cor pulmonale features include: § peripheral oedema, raised jugular venous pressure, systolic parasternal heave, loud P2 § use a loop diuretic for oedema, consider long-term oxygen therapy § ACE-inhibitors, calcium channel blockers and alpha blockers are not recommended by NICE

Induction and maintenance therapy for sarcoidosis

**Corticosteroids remain mainstay of treatment: 1) Induction: • Moderate dose oral prednisolone (20-40 mg od) • Or in selected cases with severe disease • High dose iv MP treatment (1 Gr x 3) followed by 20 mg od, then tapered 2) Maintenance: • Low dose 7.5-10 mg od **Immunosuppressants (or second line agents) • Methotrexate • Azathioprine *give these with or without hydroxychloroquine

Causes of dry and productive cough

**Dry: a) Acute: URTI (laryngitis, pharyngitis); Drugs (ACE inhibitors) b) Chronic: Lung cancer. GORD. Mesothelioma. c) Mixed: Heart failure Asthma: **Productive: a) Acute: Pneumonia (LRTI); TB. b) Chronic: Lung cancer. Bronchiectasis. Cystic fibrosis. c) Mixed: Heart failure; COPD.

Pneumoconiosis - Presentation

**History •SOB •Dry Cough •May be asymptomatic **Exam •Clubbing (asbestosis) •Bi-basal inspiratory crackles (asbestosis) •Decreased breath sounds (silicosis) •Signs of RHF or Pleural effusion **Risk factors •Occupation (coal-worker, builder) •Long history **Caused by inhalation of coal dust (coal worker), silica or asbestos (builder) particles which is directly cytotoxic and causes free-radical production by macrophages and the release of pro-inflammatory cytokines. **Exposure for over 15-20 YEARS and over time causes damage. *Silicosis - CW lung, asbestosis = asbestos i.e. builder **Long-term asbestos exposure can --> asbestosis (a FORM of pneumoconiosis) but also massively increases rates of mesotheliomas (cancer of the mesothelium) causing pleuritic chest pain also.

Hypersensitivity Pneumonitis - Presentation

**History •SOB on exertion •Dry cough •Fever and myalgia **Exam: •Clubbing (rare) •Bi-basal fine inspiratory crackles •Mild pyrexia- as Sx in the acute phase may mimic atyptical pneumonia **Risk Factors include: •Pets •Occupation! (farmer, plumber, malt-worker, mushroom-picker, birdkeeper) = BIG CLUE **In sensitised individuals', repeated inhalation of allergens can cause hypersensitivity reactions which vary depending on the antigen (may be animal proteins and microbes). In the acute phase, the alveoli are infiltrated by immune inflammatory cells. Early diagnosis and prompt allergen removal can stop, and can reverse disease progression so has a good prognosis. Chronic exposure can lead to granuloma formation and obliterative bronchitis. Examples include: - Farmer's lung (mouldy hay containing thermophilic actinomycetes) - Pigeon fancier's lung (blood on feathers and excrement) - Malt-worker's lung (Aspergillus clavatus) - Sugar-worker's lung/Bagassosis (thermoactinomyces sacchari) - Mushroom Worker's (compost with thermophilic actinomycetes) -Humidifier (water-containing bacteria) **Most ILDs are very similar; they differ by a little bit in each history (for example, here the major give away is the occupation)**

What might see on asthma examination

**History: •Cough •(Polyphonic Expiratory) Wheeze •SOB •Chest tightness (Symptoms are episodic - intermittent cough, wheeze, dysponoa/SOB -Diurnal variation (Sx worst in morning and night*//PEF low in morning)) **Examination: •May be normal •Nasal polyposis •Wheeze on auscultation • If acutely unwell then may be tachypneic, may also use accessory muscles to aid breathing (hyperinflated chest) **Risk factors include: •History of Atopy •FH of Asthma •Acute exacerbation risk/precipitating factors include cold, stress, infections, exercise, allergens (house dust mite, pets, pollen), pollution and drugs (B-blockers, NSAIDs) **Atopic triad: asthma, eczema, hayfever. Atopy is tendency to for T-lymphocyte to produce IgE by after exposure to allergens). Atopic triad = eczema, allergic rhinitis and asthma, also food allergies/urticaria

Bronchiectasis - Management

**Initial presentation: § Exercise and improved nutrition § Airway clearance therapy (postural drainage/vibration/oral hydration 2-3x daily for 15-30 mins - ((Like those vibration vests in 5 feet apart!))) § Inhaled bronchodilator e.g. Salbutamol/IB § Mucoactive agent (nebulized hypertonic saline - make it thinner) **Acute exacerbation •Antibiotics (Oral or IV): -Oral if mild-moderate existing disease -IV if severe underlying disease) •Increased airway clearance and continued maintenance therapy •Surgery (resection/transplant) if severe and unresponsive •3/+ acute exacerbations/year - may require long-term antibiotics

Classifying asthma attach

**Moderate asthma attack: • PEF at 50-75% of best or predicted • No signs of severe asthma **Severe Asthma attack: • PEF at 33-50% of best or predicted • respiratory rate ≥25/min • heart rate ≥110/min • Inability to complete sentences in one breath

Type 1 resp failure issue

**Principles of Type 1 Respiratory Failure: § Co2 is more soluble than O2 - *that's why O2 needs Hb to carry it § V/Q mismatch - either issue with ventilation or perfusion § Compensation: §Good lung cannot hyper-oxygenate (>100% sats) §Good lung *can* hyper-ventilate (remove CO2) **Ventilation issue: § lung cannot overoxygenate but CAN blow off lots of CO2 § if one bit of lung is wrong, get hypoxia as cannot compensate oxygen **Perufusion: less Hb --> less O2 --> hypoxic **Bad lung has low ventilation (V) or perfusion (Q) § Good lung *can* hyper-ventilate (remove CO2)

Environmental risk factors for sarcoidosis

**Risk factors: § Agricultural exposures § Insecticides § Microbial bioaerosols (work environments with mould/damp exposure) ** Protective factors: Cigarette smoking § may develop disease few years after stopping smoking

Type 1 and Type 2 Resp failure

**TYPE 1 One Issue: §Hypoxia § Focal § V/Q Mismatch **TYPE 2 Two Issues: §Hypoxia §Hypercapnic § Global § No Global Gas Exchange

List causes of type 1 and type 2 resp failure

**TYPE 1: §Acute asthma §Atalectasis §Pulmonary Oedema §Pneumonia §Pneumothorax §PE §ARDS **TYPE 2: §Acute severe asthma §COPD §Upper airway obstruction §Neuropathies (GBS, MND) §Drugs (opiates)

A week after discharge, Mrs Virginia is admitted to A&E again, this time with breathlessness. She is agitated but does not complain of any chest pain. She says the breathlessness came on suddenly while she was sat in her chair at home. An ECG taken in the ambulance showed sinus tachycardia but no other changes. Her oxygen saturations are 92% (on 28% oxygen), her respiratory rate is 28/min, her heart rate 112 bpm, her blood pressure 135/89 mmHg, and her temperature is 37.3.C. On examination, she has unilaterally decreased chest expansion and an area of hyper-resonant percussion, and reduced breath sounds throughout her left lung anteriorly and posteriorly. Her trachea is not deviated. What are the complications of pneumonia? What is most likely to have happened in this case?

**The complications of pneumonia include: a) Spread of infection: pleural effusion, empyema, abscess, septicaemia b) Damage to local structures: bronchiectasis, pneumothorax **Her breathlessness, apyrexia, and examination suggest a pneumothorax. **Pneumothorax is an uncommon complication of pneumonia but she also has COPD, which could have left her with bullae in her lungs that are prone to rupture (e.g. after a particularly vigorous cough). **You MUST exclude a tension pneumothorax by checking for tracheal deviation on examination. Mrs Virginia had no tracheal deviation and was stable. The signs on physical examination indicated a pneumothorax in her left lung, which was consistent with her chest radiograph. It can be difficult to distinguish a large bulla from a pneumothorax on a single chest radiograph, so in this case a comparison was made with the radiograph from her previous admission. If a previous radiograph is not available for comparison, CT of the chest will distinguish between the two. Mrs Virginia's pneumothorax was decompressed using a chest drain.

What specific signs should you look for on physical examination that would be consistent with an infectious cause? What other signs might you see, given her COPD?

**With regards to her likely infection, you should look for: § Systemic features: Is she febrile? Is she sweating? Is she tachycardic? § Respiratory distress: Is her respiratory rate increased? Is she having difficulty breathing - can she complete sentences, is she using her accessory muscles? Is she peripherally cyanosed? Is she confused (you can assess confusion with an Abbreviated Mental Test Score (AMTS); see Chapter 2). These give an idea of the severity of her condition. § Tender cervical lymphadenopathy: in a patient with a cough, this suggests infection in the upper respiratory tract. § Lungs: reduced chest expansion, focal dull percussion note, breath sounds (reduced in effusion, bronchial sounding in pneumonia), and vocal resonance. Vocal resonance distinguishes between consolidation, which increases resonance, and eff usion, which diminishes it. **Given her COPD, you should also note any: • Chest wall deformities (e.g. hyperexpansion or 'barrel chest'). • Intercostal recession: a sign of severe COPD. • Signs of right heart failure due to her COPD ('cor pulmonale'), such as peripheral oedema, raised jugular venous pressure (JVP), a parasternal heave, a loud or palpable P2 heart sound, or tricuspid regurgitation. • Asterixis: even though some COPD patients are chronic CO2 retainers, asterixis can be seen if COPD deteriorates and CO2 levels rise significantly.

What is kartageners syndrome?

**also known as primary ciliary dyskinesia. § Normally, the left testicle hangs lower than the right. § However, patients with Kartageners syndrome it is reversed. § This is due to the patient having situs inversus. § Cystic fibrosis can also present similarly if they were not diagnosed at a young age. § However, they would have other symptoms such as diabetes, diarrhoea and fat-soluble vitamin deficiencies. § Although some antibiotics may impair sperm function and motility, there is nothing in the history to suggest he is currently taking them. **Pathogenesis: § dynein arm defect results in immotile cilia **Features: § dextrocardia or complete situs inversus § bronchiectasis § recurrent sinusitis § subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)

Bronchopneumonia lung

**in infected lungs. get patches of lighter bits on lung = pus (is tougher rather than spongy). could be staph aureus. is bronchopneumonia. Now get it more commonly in people who smoke and have COPD = called acute exacerbation of COPD (get little infection, but because of poor lung --> very hypoxic and breathless) **if get lobar pneumonia: only get the consolidation in one lobe. Almost always called by streptococcus (90%). Affects all ages. Now just treat with penicillin (amoxicillin). If it's not streptococcus and GP gives amoxicillin, won't get better, then come to hospital, do cultures and find out which organism causes it. Other organism that often causes lobar pneumonia is mycoplasma - cover this with a macrolide. Hence prescribe: Penicillin (amoxcillin)+ macrolide (clarithromycin)

Pneumococcus and haemophilus influenzae

**two most common causative organisms for pleural effusion § pneumococcus (gram +ve purple/blue diplococcus) - TREAT WITH BENZYL PENICILLIN § haemophilus influenzae (gram-ve pink rod) - TREAT WITH AMOXICILLIN. **So for CAP: use amoxicillin as covers haemophilus and strep pneumoniae

Main reasons for using second line agents in sarcoidosis treatment

*Immunosuppressants are second line agents: • Methotrexate • Azathioprine • Low dose corticosteroids (7.5 -10 mg od) alone not sufficient to control disease • Need for corticosteroid sparing effects in patients requiring prednisolone long term • Intolerable corticosteroid side effect

Acute asthma management ludley

*Nebulized Ipratropium bromide is added for acute-severe or life-threatening asthma (or those with poor response to salbutamol therapy)

Immediate management of acute asthma

*Nebulized Ipratropium bromide is added for acute-severe or life-threatening asthma (or those with poor response to salbutamol therapy) Senior help should be sought BEFORE IV aminophylline is administered *slide taken from 2019 Chronic SOB by Alistair Ludley

Clinical consequences of apneoa

*treat the: § fragmented sleep § intermittent hypoxia (bad if they have other cardiac co-morbidities) § people tend to present saying am sleep **Sleep fragmentation can affect cognitive function: •Synaptic Homeostasis Hypothesis: Learning occurs via the formation of synapses •Neurones strengthen synapses when awake while interacting with the environment •Neurones renormalize synapses in sleep when the brain is 'off line'. **in UK - 1.5mil with severe sleep apnoea. **AHI = apnoei/hypopnea index - severe = >15 in an hour.

Types of non-invasive ventilation

- High flow nasal prongs -CPAP = Continuous Positive Airway Pressure- Delivers a continuous flow of oxygen at a preset pressure level -BiPAP = Bilevel Positive Airway Pressure- Delivers oxygen at two different pressure levels **Inspiratory Positive airway Pressure (IPAP) **Expiratory Positive Airway Pressure (EPAP)

Summarise the epidemiology of ARDS

1 in 6000 annually in UK

Management of acute cardiogenic pulmonary oedema

1) ABCDE Assessment. Position upright 2) § Give Oxygen if hypoxic. § High Dose IV Diuretics - FUROSEMIDE Bolus. § Treat Cause - Beta Blockers for arrhythmia. Re-Assess. 3) If improved, Regular Diuretics, Fluid Restriction, Daily Weights - lose 1kg a day (1 Litre). 4) If not improved, Consider Nitrate Infusion (i.e. GTN) if systolic BP >100 mmHg. Consider Continuous Positive Airway Pressure (CPAP) -Recruits alveoli -Drives fluid out of alveolar spaces.

Management of acute COPD

1) ABCDE assessment Are there any signs of Decompensated T2RF? 2) If yes, Call for help -> ITU/HDU for possible NIV § Oxygen - Aim Sats 98% § Bronchodilators: Salbutamol +/- Ipratropium, § Steroids: PO Prednisolone/IV Hydrocortisone. RE-ASSESS 3) If no, § Oxygen - Aim Sats 94-98% or 88-92% if T2RF Via Venturi Mask § Bronchodilators: Salbutamol +/- Ipratropium, § Steroids: PO Prednisolone/IV Hydrocortisone § Antibiotics: If needed. RE-ASSESS. 4) If not improved, send to ITU/HDU. If improved: § Continue Bronchodilators, § Steroids (5-7 days), § Wean O2 § Complete Course of antibiotics § Chest Physio - If sputum+++ § Inhaler technique & Smoking Cessation advice § Pulmonary Rehabilitation

Management of life-threatening asthma

1) ABCDE assessment Are there any signs of Severe or life threatening Asthma? **IF YES: § Call for help -> ITU/HDU § Oxygen- Aim Sats 98% § Bronchodilators: Salbutamol +/- Ipratropium, IV Magnesium § Steroids: PO Prednisolone/IV Hydrocortisone AND RE-ASSESS **IF NO: § Oxygen - Aim Sats 98% § Bronchodilators: Salbutamol +/- Ipratropium, IV Magnesium § Steroids: PO Prednisolone/IV Hydrocortisone RE-ASSESS. **If not improved --> ITU/HDU **If improved: § Continue Bronchodilators, Steroids (5-7 days), Wean O2 § Serial PEF - Discharge if PEF ≥ 75% § TAME asthma (Technique, Avoid triggers, Monitor PEF, Educate)

Once a patient has been diagnosed with chronic heart failure, there are several medications that can help reduce their mortality. What are the key trials demonstrating mortality benefi t in chronic heart failure?

1) ACE inhibitors: the SAVE1 and SOLVD2 trials both showed that ACE inhibitors can significantly reduce mortality from chronic heart failure, from 8-28% depending on how symptomatic the patient is (more symptomatic patients gain more benefit). In patients who cannot tolerate ACE inhibitors because of their side-effects (e.g. cough), the ELITE II3 study and Valsartan Heart Failure Trial4 have shown that angiotensin II receptor blockers (A2RB) are as effective as ACE inhibitors in reducing mortality. However, a third trial (RESOLVD5) had to be stopped because of increased mortality in the group receiving the A2RB. 2) β-Blockers: Several trials6 including CIBIS-II7 and MERIT-HF8 have shown that β-blockers reduce mortality from chronic heart failure by about 25%. 3) Spironolactone: the RALES9 trial found that the aldosterone receptor spironolactone reduced mortality from chronic heart failure by about 30%.

Good history-taking begins with listening to whatever the patient has to tell you, followed by open questions to avoid leading the patient's answers. You can then move on to specifi c questions that can help narrow your differential diagnosis. What specific questions might you ask someone who presents with shortness of breath?

1) About SOB 2) Risk factors 3) Associated symptoms GOING INTO DETAIL NOW: 1) About the shortness of breath: a) Timing of onset? This is crucial because vascular (e.g. PE) and mechanical (e.g. pneumothorax, foreign body) pathologies typically present suddenly. At the other end of the spectrum, it may take weeks or months before diseases such as lung cancer or pulmonary fibrosis cause noticeable dyspnoea. b) Alleviating or exacerbating factors? Most shortness of breath will be worse on exertion. However, heart failure will also be worse on lying fl at; asthma will usually be worse at certain times of the year (e.g. due to pollen allergy), in certain places (e.g. in dusty environments, or when the pets are around), during intense cardiovascular exercise (e.g. running), or in the early hours of the morning. Psychogenic hyperventilation will be worse at times of anxiety and stress. 2) Risk factors: a) Smoking? Never forget to ask about smoking and to quantify this in terms of 'pack years' smoked (1 pack = 20 cigarettes; 20 cigarettes a day for a year = 1 pack year). b) Pets? The patient may be allergic to pets, especially new ones. c) Occupational history? Ask about jobs - there are still lots of people who have been exposed to asbestos, silica dust, and coal particulates in past jobs and who are at risk of pneumoconioses. d) Medications? Certain drugs can cause pulmonary fibrosis, e.g. amiodarone, methotrexate, cyclophosphamide, bleomycin, hydralazine, busulphan. e) Nutritional status? Even in today's Western societies, some patients present with malnourishment - typically elderly patients who live alone on a 'tea and toast' diet or homeless people with alcoholism who fail to maintain an adequate diet. Such patients are at risk of anaemia and thus shortness of breath. 3) Associated symptoms a) Cough? A cough points strongly towards a respiratory pathology. The nature of the cough is important: Is it productive? What colour is the sputum? Is there any blood? When does the cough occur? What does the cough sound like? A persistent, productive cough over the last few days suggests pneumonia; a persistent, productive cough on most days of the past 3 months and spanning years suggests chronic bronchitis; a dry cough present mainly during the episodes of shortness of breath or at night suggests asthma, but may also be a feature of left ventricular failure; blood-stained sputum may suggest a PE, lung cancer, or a cavitating pneumonia. Certain pathologies are associated with characteristic sounding coughs - croup is said to sound like a barking seal, whereas recurrent laryngeal nerve palsy (sometimes associated with lung cancer) can produce a bovine cough. b) Chest pain? If there is chest pain, is it pleuritic? Pleuritic chest pain can suggest pneumonia, a PE, or a pneumothorax, because these often involve the parietal pleura. Non-pleuritic chest pain could indicate a cardiovascular pathology. c) Muscular weakness or fatigue? Neuromuscular diseases (e.g. Guillain- Barr. syndrome, myasthenia gravis, Lambert-Eaton syndrome, polymyositis, motor neuron disease) will usually be accompanied by muscular weakness or fatigueability. d) Tender limbs? Pulmonary emboli can originate from anywhere in the venous system. Patients usually only notice deep vein thrombosis (DVT) if it occurs in a limb as this will usually cause inflammation - a swollen red, tender, warm, shiny looking limb. approximately 35% of fatal PEs originate from calf DVTs. e) Weight loss? Night sweats? Loss of appetite? These are 'red flag' signs that suggest that a highly metabolic, systemic inflammatory process is going on - often a cancer. Always ask these questions, regardless of the presentation. f) Loss of blood? Anaemia can cause or exacerbate shortness of breath, so always ask about heavy menstrual bleeding (in women) and melaena.

You are called to see a 39-year-old female in the medical assessment unit who has been bought in from home by ambulance with severe shortness of breath. She is able to give a history but is extremely short of breath, which has increased over the previous 24 hours. She has noted intermittent shortness of breath and central chest discomfort over the past few months and has also experienced a cough, associated with wheeze, that troubles her in the early morning. Sputum has been clear and there has been no haemoptysis. Her exercise tolerance has reduced and she has experienced dyspnoea on exertion. She has no other symptoms of note and no other significant medical history. She is married with 2 children and is on no medication apart from the oral contraceptive pill. On examination, she is short of breath at rest and finds it hard to complete sentences. Heart rate is 110bpm and regular, blood pressure 110/65mmHg and apyrexial. She is not cyanosed. Diffuse wheezes are audible throughout her chest. Heart sounds are normal. You do not attempt formal abdominal or neurological examination. Initial blood results (FBC, U&Es) are unremarkable. 1) Which is the most likely diagnosis? 2) Which 3 further investigations are indicated whilst she is in A+E?

1) Acute severe asthma attack - § This patient gives a good history of asthma with preceding bouts of dyspnoea and chest discomfort and nocturnal cough and wheeze. § The history of preceding symptoms makes pneumonia and PE unlikely and clinical findings do not fit for a pneumothorax § This does not fit for extrinsic allergic alveolitis, which is associated with episodic dyspnoea following exposure to allergen and a dry cough with fever (no wheeze). § There is no history of industrial dust exposure to suggest pneumoconiosis § Bronchiectasis is associated with production of large amounts of purulent sputum. 2) ECG, peak flow, blood gases. § Following initial observations and investigations, treatment of asthma should be initiated at once. It is important, where possible, to record the patients presenting peak flow, although it may be difficult to obtain in distressed patients. § Sputum culture does not need to be performed immediately and is often not needed at all, unless there is evidence suggestive of infection § There is no indication for bronchoscopy here § In the absence of clinical evidence of a large pneumothorax (which may be associated) chest radiograph can wait.

1) The patient's observations are stable and so you decide this is a simple CAP that does not require hospital admission and can be managed at home. Which antibiotic therapy would you prescribe? There is no volunteered history of drug allergy 2) Before discharge, the patient appears more unwell and, on review, your registrar decides the patient's condition is more serious and he needs to stay in. Which antibiotics do you think he should receive?

1) Amoxicillin § For non-allergic patients with clear evidence of consolidation, who can be managed at home, single agent therapy with amoxicillin is appropriate. § For those with more severe disease admitted to hospital, the combination of co-amoxiclav (to cover resistant strains of H influenzae- approximately 15%) and a macrolide (clarithromycin, erythromycin, etc) is correct. § Patients admitted to hospital with bronchopneumonia or without radiographic evidence of consolidation should not be given both antibiotics - they do not have lobar pneumonia! 2) Co-Amoxiclav and Clarithromycin. § Most hospitals use a severity scoring system to help determine where a patient should be managed and with which antibiotics. BTS guidelines suggest that patients with a CURB65 score of 3 or higher should be admitted to hospital and given dual therapy with an intravenous combination of a "broad spectrum ß-lactamase stable antibiotic such co-amoxiclav, together with a macrolide such as clarithromycin". § Those with a mild penicillin allergy (rash only) may have a 2nd or 3rd generation cephalosporin instead of the co-amoxiclav, although patients with a history of severe allergy should avoid cephalosporins as there is a risk of crossover allergy

Explain the aetiology/risk factors of asbestos-related lung disease (incl. asbestosis/ mesothelioma)

1) Asbestosis ⇒ There are three different types of asbestos Chrysotile (white asbestos) is the least fibrogenic. Crocidolite (blue asbestos) is the most fibrogenic. Amosite (brown asbestos) has intermediate fibrogenicity. ⇒ Asbestos was commonly used in the building trade hence always ask about OCCUPATION in resp history - commonly in shipyard workers! ⇒ Degree of asbestos exposure is related to degree of pulmonary fibrosis. ⇒ Inflammation gradually causes mesothelial plaques in the pleura ⇒ Causes increased risk of bronchial adenocarcinoma and mesothelioma. **RFs: o cumulative dose of inhaled asbestos o cigarette smoking 2) Mesothelioma: ⇒ It is associated with occupational exposure to asbestos but the relationship is complex. ⇒ 90% report previous exposure to asbestos, but only 20% of patients have pulmonary asbestosis. The latent period between exposure and development of tumour can be up to 45 years. ⇒ Malignant pleural mesothelioma rarely spreads to distant sites but most patients present with locally advanced disease. **RF: § asbestos exposure § asbestos exposure during home maintenance and renovation § age 60 to 85 years § male sex § family history

Explain the aetiology/risk factors for Aspergillus lung disease

1) Aspergilloma o Growth of an A. fumigates mycetoma ball in a pre-existing lung cavity (e.g. post-TB/sarcoidosis, old infarct or abscess) 2) Allergic Bronchopulmonary Aspergillosis (ABPA) o Colonisation of the airways by Aspergillus fumigatus leads to IgE and IgG-mediated immune responses o Usually occurs in atopics, ASTHMATICS and CF patients o The release of proteolytic enzymes, mycotoxins and antibodies leads to airway damage - this initially causes bronchoconstriction but as inflammation persists, permanent damage occurs causing bronchiectasis o Presents as asthma complicated by bronchial obstruction, fever, malaise, expectoration of brownish mucus plugs, peripheral blood eosinophilia, and haemoptysis. 3) Invasive Aspergillosis o Invasion of Aspergillus into lung tissue and fungal dissemination o This occurs in immunosuppressed patients (e.g. neutropenia, steroids, AIDS, leukaemias) or after broad-spectrum antibiotic therapy

Identify appropriate investigations for Aspergillus lung disease

1) Aspergilloma: o CXR ● May show a round mass with a crescent of air around it ● Usually found in the upper lobes o CT or MRI - may be used if CXR is unclear o NOTE: sputum cultures may be negative if there is no communication between the cavity colonised by Aspergillus and the bronchial tree o Strongly positive serum precipitins o Aspergillus skin test - +ve in 30% 2) ABPA: o Immediate skin test reactivity to Aspergillus antigens o Aspergillus-specific IgE radioallergosorbent test - RAST o Eosinophilia o Raised total serum IgE o Raised specific serum IgE and IgG to A. fumigatus - serum precipitins o Aspergillus in sputum o CXR ● Transient patchy shadows ● Segmental collapse or consolidation ● Distended mucous-filled bronchi ● Signs of complications: ▪ Fibrosis in upper lobes ▪ Bronchiectasis o CT ● Lung infiltrates ● Central bronchiectasis o Lung Function Tests ● Reversible airflow limitation ● Reduced lung volumes/gas transfer 3) Invasive Aspergillosis: o Aspergillus is detected in cultures or by histological examination o Bronchoalveolar lavage fluid or sputum may be used diagnostically o Chest CT and and serum Aspergillus galactomannan antigen test ● Nodules surrounded by a ground-glass appearance (halo sign) ● This is caused by haemorrhage into the tissue surrounding the fungal invasion

Generate management plan for acute asthma attack

1) Assess severity - life-threatening or severe attack? Using PEF, ability to speak, RR, pulse rate, O2 sats **ACUTE - usually presents with acute breathlessness and wheeze a) ABCDE approach b) Give O2 and monitor O2 sats, ABG, PEFR High-flow oxygen using face mask, Venturi mask or nasal cannulae. Adjust flow rates as necessary to maintain oxygen saturation of 94-98% b) 5mg salbutamol nebulised every 15 mins c) 0.5mg ipratropium bromide nebulised d) 100mg IV hydrocortisone OR 40mg PO prednisolone e) If no improvement: 1.2-2 mg IV Mg sulfate over 20mins AND get senior help ** Note: must monitor ECG for arrhythmias due to electrolyte disturbances o If still no improvement: IV aminophylline o If still no improvement: intubation and ventilation in ICU o OR, if improving within 15-20mins: § Give nebulised salbutamol every 4 hours § Prednisolone 40-50mg PO OD 5-7 days § Monitor peak flow and O2 sats, aim 94-98% with supplemental if needed o IMPORTANT: a normal PCO2 is a BAD SIGN in a patient having an asthma attack - This is because during an asthma attack they should be hyperventilating and blowing off their CO2, so PCO2 should be low SO A normal PCO2 suggests that the patient is fatiguing Overall: §OSHITME§ § patients who fail to respond require senior critical care support and should be treated in an appropriate ITU/HDU setting. Treatment options include: intubation and ventilation OR extracorporeal membrane oxygenation (ECMO) **OTHER: ● Treat underlying cause (e.g. infection) ● Give antibiotics if it is an infective exacerbation ● Monitor electrolytes closely because bronchodilators and aminophylline causes a DROP in K+ ● Invasive ventilation may be needed in severe attacks ** DISCHARGE when: ● PEF > 75% predicted ● Diurnal variation < 25% ● Inhaler technique checked ● Stable on discharge medication for 24 hours ● Patient owns a PEF meter ● Patient has steroid and bronchodilator therapy ● Arrange follow-up

On examination, Mrs Virginia looks sweaty and unwell. She is cachectic and has a 'barrel chest'. Her fingers are tar-stained. She is tachycardic and tachypnoeic with a pulse of 107 bpm and a respiratory rate of 22/min. Her temperature is 38.5.C. She has poor chest expansion, an expiratory wheeze, hyperresonant percussion note throughout but with dullness at the right lung base, and bronchial breath sounds in the same place. Vocal resonance is increased over the area of percussion dullness. You find no lymphadenopathy in the neck. She is not confused, with an AMTS of 9/10. What investigations would you like to request?

1) Blood tests: § Arterial blood gas (ABG): you will want to assess her gas exchange to monitor her progress (she should also be on pulse oximetry) and ensure she doesn't develop respiratory failure. Keep in mind that she has COPD and that her baseline may therefore be different from a 'normal' baseline, e.g. slightly elevated CO2 levels may be normal for her. § Full blood count (FBC): the white cell count should be raised in infection, with a neutrophilia if it is a bacterial infection. § C-reactive protein (CRP): will also be raised if there is an underlying infective process. § Urea and electrolytes (U&Es): the patient's U&Es may be deranged if she is dehydrated and consequently hypoperfusing her kidneys. Urea is an indicator of severity and influences prognosis. 2) Imaging: § Chest radiograph: this may reveal areas of consolidation, potentially in a lobar pattern, or a pneumothorax (which are more common in patients with COPD). § Electrocardiogram (ECG): you must perform this to rule out ischaemia or atrial fibrillation secondary to pneumonia. It may also show right heart strain in some patients with COPD. **Note: sputum cultures are rarely useful as the sputum will contain all the commensal flora that is normally found in the upper respiratory tract. However, bronchoalveolar lavage may be performed to get a sputum sample free of this flora and thereby identify the off ending organism, but this is only done if a pneumonia does not respond to conventional antibiotic treatment suggesting infection with an atypical organism.

Which lung conditions manifest over days / weeks?

1) Cancer - often normal exam, but often see in chest x ray 2) TB - often normal exam, but often see in chest x ray 3) Pneumocystis - may be in risk group, subacute breathlessness, exercise desaturation

List some broad mechanisms that can lead to shortness of breath. Give an example of a disease that falls under each of these mechanisms.

1) Insufficient oxygen entering the lungs - COPD 2) Insufficient oxygen entering the blood - emphysema 3) Insufficient oxygen reaching the tissues - anaemia 4) Increased respiratory drive - acidaemia

Identify appropriate investigations for idiopathic pulmonary fibrosis

1) Bloods o Raised CRP and immunoglobulins o ABG ▪ Normal in early disease ▪ PO2 decreases with exercise ▪ Normal PCO2, which rises in late stage disease o ANA and Rheumatoid Factor ▪ 1/3 of patients are positive for ANA or RF 2) CXR o Usually NORMAL at presentation o Early disease may show ground glass shadowing o Later stage disease shows bilateral lower zone reticulonodular shadowing, signs of cor pulmonale and, eventually, honeycombing 3) High-Resolution CT o Should be done in all suspected IPF patients. More sensitive in early disease than CXR. Might obviate the need for biopsy 4) Pulmonary Function Tests o Spirometry - Restrictive features (reduced FEV1 and FVC, with preserved or increased FEV1/FVC) o Decreased lung volumes o Decreased lung compliance o Decreased total lung capacity ● Bronchoalveolar Lavage - exclude infections and malignancy ● TC-DTPA scan may reflect disease activity ● Lung Biopsy - gold standard for diagnosis but not always needed, histological changes are referred to as usual interstitial pneumonia (UIP) ● Echocardiography - to check for pulmonary hypertension

What investigations would you like to arrange for likely CHF patient with SOB?

1) Bloods • Full blood count (FBC): looking for anaemia. • Blood cholesterol, glucose, and HbA1c: abnormal cholesterol levels (total >5 mM, low-density lipoprotein (LDL) >3 mM or high-density lipoprotein (HDL) <1 mM) and abnormal glucose levels (random >11.1 mM or fasting >7 mM) will give clues about risk factors for ischaemic heart disease, the main cause of heart failure. Mrs Finnegan is a known diabetic, so her HbA1c level will be useful as this is a measure of her glucose control over the preceding 60 days (non-diabetic HbA1c <6.5%). • Thyroid function tests (TFTs): hyperthyroidism can cause a tachyarrhythmia and high-output cardiac failure. • Urea and electrolytes (U&Es): if you think the patient might have excess fluid and therefore there is a chance you might start diuretics to offload some fluid, you need a baseline of electrolyte levels and renal function. It is best to take all the bloods now, both to avoid putting a needle in the patient twice and because an earlier baseline is better. o BNP - released when ventricular cells are excessively stretched (low specificity for heart failure) 2) Imaging • Chest radiograph: looking for signs of heart failure, pneumonia, bronchiectasis, or fibrosis (pneumothorax and collapse are unlikely given the examination findings). 3) Electrocardiogram (ECG): the ECG is nearly always abnormal in patients with heart failure (indeed, an entirely normal ECG has a negative predictive value for heart failure of about 98%). An important cause of heart failure is necrosis to areas of the heart caused by MI. Diabetics often have 'silent infarcts', which are not noticed by the patient. The presence of pathological Q-waves or a bundle branch block on the ECG would suggest a previous, full-thickness MI. 4) Other: If the history were suggestive of lung pathology (rather than cardiac pathology) as the cause of breathlessness, you might consider performing: • Peak expiratory flow rate (PEFR). Th is can be used to stratify the severity of an asthma attack in chronic asthma. • Spirometry. Th is is used to distinguish between obstructive and restrictive lung disease. In obstructive airways disease (e.g. asthma, COPD, bronchiectasis), the bronchi are narrowed by mucus such that less air can be forcibly exhaled during a single second (forced expiratory volume in 1 second; FEV1 <70% of predicted), but the total lung capacity is not reduced (forced vital capacity; FVC >70%). In restrictive airways disease (e.g. pulmonary fibrosis), the total lung volume is reduced (FVC <70%) but the amount of air that can be exhaled in the first second remains the same (FEV1 >70%).

IPF (idiopathic pulmonary fibrosis) investigations

1) Bloods, ABG, Biopsy*: a) Bloods: -CRP and Ig raised -ANA and Rheumatoid factor (1/3 patients positive for either) b) ABG normal in early disease, PO2 decreases with exercise and normal PCO2 which rises in late stage disease c) Biopsy is the gold standard (however not always appropriate/needed), but usually high-resolution CT is usually appropriate, especially sensitive for early presentation 2) CXR •Ground glass (earlier) •Reticulonodular shadowing (fibrosis) •Cor pulmonale (later) 3) High resolution CT •Ground glass appearance •Honeycombing 4) Lung function tests •Restrictive pattern (FEV1:FVC>0.7)

Hypersensitivity Pneumonitis - Investigations

1) Bloods, ABG: a) Bloods § FBC - leukocytosis, neutrophilia, lymphopenia § ESR b) ABG - reduced PO2 and PCO2 c) Serology Test for IgG to fungal/avian antigens (not diagnostic as they may be found in normal individuals) 2) CXR: •Often normal in acute episodes, but may be patchy nodular infiltrates •May show ground-glass signs, reticulonodular shadowing, cor pulmonale and honeycombing • Fibrosis may be seen in chronic cases - upper zone mottling/consolidation 3) High resolution CT: • More accurate than a CXR, helps to confirm diagnosis of chronic HP • Detects early changes • May show patchy, ground glass shadowing and nodules, extensive fibrosis 4) Lung function tests •Reduced TLC and gas transfer during acute attacks •Reversible restrictive defect (low FEV1, FVC) --> Preserved/increased FEV1/FVC ratio •Restrictive pattern (FEV1:FVC >0.7) 5) Broncho alveolar lavage •Increased cellularity (Increased lymphocytes and mast cells)

Identify appropriate investigations for pneumonia

1) Bloods: o FBC - raised WCC o U&Es o LFT o CRP o Blood cultures o ABG (assess pulmonary function) o Blood film - Mycoplasma causes red cell agglutination 2) CXR: o Lobar or multilobar (patchy) shadowing o Pleural effusion or cavitation o NOTE: Klebsiella often affects upper lobes o May detect complications (e.g. lung abscess) 3)Sputum/Pleural Fluid - MC&S 4) Urine - Pneumococcus and Legionella antigens - in severe cases, check for Legionella (sputum culture, urine antigen) 5) Atypical Viral Serology 6) Bronchoscopy and Bronchoalveolar Lavage - if Pneumocystis carinii pneumonia (immunocompromised) is suspected, or if pneumonia fails to resolve

Identify appropriate investigations for sarcoidosis

1) Bloods: o High serum ACE in 60% o High calcium ((granulomatous tissue produces ectopic 1a-hydroxylase so there is increased calcitriol which causes high Ca) o High ESR o FBC - WCC may be low due to lymphocyte sequestration in the lungs o High Immunoglobulins o LFTs - high ALP + GGT 2) 24 hr Urine Collection: o Hypercalciuria 3) Tuberculin skin test -ve in 2/3 4) CXR: o Stage 0 - may be clear o Stage 1 - bilateral hilar lymphadenopathy o Stage 2 - stage 1 with peripheral pulmonary infiltration and paratracheal node enlargement o Stage 3 - peripheral pulmonary infiltration alone o Stage 4 - pulmonary infiltration and fibrosis, bulla formation (honeycombing), pleural involvement ● High-Resolution CT Scan o Check for diffuse lung involvement ● Gallium Scan - shows areas of inflammation ● Pulmonary Function Tests - may be normal or o Low FEV1 o FVC shows restrictive picture ● Bronchoscopy and Bronchoalveolar Lavage o High lymphocytes o High CD4: CD8 ratio ● Transbronchial Lung Biopsy (or lymph node biopsy) § Tissue biopsy can be from lung, liver, lymph nodes, skin nodules or lacrimal glands § Diagnostic § Shows non-caseating granulomas consisting of: o Epithelioid cells (activated macrophages) o Multinucleate Langerhans cells o Mononuclear cells (lymphocytes)

The chest x-ray shows probable primary lung carcinoma. Which three investigations are likely to confirm the diagnosis? What are the two possible causes of the patient's chest pain?

1) Bronchoscopy, Lung biopsy, CT scan of the chest/abdomen. CT is done to define the nature and location of the mass. Abdominal CT will be included as it needs to be done as part of the staging of lung cancer. Most patients will undergo bronchoscopy. A tissue diagnosis is required in many cases of lung cancer, particularly if the staging indicates that the tumour is operable, so lung biopsy is often done. PET scanning is used in patients who have been staged by CT and are being considered for curative surgery. Bone scan will only be done if bony metastases are suspected. 2) Chest wall involvement by the tumour, Rib metastases. Chest pain is associated with complication of a primary lung nodule - chest wall involvement and presence of metastases in the bones causing a 'pleuritic' type of pain, which may be sharp, well localised and is worse with movement.

Diagnosing a PE

1) CTPA - . Gold Standard 2) if can't do CT for example if patient is pregnant, can do a V/Q scan- will demonstrate perfusion defects and a V/Q Mismatch 3) Use scoring tools to help your diagnosis i.e. Wells score and Geneva score What is PE? Venous Thrombi that pass into the pulmonary circulation causing occlusion. Normally arise from DVTs **Risk factors: • Immobilisation • Malignancy • Recent Surgery • HRT/COCP • Thrombophilias

Identify appropriate investigations for pneumothorax

1) CXR o It will show a dark area of film with no vascular markings o Fluid level may be seen if there is any bleeding o Note: a CXR should not be performed for tension pneumothorax suspicion as it can delay immediate necessary treatment 2) ABG o Check for hypoxaemia

Pneumoconiosis - Investigations

1) CXR: •Asymptomatic (simple) - micronodular mottling •Symptomatic (complicated) - bilateral lower zone reticulonodular shadowing and pleural plaques, eggshell calcification (silicosis) 2) CT: •Fibrotic changes 3) Lung function tests: •Restrictive pattern (FEV1:FVC >0.7) **Reticulonodular shadowing is like lines and dots, unlike PO shadowing which is more fluffy - image from Amir Sams DPD lecture

A 68-year-old male patient has been referred to chest outpatients with a 6-month history of cough with associated lethargy and he has also lost 4kg in weight. The cough is intermittently productive of mucus-like material and he has noticed streaks of blood also in the sputum several times. He has noted mild shortness of breath on exertion. He has no chest pain and no other symptoms of note. He is a retired dentist and is married with one child. He is a non-smoker (and has never smoked) and does not drink alcohol to excess. His only previous medical history of note is a history of what he thinks was thoracic tuberculosis when he was a child. On examination, he looks mildly underweight, but otherwise well with no clubbing. You note decreased air entry and dullness to percussion over the right lung apex, but physical examination is otherwise unremarkable. 1) What is your differential diagnosis at this stage? 2) What initial investigations would you request?

1) Carcinoma of the bronchus 2) Mycetoma (aspergilloma) 3) Reactivation of thoracic tuberculosis The initial symptom complex is concerning - cough, weight loss, haemoptysis and some shortness of breath - and lung carcinoma must be excluded. Reactivation of tuberculosis could present like this. Fibrosing alveolitis tends to present with dyspnoea, clubbing and fine late inspiratory crackles on auscultation. Asbestosis may cause lung fibrosis and pleural plaques (and lung cancer). There is no definite evidence in the history to suggest occupational exposure. Late onset asthma may cause cough, shortness of breath and wheeze - weight loss and haemoptysis are more sinister symptoms. *Aspergillus species can affect the lung in 5 ways: 1) Asthma - type I hypersensitivity 2) Allergic bronchopulmonary aspergillosis - type I and III hypersensitivity with recurrent asthma and bronchial damage and bronchiectasis. Associated with positive aspergillus skin test, elevated IgE, eosinophilia, serum precipitins. 3) Mycetoma (aspergilloma) - fungus ball forming in a pre-existing lung cavity 4) Invasive aspergillosis (in the immunosuppressed) with high mortality 6) Extrinsic allergic alveolitis - recurrent dyspnoea and dry cough and ultimately fibrosis 2) Chest radiograph, Sputum sample for microscopy and culture, Lung function tests, Sputum sample for cytology. Lung function tests are performed in many patients with dyspnoea to assess if there is an obstructive/restrictive defect or any reversibility of symptoms. Blood cultures/gases not indicated.

The chest radiograph confirms right apical opacity which contains curvilinear lucency consistent with cavitation and there is also a probable mass within the cavity, outlined by the crescent of lucency. These radiographic appearances are highly suggestive of mycetoma formation. Which of the following other conditions may cause a cavitating mass on chest radiograph?

1) Carcinoma of the bronchus 2) Squamous cell carcinoma metastasis 3) Pulmonary infarct 4) Wegener's granulomatosis 5) Bacterial lung abscess **Fibrosing alveolitis causes increased interstitial lung density (lines) and mesothelioma causes a pleural mass.

A 73-year-old man presents with a few months history of non-productive cough and 2 recent episodes of haemoptysis. He is also complaining of left sided chest pain that is not relieved by NSAIDs. The patient used to smoke occasionally. He is not on any regular medication. On examination, he is slightly breathless. His chest is clear, however, and there are no other abnormal findings. He is apyrexial. Blood results: Hb 113135-180 g/L WCC 6.74-11 x109/L Plt 350150-450 x109/L Na+ 135136-145 mM K+ 4.03.5-5.1 mM Ur 61.7-8.3 mM Cr 2562-106 µM Ca2+ 3.0 2.15-2.55 mM 1) What you do next as your initial investigation?

1) Chest x-ray - The primary pathology appears to be in the lung, so a chest x-ray will be the most rapid and valuable next step.

Management of CAP/atypical and HAP ***VERY IMPORTANT SLIDE***

1) Community-acquired pneumonia (CAP): Amoxicillin (co-amoxiclav if severe) 2) Hospital-acquired pneumonia (HAP): Staph aureus Pseudomonas aeruginosa Klebsiella § If staph: Flucloxacillin § If MRSA: Vancomycin § If pseudomonas: Tazocin + gentamicin 3) Atypical pneumonia: Clarithromycin 4) Aspiration pneumonia: Metronidazole ((Commonly: amoxicillin + clarithromycin) **Amoxicillin and co-amoxiclav = penicillin **Clarithromycin = macrolide **Flucloxacillin = penicillin **Gentamicin = aminoglycoside **Vancomycin = glycopeptide **Metronidazole = nitroimidazole **Cefuroxime = carbapenem

A 54-year-old man is referred for assessment to hospital by his GP with suspected pneumonia. 1) Which 2 aspects of his case might justify admitting him to hospital rather than managing him at home? 2) On examination, which of the following observations would indicate that inpatient management may be necessary? § Atrial fibrillation 100/min § Blood pressure 110/55 mmHg § Bronchial breathing § Cervical lymphadenopathy § Respiratory rate of 28/minute

1) Confusion and Respiratory rate of 32/min § NICE recommends using the CURB65 score for assessing the severity of pneumonia § Confusion and raised respiratory rate >30 are worrying signs that may indicate respiratory failure or sepsis. § Cough, fever, chest pain and weight loss are not in themselves indications for admission. § Other non-acute factors that may drive admission, include the patient's social situation and co-morbidity, which may affect whether it is possible for him to be managed at home. 2) Blood pressure 110/55 mmHg § A high respiratory rate suggests significant hypoxia. However, the cut off for the CURB65 severity score is a RR >= 30 breaths per minute. § Atrial fibrillation may be due to pneumonia but may well be an unrelated matter. § Bronchial breathing may occur in any pneumonia and is not necessarily a marker of severity § Cervical lymphadenopathy is unrelated to pneumonia severity. § A systolic BP <100 or a diastolic BP <60 mmHg is a sign indicating a worse prognosis.

Mr Morris tells you he has been coughing up frank blood. He feels it is a lot. When you try to quantify it, he tells you that he has found blood spotting on his handkerchief throughout the day, but he finds it difficult to quantify how much. It seems to have developed fairly rapidly, although he has had a smoker's cough for years. You are also able to confirm that the blood is bright red and almost certainly from the lungs. What symptoms apart from coughing up blood might you ask Mr Morris about? Think of key clues that would help you narrow your differential diagnosis.

1) Cough productive of sputum? Indicates lower respiratory tract infection (pneumonia, bronchitis, TB), bronchiectasis, or lung cancer. 2) Fever? More commonly associated with a lower respiratory tract infection. Night sweats may indicate TB or carcinoma. 3) Weight loss? Th is is associated with lung cancer and TB. You should consider whether the weight loss was planned or not, but significant weight loss in a relatively short period is rarely the result of dieting and exercise and should therefore be investigated. 4) Pleuritic chest pain? Pleuritic chest pain can arise following a PE or pneumonia that has spread to the pleura. 4) Shortness of breath? Try to quantify this in terms of exercise tolerance: o How far can they walk before they get breathless? o Can they climb a flight of stairs without getting breathless? Sudden-onset shortness of breath can be caused by PE, whereas a more gradual time course would be consistent with heart failure. 5) Are there any extra-pulmonary manifestations of lung cancer such as: a) Bone pain? (bone metastases) b) Dull, aching, swollen wrists/ankles? (hypertrophic pulmonary osteoarthropathy (HPOA), a rare disorder most commonly seen in patients with lung cancer) c) Cushingoid features, muscle weakness, oedema, skin hyperpigmentation? (if there is a small cell carcinoma secreting ectopic adrenocorticotropic hormone (ACTH)) d) Polyuria, polydipsia, hypotonia, hyporeflexia, muscle weakness? (hypercalcaemia secondary to bone metastases or PTH-related peptide (PTHrP)- secreting lung cancer) e) Muscle weakness? (especially proximal muscles i.e. difficulties standing and walking), autonomic dysfunction (e.g. dry mouth, constipation, urinary retention?) Eaton-Lambert syndrome is a rare neuromuscular disorder most commonly seen in patients with small cell lung cancer. 7) Has he had haematuria and/or oliguria? Theere are a number of rare conditions that can affect both the lungs and kidneys (causing a 'PULMONARY-RENAL syndrome'). The main causes of this are: a) Goodpasture's syndrome, an autoimmune condition where autoantibodies attack the lungs and the glomeruli in the kidneys. Th is is important to identify early since the patient progresses rapidly to irreversible renal failure b) Vasculitides, e.g. Wegener's granulomatosis, microscopic polyangiitis, polyarteritis nodosa c) Systemic lupus erythematosus.

DDx for bi-basal crepitations and how would you differentiate between the causes?

1) FINE a) ILD: reduced chest expansion, clubbing 2) COURSE a) Pneumonia: acute productive cough, fever, chest pain, dull percussion note b) Bronchiectasis: chronic productive cough, wheeze, clubbing c) Pulmonary oedema: raised JVP, pedal oedema, orthopnoea, hx of IHD

Which lung conditions manifest over hours/days?

1) Infection with viruses or bacteria (just upper resp tract/bronchitis (cough but no breathlessness as alveoli spared)/ pneumonia ) 2) Asthma - bronchospasm , chest X-ray may be normal as airways not affected 3) Pulmonary oedema 4) Acute hypersensitivity pneumonitis (industrial dust)

Identify appropriate investigations for tuberculosis

1) FIRST LINE: CXR 2) Then: sputum acid-fast bacilli smear (3 samples 8 hours aprt, with one being in early morning) 3) Then: GOLD STANDARD: sputum culture - can take up to 6 weeks 4) FBC ● Also, isolate patient! ● Histology: hall mark is presence of CASEATING GRANULOMAS. Note: if histology + clinical picture are consistent with TB, start treatment without waiting for culture results. ● CXR: a) Primary Infection ▪ Peripheral consolidation ▪ Hilar lymphadenopathy b) Miliary Infection ▪ Fine shadowing c) Post-Primary ▪ Upper lobe shadowing ▪ Streaky fibrosis and cavitation ▪ Calcification ▪ Pleural effusion ▪ Hilar lymphadenopathy ** Treatment: RIPE o All 4 drugs are started at same time: rifampicin, isoniazid, pyrazinamide and ethambutol o First 2 given for 6 months o Second 2 for 2 months only o Sputum cultures will be repeated during treatment until 2 consecutive -ves

Mrs Virginia is a 78-year-old lady who presents with a persistent cough. What specific questions should you ask her in the history?

1) First, ask open questions about the cough itself: a) Acute or chronic? The British Thoracic Society (BTS) defines acute as <3 weeks and chronic as >8 weeks. Between 3 and 8 weeks the cough may be due to recovering acute illness or developing chronic illness. b) Constant or intermittent? A cough that is intermittent may suggest an extrinsic trigger (e.g. if the patient only coughs at work there may be an allergy to something in the workplace). A cough that is constant suggests an intrinsic cause. c) Productive or dry? The presence of sputum indicates inflammation and/ or infection. Patients with chronic obstructive pulmonary disease (COPD) have chronically inflamed airways and often produce white or clear sputum. Patients with infection have yellow or green sputum. Asthmatics may also produce yellow sputum. Particularly large volumes of green or rusty sputum may be coughed up in bronchiectasis and lung abscesses. d) Blood? More specifically: i) Blood-streaked sputum? Suggests infection ((e.g. atypical pneumonia - Klebsiella pneumonia)) or bronchiectasis. ii) Pink and frothy sputum? Suggests pulmonary oedema. iii) Frank blood (haemoptysis)? tuberculosis (TB), lung cancer, pulmonary embolus, bronchiectasis, or other rarer causes (e.g. Wegener's granulomatosis, Goodpasture's syndrome). e) Timing? Asthma is classically worse at night. Pulmonary oedema or gastro-oesophageal reflux disease (GORD) can also be worse at night due to the positional effects of lying flat. Patients often report sleeping propped up on pillows to mitigate these effects. Trigger factors such as pets, cold weather, or exercise indicate asthma, as does a worsening in spring/summer. f) Character? A wheezy cough suggests airway obstruction due to asthma or COPD. A bovine cough (breathy) is characteristic of vocal cord paralysis. A dry cough is suggestive of pulmonary fi brosis. A gurgling cough is suggestive of bronchiectasis. Pertussis infection causes a 'whooping' cough. **2) Second, ask directed questions about factors that might be triggering the cough: • Smoking? • Asthma? • Allergies? New pets, new house, new job (exposure to allergens)? • Recent rhinitis/sinusitis? • History of GORD? • Drug history? Certain drugs (e.g. angiotensin-converting enzyme (ACE) inhibitors) can cause a cough. • Travel? Th e patient may have visited an area of the world where TB is highly prevalent (e.g. Asian subcontinent, Central Asia, sub-Saharan Africa). **Third, ask about factors that might be associated with the cough and give you clues about the underlying cause: a) Fevers, night sweats, rigors, weight loss? These suggest malignancy, TB, or another severe infection. b) Breathlessness?This would be in keeping with asthma, COPD, pneumonia, or pulmonary oedema but rarer in lung cancer or GORD. c) Chest pain, particularly pleuritic chest pain? This may indicate pneumonia, pneumothorax, pulmonary embolism, or viral pleurisy. Equally it may be due to muscle strain secondary to vigorous coughing, or a fractured rib following trauma. d) Wheeze? Th is suggests obstruction of the airways such as that found in asthma, COPD, or tumours compressing an airway.

Which lung conditions manifest over seconds/minutes?

1) Foreign body (rare in adults, obvious history) 2) pneumothorax 3) pulmonary embolism (some marker of resp distress, Orthopnea, right heart strain, usually normal chest x ray and exam, D dimer helpful if negative, cough not a feature) 4) anaphylaxis (usually has circulatory failure too) - get urticarial rash. if was non-blanching rash - meningococcal meningitis/sepsis

Which differentials are associated with coughing up: 1) Frank blood 2)Blood-streaked sputum 3) Frothy sputum

1) Frank blood- Suggest vascular problem (e.g. erosion of cancer into a blood vessel) 2) Blood-streaked sputum - Lung infections can cause this. Chronic production of large amounts of blood-stained sputum suggests bronchiectasis. 3) Frothy sputum -Pulmonary oedema

Mr Morris is a smoker with a 50-pack-year history, having started when he was conscripted into the navy and given cigarettes each week as part of his compensation (a common story in his generation). As a retired electrician, he has almost certainly had some exposure to asbestos, but denies ever having worked too closely with it as he was primarily concerned with residential housing. He has no history of lung disease. He has not travelled beyond the UK 'for many years' and has not been immunized against TB. He has no risk factors for a DVT/PE other than his smoking history. He is not taking aspirin or warfarin. The GP conducts a full physical examination, beginning by simply inspecting Mr Morris. The GP then examines his hands, head, neck, and chest. The examination is completed by checking his abdomen and his neurological status. Think of how the diseases mentioned in your differential might manifest during the examination: What signs should the GP particularly look out for on examination of this gentleman?

1) General inspection from the end of the couch: a) Hoarse voice: ?invasion of recurrent laryngeal nerve by cancer b) Purpuric rash or petechiae: ?vasculitis affecting lungs c) Cushingoid appearance (moon face, buffalo hump on neck, fat on abdomen, wasted limbs): ?lung cancer secreting ACTH d) Cachexia 2) Hands: a) Clubbing: ?lung cancer, lung abscesses, bronchiectasis b) Tar stains: ?smoker c) Wasting of the dorsal interossei: ?invasion of T1 nerve root by apical lung cancer (Pancoast tumour) 3) Arms: − Hypotonic, hyporeflexive, weak arms: ?hypercalcaemia due to bone metastases from lung cancer 4) Face: a) Swollen face: ?obstruction of superior vena cava by tumour b) Bleeding from oral or nasal mucosa: ?source of blood, i.e. not true haemoptysis c) Saddle nose: ?Wegener's granulomatosis d) Horner's syndrome (miosis, ptosis, and anhydrosis, i.e. small pupil, droopy eyelid, and lack of sweating): ?invasion of the sympathetic supply to the face by apical lung cancer e) Jaundice: ?liver cancer which has spread to the lungs or vice versa f) Focal neurology: ?brain metastases from lung cancer 5) Neck: a) Cervical lymphadenopathy, non-tender: ?TB, bronchial carcinoma b) Left supraclavicular lymphadenopathy (Virchow's node): ?GI malignancy which may have metastasized to the lungs c) Tracheal deviation: ?lung collapse secondary to a large mass such as a tumour or abscess 6) Chest: a) Asymmetrical lung expansion: ?lung pathology in side of reduced expansion b) Dullness to percussion: ?pneumonia, lung abscess, pleural effusion due to cancer c) Stridor: ?tumour or foreign body obstructing bronchus d) Crackles: ?pneumonia, left ventricular failure, bronchiectasis e) Pleural rub: ?mesothelioma, pleuritis from pneumonia, distal PE causing infarction and associated pleurisy 7) Abdomen: − Hepatomegaly: ?liver malignancy which can spread to the lungs, and vice versa 8) Legs: − Unilateral signs of DVT? A DVT may have caused a PE. Look for a unilaterally inflamed leg, unilateral pitting oedema, tenderness over the deep veins or distended, non-varicose superficial veins.

Explain the aetiology/risk factors for asthma

1) Genetic Factors o Family history o Atopy (tendency for T lymphocytes to drive production of IgE on exposure to allergens) 2) Environmental Factors o House dust mites o Pollen o Pets o Cigarette smoke o Viral respiratory tract infections o Aspergillus fumigatus spores o Occupational allergens **Pt history will sound like: •Recurrent episodes •Variation (worst in morning & evening) •History of atopy •Family History •Smoker •Occupation •Pets

A 36-year-old male, of no fixed abode, was brought to the ED collapsed. Symptoms were of increasing weakness, loss of appetite, and weight loss "for some time". On direct questioning, he admitted to cough productive of green sputum, and there had been one episode of coughing blood clots "a few days ago". Until recently he had drunk at least 4 litres of strong cider a day. On examination, heart rate is 104bpm, BP 105/70mmHg, respiratory rate 24/min and temperature 38.4 degrees Celsius. He was unkempt and severely cachectic. A number of scars over veins were noted making venous access difficult. There were crackles over the left anterior chest. Some small firm mobile lymph nodes were palpable in both supraclavicular fossae and axillae. The CXR showed extensive infiltration in the left upper and middle zones, with appearances suggesting cavitation and some elevation of the left hilum, and lesser infiltration in the right upper zone. 1) Which four conditions should be considered in your differential diagnosis? 2) Which three of the following investigations would be most appropriate?

1) HIV/AIDS with atypical infection Multiple 2) Staphylococcal lung abscesses related to IV drug use 3) Pulmonary tuberculosis 4) Necrotising aspiration pneumonia **This patient is immunocompromised. He has evidence of cavitation on his chest radiograph and is acutely unwell. Aspiration pneumonia, cavitating pneumonia, atypical infection such as TB or secondary to HIV, should all be considered in the first instance. Cavitating malignancy would be less likely in a patient of this age with this presentation but would need to be considered if initial treatment was ineffective. The appearances would not be typical for pulmonary haemorrhage or cardiac failure. 2) Sputum for MC&S and AFB, HIV blood test and CT chest and abdomen. Sputum should be sent for microbiology including AFBs and also to cytology. Blood cultures should be undertaken. An HIV test is indicated. CT of the chest and abdomen is indicated to further assess the degree of lung abnormality and possible abscess which may require drainage, also evaluating mediastinal and abdominal lymph nodes and the liver and spleen.

1) This patient has a severe acute asthma attack. Which first-line treatments would you instigate? 2) Your patient starts to improve rapidly following initial treatment and it is decided to admit her to the ward for ongoing care. Which treatments would now be appropriate?

1) High dose oxygen by mask 2) Salbutamol 2.5mg nebulised with O2 3) Ipratropium bromide 0.5mg nebulised with O2 4) Hydrocortisone 100mg IV § Oxygen should be continued until the PaO2 has normalised § Salbutamol (and ipratropium bromide) need to be administered at once by nebuliser. § Aminophylline can be given as an IV infusion but is usually reserved for patients who do not respond to initial treatment. § High-dose steroids are also needed to reduce inflammation, either IV or as oral prednisolone 30-60mg (reducing dose). § Management advice for acute severe asthma is provided in the BTS / Sign Guidelines (2016) 2) 1) Continue O2 at lower dose 2) Commence oral steroids 3) 4 hourly nebulised Salbutamol 4) Monitor peak flow and oxygen saturations **You can now reduce oxygen dose, steroid dose can come down and nebuliser intervals can also reduce. Close monitoring is still needed with escalation of treatment if her observations worsen There is no indication in this scenario for antibiotic treatment or Aminophylline infusion

A 65-year-old female presents to medical outpatients with a 6-week history of increasing pain in her right shoulder. This pain is continious, worse at night and when she lies on the shoulder, and she has also noted some radiation of pain down her right arm in certain positions. She has no cough, nausea or vomiting and no urinary or bowel symtoms of note. She is an ex-smoker, having smoked 20 a day for 25 years and she gave up 5 years previously. She is taking co-dydramol for the pain, but no other medication and does no drink excessive alcohol. She is married but has no children. On examination, her pulse is 80bpm and regular, blood pressure 130/65 mmHg and she is apyrexial. 1) As you examine her sclera, you notice that her right pupil is smaller than the left and appears constricted and there is some drooping of her eyelid. What might explain these findings? 2) You continue your physical examination and you note severe discomfort in the right shoulder when the patient abducts her arm. She is tender to palpation over the supraclavicular region. Cardio-respiratory and abdominal examination is unremarkable apart from dullness to percussion and reduced air entry at the right lung apex. What might explain the shoulder pain? 3) Which of the following initial investigations would you request at this point? 4) The chest radiograph confirms abnormal soft tissue and rib destruction at the right lung apex. What is this lesion likely to represent?

1) Horner's syndrome. This patient has a Horner's syndrome - proptosis, miosis, enophthalmos and anhydrosis (depending on level of disruption to sympathetic chain). 3rd nerve palsy (superior oblique muscle) causes pupillary dilatation and a Holmes-Adie pupil (benign condition) is moderately dilated and poorly reactive to light. Opiates may cause pupillary constriction (bilateral) but not ptosis. 2) Superior sulcus lung carcinoma. When combined with the eye findings the shoulder symptoms are highly suggestive of superior sulcus/apical lung carcinoma (Pancoast tumour). 3) Chest radiograph 4) An apical lung carcinoma (superior sulcus - Pancoast tumour) - Pancoast tumour is the only condition from the list which causes rib destruction.

measures of 'disease activity' in sarcoidosis

1) Imaging: a) HRCT patterns b) FDG-PET 2) Bronchoalveolar lavage: lymphocytosis 3) -Serum markers: inflammatory markers, ACE, IL2R, chitotriosidase, 24- hour urinary calcium 4) -Serial Lung Function Testsuse combination of imaging, lavage, serum markers , lung function tests

Stepwise treatment of asthma

1) Inhaled SAB2A PRN + Add inhaled steroid as needed 2) Daily low dose ICS 3) Low dose ICS + LABA 4) Medium dose ICS + LABA 5) High dose ICS + LABA * ICS-formoterol - LABA

COPD management BTS guidelines 2020

1) MILD: SABA or SAMA (e.g. Salbutamol or Ipratropium Bromide) 2) MODERATE SABA + LABA or SAMA + LAMA (e.g. + Salmeterol or Tiotropium) 3) SEVERE: LABA + LAMA or LABA + ICS (e.g. Salmeterol + Tiotropium or Symbicort) 4) V SEVERE LABA + LAMA + ICS **SABA = short acting beta-agonist, SAMA = short acting muscarinic antagonist, LABA = long-acting beta agonist, LAMA = long acting muscarinic antagonist and ICS = inhaled corticosteroid

Oxygen delivery devices and flow rates

1) Nasal cannulae: As with all oxygen delivery devices, there is a significant amount of variability depending on the patient's breathing rate, depth and how well the oxygen delivery device is fitted. Below are some guides to various oxygen flow rates and the approximate percentage of oxygen delivered:4 1L / min - 24% 2L/ min - 28% 3L/ min - 32% 4L / min - 36% 2) Simple face mask: The oxygen delivery of simple face masks is highly variable depending upon oxygen flow rate, the quality of the mask fit, the patient's respiratory rate and their tidal volume. Simple face masks can deliver a maximum FiO2 of approximately 40%-60% at a flow rate of 15L/min. These masks should not be used with flow rates less than 5L/min.³ 3) Reservoir mask (also known as a non-rebreather mask): Reservoir masks deliver oxygen at concentrations between 60% and 90% when used at a flow rate of 10-15 l/min.³ The concentration is not accurate and will depend on the flow of oxygen as well as the patient's breathing pattern. These masks are most suitable for trauma and emergency use where carbon dioxide retention is unlikely. 4) Venturi masks: A Venturi mask will give an accurate concentration of oxygen to the patient regardless of the oxygen flow rate (the minimum suggested flow rate is written on each). Venturi masks are available in the following concentrations: 24%, 28%, 35%, 40% and 60%. They are suitable for all patients needing a known concentration of oxygen, but 24% and 28% Venturi masks are particularly suited to those at risk of carbon dioxide retention (e.g. patients with chronic obstructive pulmonary disease).³

Mr Morris' pulse is 78 bpm, his blood pressure is 132/66 mmHg, his respiratory rate is 14/min and his temperature is 36.5°C. The positive findings on examination of Mr Morris include tar stains on his hands and a palpable liver edge 2 cm below the ribs. There were no abnormal findings on examination of Mr Morris' respiratory system. Mr Morris gets referred to the respiratory clinic as an outpatient. He is referred urgently because of his haemoptysis, weight loss, and hepatomegaly. You are the Registrar at this clinic and you confirm the history and examination findings obtained by the GP. Which investigations should you request and why?

1) Oxygen saturations, which form part of the vital observations and help you to understand the severity of the underlying pulmonary disease causing the haemoptysis. 2) Blood tests: a) Full blood count (FBC) looking for anaemia, which reflects the magnitude and duration of bleeding or which may be a manifestation of an underlying malignancy. You are also looking for a raised white cell count indicating an infectious or inflammatory process. b) C-reactive protein (CRP) which will be raised in infection, inflammation, and some cases of malignancy. c) Clotting screen, for a bleeding disorder which may be exacerbating if not directly causing the haemoptysis. d) Urea and electrolytes (U&Es) for renal involvement, as in Goodpasture's syndrome or Wegener's granulomatosis, which can affect the kidney and the lung. e) Calcium, phosphate, and alkaline phosphatase (ALP) for bone metastasis from a primary lung cancer. f) Liver enzymes for liver involvement of a cancer. 2) Urine test: urinalysis looking for haematuria, suggesting pulmonary-renal syndrome. 3) Imaging: chest radiograph **Note: if TB is suspected, strenuous efforts should be made to obtain specimens or tissue from which to culture the organism (particularly given the growing prevalence of resistant strains). The skin sensitivity tests (Heaf, Mantoux) and newer T-cell based assays (e.g. Quantiferon, ELIspot) are only useful to determine latent TB infection and tell you nothing about disease activity. As many people are infected but not diseased, these tests are of little diagnostic value. They are used in contact tracing to see if somebody who has been exposed to open TB has become infected.

Causes of pleuritic chest pain

1) PE 2) Pneumonia 3) Pleuritis 4) Pericarditis 5) Pneumothorax

ABG sequence of interpreting

1) PaO2 2) pH 3) PaCO2 4) HCo3- 5) BE OPCHB

Different types of pneumonia

1) Pneumococcal pneumonia: § commonest bacterial pneumonia. § Common in elderly, alcoholics, post-splenectomy, immune-suppressed, patients with HF/lung disease § CXR: lobar consolidation § Tx: amoxicillin, benzylpenicillin or cephalosporin 2) Staphylococcal: § May complicate influenza or occur in young, elderly, IV drug users or pts with underlying disease. § Bilateral cavitating bronchopneumonia § Tx: flucloxacillin +/- rifampicin 3) Klebsiella: § Rare § Occurs in elderly, diabetics and alcoholics § Can cause HAP § Cavitating pneumonia esp of upper lobes § Tx: cefotaxime or imipenem 4) Pseudomonas: § Causes HAP § Tx: anti-pseudomonal penicillin, ceftazidime, meropenem or ciprofloxacin + aminoglycoside 5) Mycoplasma pneumoniae: § Occurs in epidemics about every 4 years § Presents with flu-like symptoms followed by a dry cough § CXR: reticular-nodular shadowing or patchy consolidation often of 1 lower lobe § Can cause autoimmune haemolytic anaemia 6)Legionella pneumophilia: § Colonises water tanks kept at <60 degrees - i.e. hotel air-conditioning and hot water systems § Flu-like systems then dry cough and dyspnoea. § Causes hyponatremia § CXR: bi-basal consolidation § Tx: fluoroquinolone for 2-3w or clarithromycin 7) Chlamydophilia pneumoniae: § Biphasic illness: pharyngitis, hoarseness, otitis then pneumonia § Diagnosis: chlamydophilia complement fixation test, PCR invasive samples § Tx: doxycycline or clarithromycin 8) Chlamydiophilia psittaci: § Causes psittacosis - an ornithosis acquired from infected birds, esp parrots § Causes headache, fever, dry cough, lethargy, anorexia and D&V § Diagnosis: Chlamydophilia serology § Tx: doxycycline or clarithromycin 9) Viral pneumonia: § Commonest cause: influenza § Others: measles, CMV, varicella zoster 10) Pneumocystis pneumonia: § Pneumonia in immunosuppressed § Responsible organism: pneumocystis jiroveci § Dry cough, exertional dyspnoea, low PaO2, fever, bilateral crepitations § CXR: bilateral perihilar interstitial shadowing § Tx: high dose co-trimoxazole or pentamidine by slow IVI for 2-3w

Different types of pneumonia: Chlamydophilia pneumoniae

Different types of pneumonia: Klebsiella

Different types of pneumonia: Legionella pneumophilia

Different types of pneumonia: Mycoplasma

Different types of pneumonia: Pneumococcal pneumonia

What questions should you ask about the haemoptysis?

1) What is he coughing up? a) Frank blood: this is suggestive of a vascular problem such as a ruptured blood vessel (invasive cancer, bronchiectasis, TB, mycetoma), a ruptured arteriovenous malformation, or a vascular-bronchial fistula. b) Blood-streaked sputum: any infection of the lungs can cause this; however, in the context of chronic production of large volumes of sputum this would suggest bronchiectasis. c) Pink frothy sputum: this suggests pulmonary oedema (secondary to, for example, left ventricular failure or severe mitral stenosis). 2) How much is he coughing up? Try to help the patient quantify this by comparing with amounts they might know - a teaspoon, a tablespoon, an eggcup, or more - especially as even a small amount of coughed-up blood will be alarming and seem like a lot to many patients. Massive haemoptysis can be caused by erosion of a pulmonary blood vessel. 3) How suddenly did it start, and has it got worse progressively? Sudden onset is consistent with pulmonary embolism (PE) or erosion of a cancer into a large pulmonary blood vessel. Gradual onset argues for a progressive condition such as lung cancer or bronchiectasis.

Different types of pneumonia: Pneumocystis pneumonia

Different types of pneumonia: Pseudomonas

Different types of pneumonia: Staphylococcal

Different types of pneumonia: Viral pneumonia

Primary and secondary pneumothroax

1) primary mostly in young tall men, smokers, marfans § cause is bleb that bursts 2) in secondary is due to underlying - e.g. COPD alveolar bullae burst

Presentation of anaemia and SOB

Presentation of bronchiectasis

Presentation of chronic asthma

Presentation of pulmonary fibrosis

We already know that Mrs Finnegan's dyspnoea has developed over several months. What key clues on history and examination will help you differentiate between the potential diagnoses? Try to think of key clues for the most common diagnoses in the 'weeks to months' column above.

1) • COPD − Remember that COPD is a bracket term encompassing chronic bronchitis and emphysema. − History of chronic bronchitis (a clinical diagnosis, based on the presence of a cough, productive of sputum (~10 mL daily), on most days of 3 months for 2 consecutive years) and permanent, largely irreversible, shortness of breath. − Presence of risk factors suggesting a cause for COPD: − Smoking (usually more than 20 pack years) − Occupational exposure to lung irritants, e.g. in coal miners, tunnel workers − α1-Antitrypsin deficiency (liver failure, family history). − Signs of COPD: − Hyperexpanded chest − Breathing through pursed lips − Reduced air entry/chest expansion − Hyper-resonant percussion note (particularly resonance over the heart and liver). 2) Chronic asthma − History of transient, reversible cough, wheeze and shortness of breath - often worse at night, during exercise, or when exposed to allergens or cold − Presence of associated atopic conditions personally or in family members (eczema, hayfever, allergies, nasal polyps) − Symptoms may be exacerbated by drugs such as non-steroidal antiinflammatory drugs (NSAIDs), aspirin, β-blockers (including those in eye drops used for glaucoma) − Wheeze on auscultation of the lungs. 3) Pulmonary fibrosis − History of exposure to asbestos, silica, or coal (pneumoconioses causing fibrosis), exposure to drugs (e.g. methotrexate) − Signs on examination include: − Clubbing (in usual interstitial pneumonitis) − Reduced air entry/chest expansion − Late inspiratory, fine crackles (often heard throughout the chest rather than just the lung bases as in pulmonary oedema). 4) Heart failure − History of shortness of breath on exertion, orthopnoea (breathless when lying flat), paroxysmal nocturnal dyspnoea (waking up short of breath) − Presence of risk factors suggesting a cause for heart failure: − Ischaemic heart disease (smoking, diabetes mellitus, hypercholesterolaemia, hypertension, South Asian descent, strong family history) − Other atherosclerotic disease (e.g. stroke, transient ischaemic attack (TIA), limb claudication) - Hypertension ( − can cause heart failure by itself, in the absence of ischaemic heart disease) − Valvular disease (e.g. rheumatic fever, endocarditis, Marfan's syndrome) − Cardiomyopathy **Signs on examination include: − Displaced apex beat − Third and fourth heart sounds − Crackles in both lung bases − Raised jugular venous pressure (JVP), hepatomegaly, peripheral oedema (ankles, sacrum). 5) Anaemia − History of bleeding (menorrhagia, melaena, haematochezia) or malnutrition ('tea and toast' diet in elderly, poor diet of homeless). Fatigue as well as shortness of breath on exertion − Signs of peripheral (fingers) or central (tongue) cyanosis. Specific signs such as koilonychia, glossitis, and angular stomatitis (all rare). Checking for conjunctival pallor is routinely done but is unreliable. 6) Bronchiectasis would be suggested by a history of productive cough and recurrent chest infections, or a history of cystic fibrosis. 7) Obesity, kyphoscoliosis, ankylosing spondylitis can be excluded on inspection. 8) Physical deconditioning is a diagnosis of exclusion.

Different types of pneumonia: chlamydiophilia nsittaci

Describe the pattern of cough in: Pneumonia, Chronic bronchitis, Asthma

1) Pneumonia 3-4 day history of persistent, productive cough - 2) Chronic bronchitis Persistent, productive cough on most days of the past 3 months and spanning years - 3) Asthma Dry cough present mainly during episodes of shortness of breath or at night

§ A 24-year-old previously fit and healthy policeman presents to the ED complaining of painful ankles, difficulty walking and general malaise and ill-health. His symptoms started 5 days ago with a 'flu-like illness. He had felt unwell, with a dry throat, low energy levels and fatigue. He had ignored the symptoms initially but yesterday he felt so unwell that he called in sick to work. This morning, he woke up with bilateral ankle pain and swelling. The pain is so bad that he can barely walk. § On examination, he has a low-grade fever of 37.5°C, looks unwell and has bilateral ankle joint swelling consistent with effusions. 1) Which 2 of the following would be top of the list of your differential diagnosis? 2) He has erythema nodosum. Which 3 of the following investigations would be most helpful in reaching the diagnosis? § Aspirate synovial fluid from the ankle joints for culture and crystals § ASO (Anti-Streptolysin O) Titres § Autoimmune profile § Chest X-ray § IgM Rheumatoid Factor § Renal biopsy § Throat swab § X-ray ankle joints

1) Post-streptococcal reactive arthritis or Acute sarcoid. This is not a typical presentation of rheumatoid arthritis or systemic lupus erythematosis (although they could feasibly present acutely like this). Post-streptococcal reactive arthritis and sarcoidosis are the most likely diagnoses. Septic arthritis would be unusual in a fit healthy young man and would usually be a monoarthritis. Lyme disease usually starts with a typical rash (erythema chronicum migrans) and then can cause arthritis several weeks later. 2)Throat swab, Chest X-ray, ASO (Anti-Streptolysin O) Titres. § A chest X-ray is needed to look for features of sarcoidosis. § Throat swab and ASO titre are aimed at confirming / excluding streptococcal disease § X-ray of acutely swollen ankles will probably show soft tissue swelling contribute diagnostically. § Even septic arthritis does not cause abnormal radiographic changes for several weeks. § An autoimmune profile and rheumatoid factor would likely be done as part of the diagnostic screen but mostly for exclusion . § Joint aspiration is invasive and would only be indicated if you suspect septic arthritis. That is one of the least likely diagnoses in this case and this can be deferred whilst other more relevant tests are done first. If no clear diagnosis is reached then aspiration may be required.

Generate a management plan for pulmonary embolism

1) Primary Prevention: o Compression stockings o Heparin prophylaxis for those at risk o Good mobilisation and adequate hydration 2) If haemodynamically stable: o O2 o Anticoagulation with LMWH or rivaroxaban o Switch over to oral warfarin for at least 3 months ▪ Maintain INR 2-3 o Analgesia 3) If haemodynamically UNSTABLE (massive PE): o Resuscitate o O2 o IV fluids o Thrombolysis with tPA may be considered if cardiac arrest is imminent 4) Surgical or radiological: o Embolectomy o IVC filters - sometimes used for recurrent PEs despite adequate anticoagulation or when anticoagulation is contraindicated

Asthma management BTS thoracic society 2020 guidelines

1) SABA (e.g. Salbutamol) •2) SABA + low-dose ICS (e.g. Salbutamol + Beclometasone) •3) SABA + low-dose ICS + LTRA (e.g.. Salbutamol, Beclometasone and Monteleukast) •4) LABA + low-dose ICS +/- LTRA (e.g. Symbicort (Budesonide+Formoterol) •5) LABA + high-dose ICS (+/- LTRA) •6) Trials such as Theophylline (long-acting muscarinic antagonist) •7) Oral Corticosteroids e.g. Prednisolone **Note: •Check inhaler technique •Patient adherence •Encourage smoking cessation and weight loss advice if applicable § Abbreviations: **SABA = short acting beta-agonist, ICS = inhaled corticosteroid, LTRA = leukotriene receptor antagonist, LABA = long-acting beta agonist Write it out many times as this is really important and also v clinically relevant and common (asthma and COPD tx)!

A 35-year-old Caucasian female presents to her GP with a two-week history of dry cough, increasing breathlessness, aches and pains and mild weight loss. On examination, her general appearance is unremarkable. She has a temperature of 37.0°C, pulse 92 per minute regular and blood pressure 126/85 mmHg. There is tender lymphadenopathy of the superficial cervical chain, supraclavicular and inguinal lymph nodes. Heart sounds appear normal and chest examination is unremarkable. Her abdomen is soft and non-tender there is evidence of red, firm, non-tender nodules distributed on the anterior surface of both shins. Neurological examination is normal. Results of initial investigations including full blood count, urea and electrolytes and ECG are normal. 1) Which 4 of these conditions should you include in your differential diagnosis? 2) Which 4 nitial investigations would be most helpful to confirm the diagnosis?

1) Sarcoidosis, Tuberculosis, Lymphoma, Infectious mononucleosis. Given her lymphadenopathy, you need to consider sarcoidosis, infectious mononucleosis and lymphoma. Tuberculosis is also a possibility but would be unusual in a young female caucasian unless immunocompromised or exposed to TB. The story does not really fit for Legionnaire's, extrinsic allergic alveolitis or asthma 2) § Serum angiotensin converting enzyme (ACE) § Lymph node tissue biopsy § Chest x-ray (CXR) § Serum calcium **Blood cultures are unlikely to be helpful here (they are useful in system infection but are not useful in diagnosing lymphoma, TB or sarcoidosis). **A bone scan may be useful in metastatic disease but would not be an appropriate investigation in this patient. **Serum ACE is raised in 2/3 of patients with sarcoidosis, although it is not specific for sarcoidosis. **CXR would be a useful investigation of choice. **Serum calcium may be raised in lymphoma or sarcoidosis (although not a specific test it is a useful marker) **Although invasive, lymph node biopsy may be diagnostic **Lung function tests would be unlikely to be abnormal at the early stage of the disease. **Thyroid function tests are a useful general screen in such a patient but would not be abnormal in sarcoidosis or help in confirming any of the other diagnoses.

Which different classes of inhaled drugs are used in obstructive airways disease (asthma and/or COPD)? What is the mechanism of action of each drug?

1) Short-acting bronchodilators: − Salbutamol (UK: blue, 'Ventolin'): selective β2-agonist. Acts on a G-protein-coupled receptor, activating adenylate cyclase and increasing the formation of cAMP, leading to relaxation of the smooth muscle lining the airways. − Ipratropium (UK: white + green, 'Atrovent'): antimuscarinic/cholinergic. Antagonizes muscarinic acetylcholine receptors in the airways, preventing parasympathetic-mediated smooth muscle contraction. Often used in COPD, but less often in asthma. − Salbutamol + ipratropium (UK: white + orange, 'Combivent'). 2) Inhaled steroids − For example beclometasone, budesonide (UK: brown inhalers), fl uticasone (UK: orange inhaler). Work by affecting intracellular transcription of various proteins to reduce inflammation in the airways. Used in asthma and COPD as second-line treatment. 3) Long-acting bronchodilators − Salmeterol, formoterol: long-acting β2-agonist (LABA). Mechanism like the short-acting variant. − Tiotropium: long-acting anticholinergic (LACA). Mechanism like the short-acting variant. Used in COPD but not asthma. − Long-acting bronchodilators can also be combined with inhaled steroids, e.g. budesonide + formoterol (UK: red, 'Symbicort') or fluticasone + salmeterol (UK: purple, 'Seretide'). 4) Oxygen. Don't forget that this is a drug! It may be given acutely, e.g. in an ambulance or in hospital, or long-term, e.g. in severe COPD. Oral drugs are also sometimes used, including oral steroids, xanthine derivatives (theophylline, aminophylline), leukotriene antagonists (montelukast), and cromones (sodium cromoglycate, nedocromil sodium)

Types of LUNG CANCERS

1) Small cell: (20%) § Tend to be central tumours § Aggressive malignancy (2/3 have distant metastasis at presentation) § Treated with chemotherapy § Associated with SIADH (causes hyponatremia) 2) Non-small cell includes adenocarcinomas, squamous cell carcinomas, large cell carcinomas and carcinoid tumours (80%) a) Squamous cell carcinomas: § Treated with radiotherapy § Associated with PTHrp release which leads to hypercalcaemia § Cavitating lesion on CXR b) Adenocarcinoma: § Located peripherally § More common than others in non-smokers c) Large cell: poor prognosis

Mr Morris has had a cough for years, but it is only productive when he is unwell. He has not been unwell recently, although he notes that he has unintentionally lost weight - he estimates a stone (about 6.5 kg) in the last 6 months. He has no pleuritic chest pain, but gets breathless after climbing just one flight of stairs at home. He attributes this to his age, and lack of exercise. He has had no urinary symptoms. What features about Mr Morris' past history will help you narrow your differential diagnosis even further?

1) Smoking history? Smoking is the most significant risk factor for lung cancer. Quantify how much he smokes or smoked using the average number of cigarettes smoked a day and the number of years smoked, i.e. when he started and, if relevant, quit. Someone who smoked 10 cigarettes a day for 30 years is said to have smoked for 15 pack years (10 cigarettes = 0.5 packs; and 0.5 × 30 years = 15 pack years). 2) Exposure to asbestos or other inhaled industrial substances? For example silica (i.e. stone cutter's dust), coal, radon, arsenic, haloethers, polycyclic aromatic hydrocarbons. Such exposure is a risk factor for lung cancer and, in the case of asbestos, mesothelioma. 3) Prior lung disease? This may indicate a chronic condition, such as TB or bronchiectasis, or a vulnerability to repeated infections (e.g. pneumonias) that you may wish to investigate further. 4) Did he grow up abroad or travel recently? If yes, which country? Has he been vaccinated for TB? TB is endemic in many countries, particularly the Asian subcontinent and southern African states, and patients can be relatively asymptomatic for extended periods of time. 5) Does he have risk factors for a deep vein thrombosis (DVT)/pulmonary embolus (PE)? These include prolonged stasis (bed rest or long-haul flight), blood vessel damage from recent trauma or surgery, malignancy causing hypercoagulable blood, other clotting abnormalities, or a history of previous venous thromboembolism. Also ask about a painful swollen limb, particularly leg, which could be a DVT leading to a PE. 6) Is he on anticoagulant medications or does he have a known bleeding diathesis (tendency)? These can increase the risk and/or magnitude of internal haemorrhage

Gold standard investigation for COPD

1) Spirometry •<70% FEV1:FVC (obstructive pattern) •Reduced PEFR, Increased Lung Volumes § is the gold standard - shows irreversibility pre and post bronchodilator 2) CXR •Barrel chest, hyperinflated lungs (>6 anterior ribs, flattened hemi diaphragm) and elongated cardiac silhouette 3) Bloods, ABG: - increased Hb, HCT (secondary polycythaemia), ABG if acutely unwell/raised pCO2 and hypoxia 4) Others: A1AT levels, serial peak flow measurements ( if asthma is a potential differential), ECG/Echo for cardiac assessment if there are features of cor pulmonale **FEV1 and Severity: § >80 % = Mild § 50-79% = Moderate § 30-49% = Severe § <30% = Very Severe

Explain the aetiology/risk factors of pneumothorax

1) Spontaneous: o Occurs in people with typically normal lungs o Typically in tall, thin males o It is probably caused by the rupture of a subpleural bleb (bulla) 2) Secondary: o Occurs in patients with pre-existing lung disease (e.g. COPD, asthma, TB, pneumonia, lung abscess, CF, lung cancer, sarcoidosis) 3) Traumatic: o Caused by penetrating injury to the chest o Often iatrogenic (e.g. during jugular venous cannulation, thoracocentesis, transbronchial biopsy, subclavian CVP line insertion, +ve pressure ventilation) 4) Risk Factors o Collagen disorders (e.g. Marfan's syndrome, Ehlers-Danlos syndrome) 5) Tension pneumothorax

Bronchiectasis - Investigations

1) Sputum culture and sensitivity: •Common organisms include P. Aeruginosa, H. influenzae, Mycobacteria, Klebsiella, S. pneumonia, S. aureus. 2) CXR: •Dilated bronchi (tramline shadows -- parallel lines running from the hilum to the diaphragm) •Fibrosis •Pneumonic consolidation •Atelectasis (collapse due to no use) 3) High-resolution CT: -= best diagnostic tool •Dilated bronchi with thickened walls (SIGNET RING sign) •Assess distribution and extent of disease •Others = Spirometry, sweat electrolytes (CF), aspergillus skin prick test

Outline the management of COPD.

1) Stop smoking 2) Inhaled therapy (Beta-2 agonists and steroids) 3) Pulmonary rehabilitation (physiotherapy, exercise etc.) 4) Vaccination 5) Non-invasive ventilation 6) Long-term oxygen use 7) Manage exacerbations

Mrs Finnegan went for echocardiography. This showed anterior akinesia and a left ventricular ejection fraction of 36%. Coronary angiography showed patent graft vessels but an occluded left anterior descending artery, plus severe stenosis of the right coronary and circumflex arteries. Based on this, it is fair to proceed based on a working diagnosis of congestive heart failure secondary to ischaemic heart disease. What drug treatments would you offer this lady? Don't worry about specific drugs. Try to think what types of drug might help with: (1) her symptoms (too much fluid in lungs and limbs), (2) the pathological mechanism involved in heart failure, and (3) the underlying cause of the problem (atherosclerosis, in her case).

1) Symptomatic relief: her symptoms are largely due to her left ventricular failure (pulmonary oedema). You should treat this as follows: − In those patients presenting with acute pulmonary oedema (i.e. not our patient) - sit upright, give oxygen, and reduce cardiac pre-load with vasodilators such as morphine, nitrates, and furosemide. − Chronically - with a loop diuretic such as furosemide, which may be combined with the potassium-sparing diuretic spironolactone. 2) Pathophysiological mechanism: reduced cardiac output activates two physiological systems that actually worsen the situation in heart failure: sympathetic and the renin-angiotensin systems. Greater sympathetic activation increases heart rate and contractility via β-adrenergic receptors. This increases the heart's oxygen demand, which may already be compromised in heart failure (particularly if secondary to ischaemic heart disease), and at higher heart rates filling time and therefore cardiac output may be further reduced. Activation of the renin-angiotensin system results in increased water retention, leading to fluid overload. Logically, therefore, addressing the unhelpful response of these two systems is associated with improved mortality: − Reduce the oxygen demand of the heart: heart failure is usually due to not enough blood reaching the hard-working myocytes, which start to die. One way of treating this is to use a β-blocker which slows the heart beat, although β-blockers must never be used if patient is in acute LVF. The patient won't like it (as a slower beating heart will make them feel tired and lethargic) but the many double-blinded, randomized controlled trials have shown that the patient will live longer. The trick is to start with a small dose of β-blocker and increase it very slowly. − Inhibit the renin-angiotensin-aldosterone system: angiotensin-converting enzyme (ACE) inhibitors limit activation of the renin-angiotensin- aldosterone pathway, thus reducing reabsorption of sodium and water from the kidneys. Several double-blinded, randomized controlled trials have now shown that ACE inhibitors reduce mortality in heart failure. Angiotensin II receptor blockers (ARBs) may be used as an alternative to ACE inhibitors. NICE guidelines suggest that aldosterone antagonists such as spironolactone can also be used. 3) Underlying cause: the most common cause of heart failure is atherosclerosis of the coronary arteries and you should consider addressing this. There are various ways of preventing atherosclerosis getting worse (and maybe even helping the body start to reverse it): statins to reduce cholesterol levels and prevent progression of the atheroma; aspirin to reduce the risk of thrombosis leading to heart ischaemia or infarction; and medication for diabetes mellitus if the patient is diabetic, as uncontrolled diabetes leads to hyperglycaemia which accelerates atherosclerosis. In advanced heart failure, treatments can include digoxin, cardiac resynchronization therapy (biventricular pacemakers), implantable cardioversion devices (ICDs), mechanical assist devices, or heart transplantation. Also, in addition to drug treatments, your management should include conservative measures, such as advice to adopt a healthy (low-salt) diet, minimizing alcohol intake, and taking regular exercise.

Management of COPD

1) TREATING STABLE COPD: ● General o Patient education -Stop smoking o Encourage exercise o Treat poor nutrition or obesity o Influenza AND pneumococcal VACCINATION o Pulmonary rehabilitation/palliative care o PRN short-acting antimuscarinic (ipratropium) or short acting b2 agonist (salbutamol) 2) ● MANAGEMENT OF CHRONIC COPD o Initiate short-acting b2-agonist (SABA)/short-acting muscarinic antagonist (SAMA) o Then: ▪ If FEV1>50%: long-acting b2-antagonist (LABA) OR long-acting muscarinic antagonist (LAMA) If worsens: add inhaled corticosteroids (ICS) ▪ If FEV1 <50%: LABA + inhaled corticosteroid (ICS) in combined inhaler or LAMA If worsens: add ICS ● SABA example: salbutamol ● SAMA: ipratropium ● LABA: salmeterol ● LAMA: tiotropium ● Inhaled corticosteroids: beclomethasone ● Symbicort - budeonside + formotrel ● If remain symptomatic o Refer to specialist o Consider steroid trial, home nebulisers, theophylline/aminophylline ● Regular oral steroids should be avoided if possible ● Indications for surgery: recurrent pneumothoraces, isolated bullous disease, lung volume reduction surgery ● Pulmonary rehabilitation: o Oxygen therapy (LTOT): § For those who stop smoking only § Consider if: § PaO2 < 7.3 kPa on air during a period of clinical stability § PaO2: 7.3-8 kPa and signs of secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema or pulmonary hypertension 3) MANAGEMENT OF ACUTE EXACERBATIONS OF COPD - usually occurs in Winter due to viral or bacterial infections o Controlled O2 therapy using 24% Venturi Mask aiming for sats at 88-92%. Adjust according to ABG, aiming PaO2>8kPa o 5mg nebulised salbutamol + o 0.5mg nebulised ipratropium + o 200mg IV hydrocortisone OR 40mg PO prednisolone o Then: 500mg/8hr amoxicillin o If no improvement: IV aminophylline o If no improvement: biphasic NIV (BiPAP) o If no improvement: intubation and ventilate in ICU § Prevention of infective exacerbations: pneumococcal and influenza vaccination

Generate a management plan for pneumothorax

1) Tension Pneumothorax (EMERGENCY) o Maximum O2 o Needle decompression: Insert large bore needle into 2nd intercostal space MCL on affected side, just above the 3rd rib to avoid neurovascular bundle below rib. o Up to 2.5 L of air can be aspirated o Stop if patient coughs or resistance is felt o THEN chest drain o Follow-up CXR 2 hrs and 2 weeks later 2) Chest Drain with Underwater Seal: o Performed if: ▪ Aspiration fails ▪ Fluid in the pleural cavity ▪ After decompression of a tension pneumothorax o Inserted in the 4th-6th intercostal space midaxillary line (safe triangle) - avoids long thoracic nerve and artery 3) Recurrent Pneumothoraces o Chemical pleurodesis (fusing of visceral and parietal pleura with tetracycline or calc) o Surgical pleurectomy 4) Advice: o Avoid air travel until follow-up CXR confirms that pneumothorax has resolved o Avoid diving

You are called to see a 19-year-old man in the ED who has presented with chest pain and shortness of breath. He is able to give a history and is mildly short of breath at rest. He developed pain over his right chest earlier that day whilst running for a bus and this has worsened over the past 4 hours. The pain catches him on inspiration in particular although this is not worsening. He has no cough or haemoptysis and is otherwise fit and well. He does not smoke or drink excess alcohol and is on no medication. On examination, he is short of breath at rest but is not pale or cyanosed. Heart rate is 100bpm, blood pressure is 115/65 mmHg and he is apyrexial. His heart sounds are normal. The trachea appears mildly deviated to the left. There is reduced air entry and hyper-resonance to percussion in the right hemithorax. 1) What is the most likely diagnosis at this point?

1) Tension pneumothorax. The history of pleuritic chest pain and shortness of breath combined with reduced lung air-entry and hyperresonance is indicative of a pneumothorax. Pleural effusions are dull to percussion. The presence of tracheal deviation away from the affected side suggests mediastinal shift and a large volume pneumothorax under tension (not a small apical pneumothorax). This patient is not yet compromised but is likely to be very ill very soon - younger patients can deteriorate very suddenly. If you suspect a tension pneumothorax do not delay your treatment by arranging chest radiographs etc. - drain the air before cardiorespiratory compromised occurs.

On the post take round, it was established that the patient had been an IV drug user. He had recently moved down from London, having spent 3 years in India and South-East Asia in the 1990s. He had been treated for pulmonary tuberculosis 3 years ago at another UK hospital but had been lost to follow-up. He had a close friend who had died of HIV/AIDS with TB. Later the same day, the laboratory reported AFBs seen on direct sputum smear, with a negative HIV blood test. What pieces of the following information that could be obtained from his previous hospital would be most useful? The drugs he was treated with before, Previous Chest X-ray appearances, The drug sensitivities of his previous TB infection, Previous HIV status, Information on duration of and adherence to treatment Last liver function test results

1) The drugs he was treated with before 2)The drug sensitivities of his previous TB infection 3)Information on duration of and adherence to treatment **In the context of a likely diagnosis of TB, the most important previous information will relate to the previous TB infection and related drug sensitivities - a history of compliance with treatment or otherwise is also important. The previous chest x-ray and blood results are not important at this stage in making a diagnosis, noting it is always good practice to compare with previous imaging and blood findings if these are available.

A 60-year-old man presented with right-sided chest pain, dyspnoea and a recurrent right sided pleural effusion without any apparent cause at the time of presentation. After 2 years he died. 1) Look at the postmortem image below. Which of the following correctly describes this appearance? 2) Which is the most likely diagnosis in this case? 3) What aspect of the clinical history is important to enquire about if this condition is suspected?

1) There is pleural tumour encasing the lung 2) Mesothelioma of the pleura. This tumour arises from the mesothelial cells of the pleura and spreads initially via the pleural space to encase the lung. 3) Occupational history. In the UK, virtually all cases of mesothelioma are due to exposure to asbestos. It is important to enquire about asbestos exposure which is usually occupational exposure. In particular: boilermakers, plumbers, heating engineers, electrical engineers and anyone working with building materials may have been exposed.

1) On investigation, which of the following would suggest pneumonia case may be a high risk case? 2) Which of the following would suggest this pneumonia may be complicated by underlying pulmonary disease? § CRP of 200 (normal <5) § Lobar consolidation on CXR § Reduced lung volume on affected side § Urea >10 mmol/L (normal range 3-6.5) § WBC 14.0 (normal 4-10x109/L)

1) Urea >10 mmol/L (normal range 3-6.5) o High risk cases may be identified by the CURB-65 score, the elements of which are: Confusion, raised Urea, high Respiratory rate, low Blood pressure and over 65. § Renal impairment is an adverse risk factor (whether it is pre-existing or due to dehydration/sepsis). § Lobar consolidation on CXR, raised CRP and an elevated WBC are common with pneumonia and can occur in patients at lesser levels of risk. § Reduced lung volume may indicate an obstructing lesion (i.e. lung cancer) but is not of itself a risk factor 2) Reduced lung volume on affected side. Reduced lung volume on affected side suggests there may be a proximal lesion (most likely lung cancer), a parapneumonic effusion/pleural empyema, or there is old disease affecting that side. Either way it's not a simple CAP.

When to involve ITU in asthma attack

1. acute severe or life-threatening asthma, who is not responding to treatment 2. Requiring ventilatory support **How they help: § higher level oxygen - optiflow - can deliver up to 60L/min). on ward can only do max of 15L/min. § ventilation

biPAP in COPD

1.CPAP (Continuous Positive Airway Pressure) - tx. T1 respiratory failure (e.g. sleep apnoea) 2.Bi-PAP (Bi-level PAP) - tx T2 respiratory failure (e.g. COPD)

Summary for OSA

1.Sleep Apnoea is caused by changes in the control of breathing, occlusion of the pharyngeal airway leads to obstructive sleep apnoea (OSA) 2.The global prevalence of OSA is increasing, due to links with obesity 3.OSA is associated with arousals from sleep, symptoms of excessive daytime sleepiness and in some people it can also be linked to cardiovascular disease 4.The NICE recommended treatment, for people with moderate to severe OSA plus symptoms of sleepiness is continuous positive airway pressure (CPAP) 5.Adherence to CPAP treatment varies in patients with OSA 6.Alternative treatments are available, although the clinical and cost effectiveness of these treatments sometimes needs to be established 7.Despite being common, awareness and research into OSA is limited

Just as you start to write up the drugs, the patient's wife mentions that he is allergic to penicillin. You elicit a history of an urticarial rash 15 years ago. Assuming that the history is correct, what is the approximate risk of an allergic reaction if you were to give him a cephalosporin such as cefuroxime?

7%. It's said to be 7-10%, and probably towards the lower end of this range.

In uncomplicated pneumonia, how quickly would you expect consolidation to disappear in 95% of patients?

6 weeks. While consolidation can clear quickly, 5% of patients with uncomplicated pneumonia will still have some consolidation at 6 weeks. Unless there are other reasons to suspect lung cancer, it is not appropriate to bronchoscope patients for persistent consolidation (to exclude lung cancer) until at least six weeks after presentation.

The image below was taken from a CTPA study at the level of the main pulmonary arteries. Order the parts of anatomy in descending order (first to last) as labelled A-F.

A - ascending aorta B - descending aorta C - SVC D - main pulmonary trunk E - Thrombus right pulmonary artery F - Thrombus in left pulmonary artery

What management for this CXR?

A - chest drain insertion

What thinking in someone who keeps pigeons

extrinsic allergic alveolitis (bilateral reticular nodular shadowing). bird fanciers lungs

Give a differential for a solitary coin lesion on a chest radiograph.

A coin lesion could be: • Parenchymal tumour: benign, primary lung cancer, secondary lung cancer • Lymph node: lymphoma • Granuloma: TB, sarcoidosis • Abscess • Hamartoma • Foreign object

Mixed respiratory and metabolic acidosis

A mixed respiratory and metabolic acidosis would have the following characteristics on an ABG: ↓ pH ↑CO2 ↓HCO3- Causes of mixed respiratory and metabolic acidosis include: Cardiac arrest OR Multi-organ failure

Mixed respiratory and metabolic alkalosis

A mixed respiratory and metabolic alkalosis would have the following characteristics on an ABG: ↑ pH ↓ CO2 ↑ HCO3- Causes of mixed respiratory and metabolic alkalosis: § Liver cirrhosis in addition to diuretic use § Hyperemesis gravidarum § Excessive ventilation in COPD

You see a 70-year-old man diagnosed with hypersensitivity pneumonitis following a four-month history of shortness of breath at rest and cyanosis. Which of the following does not fall under the category of hypersensitivity pneumonitis? A.Coal worker's lung B.Pigeon fancier's lung C.Mushroom picker's lung D.Farmer's lung E.Malt worker's lung •

A.Coal worker's lung A - this is silicosis (pneumoconiosis)

List the features of heart failure seen on CXR

ABCDE: § Alveolar shadowing § Kerley B lines § Cardiomegaly § Upper lobe diversion § Pleural effusion

Ix for ARDs

ARDS can be defined by the 'Berlin' Criteria. A simplified version is: §Alternative cause (cardiogenic pulmonary oedema) §Rapid onset i.e <1 week §Dyspnoea §Similar on CXR **Investigations: §ABG §CXR/CT §Echocardiogram §Covid Swab **Treat underlying cause + Be aware it exists

A respiratory review is arranged and in view of his weight loss and failure to improve a bronchoscopy is arranged, which shows a tumour obstructing the orifice of his right lower lobe. Biopsies are taken. After a few further days of antibiotic therapy his general condition improves markedly and his temperature settles. Which is currently the most common histological subtype of lung cancer?

Adenocarcinoma. Most common subtypes of lung cancer: § Adenocarcinoma approx 40% § Squamous cell carcinoma approx 25-30% § Small cell carcinoma approx 15% § Large cell undifferentiated approx 10% § Rare types are bronchoalveolar carcinoma and carcinoid, both approx 1% of all tumours, and unrelated to smoking § If a diagnosis of lung cancer is made then further assessments are made in order to determine his general level of fitness for treatment, starting with history and examination, and comorbidities which may preclude surgical or other radical treatment. Staging assessments again begin with clinical assessment eg palpation of supraclavicular nodes, hepatomegaly etc to CT scan thorax and upper abdomen (down to the level of the adrenal glands) to stage the primary tumour, regional and distant nodes, and distant metastatic spread (TNM classification). Only 5-10% of newly diagnosed lung cancer patients are suitable for potentially curative resection.

List 3 investigations for pneumoconiosis

Also on HRCT - * nodular opacities, micronodular shadowing; eggshell calcification (silicosis)

V/Q mismatch

An imbalance in the amount of oxygen received in the alveoli and the amount of blood flowing through the alveolar capillaries **low oxygen levels --> pulmonary vasoconstriction - to divert blood towards places that have more oxygen --> BUT issue w/ COVID is that almost all of the lung is poorly ventilated hence get vasoconstriction everywhere causing pulmonary hypertension

Tx of PE

Are they haemodynamically stable? i.e. SBP <90 mmHg **YES: (Submassive/Small PE) §Respiratory support §Anticoagulation § Anticoagulants: §Fondaparinux/Heparin for 5 days §Warfarin for 3 months **NO (Massive PE) §Respiratory support §1st line: Thrombolysis §2nd line: Embolectomy § IV Thrombolytics (fibrinolytics): §Alteplase §Streptokinase

4 causes of basal creps

§ heart failure, pneumonia, bronchiectasis, IPF **superimposed bronchiectasis caused by: § Pseudomonas aeruginosa § Strep pneumoniae § Haemophilus influenzae

You are told by your registrar that a 69-year-old man has been admitted to the chest ward with dyspnoea, cyanosis and finger clubbing. His chest x-ray shows bilateral lower zone reticulo-nodular shadowing. From the list below, which is the most likely diagnosis? A.Bronchiectasis B.Pulmonary fibrosis C.Bronchogenic carcinoma D.Bronchitis E.COPD

B.Pulmonary fibrosis

A 72-year-old atopic man attends the GP complaining of increased shortness of breath and a nocturnal cough which is productive of clear sputum. The GP notes the gentleman has a history of diagnosed COPD and decides to review his medications. The man hands the GP his inhaler, a SABA. After conducting spirometry, the GP calculates an FEV1 of 40% expected. What is the next most appropriate treatment step? A.Replace the SABA with a LAMA and add an ICS B.Replace the SABA with an LABA and add an ICS C.Add a LABA D.No medication alterations required E.I need to conduct more tests to determine what medications to review

B.Replace the SABA with an LABA and add an ICS **the atopic features suggest the gentleman may respond to steroids

The diagnosis is sarcoidosis. Which 2 of the following should be included in the immediate management plan for this patient?

Bed rest and Follow up in the rheumatology clinic § Antibiotics are not needed for sarcoidosis, nor are iv steroids. § Bed rest is important whilst the ankles are inflamed. § Generally, these patients can be managed in the community with appropriate advice (this would include ensuring appropriate analgesia) § A follow-up appointment should be organised with a Rheumatologist and/or Respiratory team. . § Bronchoscopy is not usually required

You are asked to see a 43-year-old male patient in the medical assessment unit who has been referred by his GP with a cough and shortness of breath. The patient is single, lives in sheltered communal housing, and has a history of alcohol misuse over many years. He is able to provide you with a history. He has felt unwell for 3-4 weeks and has had a cough productive of green/brown sputum for 10 days. He has noted some streaks of blood in the sputum and has had pain over his right and left chest, worse on inspiration. He has felt short of breath and also sweaty, more so at night. He is not eating and has lost 2-3kg in weight. He is not on any medications and denies any significant previous medical history. He smokes 15-20 roll-up cigarettes per day and is still drinking alcohol although he claims this is "under control." He lives in the shelter at times but does spend nights also sleeping rough. On examination, he looks unkempt and underweight. He is clammy and feels hot. Heart rate is 85bpm and regular, BP 140/70mmHg and temperature 38ºC. He has small, tender nodes present in the anterior triangles of his neck. Cardiac and abdominal examination is normal. His respiratory rate is raised and widespread coarse cackles are present on auscultation throughout his lungs. Blood results: Hb 140135-180 g/L WCC 174-11 x109/L Plt 226150-450 x109/L Na+ 138136-145 mM K+ 4.03.5-5.1 mM Ur 6.81.7-8.3 mM ESR 680-15 mm/h Urine dip: normal 1) Which 2 of these diagnoses is most likely? 2) Which 5 of these initial investigations would you undertake?

Bacterial pneumonia, Pulmonary tuberculosis. § This patient presents with symptoms and signs consistent with an infective process. § Although he may have bacterial pneumonia, in the clinical context of homelessness and alcohol misuse tuberculosis (TB) must be excluded. § Mycoplasma tends to present with malaise and a dry cough as does pneumocystis. § Underlying bronchial carcinoma should always be considered in patients with recurrent or non-resolving pneumonia and follow up clinically and radiologically is imperative. Alveolar cell carcinoma is rare and may present with profound production of watery sputum. 2) § Sputum sample x 3 for microbiology § ECG § Blood gases § Blood cultures § Chest radiograph o Most of these investigations would form part of your initial management of any patient presenting with acute respiratory illness of suspected infective cause o Because of the suspicion of TB, multiple sputum samples for Ziehl-Nielsen (ZN) staining and tuberculous culture are recommended. Urgent Gram-stain may also demonstrate a conventional or co-existing bacterial cause. o Some units will offer a TB polymerase-chain reaction test which can provide a rapid diagnosis. Bronchoscopy may be helpful if sputum samples are negative. Immunological testing for TB (tuberculin, Heaf etc) are generally used for screening.

Patient's clinical condition in ABG

Before getting stuck into the details of the analysis, it's important to look at the patient's current clinical status, as this provides essential context to the ABG result. Below are a few examples to demonstrate how important context is when interpreting an ABG: § A 'normal' PaO2 in a patient on high flow oxygen: this is abnormal as you would expect the patient to have a PaO2 well above the normal range with this level of oxygen therapy. § A 'normal' PaCO2 in a hypoxic asthmatic patient: a sign they are tiring and need ITU intervention. § A 'very low' PaO2 in a patient who looks completely well, is not short of breath and has normal O2 saturations: this is likely a venous sample.

Which one of the following is NOT a risk factor for multi-drug resistant tuberculosis?

Being age 20-30 years. Age per se is not a risk factor for drug resistance. Should request PCR probe for rifampicin resistance Use standard 4 drug regime plus streptomycin and ciprofloxacin. Due to previous history and possibility of drug resistance, a standard 4 drug regime is not suitable in this patient. Assuming response to treatment and no significant abscess formation on CT, surgical intervention / radiological percutaneous drainage would not be indicated. In-patient treatment, certainly initially, would be warranted.

A chest X-ray was performed (image below). What does the CXR show?

Bilateral hilar lymphadenopathy

A chest radiograph was performed and is shown below. What abnormality is present?

Bilateral hilar lymphadenopathy. This patient has prominent, bulby and symetrically enlarged hila consistent with bilateral lymphoderopathy. Sarcododsis, lymphoma & TB can all cause this apperance although it is most frequently observed with sarcodosis. The lungs appear normal, although patient has clinical evidence of pulmonary involvement-CT may be helpful to delineate lung changes.

What are Reed-Sternberg cells?

Binucleate lymphocytes - associated with Hodgkin's lymphoma

List a cause of gradual-onset haemoptysis

Bronchiectasis (and other progressive diseases)

You strongly suspect a diagnosis of mycetoma. What other investigations may be helpful?

Bronchoscopy, Aspergillus skin test, Serum precipitins, Repeat sputum samples for culture, Computed tomography thorax. **Aspergillus skin test is positive in 30%. Serum precipitins often strongly positive for Aspergillus, which may also be found in sputum. Computed tomography will delineate lung apex in more detail and mucus plugs may be found at bronchoscopy.

Travel of granulomas in sarcoidosis

granulomas follow lymphatic pathway, follow broncho-vascular bundle --> interlobular septum --> pleura

Which of the following is not a respiratory cause of clubbing? A.Squamous cell lung cancer B.Interstitial lung disease C.COPD D.Cystic fibrosis E.An empyema

C. COPD **Respiratory causes of clubbing •Malignancy •Empyema (lung abscess) •Interstitial lung disease •Cystic Fibrosis

A tall 26-year-old woman comes into the GP complaining of chronic fatigue. Upon further questioning she reports that she 'can never get a good night's sleep' and that she tends to fall asleep a lot at her workplace as a call centre customer service representative. She also mentions that she thinks it may have something to do with a condition her mother had. The only significant finding upon examination is patches of stretchy skin, especially around the neck area. What is the most likely underlying condition leading to disrupted sleep? A.Obesity B.Bad sleeping position C.Marfan's syndrome D.Down's syndrome E.Chronic fatigue syndrome

C. Marfan's syndrome

What this CXR show?

COPD FEV1/FVC < 70 = obstructive. § hyperinflated lungs with flattened diaphragm

Pink puffers and blue bloaters

COPD types, blue bloater = chronic bronchitis, pink puffer = emphysema. § PINK PUFFERS AND BLUE BLOATERS Patients with bronchitis can be described as BLUE BLOATERS as they have REDUCED alveolar ventilation with a low PaO2 and high PaCO2. The high CO2 levels causes cyanosis - but they are not breathless and may go on to to develop cor pulmonale. Their respiratory centres are relatively insensitive to CO2 and they rely on hypoxic drive to maintain respiratory effort. § Patients with emphysema can be described as PINK PUFFERS as they have INCREASED alveolar ventilation, a near normal PaO2 and a normal/low PaCO2. These patients use pursed lip breathing to oxygenate their blood. They are breathless but not cyanosed, and may progress to T1 resp failure.

How is obstructive sleep apnea treated?

CPAP is recommended for patients with moderate to severe OSA and symptoms of sleepiness

Which imaging modality is most useful for diagnosing bronchiectasis?

CT chest - shows dilated bronchi

What form of imaging is most useful in a patient presenting with haemoptysis?

CXR - look for mass lesions, diffuse alveolar infiltrate, hilar lymphadenopathy etc.

Assessing the acutely unwell resp patient

Call for help!! § Airway - Patent?, Stridor? Obstructed? - IF yes 2222 § Breathing - Speech(full sentences?), RR, Sats, ABG, auscultation, CXR § Circulation - HR, BP, CRT, ECG § Disability - GCS, Glucose, Pupils, Neuro-exam § Exposure/Everything else - Abdomen, Signs of overload *** Re-assess!!!!

Causes of metabolic alkalosis

Causes of metabolic alkalosis = either dec H+ or inc HCO3- § GI loss of H+ - vomiting § Renal loss of H+ - loop and thiazide diuretics

Causes of restrictive lung disease

Causes of restrictive lung disease can be pulmonary or non-pulmonary in origin. 1) Pulmonary causes of restrictive lung disease include: a) Pulmonary fibrosis b) Pneumoconiosis c) Pulmonary oedema d) Lobectomy/pneumonectomy e) Parenchymal lung tumours 2) Non-pulmonary causes of restrictive lung disease include: a) Skeletal abnormalities (e.g. kyphoscoliosis) b) Neuromuscular diseases (e.g. motor neuron disease, myasthenia gravis, Guillan-Barre syndrome) c) Connective tissue diseases d) Obesity or pregnancy

Which of the following would be the next investigation of choice to confirm your diagnosis of PE?

Computed tomography pulmonary angiography (CTPA). CTPA is the imaging investigation of choice for the diagnosis of suspected pulmonary embolism. As a modality CTPA is relatively non-invasive although it does involve intravenous injection of iodinated contrast and also the use of ionising radiation. It is not suitable for patients with a history of iodine allergy or renal impairment which may be worsened by the use of iodinated contrast. V/Q scans are being used less but do have a role in patients with renal failure or contrast allergy. MR angiography has not been widely investigated and both MR and V/Q nuclear medicine investigations are not appropriate in shocked patients. Conventional pulmonary angiography is performed via introduction of the catheter into a femoral vein which is then manipulated around the right heart into the pulmonary arteries and contrast injected. This is not widely used now as a diagnostic tool but is used for direct delivery of thrombolysis. Ultrasound is not indicated in this situation and is primarily used to diagnose lower limb deep venous thrombosis and not pulmonary embolus.

What is the most common cause of heart failure?

Coronary artery atherosclerosis

Less typical CT patterns in sarcoidosis

hence here would need histology to confirm

What is gold standard investigation for diagnosing bronchiectasis?

high resolution CT - signet ring sign

A 26-year-old bus driver presents to the GP complaining of a worsening shortness of breath. On examination, the patient is afebrile, has a BP of 110/85 and has a marked wheeze on auscultation. The only medications the patient is on is Salbutamol, PRN. What is the next most appropriate treatment step as per the treatment guidelines for this condition? A.Replace the blue inhaler with a brown, low-dose inhaled corticosteroid B.Replace the blue inhaler with a long-acting beta-agonist medication C.Replace the blue inhaler with a long-acting muscarinic agonist D.Add an inhaled low-dose corticosteroid to her medications, taken OD E.Add oral corticosteroid tablets to her medications, taken OD

D.Add an inhaled low-dose corticosteroid to her medications, taken OD

A 65-year-old man with a medical background of benign prostatic hyperplasia, presents to the GP with a 1 week history of worsening shortness of breath on exertion. He has a temperature of 38.5C, reports no weight loss but does mention some mild fatigue from his 'pet pigeons keeping him up all night' recently. On auscultation, the GP can determine fine, bi-basal inspiratory crackles. What is the most likely diagnosis? A.COPD B.Lung cancer C.Bronchiectasis D.Hypersensitivity pneumonitis E. Idiopathic pulmonary fibrosis

D.Hypersensitivity pneumonitis

What does this CXR show?

DDx - fibrosis (reticular nodular shadowing (lines + dots)) FEV1/FVC > 70 --> restricted

Recognise the presenting symptoms of pulmonary embolism

Depends on the SITE and SIZE of the embolus ● Small - may be ASYMPTOMATIC ● Moderate: o Sudden-onset SOB o Cough o Haemoptysis o Pleuritic chest pain ● Large (or proximal) o As above and: ▪ Severe central pleuritic chest pain ▪ Shock ▪ Collapse ▪ Acute right heart failure ▪ Sudden death ● Multiple Small Recurrent: o Symptoms of pulmonary hypertension

The chest radiograph is shown below. What does this show?

Diffuse nodular infiltrates present in both lungs. TB on a chest radiograph can have a variety of appearances. Primary TB often causes no symptoms and calcifications may be seen where a lesion has healed. Reactivation can cause pneumonic consolidation, cavitation, lymphadenopathy or nodular densities (miliary TB = multiple small nodules 1-2mm in size).

His chest radiograph is shown below. What are the radiological findings?

Diffuse reticular/interstitial density in both lungs. This patient has small volume lungs with an increase in interstitial / reticular ("net-like") density in keeping with lung fibrosis. The appearances are non-specific and do not usually give a cause of the condition.

A 58-year-old man with known COPD, diagnosed eight months ago, attends your clinic with persistent shortness of breath despite stopping smoking and using his salbutamol inhaler (given to him at the time of diagnosis), which he finds he is using more frequently. You assess the patient's lung function tests that have been recorded just before he saw you in clinic on this occasion. His FEV1 = 65 per cent of the predicted value. Oxygen saturations are 95 per cent on room air, respiratory rate in 18, and his temperature is 37.1°C. From the list below, select the next most appropriate step in this patient's management. A.40 mg daily oral prednisolone for 5 days B.Start long-term oxygen therapy C.Start inhaled corticosteroid therapy D.Add oral theophylline therapy E.Add a long-acting β2 agonist inhaler

E. Add a long-acting β2 agonist inhaler (Taken from 500 SBA's by Sukhpreet et al)

A 17 year-old girl presents to the local A&E complaining of worsening shortness of breath, despite use of what she describes as her 'blue inhaler'. On examination her oxygen saturations are 95%, she is afebrile and has a BP of 101/67. The attending physician takes an ABG and the results are shown below. Grade the severity of this asthma attack. pH: 7.25 pCO2: 7.4 kPa (4.5-6.0) pO2: 10.4 kPa (>10.5) HCO3: 23 mmol/l A.I cannot tell from the information available B.Moderate C.Acute severe D.Life threatening E.Near fatal

E.Near fatal

From age 55 up to the time of presentation, this patient worked as a boilermaker. He also worked as a heating engineer from age 30-40. Which of these two employments is more likely to have caused his mesothelioma?

Employment age 30 - 40 (heating engineer). The "lead time" between asbestos exposure and development of mesothelioma is almost always more than 20 years. It is therefore important that enquiries about the occupational history go back in detail to the patients' early career. Identifying which of several employments was the relevant exposure might be important if the relatives claim compensation.

Erythema nodosum is associated with what?

Erythema nodosum is associated with: § Infections (streptococcal = commonest infectious cause); TB; Mycoplasma pneumonia; psittacosis; Yersinia, Salmonella and Campylobacter gastroenteritissystemic fungal infections including histoplasmosis, blastomycosis, coccidioidomycosis); § Sarcoidosis § Inflammatory bowel disease (Crohn's disease and Ulcerative colitis) § Neoplasia (leukaemia, Hodgkin's disease) § Drugs especially sulfonamides and oral contraceptives § Pregnancy.

What is this rash?

Erythema nodosum. Erythema nodosum is associated with: § Infections (streptococcal = commonest infectious cause); TB; Mycoplasma pneumonia; psittacosis; Yersinia, Salmonella and Campylobacter gastroenteritissystemic fungal infections including histoplasmosis, blastomycosis, coccidioidomycosis); § Sarcoidosis § Inflammatory bowel disease (Crohn's disease and Ulcerative colitis) § Neoplasia (leukaemia, Hodgkin's disease) § Drugs especially sulfonamides and oral contraceptives § Pregnancy.

The image below is of the patient's legs. What clinical sign does it show?

Erythema nodosum. This image demonstrates erythema nodosum (EN). There are rounded, erythematous and raised lesions present on the anterior shins. EN can be associated with streptococcal infection, TB, sarcoidosis, drugs, inflammatory bowel disease and histoplasmosis.

The patient's ECG trace is shown in figure 2. What best describe the ECG findings?

First degree AV block and right bundle branch block. See the ECG strip in the image below. The ECG demonstrates 2 main waveform abnormalities: 1) first degree AV block: note markers in lead 2 showing the lengthened PR interval 2) right bundle branch block: note the wide secondary R-wave in the right chest leads arrowed in V1, and the deep S-wave arrowed in V6

ground glass vs consolidation

Ground-glass opacification/opacity (GGO) is a descriptive term referring to an area of increased attenuation in the lung on computed tomography (CT) with preserved bronchial and vascular markings. § seen including tuberculosis, nonspecific interstitial pneumonia, sarcoidosis

Presentation of idiopathic pulmonary fibrosis

History: •SOB on exertion •Dry cough with no wheeze •Fatigue/weight loss •Exam: •Clubbing •Bi-basal FINE inspiratory crackles (like snow crunching) • Late stage disease may show RHF signs •Cyanosis **Risk factors: •Animal and vegetable dusts •Smoking •Drugs = -Methotrexate (antimetabolite) - RhA/AI, Bleomycin (chemo drug) and Amiodarone (arrythmias) • Occupation - exposure to wood/metal/dusts **IPF - Chronic inflammatory condition of the lung, resulting in fibrosis of the alveoli and interstitium. § Fibrosis = excess collagen in connective and interstitial tissue causing thickening. It is RARE, with 6/100,000 affected. § Occurs in genetically predisposed individuals

Bronchiectasis - Presentation

History •Persistent cough with COPIOUS purulent sputum (> laid flat) •Breathlessness •Intermittent haemoptysis •Symptoms tend to begin after an acute respiratory illness and worsen during this period Exam: •Clubbing •Coarse inspiratory crackles (usually at lung base, shift with coughing) - like in COPD as something blocking the airways (mucus) •High-pitched inspiratory wheeze

Examination signs of COPD patient

History •SOB •Chronic Productive Cough •Wheeze Exam •Inspection - Tar staining, Cyanosis and Barrel Chest, may have Asterixis, purse-lipped breathing •Palpation - Reduced lung expansion and Hyperresonance •Auscultation - Wheeze, Coarse crackles •May see signs of RHF (secondary to pulmonary hypertension)) **Risk Factors include: •Smoking !! •FHx •Alpha-1 antitrypsin deficiency **Notes: § Cough with clear sputum usually, may be tinged if infective exacerbation. § A1AT - deficiency of this enzyme. Rare* but consider if patient is young/non-smoker/FHx of A1AT but has COPD symptoms § Coarse crackles are like rubbing hair between your ringers, fine crackles (as seen in fibrosis) are like snow-crunching sounds. Coarse is due to airway clogging.

What will most asthma patients be on?

ICS/LABA combination

What are the key cytokines that drive clinical manifestations of asthma

IL-4,5,13 --> B cell class switching and IgE production --> basophil and mast cell degranulation --> all of effects

Mepolizumab

IL-5 antagonist. Get this injection (IV/SC) every 4 week --> measure exacerbations and FEV1. There is reduction of about 50% of exacerbations (reduced IgE). And improvement in FEV1. Also improvement in QoL (SGRQ score)

What is interstitial lung disease?

ILD is a term which includes a large group of disorders that cause scarring (fibrosis) of the lungs. These include: •Idiopathic pulmonary fibrosis •Hypersensitivity pneumonitis (EAA) •Pneumoconiosis •Sarcoidosis

What diagnoses should you be concerned about regarding haemoptysis?

INVITED MD: 1) Infective: pulmonary tuberculosis (TB), bronchitis, pneumonia, lung abscess, mycetoma 2) Neoplastic: primary lung cancer, metastatic lung cancer 3) Vascular: pulmonary infarction, left ventricular failure, bleeding diathesis, arteriovenous malformation, vascular-bronchial fistula 4) Inflammatory: Wegener's disease, Goodpasture's syndrome, systemic lupus erythematosus, hereditary haemorrhagic telangiectasia (Osler-Weber-Rendu syndrome), polyarteritis nodosa, microscopic polyangiitis 5) Traumatic: iatrogenic (lung biopsy, post-intubation), wounds (broken rib) 6) Endocrine: (none) 7) Degenerative: bronchiectasis 8) Metabolic: (none) 9) Drugs: warfarin (bleeding diathesis), crack cocaine use **The most common causes are INFECTIONS and EXACERBATIONS of chronic obstructive pulmonary disease (COPD), but these should never be assumed to be the cause. Lung cancer is a 'MUST EXCLUDE' diagnosis in a presentation of haemoptysis. Note that up to a third of cases of haemoptysis have NO identifiable cause.

Hypoxaemia

If PaO2 is <10 kPa on air, a patient is considered hypoxaemic. If PaO2 is <8 kPa on air, a patient is considered severely hypoxaemic and in respiratory failure.

Define Interstitial lung disease

Interstitial lung disease (ILD) is an umbrella term for a large group of disorders that cause scarring (fibrosis) of the lungs. The scarring causes stiffness in the lungs which makes it difficult to breathe.

How would you treat massive PE immediately?

Intravenous or intra-arterial infusion of thrombolytic agent In a case of massive pulmonary embolus the most appropriate treatment, depending on local availability of services, is urgent pulmonary angiography and then direct perfusion of thrombolytic drugs into the pulmonary arteries to dissolve the thrombus. Thrombolysis can also be administered via a peripheral intravenous route if local radiological expertise is not available or in less severely compromised patients. Surgical thrombectomy is an alternative within cardiothoracic units but is significantly more invasive than thrombolysis infusion. Subcutaneous low molecular weight heparin therapy and subsequent oral anticoagulation are used for smaller pulmonary emboli and are not appropriate acutely for massive pulmonary embolus although these agents will be needed subsequently for longer term treatment following dissolution of the acute thrombus. Remember there are several contra-indications to the use of thrombolytic agents (e.g. streptokinase, urokinase, r-TPA - recombinant - Tissue Plasminogen Activator). These include: § recent haemorrhage, trauma, surgery § suspected or known aortic dissection § suspected or known peptic ulcer disease § previous allergy to agent e.g streptokinase § previous history of suspected or known haemorrhagic intracerebral event § severe hypertension

What does this x-ray show

Is a left lower lung collapse --> hence also tracheal deviation to the left

Mixed acidosis/alkalosis

It's worth mentioning that it is possible to have a mixed acidosis or alkalosis (e.g. respiratory and metabolic acidosis/respiratory and metabolic alkalosis). § In these circumstances, the CO2 and HCO3- will be moving in opposite directions (e.g. ↑ CO2 ↓ HCO3- in mixed respiratory and metabolic acidosis). Treatment is directed towards correcting each primary acid-base disturbance. You can see some causes of mixed acidosis and alkalosis below

A 70-year-old female attends the ED with complaints of sharp chest pain, fever and shortness of breath. She has been a heavy smoker for 40 years and has a productive cough. On examination, she appears distressed with a respiratory rate of 40/min and oxygen saturations of 83% on air. Chest auscultation reveals reduced breath sounds and bronchial breathing on the left side. 1) What does CXR show? 2) What are the two most likely causes? 3) What are the four most appropriate investigations to confirm the diagnosis?

Left lung collapse/consolidation. There is considerable mediastinal shift to the left so there must be a considerable loss of lung volume on that side. Also there is an air bronchogram of at least one of the larger bronchi indicating consolidation. 2) Pneumonia. Obstruction of left bronchus. Both the left obstruction of the main bronchus and pneumonia would give such CXR appearance. A foreign body may cause collapse, but would not result in consolidation. 3) § Bronchoscopy +/- biopsy § CT chest § Sputum microscopy and culture § Blood culture **In patients with suspected infection, it is essential to obtain culture samples early, ideally before the initiation of empiric antibiotics. Arterial blood gases may be helpful in assessing the severity of illness, but it will NOT be diagnostic of a specific condition. The patient is too ill to perform formal lung function tests. Appropriate imaging will help to confirm or exclude the most likely pathology.

CXR showing tension pneumothorax

Left-sided tension pneumothorax. Life threatening condition defined as air trapped in the pleural cavity under a positive pressure, causing cardiopulmonary compromise

Sarcoidosis may be a family of diseases

Lofgren's disease has very distinct genetic associations (HLA DR3, CCR2), demographics and clinical findings • Different HLA associations with different organ involvement (uveitis, cardiac) • Different HLA associations with acute (HLA-DR3) and chronic (HLA-DR14 and 15) disease

He has small volume lungs with reticular/interstitial density seen bilaterally. What are these appearances consistent with?

Lung fibrosis. Emphysema and asthma tend to cause lung hyperinflation. The chest film is often normal in asthma. Bronchiectasis causes ring shadows with bronchial wall thickening.

What drives respiration?

Mainly the arterial pH (closely related to pressure of CO2) which is detected by chemoreceptors (carotid and aortic bodies and peripheral chemoreceptors) and signals to the respiratory centre

Bronchoscopy is undertaken (image below) and reveals the following obstructive lesion in the left main bronchus. What is the diagnosis likely to be?

Malignant bronchial tumour. there is a fungating mass invading the bronchial lumen. Malignant bronchial tumour is the most likely diagnosis given the bronchoscopy appearance.

A 29-year-old African woman has presented to the medical assessment unit with increasing shortness of breath, a dry cough and weight loss. 1) Her chest radiograph is shown below. What abnormality do you see? 2) Which of the following would you consider to be the most likely explanation for the radiological appearances? 3) Would counselling and HIV testing be indicated?

Miliary nodular lung densities. Multiple small nodules (1-2mm in size) are seen throughout both lungs with some patchy consolidation seen in the left lower zone. There are a number of causes of this type of nodular appearance, also known as miliary, with tuberculosis the most likely in a young African or Asian immigrant with these symptoms. 2) Tuberculosis. Sarcoid, metastases, occupational lung disease and extrinsic allergic alveolitis can also cause military shadowing. 3) Yes. Immunosuppression due to HIV infection should be excluded.

What are the severities of COPD

Minimally reversible airflow obstruction characterised by an FEV1/FVC ratio of <0.7. ** Severity classified by FEV1: § Mild FEV1 >80% predicted § Moderate FEV1 50-80% Predicted § Severe - FEV1 30-50% Predicted § Very severe - FEV1 <30% Predicted **GOLD Criteria for the management of COPD based on symptoms, exacerbation and severity of obstruction

Your history-taking reveals that Mrs Finnegan is a retired office worker who is diabetic and takes 'aspirin, a pill for the diabetes, and a water tablet for blood pressure'. Her past medical history is significant for an anterior myocardial infarction (MI) 5 years ago, after which she received a single vessel coronary artery bypass graft (CABG). Her parents 'died of old age' and her only sister died of lung cancer. She smoked about 10 cigarettes a day from her early 20s until her late 60s. She has slept propped up with several pillows for the last few years as this is 'more comfortable'. She becomes short of breath when gardening or walking uphill, but feels much better if she stops to catch her breath for a minute. She has not had any cough, chest pain, or dark or bloody faeces or urine. She has not lost any weight, had any night sweats, or noticed any change in appetite. However, she is worried that she may have lung cancer like her sister and was hoping you might be able to do some test to rule that out. On examination, there are no signs of cyanosis or anaemia. Her blood pressure is 155/80 mmHg and her heart rate is 85 bpm and regular. There is no cervical lymphadenopathy. Her JVP is elevated to 6 cm above the angle of Louis and her apex is most prominent lateral of the mid-clavicular line, in the sixth intercostal space. There is a median sternotomy scar from her CABG 5 years ago. There are no heaves or thrills, and auscultation reveals no murmurs. Chest expansion is symmetrical and resonant to percussion. The trachea is central and breath sounds are heard throughout both lungs, albeit with crackles in both lung bases. Her liver is not enlarged or tender but there is pitting oedema in both ankles. Abdominal examination is normal. Neurological examination is also normal. Mrs Finnegan's history and examination are consistent with a particular diagnosis for her shortness of breath, but this should be confirmed or refuted with basic investigations. Given the history and examination, what is the most likely cause of Mrs Finnegan's shortness of breath?

Mrs Finnegan is an elderly lady with shortness of breath and significant risk factors for both cardiovascular disease (ex-smoker, hypertension, diabetes mellitus, previous MI) and respiratory disease (>20 pack years of smoking). However, she gives a clear history of predictable shortness of breath on exercise that is relieved by rest. She has orthopnoea, and has a displaced apex beat, bilateral pulmonary oedema, and ankle oedema. Put together, this all suggests that Mrs Finnegan likely has congestive heart failure that is causing reduced cardiac output, pulmonary oedema, and peripheral oedema.

Mrs Finnegan's ECG shows pathological Q waves in leads V1-V4. Her FBC is normal. Her glucose is 6.2 mM and her HbA1c is 6.8%. Her total cholesterol = 6.2 mM, LDL = 3.1 mM and HDL = 1.1 mM. What is the diagnosis for Mrs Finnegan? Can you identify any risk factors for this diagnosis in her history and investigations?

Mrs Finnegan is probably suffering from congestive cardiac failure as she has signs of both left ventricular failure (bibasal crackles suggestive of pulmonary oedema, and a displaced apex beat as well as a chest radiograph showing bilateral pulmonary oedema) and right ventricular failure (peripheral oedema and a raised JVP). Heart failure is a syndrome, not a true pathological diagnosis. Mrs Finnegan's heart failure could be due to any number of causes (e.g. hypertension, valvular disease, alcohol-induced cardiomyopathy) but it is important to remember that the most common cause of heart failure is ischaemic heart disease and that this patient has significant risk factors for this pathology: • She smoked 10 cigarettes (half a pack) every day for 40 years = 20 pack years. • She has diabetes mellitus. • Her total cholesterol (6.2 mM) and LDL (3.1 mM) are elevated. • Her hypertension is not well controlled (155/80 mmHg). National Institute for Health and Clinical Excellence (NICE) guidelines recommend a target blood pressure of <140/85 mmHg for most people, <130/80 mmHg for diabetics or <125/75 mmHg for patients with proteinuria. Th e absence of angina in Mrs Finnegan does not exclude ischaemic heart disease since patients with diabetes mellitus may have 'silent' ischaemia.

Mrs Virginia's chest radiograph is shown in Fig. 7.1. How would you interpret this radiograph?

Mrs Virginia's chest radiograph shows an area of dense opacity in the right side of her chest. Th e dense pattern confined to a discrete area of lung is in keeping with consolidation. Given that the right hemidiaphragm is still visible but the right heart border has been obscured this is therefore likely to represent consolidation in the right middle lobe - which is consistent with the clinical findings on examination.

Mrs Virginia says that she has had a cough for months but that over the last few days she has been 'coughing more, and more muck has been coming up'. She says that the sputum is yellow-green, but there has been no blood. There appear to be no triggers or periodicity. In her history she reveals that she is a long-term smoker (60 years smoking 10 a day = 30 pack years) and has a diagnosis of COPD. She says she walks a mile a day to the shops and back, and has no history of asthma, allergies, or reflux. She uses inhalers for her COPD ('a dry powder one, a blue spray, and a brown spray') but is not on home oxygen and takes no other medications. Reassuringly, she has had no night sweats, rigors, or weight loss, and is no more breathless than usual. However, she says she has felt a little hot over the last day. She has not been abroad 'since the war', although she went on a Saga holiday in Eastbourne the previous summer. What is the differential diagnosis of cough? Try thinking about conditions which present acutely or chronically, and whether the cough would be dry or productive? Which of these are most likely given this lady's presentation?

Mrs Virginia's complaint is an acute worsening of her productive cough. Th is therefore narrows the differential down to an infectious cause. Of those, the absence of constitutional features (e.g. weight loss, night sweats) or foreign travel makes TB unlikely.

Stage 2 Sarcoidosis

Multiple miliary peribronchiolar nodules are scattered diffusely throughout both lungs. In addition, BOTH HILAR REGIONS ARE ENLARGED due to lymph node enlargement.

What is third step in ABG?

PaCO2: At this point, prior to assessing the CO2, you already know the pH and the PaO2. So for example, you may know your patient's pH is abnormal but you don't yet know the underlying cause. It could be caused by the respiratory system (abnormal level of CO2) or it could be metabolically driven (abnormal level of HCO3-). Looking at the level of CO2 quickly helps rule in or out the respiratory system as the cause for the derangement in pH.

Define type II respiratory failure.

PaO2 < 8 kPa PaCO2 > 6.5 kPa **Treatment: § Controlled oxygen therapy (maintain oxygen sats 88-92%) § Improve ventilation (if CO2 fails to drop with oxygen therapy) § Treat underlying cause

Can cure bronchiectasis?

NO, is irreversible. § conservative to help reduce infections - exercise, good diet; vaccinations; airway clearance (chest physio, high frequency oscillation devices, nebulised hypertonic saline) § pharm: IB Abx, oral Abx (prophylactic) § surgical - localised resection **Complications: •Recurrent infections •Cor pulmonale (RHF) •Respiratory failure

Where to keep TB patient?

Negative pressure isolation room This patient will need to be treated in isolation with appropriate precautionary measures for staff, a negative pressure environment is important to prevent spread of airborne microbes.

Pattern of nodules in sarcoidosis

Nodular Pattern: Bronchocentric Peri-fissural Subpleural

A CXR is shown below. Which of the following best describes the radiographic findings?

Normal film. CXR is normal. A normal CXR is not uncommon with a pulmonary embolus but is helpful in excluding other pathologies such as pneumothorax and pneumonia. Abnormalities to look out for in a massive pulmonary embolus would include abrupt cut off of a dilated pulmonary artery secondary to embolus with associated pulmonary oligaemia (this finding may be subtle). Areas of linear atelectasis and consolidation can also occur with smaller lesions.

What is pressure in pleural space?

Normal pressure is -5 to -8 cm H20. Pneumothoraces can be classified as primary and secondary

Adherence to CPAP in Patients with OSA

Not all patients are able to tolerate CPAP treatment

How to initially treat symptomatic pulmonary disease, cardiac and neurological sarcoidosis?

Oral high dose Prednisolone (40mg/24hr)

Non-pharmacological interventions for COPD

Other treatment: •Smoking cessation advice •Annual flu vaccinations •Pneumococcal vaccination •Lung volume reduction surgery may show improved survival rates, as well as long term O2 therapy **Long term O2 therapy is only given if: •Patients have a PO2 < 7.3 kPa •PO2 of 7.3-8 kPa and one of the following: secondary polycythemia, nocturnal hypoxemia, peripheral oedema or pulmonary hypertension * *COPD are often smokers and hence very dangerous to keep oxygen at home!

How would you treat tension pneumothorax?

Oxygen by mask, Analgesia as needed, Undertake immediate therapeutic aspiration of air percutaneously, Prepare patient for insertion of chest drain. Therapeutic aspiration of air should be undertaken (needle or venflon) to relieve tension and improve patient condition. For a pneumothorax of this size needle aspiration alone is unlikely to be sufficient and a chest-drain will be needed. This can be prepared while you aspirate air from the chest. Sites for aspiration/drain:- - 2nd intercostal space, mid-clavicular line - 6th intercostal space, mid-axillary line

Which infectious agents most associated with sarcoidosis?

P. acnes and mycobacteria. § but significant heterogeneity between studeis, especially ones with mycobacteira. § most on P.acnes were on japanese patients § unidentified organisms may be the cause in proportion of cases § colonising microbes might cause disease by their antigenic or adjuvant properties rather than infection

what does this CXR and CT show?

PE. Management of LMWH

What see on inspection in idiopathic pulmonary fibrosis

Patient History: •Animal/vegetable dusts •Smoking status •Occupation •Drugs: §Bleomycin §Methotrexate §Amiodarone **Aetiology: § Genetically predisposed host (e.g. surfactant protein mutations); recurrent alveolar damage results in cytokine release, activating fibroblasts, differentiating into myofibroblasts and increased collagen synthesis § Drugs can produce similar illnesses (bleomycin, methotrexate, amiodarone) § Risk Factors: smoking, occupational exposure to metal/wood, chronic micro-aspiration, animal/vegetable dusts **will have SOBOE, no wheeze, dry cough.

You review the chest radiograph (image below). What does this show?

The left lower lobe has collapsed - this can be seen in the image below as a triangular area of increased density behind the heart (arrows) with loss of clarity of descending aorta and diaphragm. This is likely to be due to a retained mucus plug - treat by physio and follow-up chest x-ray. Involve chest team (bronchoscopy) if collapse fails to resolve.

Which occupational disease is associated with chronic dust inhalation?

Pneumoconiosis

CURB-65

Point scoring system used for evaluating the risk of mortality with pneumonia. ● Assess severity using the British Thoracic Society Guidelines: o CURB-65 is a simple, validated scoring system o 1 point for each: ▪ Confusion - abbreviated mental test <8 ▪ Urea >7mmol/l ▪ Respiratory rate greater than or equal to 30 ▪ BP < 90 systolic and/or 60 diastolic ▪ Age greater than/equal to 65 o 0 - 1: home treatment if possible o 2: hospital therapy o 3 or more: severe pneumonia - consider ICU

Asbestosis CXR

Posterior-anterior view of the chest with 'mesa'-like pleural thickening of the left diaphragm and 'in-profile' pleural thickening of the mid zones of both the left and right lungs

Potential causes of type 2 respiratory failure

Potential causes of type 2 respiratory failure: § Increased airways resistance - COPD/asthma § Reduced breathing effort - drug effects (e.g. opiates)/brain stem lesion/extreme obesity § A decrease in the area of the lung available for gas exchange - chronic bronchitis § Neuromuscular problems - Guillain-Barré syndrome/motor neuron disease § Deformity - ankylosing spondylitis/flail chest

Which of the following statements concerning mycetoma are true? Previous tuberculosis is a predisposing factor, Previous sarcoidosis is a predisposing factor, Smoking is a risk factor, Oral antifungal agents are the treatment of choice, Surgery is indicated for solitary symptomatic lesions, Mycetoma is a cause of massive haemoptysis.

Previous tuberculosis is a predisposing factor, Previous sarcoidosis is a predisposing factor, Surgery is indicated for solitary symptomatic lesions, Mycetoma is a cause of massive haemoptysis. Oral treatments are of limited use. Percutaneous antifungal injection can be helpful. Asymptomatic lesions may not need treatment. Surgical excision is the treatment of choice.

Primary vs secondary cancer CXR

Primary lung cancer: •Consolidation (usually heterogenous) •(Bi-hilar lymphadenopathy) •(Pleural effusions) (Cavitating lesions - usually SqCC) **Secondary lung cancer: •Coin shaped lesions (cannonball mets)

What is your differential diagnosis for shortness of breath in a post-operative patient? What key clues will help you identify the most likely cause? How will you manage each cause?

Pulmonary Oedema PE Atelectasis Pneumonia (aspiration) Pneumothroax

You are asked to see a 62-year-old female on the ward who has developed severe shortness of breath. This has been of sudden onset and is associated with mild central chest discomfort but no significant cough or sputum production. The patient has recently been moblised following admission and treatment for a chest infection. The patient is not taking other medication and has no other significant medical history of note. On examination, she is unwell, appears pale, clammy and poorly perfused peripherally. She has a temperature of 37.2°C, pulse 110bpm regular and blood pressure 80/50 mmHg. There is elevation of the jugular venous pressure but heart sounds appear normal and chest examination is unremarkable. Her abdomen is soft and non-tender there is no evidence of lower limb oedema and no significant abnormality is apparent on initial neurological examination. Results of initial blood investigations including full blood count and urea and electrolytes are available with no significant abnormalities. 1) Which of the following is the most likely clinical diagnosis? 2) What further initial investigations would be helpful following initial resuscitation?

Pulmonary embolism. The most likely diagnosis is that of a massive pulmonary embolism. The combination of sudden severe shortness of breath, shock and elevation of jugular venous pressure secondary to right heart strain are consistent with this diagnosis. Pulmonary embolism may be associated with central chest discomfort only when massive and indeed chest pain may not be a feature. Smaller emboli may present with more pleuritic type chest pain and haemoptysis. The normal chest examination would make pneumothorax and pneumonia less likely and the history is not typical for myocardial infarction (severe central chest pain, crushing in nature with radiation often to left arm or jaw) or aortic dissection (central chest pain which may radiate to the back and is often described as "tearing" in nature). 2) Initially an ECG, ABG and CXR are indicated. D-dimer is a protein produced by the action of plasma on cross linked fibrin and raised levels may occur in venous thromboembolic disorders. D-dimer however may also be raised in a number of other conditions including recent bed rest (as in this case), surgery and malignancy and in these patient groups D-dimer estimation is not specific for pulmonary embolus. Troponin levels likewise can be elevated in both myocardial infarction and pulmonary embolus.

Mrs Finnegan's erect postero-anterior (PA) chest radiograph. What does it show?

Remember to go through radiographs systematically. • Check the patient details are correct: none are shown here for confidentiality. • Check the radiograph is technically adequate: full coverage, good penetration, not rotated, adequate inspiration. Th is radiograph is rotated to the right. • Present your findings logically. Mrs Finnegan's radiograph shows a reticular pattern of opacification throughout both lung fields, which is much denser in the lower zones bilaterally. There is upper lobe diversion of the pulmonary veins in both lung fields. The heart shadow is significantly enlarged. There are faintly visible sternal sutures (from her CABG) and a small amount of fluid in the transverse fissure.

If PaO2 in ABG is v low what you think?

Remember to think about the context i.e. are they on high flow oxygen or if they are well but PaO2 is very low, likely a venous sample!

Recognise the signs of pulmonary embolism on physical examination

Severity of PE can be assessed based on associated signs: ● Small - often no clinical signs. There may be some tachycardia and tachypnoea ● Sudden onset ● Moderate: o Tachypnoea o Tachycardia o Pleural rub o Low O2 saturation (despite O2 supplementation) o Pyrexia o Hypotension ● Massive PE: o Shock o Cyanosis o Signs of right heart strain: ▪ Raised JVP ▪ Left parasternal heave ▪ Accentuated S2 heart sound ● Multiple Recurrent PE: o Signs of pulmonary hypertension o Signs of right heart failure

Causes of respiratory alkalosis

Respiratory acidosis is caused by inadequate alveolar ventilation leading to CO2 retention. A respiratory acidosis would have the following characteristics on an ABG: ↓ pH ↑ CO2 ** Causes of respiratory acidosis: § Respiratory depression (e.g. opiates) § Guillan barre - paralysis = poor ventilation § Asthma § COPD § Iatrogenic (incorrect mechanical ventilation settings) **Causes of respiratory alkalosis:- excessive ventilation Respiratory alkalosis is caused by excessive alveolar ventilation (hyperventilation) resulting in more CO2 than normal being exhaled. As a result, PaCO2 is reduced and pH increases causing alkalosis. A respiratory alkalosis would have the following characteristics on an ABG: ↑ pH ↓ CO2 § Anxiety § Pain - inc RR § Hypoxia (---> increased alveolar ventilation in an attempt to compensate.) § Pulmonary embolism § Pneumothorax § Iatrogenic (e.g. excessive mechanical ventilation)

Causes of respiratory acidosis

What is the diff erence between type I and type II respiratory failure? What are some of the causes?

Respiratory failure is defined as impairment of pulmonary gas exchange sufficient to result in hypoxaemia (PaO2 <8 kPa or 60 mmHg) and/or hypercapnia (PaCO2 >6 kPa or 45 mmHg). It is divided into two types depending on whether CO2 is expelled (and therefore normal or low) or retained (and therefore raised): 1) Type I respiratory failure • Pathology: this is a problem with one gas (oxygen), i.e. hypoxaemic respiratory failure. It is caused by a VENTILATION-PERFUSION MISMATCH in the lungs, with ventilation of the unaffected alveoli normal. Compensatory hyperventilation increases CO2 removal but not O2 saturation as blood leaving the unaffected alveoli is already saturated. • Causes: any lung disease, e.g. asthma, COPD, pneumonia, pulmonary fibrosis, pulmonary oedema. 2) Type II respiratory failure • Pathology: this is a problem with two gases (oxygen and carbon dioxide), i.e. hypercapnic respiratory failure (low PaO2 and a raised PaCO2). This is caused by VENTILATORY FAILURE, i.e. impairment of the respiratory 'bellows', resulting in alveolar hypoventilation. • Causes: − Decreased respiratory drive, e.g. opiates, central neurological damage (stroke, head trauma) − Impaired lung movements, e.g. chest wall deformity (as in Duchenne's muscular dystrophy for example), neuromuscular impairment (as in motor neuron disease) − Lung pathology, e.g. long-standing COPD, pulmonary fibrosis.

The chest radiograph is shown below. Which statement below best describes the findings?

Right upper zone opacity containing central cavity. Magnification view of the right upper zone shown below (image below) demonstrates a crescentic lucent line (arrows) which represents air between the central fungus ball and the lining of a pre-existing cavity. This cavity is likely to relate to previous tuberculous exposure.

Biochemical investigations demonstrate an elevated serum ACE (angiotensin converting enzyme) level and a mildly elevated corrected serum calcium. What do you now think is the most likely clinical diagnosis?

Sarcoidosis. Sarcoidosis is the most likely unifying diagnosis. Lymph node biopsy can also help by demonstrating non-caseating granulomata. Sarcoidosis is a multisystem disorder of unknown aetiology characterised by the accumulation of T lymphocytes and macrophages and the formation of non-caseating granulomas. Its prevalence is 10 to 40 per 100,000. It is more common in women and Afro-Caribbeas. The respiratory system is most commonly involved, usually in the form of adenopathy and parenchymal lung disease. Less common manifestations involve the skin, usually as erythema nodosum (bilateral tender red nodules on the lower extremities). Ocular involvement can include uveitis and papilloedema. CNS manifestations include facial nerve palsy (usually CN VII). Cardiac abnormalities can include conduction problems, heart failure, and arrhythmias. The diagnosis is established by obtaining biopsies of affected organs and by excluding other granulomatous conditions, such as fungal disease and TB, and other causes of lymphadenopathy, such as neoplasia. Bronchoscopy and transbronchial biopsy may be needed. The central nervous system is affected in 1-5% of patients with sarcoidosis; this involvement can lead to neurologic problems. Elevated levels of ACE are seen in 40% to 90% of patients. ACE is a product of macrophages and therefore an indicator of granuloma burden in the tissues. ACE levels are elevated in the serum and may be correlated with disease activity. Hypercalcaemia is present in 10% of patients and is due to increased production of 1,25-dihydroxyvitamin D by macrophages. Monitoring levels is essential during routine follow-up. Patients with bilateral hilar lymphadenopathy alone do not require treatment. In acute symptomatic sarcoidosis bed rest and NSAIDs are initially indicated. Treatment with corticosteroids are reserved for patients with uveitis, hypercalcaemia, parenchymal lung disease and neurological or cardiac involvement. Steroids are able to acutely suppress symptoms, but have not been shown to alter the long term course of the disease. Steroids are given at high dose orally for 4-6 weeks and then reduced over a longer period, up to a year, with dose increases used for disease flare-ups.

Which cancers most commonly metastasize to the lungs?

Secondary lung cancers are most commonly the result of metastasis from the following primary cancers: • Colorectal • Breast • Renal • Female genital tract: cervix, ovary **Note that metastatic lung cancer rarely cause haemoptysis as they are spreading haematogenously and therefore tend to be deep in the interstitium rather than endobronchial.

Cardiac sarcoidosis

Seen in 5% of cases, but autopsy sees 25%. associated with increased risk of death. § Imaging studies with newer imaging modalities (MRI/PET): 4%-55% asymptomatic cardiac involvement in pts with systemic sarcoidosis

Management of pneumonia based on CURB-65 score

Severity Scoring (CAP) •CURB-65 •Confusion ≤8 (AMTS) •Urea >7 mmol/L •RR >30 •BP <90/60 mmHg •Age >65 **Score of 1 = GP Score of 2 = A&E (+ short stay) Score of 3+ = Admission (± consider ICU) **Acute: •Oxygen (+ sit up patient) •IV fluids •IV painkillers •IV antibiotics •CPAP (if required)

COPD acute management

Slides from 2019 MedEd Lecutre by A. Ludley *** § For example an infective exacerbation like pneumonia may cause worsening of the symptoms and therefore a low FEV1%* **Non-Invasive Ventilation (NIV) 1.CPAP (Continuous Positive Airway Pressure) - tx. T1 respiratory failure (e.g. sleep apnoea) 2.Bi-PAP (Bi-level PAP) - tx T2 respiratory failure (e.g. COPD)

How might your management have been altered if Mrs Virginia had a history of weight loss, night sweats, blood-streaked sputum, and had just returned from Pakistan, where she had lived most of her adult life working as a teacher?

Such a history would make you suspect a diagnosis of TB. TB is contagious, airborne, difficult to treat, and potentially fatal. Patients suspected of having active TB are isolated in a side room until the diagnosis is either excluded by three negative sputum samples or confirmed and treatment commenced.

What symptom can occur as a result of obstruction of the superior vena cava by an apical lung tumour?

Swelling of the face, neck and arms

Sleep fragmentation can affect cognitive function

Synaptic Homeostasis Hypothesis: Learning occurs via the formation of synapses •Neurones strengthen synapses when awake while interacting with the environment •Neurones renormalize synapses in sleep when the brain is 'off line'.

Definition of pulmonary sarcoidosis

Systemic disorder of unknown cause(s) characterised by formation of noncaseating granulomas, affecting the lung in >90% of cases. § can also affect lots of symptoms e.g. nervous, ocular § don't know what is the initial event for these non-caseating granulomas

What is an anion gap in ECG

The anion gap (AG) is a derived variable primarily used for the evaluation of metabolic acidosis to determine the presence of unmeasured anions. To work out if the metabolic acidosis is due to increased acid production or ingestion vs decreased acid excretion or loss of HCO3- you can calculate the anion gap. § The normal anion gap varies with different assays but is typically between 4 to 12 mmol/L. § Anion gap formula: Anion gap = Na+ - (Cl- + HCO3-) **An increased anion gap indicates increased acid production or ingestion: a) Diabetic ketoacidosis (↑ production) b) Lactic acidosis (↑ production) c) Aspirin overdose (ingestion of acid) **A decreased anion gap indicates decreased acid excretion or loss of HCO3-: a) Gastrointestinal loss of HCO3- (e.g. diarrhoea, ileostomy, proximal colostomy) b) Renal tubular acidosis (retaining H+) c) Addison's disease (retaining H+)

Signs seen in sarcoidosis

The clinical presentation of acute flu like illness, mild pyrexia, malaise, erythema nodosum, arthralgia or arthritis and bilateral hilar lymphadenopathy is typical of acute sarcoidosis. Sarcoidosis is a multisystem granulomatous disorder of unknown aetiology.

Name several causes of clubbing

There are many of these and you should structure it somehow - for example by physiological system: 1) Cardiovascular: a) Infective endocarditis (subacute bacterial endocarditis) b) Congenital cyanotic heart disease c) Atrial myxoma d) Axillary artery aneurysm e) Brachial arteriovenous fi stula 2) Respiratory a) Pulmonary fibrosis b) Suppurative lung diseases: abscess, empyema, cystic fibrosis, bronchiectasis c) Bronchial carcinoma, mesothelioma d) TB 3) Gastrointestinal a) Inflammatory bowel disease b) Cirrhosis c) Malabsorption, e.g. coeliac disease d) Gastric lymphoma e) Liver abscess f) Liver or bowel cancer 4) Other a) Congenital clubbing b) Thyroid acropachy

A chest x-ray is done and is shown below. Which one of the following is seen?Which one of the following is the most likely diagnosis at this stage?

There is a mass in the left upper zone. Lung cancer. There is an obvious large mass on the chest x-ray. In a patient of this age who presents with haemoptysis, lung cancer must be the most likely diagnosis. Lymphoma of the lung is usually associated with mediastinal node enlargement. A-V malformations are usually smaller, well-defined masses.

Treatment for sarcoidosis first and second line

Toxicity of immunosuppression: • High dose oral corticosteroids long term • Second line agents: a) Methotrexate b) Azathioprine c) Others **• Low dose prednisolone ≤ 7.5 -10 mg od

Treatment for tension pneumothorax

Treatment : § Emergency Needle decompression § High Flow oxygen (via NRB mask) § Chest Drain

Centor Criteria

Used to ID streptococcal pharyngitis, need 3/4: 1. fever 2. tonsillar exudate 3. tender anterior cervical LAD 4. lack of cough

Type 2 respiratory failure

Type 2 respiratory failure involves hypoxaemia (PaO2 is <8 kPa) with hypercapnia (PaCO2 >6.0 kPa). It occurs as a result of alveolar hypoventilation, which prevents the patient from being able to adequately oxygenate and eliminate CO2 from their blood. **Hypoventilation can occur for a number of reasons including: § Increased resistance as a result of airway obstruction (e.g. COPD). § Reduced compliance of the lung tissue/chest wall (e.g. pneumonia, rib fractures, obesity). § Reduced strength of the respiratory muscles (e.g. Guillain-Barré, motor neurone disease). § Drugs acting on the respiratory centre reducing overall ventilation (e.g. opiates).

Obstructive spirometry pattern

Typical spirometry findings in obstructive lung disease include: § Reduced FEV1 (<80% of the predicted normal) § Reduced FVC (but to a lesser extent than FEV1) § FEV1/FVC ratio reduced (<0.7)

What is fourth step in ABG interpretation?

We now know the pH and whether the underlying problem is metabolic or respiratory in nature from the CO2 level. Piecing this information together with the HCO3- we can complete the picture: § HCO3- is a base, which helps mop up acids (H+ ions). § So when HCO3- is raised the pH is increased as there are less free H+ ions (alkalosis). § When HCO3- is low the pH is decreased as there are more free H+ ions (acidosis). 1) Is the HCO3- normal or abnormal? 2) If abnormal, does this abnormality fit with the current pH (e.g. ↓HCO3- and acidosis)? 3) If the abnormality doesn't make sense as the cause for the deranged pH, it suggests the cause is more likely respiratory (which you should have already known from your assessment of CO2).

High flow nasal prongs

much thicker tube compared to normal nasal prongs to allow for higher pressure. prongs also connected to unit to allow for more pressure and humidify the air - provides small PEEP (about 3)

List some differentials for sudden-onset (seconds to minutes) shortness of breath.

§ Bronchospasm (e.g. acute asthma) § Anaphylaxis § Laryngeal oedema § PE Pneumothorax § Foreign body § Hysterical hyperventilation

What's first step when looking at ABG?

Your first question when looking at the ABG should be "Is this patient hypoxic?" as hypoxia is the most immediate threat to life. PaO2 should be >10 kPa when oxygenating on room air in a healthy patient. If the patient is receiving oxygen therapy their PaO2 should be approximately 10kPa less than the % inspired concentration FiO2 (so a patient on 40% oxygen would be expected to have a PaO2 of approximately 30kPa).

emphysema

a condition in which the air sacs of the lungs are damaged and enlarged, causing breathlessness.

Protocol for suspected cardiac sarcoidosis

a) Cardiac MRI b) FDG-PET alongside resting myocardial perfusion scan **PET tends to be more sensitive than MRI: however, whether isolated PET positivity has prognostic significance remains to be established

What is spirometry? Use? What measures does it provide?

a) assessing lung function by measuring the volume of air that the patient is able to expel from the lungs after a maximal inspiration. b) It is a reliable method of differentiating between obstructive airways disorders (e.g. chronic obstructive pulmonary disease, asthma) and restrictive diseases (e.g. fibrotic lung disease). It can also help to monitor disease severity. This guide aims to provide a basic approach to spirometry interpretation. c) Spirometry provides several important measures including: 1) Forced expiratory volume in 1s (FEV1): the volume exhaled in the first second after deep inspiration and forced expiration, similar to PEFR. 2) Forced vital capacity (FVC): the total volume of air that the patient can forcibly exhale in one breath. 3) FEV1/FVC: the ratio of FEV1 to FVC expressed as a percentage. Values of FEV1 and FVC are expressed as a percentage of the predicted normal for a person of the same sex, age and height. **FEV1: >80% predicted **FVC: >80% predicted **FEV1/FVC ratio: >0.7

Which inherited condition can cause emphysema and liver disease?

a1-antitrypsin deficiency

What is ARDS and its causes?

acute respiratory distress syndrome. § ARDS is a form of Hypoxaemic Acute Lung Injury § causes include: drugs, ventilation, near drowning, severe burns, sepsis, pneumonia, transfusion reactions, COVID-19 **Note: particularly common in critically ill (ITU)

How to tell hyper-inflated lungs on CXR

also flattened diaphragms. >6 anterior ribs or 10 posterior ribs at MCL

What is the definition of severe asthma

§ poor symptom control, frequent severe exacerbations, airflow limitation § poorly controlled despite the high dose ICS + controller therapy / or requires this therapy to stop it being uncontrolled § step 4 or 5

A 24-year-old female presents with episodic wheezing and shortness of breath for the past 4 months. She has smoked for the past 8 years and has a history of eczema. Examination of her chest is unremarkable. Spirometry is arranged and is reported as normal.What is the most appropriate next steps? a) Trial of a salbutamol inhaler b) Fractional exhaled nitric oxide + spirometry/bronchodilator reversibility test c) Baseline FEV1 repeated following inhaled corticosteroids d) Arrange a chest x-ray e) Trial of a salbutamol inhaler and low-dose inhaled corticosteroi

b. Adults with suspected asthma should have both a FeNO test and spirometry with reversibility. § NICE guidance has radically changed how asthma should be diagnosed. It advocates moving anyway from subjective/clinical judgements are more towards objective tests. § There is particular emphasis on the use of fractional exhaled nitric oxide (FeNO). § Nitric oxide is produced by 3 types of nitric oxide synthases (NOS). One of the types is inducible (iNOS) and levels tend to rise in inflammatory cells, particularly eosinophils. Levels of NO therefore typically CORRELATE with levels of INFLAMMATIO. § Other more established objective tests such as spirometry and peak flow variability are still important. § All patients >= 5 years should have objective tests. Once a child with suspected asthma reaches the age of 5 years objective tests should be performed to confirm the diagnosis. **Patients >= 17 years: § patients should be asked if their symptoms are better on days away from work/during holidays. If so, patients should be referred to a specialist as possible occupational asthma § all patients should have spirometry with a bronchodilator reversibility (BDR) test § all patients should have a FeNO test **Patients 5-16 years: § all patients should have spirometry with a bronchodilator reversibility (BDR) test § a FeNO test should be requested if there is normal spirometry or obstructive spirometry with a negative bronchodilator reversibility (BDR) test **Patients < 5 years- diagnosis should be made on clinical judgement **TESTS: 1) FeNO: § in adults level of >= 40 parts per billion (ppb) is considered positive § in children a level of >= 35 parts per billion (ppb) is considered positive **Spirometry: § FEV1/FVC ratio less than 70% (or below the lower limit of normal if this value is available) is considered obstructive **Reversibility testing: § in adults, a positive test is indicated by an improvement in FEV1 of 12% or more and increase in volume of 200 ml or more § in children, a positive test is indicated by an improvement in FEV1 of 12% or more

Stage 1 Sarcoidosis

bilateral hilar lymphadenopathy

What is shown here?

bilateral hilar lymphadenopathy e.g. Infection (TB), inflammation (sarcoidosis), malignancy (lymphoma)

BiPAP

bilevel positive airway pressure - additional bit of pressure during inspiration to aid ventilation. used in type 2 resp failure

What happens to airways in asthma

bronchoconstriction, airway wall thickening and mucus hypersecretion

What does IL-13 contribute to

contributes to mucus hypersecretion and airway remodelling

Lanky Schmidt is a tall, 29 year old male. He has presented to A+E feeling short of breath. He has right sided pleuritic chest pain. He is a non-smoker and otherwise healthy. A chest radiograph shows a right sided pneumothorax 11mm in diameter. How should the medical team proceed? a)Reassure and Discharge b)Observe for 6 hours and give O2 c)Chest drain insertion and give O2 d)Needle Aspiration and give O2 e)Immediate wide bore cannula insertion at 2nd intercostal space

d) needle aspiration and give O2

Decompensated respiratory acidosis means needs...

needs assisted ventilation (invasive or non-invasive)

Do lungs have pain nerves

Management of pneumothorax

distance is from periphery to lung . § Primary <2cm --> discharge and repeat CXR. >2cm --> aspiration (chest drain if unsuccessful) § Secondary <2cm --> aspiration. >2cm --> chest drain

x ray from covid pt

fibrosis, pus and patchy shadowing

Stage 4 sarcoidosis

fibrosis. get hilar being pulled up because upper regions are more involved in sarcoid/TB and hypersensitivity pneumonitis --> hence get more fibrosis at the top --> pulls up hilum

Bullae

fluid filled blisters

Pleural rub

friction rub caused by inflammation of the pleural space § best heard in lower anterior lungs and lateral chest. Is like a CREAKING sound

Systems biology of asthma in precision medicine

from clinical phenotypes ---> moleclar phenotypes --> specific treatment --> measure biological responses (can then determine if it's lifestyle/genes affecting)

Type 2 Resp failure issue

global problem; cannot oxygenate or blow off CO2 --> hypoxic and hypercapnic

What shown here?

globular enlarged heart = pericardial effusion

Pathways for granulomas in sarcoidosis

in majority, granulomas resolve. in minority --> firbosis and chronic disease

Tx for tension pneumothorax

just above the 3rd rib 2nd ICS MCL (orange/grey cannula) **managing other pneumothoraces: § chest drain (safe triangle - lateral edge of pec major, base of axilla, 5th ICS, lateral edge of lat dorsi) § needle aspiration (insert needle into 2nd MCS ICL, sterile, then continue draining

What is second step in ABG?

looking at pH: § Acidotic: pH <7.35 § Normal: pH 7.35 - 7.45 § Alkalotic: pH >7.45 We need to consider the driving force behind the change in pH. Broadly speaking the causes can be either metabolic or respiratory. The changes in pH are caused by an imbalance in the CO2 (respiratory) or HCO3- (metabolic). These work as buffers to keep the pH within a set range and when there is an abnormality in either of these the pH will be outside of the normal range. As a result, when an ABG demonstrates alkalosis or acidosis you need to then begin considering what is driving this abnormality by moving through the next few steps of this guide.

What is barrel chest a sign of?

lung hyperinflation

Typical sarcoid imaging

may not need histology to confirm

what does x ray show

midline sternotomy wires --> from cabg and valve replacement surgery § pleural effusion - blunting of costophrenic angle and meniscus sign

lung mesothelium

monolayer of mesothelial cells that blanket the chest wall and lungs on the parietal and visceral surfaces, respectively. The normal mesothelial cell layer appears smooth, glistening, and semi-transparent.

Which of the following most accurately describes ARDS? a)Hyaline Membrane Disease b)A Type 2 Respiratory failure due to acute lung injury c)A Non-Cardiogenic Pulmonary Oedema d)A Respiratory distress secondary to severe sepsis e)Long-term respiratory sequelae of childhood rheumatic fever

non-cardiogenic pulmonary oedema

Position of chest drain

o Inserted in the 4th-6th intercostal space midaxillary line (safe triangle) - avoids long thoracic nerve and artery

cystic fibrosis lung

o is a cause of bronchiectasis (get big airways as cilia can't clear out pus) --> bacteria culminate here o get large light patchy areas o end up with pseudomonas bacteria. § in child CF is common cause. in adults various causes § lighter area in lung means its pus (will see as consolidation on X-ray and hear as bronchial breathing)

Below are the results of the arterial blood gas estimation on air. Which results are abnormal? pH 7.42, pO2 6.5kPa, pCO2 3.2kPa, BE +2.3.

pO2 6.5kPa, pCO2 3.2kPa. The arterial blood gas results demonstrate hypoxia and hypocapnia which is in keeping with pulmonary embolism and is as a result of arterial desaturation secondary to decreased pulmonary flow and also associated hyperventilation reducing carbon dioxide levels.

lobar pneumonia

pertaining to the lobe(s); diseased state of the lung (infection of one or more lobes of the lung)

What does plaques mean on CXR?

plaques - from asbestos. NOT the same as asbestosis (that is fibrosis due to asbestos)

mesothelioma CXR

pleural thickening and pleural plaque from asbestos. pleural effusions. § Left image shows pleural thickening + pleural effusion (CXR) § Upper right image shows pleural plaques (CXR) § Bottom right image shows subtle pleural thickening (CXR) - therefore use history i.e. asbestos exposure to help confirm the diagnosis

Sudden onset SOB

pneumothorax, PE or FB

PEEP

positive end-expiratory pressure - common mechanical ventilator setting in which airway pressure is maintained above atmospheric pressure § graph x axis is time, y axis is Paw cm H20. Go for pressure around 5-10 cm H20

Positive pressure breathing vs normal

positive pressure pushes air into teh lungs, as opposed to normal breathing where we create negative pressure. § can either be non-invasive or invasive with tube going directly into lungs

Improving ventilation using ventilator

pressure if always positive

What is the most likely diagnosis for this?

pulmonary oedema

addition of formoterol to budesonide... what effect?

reduces frequency of severe exacerbations (this means exacerbation requiring treatment either at home or hospital)

A 17-year-old patient presents to A&E complaining of a tight feeling in their chest, shortness of breath and some tingling in their fingers and around their mouth. They have no significant past medical history and are not on any regular medication. An ABG is performed on the patient (who is not currently receiving any oxygen therapy). An ABG is performed and reveals the following: PaO2: 14 (11 - 13 kPa) || 105 mmHg (82.5 - 97.5 mmHg) pH: 7.49 (7.35 - 7.45) PaCO2: 3.6 (4.7 - 6.0 kPa) || 27 mmHg (35.2 - 45 mmHg) HCO3-: 24 (22 - 26 mEq/L)

resp alkalosis. § Oxygenation (PaO2): A PaO2 of 14 on room air is at the upper limit of normal, so the patient is not hypoxic. § pH: A pH of 7.49 is higher than normal and therefore the patient is alkalotic. The next step is to figure out whether the respiratory system is contributing the alkalosis (e.g. ↓ CO2). § PaCO2: The CO2 is low, which would be in keeping with an alkalosis, so we now know the respiratory system is definitely contributing to the alkalosis, if not the entire cause of it. The next step is to look at the HCO3- and see if it is also contributing to the alkalosis. § HCO3-: HCO3- is normal, ruling out a mixed respiratory and metabolic alkalosis, leaving us with an isolated respiratory alkalosis. § Compensation: There is no evidence of metabolic compensation of the respiratory alkalosis (which would involve a lowered HCO3-) suggesting that this derangement is relatively acute (as metabolic compensation takes a few days to develop). § Interpretation: Respiratory alkalosis with no metabolic compensation. The underlying cause of respiratory alkalosis, in this case, is a panic attack, with hyperventilation in addition to peripheral and peri-oral tingling being classical presenting features.

Causes of bronchiectasis

resp clubbing (4 causes): bronchiectasis, Idiopathic pulmonary fibrosis, lung cancer, tuberculosis

TB RIPE

rifampicin, isoniazid (these first two are safest), pyrazinamide and ethambutol. Give these 4 antibiotics for 2 months. In this time waiting for sensitivities back. If resistant to some, then stop 2 with most side effects (pyrazinamide and ethambutol)

55 y/o with breathlessness. Smoker and diabetic. O/Es: reduced expansion on R, reduced tactile vocal fremitus (R), dull percussion on R, reduced breath sounds on R. DDx? Most useful investigation?

right sided pleural effusion. *reduced vocal resonance - fluid * increased vocal resonance with pneumonia/consolidation + loud bronchial breath sounds *not pulmonary oedema as that's bilateral § most useful Ix = CXR. Then do a pleural tap. Then send the fluid to: a) CLINICAL CHEMISTRY lab (to see how much protein - is it a transudate (<30g/dL - caused by HR) or exudate (>30g/dL - caused by infection or cancer) b) MICROBIOLOGY - they'll do microscopy (gram staining - most likely are Pneumococcus (strep pneumoniae) AND haemophilus influenzae , culture + sensitivity (grow the bacterial and see which Abx kill or stop growth - 48 hours results come back) c) CYTOLOGY

Preventing PE

stockings and LMwH § NICE guidelines state everyone must be VTE risk assessed within 24 hours of hospital admission. A standard checklist is followed. §Mechanical: Anti-embolic stockings §Pharmacological: Low-molecular-weight Heparin "TEDs & Tinz"

What is haemoptysis?

the coughing up of blood or blood-stained mucus from the bronchi, larynx, trachea, or lungs

air fluid level

the flat line between air (darker) and fluid (whiter) ; often seen in abscess

Asthma establishing the diagnosisis

there is a diagnostic delay... § symptoms are non-specific § some patients have poor symptom perception § isolated symptoms may be present - cough

Cough variant asthma case

type of asthma: -chronic non-productive, nocturnal cough without wheezing or dyspnea - Cough is only symptom -Significant airway inflammation -Diagnosis is often delayed - precipitating stimuli are same as classical asthma - Bronchospasm is not severe enough to cause airflow obstruction - 50% of cases are children <6, 15% are adults >50. within 5 years, 75% develop wheeze. - PFT may be normal, AHR + to histamine - Relief with inhaled steroids (>6/52 weeks) - relapse on treatment withdrawal § investigations: peak flow, spirometry, CXR, skin prick test, histamine challenge

What is the CAGE questionnaire?

you can try the CAGE questions to detect alcohol dependence. An answer of 'yes' to two or more of the following questions is a fairly accurate detector of alcohol abuse and dependence: 1) H ave you ever felt you need to Cut down on your drinking? 2) H ave people Annoyed you by criticizing your drinking? 3) H ave you ever felt Guilty about your drinking? 4) H ave you ever needed an Eye-opener to steady your nerves in the morning?

Management for covid or any other disease

§ ABCDE assessment § history § examination § Investigation § Treatment

Granuloma formation in sarcoidosis

§ APC --> HLA class 2 --> CD4 --> amplification of immune respones

If your patient fails to respond to initial treatment of CAP, which of the following should be considered as a possible cause?

§ Abscess formation § Possible underlying tumour § Incorrect antibiotic or antibiotic dose § Wrong initial diagnosis **Failure to respond - consider: § Wrong diagnosis initial diagnosis eg TB, PEs, vasculitis. pulmonary eosinphilia § Obstructing bronchial lesion eg cancer, FB § Antibiotic resistance or incorrect choice of antibiotic or dose § Antibiotic malabsorption or allergy § Unrealistic expectation, particularly with comorbidity, in the elderly and in overwhelming infection § Immunosuppressed patient § Pleural empyema formation § Abscess formation § Metastatic infection, phlebitis at cannulation site § Secondary PEs from bed rest

In relation to community-acquired pneumonia, which 3 of the following are true? § Abscess formation suggests Staphylococcus aureus infection § Mycoplasma pneumonia is easily recognised from CXR § Persistent fever in spite of antibiotics suggests possible empyema § Pneumocystis is a common pathogen § Streptococcus pneumoniae is the commonest cause

§ Abscess formation suggests Staphylococcus aureus infection § Persistent fever in spite of antibiotics suggests possible empyema § Streptococcus pneumoniae is the commonest cause **Feedback: § Abscess formation occurs with Staphylococcus aureus and Klebsiella infection. §Streptococcus pneumoniae is by far the commonest cause of CAP, even in mycoplasma epidemic years. § There is no distinct CXR pattern for mycoplasma or legionella vs pneumococcal pneumonia. The clinical picture is "atypical", not the radiograph! § Patients with persistent fever despite appropriate antibiotic therapy should be assessed for possible empyema. Ultrasound can be very helpful as it distinguishes well between solid and fluid. § Pneumocystis is rare, even in people who are immunosuppressed. When faced with an immunosuppressed patient with pneumonia, remember that common things are still common, but these patients can get other pathogens which don't normally affect people with normal immune function.

Which diseases can cause insufficient oxygen to be delivered across the body?

§ Anaemia § Reduced cardiac output (e.g. heart failure, aortic stenosis) § Shock (e.g. sepsis, hypovolaemia)

Licensed biologics against Type 2 inflammation

§ Anti-Ige: omalizumab (recommended for allergic asthma) § more recently anti IL-5 and anti-IL-5Ra § more recently Anti-IL4 and antiIL-4Ra/anti-IL13 **this is recommended in step 5 in the stepwise GINA pathway

Pancoast Tumours

§ Apical lung cancer § Usually non-small cell tumours § Location means they can affect nerves and vessels § Can invade sympathetic plexus in the neck (causing ipsilateral Horner's) and brachial plexus (causing arm pain and weakness) and recurrent laryngeal nerve (causing hoarse voice and bovine cough) § Can compress SVC causing increased venous pressure leading to flushed appearance and oedema of face and arms. § There will also be decreased VR to the lungs causing SOB

How should Mr Morris (haemoptysis patient) be managed, both acutely and in the longer term?

§ As always, you should check his need for resuscitation (Airway, Breathing, Circulation, ABC). § From the examination we know that he is in a stable condition. § Were his haemoptysis more serious, you would want to stop the bleeding and prevent aspiration of blood as well. § In the longer term, having had his diagnosis confirmed and his tumour staged, on an outpatient basis, Mr Morris should be referred to the multidisciplinary team (MDT) for management. § Management will depend on the results from histology (grade) and the stage (spread) of the tumour as discussed in the Viva questions.

How are lung neoplasms classified? How do they respond to treatment?

§ As for all neoplasms, lung neoplasms can at first be divided into benign and malignant. § Malignant tumours in turn can be classified as primary or secondary. § Broadly speaking, the primary malignant lung cancers are then classified in two groups based on histology: 1) Non-small cell lung cancer (NSCLC, 80%) − Subdivided into adenocarcinoma (30-40%), squamous (20-30%), large cell carcinoma (10%), and others (5%) − If localized, attempt to remove surgically or treat with radiotherapy − Otherwise responds poorly to chemotherapy and has poor prognosis if disseminated 2) Small cell lung cancer (SCLC, 20%) − Responsive to CHEMOtherapy, although rapid relapse is common. Chemotherapy is given mainly because it improves symptoms rather than mortality − Early metastasis therefore surgery is not the therapy of choice Haemoptysis is more common in SQUAMOUS cell carcinoma, which usually affects lung tissue closer to the hilar region and thus the blood has relatively little distance to travel before being coughed up.

What to ask about asthma in OSCE?

§ Ask about factors which exacerbate symptoms e.g. cold, exercise, dust § Is it better on weekends? May be occupation related § Ask about recent travel § Recent change in house? § Any pets? § What time of day is it worse? - tends to be worse in morning and at night

List some significant features of the past medical history in a patient presenting with cough.

§ Asthma § GORD § Rhinitis/sinusitis § Heart failure § Recent chest infection

What are recognised causes of pneumothorax?

§ Asthma § Marfan's syndrome § Chronic obstructive airways disease § Mechnical ventilation § Rib fracture § Central line insertion **It is usual to perform a chest radiograph following central line insertion, or attempted insertion, to exclude pneumothorax as well as to confirm line position. Rupture of a bulla is a cause of pneumothorax especially in patients with COPD. A large bulla can mimic a pneumothorax and should not be drained! If unsure check radiograph findings with a senior colleague. High positive inspiratory pressures during mechanical ventilation can lead to a pneumothorax. Marfan's syndrome is a connective tissue disorder and patients can present a pnuemothorax. This is the result of a tear in the visceral pleura due to the rupture of a subpleural bulla.

When is asthma most commonly seen?

§ Asthma is defined as " a chronic inflammatory airway disease which is characterised by reversible airway obstruction" § Type 1 hypersensitivity reaction, in which there is: •Bronchoconstriction (variety of stimuli) •Mucosal swelling and inflammation due to mast cell and basophil degranulation •Increased mucus production § Epidemiology: -Affects 10% children and 5% of adults -Usually seen in younger patients and peaks at 5 years of age, however most children outgrow it

Asthma vs COPD

§ Asthma usually involves acute (temporary) increases in airway resistance whereas COPDs are associated with chronic (long-lasting) increases in airway resistance. § - differentiating between the 2 is therapeutically relevant as *inhaled corticosteroids are the primary long term intervention for asthma whereas long acting anticholinergic inhaler is generally preferred for COPD* - most efficient test to *differentiate asthma + COPD = spirometry before and after administration bronchodilator (albuterol) I. pts with asthma show significant reversal (>12% increase in FEV1) in airway obstruction after administration of bronchodilator

Why do we get short of breath at altitude? What is the pharmacological mechanism of action of the altitude sickness drug acetazolamide ('Diamox')? How might this influence breathlessness at altitude?

§ At altitude, there is a lower partial pressure of oxygen in the environment. Thus there is a smaller concentration gradient driving oxygen from air in the alveoli into the blood. As a result there is a reduction in gas exchange, leading to hypoxia. This causes breathlessness and compensatory hyperventilation to correct the hypoxia. § The hyperventilation causes a respiratory alkalosis, which makes one feel lightheaded. § One either feels breathless (from hypoxia) or dizzy (from hyperventilation). Acetazolamide inhibits carbonic anhydrase, an enzyme that catalyses the conversion of CO2 and H2O into HCO3- and H+. There are two theories as to how this might alleviate breathlessness: 1) The first suggests the inhibition of carbonic anhydrase leads to a build-up of CO2, stimulating the respiratory centre and increasing the ventilatory drive. 2) The other theory suggests that the inhibition of carbonic anhydrase in the kidneys leads to a bicarbonaturia and hence a metabolic acidosis, which off sets the respiratory alkalosis due to hyperventilation at altitude. The acidosis caused by acetazolamide enables one to hyperventilate at altitude (thus reducing hypoxia and shortness of breath) without becoming lightheaded from the alkalosis that would otherwise result from hyperventilating.

Outline the management of asthma

§ Avoid triggers § Bronchodilation: a) Beta-2 agonists (e.g. salbutamol) b) Anti-muscarinics (e.g. ipratropium bromide) c) Phosphodiesterase inhibitors (e.g. aminophylline) § Reduce immune response in the lungs

What Abx for prophylaxis of COPD

§ Azithromycin is the standard antibiotic prophylaxis in patients with COPD. § Amoxicillin is usually the first-line antibiotic in the management of infective exacerbations of COPD.

What is fifth step in ABG interpretation?

§ BE. § The base excess is another surrogate marker of metabolic acidosis or alkalosis: 1) A high base excess (> +2mmol/L) indicates that there is a higher than normal amount of HCO3- in the blood, which may be due to a primary metabolic alkalosis or a compensated respiratory acidosis. 2) A low base excess (< -2mmol/L) indicates that there is a lower than normal amount of HCO3- in the blood, suggesting either a primary metabolic acidosis or a compensated respiratory alkalosis.

Investigations for bronchiectasis

§ Basic observations § Bedside tests •Sputum MCS •Sweat test (cystic fibrosis) •Genetic testing (PCD, Young's) § Bloods: •FBC •CRP •ABG •Blood culture § Imaging: •CXR High resolution CT (HR-CT

Bi-PAP

§ Bi-level : high level inspiratory pressure, low level expiratory pressure --> so give pressure to make sure airways stay open and don't collapse. Used in T2RF

A 78-year-old man has been admitted with an infective exacerbation of chronic obstructive pulmonary disease (COPD). He has been treated with controlled oxygen therapy, nebulised bronchodilators, steroids and antibiotics. Two hours after admission a blood gas is performed: pH - 7.31 Pa02 - 7.8kPa Pa C02 - 9kPa HCO3-36 mmol/l **What is the next most appropriate management step?

§ BiPAP. § For patients with persistent hypercapnic ventilatory failure despite optimal medical therapy, non-invasive ventilation should be considered.

What is gold standard for idiopathic pulmonary fibrosis?

§ Biopsy is the gold-standard but not always appropriate. High-resolution CT is usually appropriate § CXR for late presentation § HR-CT for early presentation

CXR and HRCT in idiopathic pulmonary fibrosis

§ Biopsy is the gold-standard but not always appropriate. High-resolution CT is usually appropriate § CXR for late presentation. § HR-CT for early presentation, **Prognosis poor, average life expectancy is around 3-4 years

Air bronchograms

§ Black areas in a lung scan; indicate areas with air in them. § alveoli filled with pus, air filled in terminal broncihole surrounded by areas of pus so stands out

What is the diff erence between bronchitis and pneumonia, and between broncho- and lobar pneumonia?

§ Both are lower respiratory tract illnesses, but bronchitis is a disease of the airways whereas pneumonia is a disease of the alveoli. § In bronchitis, airways inflammation leads to excess mucus production and partial airway obstruction. § In pneumonia, pus accumulates in the alveoli impairing gas exchange and appearing as consolidation on a chest radiograph. Pneumonia can be classified by the pattern of anatomical involvement. § In bronchopneumonia, focal areas are affected in a patchy distribution that may involve one or more lobes. § Lobar pneumonia, as the name suggests, involves most or all of a single lobe.

Bronchiectasis definition

§ Bronchiectasis can be defined as "a lung airway disease characterised by CHRONIC bronchial dilation and IMPAIRED mucocilliary clearance and FREQUENT bacterial infections. § Causes: •Idiopathic (50%) •Congenital (e.g. Cystic Fibrosis) •Post-infective (TB, Pneumonia) •Others include: Host immunodeficiency, Obstruction (foreign body, tumour), GORD, Inflammatory disorders, ABPA § Epidemiology •Most commonly seen in childhood **Chronic lung inflammation which causes fibrosis and permanent dilation of the bronchi as a result of destruction to the wall's elastic and muscular components. This then causes mucus pooling, therefore increasing the risk of respiratory infections. **Many causes: § Congenital - CF is the most common cause, others include Young's syndrome, A1AT deficiency, ciliary dyskinesia) ABPA = allergic bronchopulmonary aspergillosis

How does CO2 made blood acidic?

§ CO2 binds with H2O and forms carbonic acid (H2CO3) which will decrease pH. When a patient is retaining CO2 the blood will, therefore, become more acidic from the increased concentration of carbonic acid. When a patient is 'blowing off' CO2 there is less of it in the system and, as a result, the patient's blood will become less acidotic and more alkalotic. § The idea of 'compensation' is that the body can try and adjust other buffers to keep the pH within the normal range. If the cause of the pH imbalance is from the respiratory system, the body can adjust the HCO3- to counterbalance the pH abnormality bringing it closer to the normal range. This works the other way around as well; if the cause of a pH imbalance is metabolic, the respiratory system can try and compensate by either retaining or blowing off CO2 to counterbalance the metabolic problem (via increasing or decreasing alveolar ventilation). § So we need to ask ourselves: 1) Is the CO2 normal or abnormal? 2) If abnormal, does this abnormality fit with the current pH (e.g. if the CO2 is high, it would make sense that the pH was low, suggesting this was more likely a respiratory acidosis)? 3) If the abnormality in CO2 doesn't make sense as the cause of the pH abnormality (e.g. normal or ↓ CO2 and ↓ pH), it would suggest that the underlying cause for the pH abnormality is metabolic.

Causes of obstructive lung disease

§ COPD § Asthma § Emphysema § Bronchiectasis § Cystic fibrosis

List some differentials for gradual-onset (weeks to months) shortness of breath

§ COPD § Chronic asthma § Heart failure § Pulmonary fibrosis § Anaemia § Bronchiectasis

RFs for PE

§ CT, s'il vous plait **C: §Cancer §Chemo §Cardiac Failure §COPD §Factor C deficiency **T: §Trauma §Time (age) §Thrombocytosis **S: §Stasis §Surgery §Factor S deficiency **V: §Varicose veins §Virchow's Triad §Factor V Leiden **P: §Pill (OCP) §Pregnancy §Puerperium §Previous VTE §Polycythaemia §Paraprotein deposition ****Why? Because you will be asking the radiologist for a CTPA***

PMH in COVID

§ CVD, DM, HTN, Chronic lung disease e.g. COPD, Cancer, CKD, obesity, smoking

List some causes of blood-stained sputum.

§ Cavitating pneumonia § PE § Lung cancer § Bronchiectasis

List some signs of respiratory pathology that can be seen in the neck

§ Cervical lymphadenopathy § Tracheal deviation

List some signs of COPD on physical examination

§ Chest wall deformity (e.g. barrel chest) § Breathing through pursed lips § Use of accessory muscles § Reduced chest expansion § Prolonged expiratory phase

Which 5 of the following are associated with idiopathic pulmonary fibrosis? § Clubbing § Diffuse lung fibrosis § Late inspiratory crepitations § Obstructive defect on lung function tests § Restrictive defect with reduced transfer factor on lung function tests § Increased risk of lung carcinoma § Increased risk of bronchiectasis

§ Clubbing § Diffuse lung fibrosis § Late inspiratory crepitations § Restrictive defect with reduced transfer factor on lung function tests § Increased risk of lung carcinoma **Ideopathic pulmorary fibrosis causes infiltration with inflammatory cells and fibrosis and ultimately respiratory failure. **CRP, immunoglobulins, and ANA and rheumatoid factor may be increased. **It causes a restrictive defect on lung function testing with decreased transfer factor (unlike the obstructive defect seen with COPD) **It is associated with an increased incidence of lung carcinoma.

List some signs of interstitial lung disease on physical examination

§ Clubbing § Reduced chest expansion § Late inspiratory fine crackles

what would see on inspection, palpation, auscultation in COPD

§ Coarse crackles = 'hair-like' sounds (emulate by rubbing hair between your fingers) - to do with stuff clogging the airways § Fine crackles = 'snow-crunching' sounds - to do with air bubbling through exudate (so is caused by stuff like pneumonia) § RHF = Right Heart Failure ***Causes of clubbing***: •Most common is idiopathic (50%) **Respiratory causes: •Malignancy • Interstitial lung disease •Empyema lung abscess •Cystic fibrosis NOT COPD **CVS causes: •Malignancy •Infective (bacterial) Endocarditis •Tetralogy of Fallot •Congenital cyanotic heart disease •Atrial myxoma **GI causes: •Malignancy •Coeliac's disease •IBD Cirrhosis Signs of clubbing •Boggy nail bed •Loss of Lovibond's angle (should be less than 180 degrees) •'Drumsticking' of fingers •Increased longitudinal curvature of nail

This patient had acid-fast bacilli (AFB) present in his sputum. He remains in hospital. How should he be treated now? Choose 5 options § Commence multiagent antiberculous chemotherapy orally § Continue barrier nursing in side-ward § Ensure patient compliance with medication is directly observed § Arrange tuberculin skin test § Discuss HIV testing with patient § Arrange contact tracing § Commence single agent antituberculous chemotherapy orally

§ Commence multiagent antiberculous chemotherapy orally § Continue barrier nursing in side-ward § Ensure patient compliance with medication is directly observed § Discuss HIV testing with patient § Arrange contact tracing O Multi-agent therapy should be commenced as soon as the diagnosis is confirmed O Isolation measures should continue whilst he remains an inpatient O HIV is an important risk factor for TB and so should be recommended O Patient compliance is vital, as is contact tracing (although both of these may be difficult given his social background).

What symptoms are associated with hypercapnia?

§ Confusion § Reduced consciousness level § Asterixis § Bounding pulse

List some causes of interstitial lung disease

§ Congenital - neurofibromatosis, Gaucher disease § Systemic inflammatory disease - rheumatoid arthritis, ankylosing spondylitis, sarcoidosis § Chemicals - asbestos, silica § Drugs - methotrexate, amiodarone, nitrofurantoin, cicosporin § Hypersensitivity - Bird-fancier's lung § Radiation § Idiopathic

List some important symptoms that may be associated with haemoptysis. State the underlying pathology that may cause the symptoms.

§ Cough productive of sputum - suggests lower respiratory tract infection or bronchiectasis § Fever - associated with lower respiratory tract infections § Weight loss - systemic feature of lung cancer and TB § Pleuritic chest pain - PE or pneumonia § Shortness of breath - clarify whether it is sudden-onset (e.g. PE) or gradual-onset (e.g. heart failure) § Haematuria/Oliguria

What can cause abnormalities in the expiratory volume-time graph in spirometry?

§ Coughing during expiration § Extra breath during expiration § Slow start to forced expiration § Sub-maximal effort

What is indicative of possible life-threatening acute asthma?

§ Cyanosis § Exhaustion and poor respiratory effort § Bradycardia § Hypotension § pH 7.25 on ABG § pCO2 6kPa § Silent chest on auscultation **Watch carefully for these factors. A 'silent' chest in an unwell asthmatic patient should ring alarm bells as should evidence of physical exhaustion § Acidosis, severe hypoxia, or CO2 retention are all indicative of respiratory failure on blood gases. Involve anaesthetists early and initiate ventilation if necessary before severe compromise occurs. § Bradycardia is concerning but moderate tachycardia is common and occurs as a side-effect of salbutamol and aminophylline - it is not an ominous sign.

List some signs of anaemia on physical examination

§ Cyanosis § Koilonychia (if severe iron deficiency) § Glossitis § Angular stomatitis § Conunctival pallor

§ reduced air entry with wheeze § red hot swollen tender calf § hypotensive , tachycardic § DDx? What GP to do?

§ DVT/ cellulitis, COPD exacerbation, septic? § as patient is acutely unwell, would refer to hospital for management - GP arrange for ambulance § will need doppler, bloods (D-dimer), CTPA, CXR § analgesia, oxygen, DOACs

Causes of acute pulmonary oedema

§ Defined as an accumulation of fluid within the lung parenchyma, resulting in impaired gaseous exchange. § Causes: a) Cardiogenic - Heart Failure, Arrhythmia, Myocardial Infarction b) Renal - Acute, severe Kidney failure c) Acute respiratory distress syndrome (ARDS) - Caused by lung injury, i.e. infection (Cov-Sars-2) § multiple causes § Different causes may mean different treatment approaches - TREAT THE CAUSE

What is infective organism in TB?

§ Definition: infection by Mycobacterium tuberculosis, which causes multi-systemic disease §Risk factors: •Travel •South Asians/India/Bangladesh •Immunocompromised (HIV infection) § Signs and Symptoms: General: •FLAWS •SOB •Cough (+ green sputum) •Haemoptysis •Lymphadenopathy **STAGES: § Primary: initial infection (often asymptomatic, can be pulmonary) § Latent: asymptomatic infection § Post-primary: reactivation usually when immunocompromised (severe symptoms) § Miliary: lymphohaematogenous dissemination of TB **More likely to catch TB from: Relatives > Strangers

List three key features of the history of presenting complaint of haemoptysis

§ Describe what you are coughing up. § How much was coughed up? § Did the haemoptysis occur suddenly or come on gradually?

Review of clinical findings reveals a likely diagnosis of Pancoast lung carcinoma with brachial plexus and rib involvement and also Horner's syndrome. This is due to disruption of the sympathetic chain. Wat conditions are associated with Horner's syndrome?

§ Diabetes mellitus § Cerebrovascular disease § Demyelination § Trauma § Carotid aneurysm § Carotid dissection § Skull base tumour **All of these conditions are associated with Horner's syndrome apart from COPD.

How does diabetic ketoacidosis lead to metabolic acidosis?

§ Diabetic ketoacidosis arises because of a lack of insulin in the body. § The lack of insulin and a corresponding elevation of glucagon leads to increased release of glucose by the liver, but an inability for cells to utilise the glucose. § High serum glucose levels result in increased urinary excretion of glucose, taking water and solutes along with it in a process known as osmotic diuresis (this leads to polyuria, dehydration and polydipsia). § The absence of insulin also leads to the release of free fatty acids from adipose tissue (lipolysis) as the body needs to generate energy from a source other than glucose. These fatty acids are converted into ketone bodies to be used as an energy source. § The ketone bodies cause the blood to become more acidic (metabolic acidosis). The body attempts to compensate for the metabolic acidosis by hyperventilating to blow off CO2 and thereby increase pH. § This hyperventilation, in its extreme form, may be observed as Kussmaul respiration. ***Bedside investigations to do: bloods, ABG, IV fluids, Capillary blood glucose, Urinalysis:(Glucose +++Ketones +++)

Gold stages for COPD

§ Diagnostic tests include pulmonary function tests, chest x-ray, chest computed tomography scan, oximetry, and arterial blood gas analysis. § Patients should be encouraged to stop smoking or occupational exposure and be vaccinated against viral influenza and Streptococcus pneumoniae. § Treatment options include bronchodilators, inhaled corticosteroids, and systemic corticosteroids. § Long-term oxygen therapy improves survival in severe COPD.

Which 3 of the following actions would you take urgently now?

§ Discuss case and antibiotic use urgently with microbiology § Arrange urgent review by chest team § Move patient to side room and introduce respiratory isolation procedures § Commence antibiotics; if possible once you have discussed the case with microbiology. Sputum findings will ultimately dictate what is used but it may be necessary to commence conventional antibiotic agents intravenously prior to results of sputum stain/culture. § The patient does not need hospital transfer at this stage but the local chest physicians should be involved early in proceedings. A patient with suspected TB should be cared for in a side room with respiratory isolation § Bronchoscopy is only indicated if sputum is unobtainable or not diagnostic (as some risk to both the patient and endoscopy staff).

List some signs of heart failure on physical examination

§ Displaces apex beat § S3 and S4 heart sounds § Bibasal crackles § Raised JVP § Hepatomegaly § Peripheral oedema

The most likely diagnosis is that of acute massive pulmonary embolism. With regard to ECG changes in acute massive pulmonary embolus which of the following statements are true? § ECG abnormalities are common and are seen in most patients § The ECG may be normal § Right bundle branch block may occur § Left sided ECG abnormalities exclude the diagnosis of pulmonary embolus § S1 Q3 T3 pattern is the commonest ECG abnormality

§ ECG abnormalities are common and are seen in most patients § The ECG may be normal § Right bundle branch block may occur The ECG is normal in up to 15% of cases. The so called "S1 Q3 T3" pattern associated with acute massive pulmonary embolus is relatively rare. Other non-specific ECG abnormalities are more common including sinus tachycardia, atrial fibrillation, first degree AV block and right bundle branch block. Left sided ECG abnormalities are unusual but may occur in acute massive pulmonary embolus.

Drugs for asthma

• Quick relief meds: short-acting/long-acting beta 2 agonists (albuterol-bronchodilator) (SABA/LABA), anticholinergics (SAMA/LAMA), **Long term control: inhaled corticosteroids (prevent inflammation of chronic asthma) (ICS), leukotriene receptor antagonist **Combinations: LABA/ICS, LABA/LAMA, LABA/LAMA/ICS ( triple therapy) • Metered-dose inhalers and dry powder inhalers

What is Eisenmenger's syndrome?

§ Eisenmenger's syndrome describes the situation where a left to right cardiac shunt becomes a right to left (or bidirectional) shunt. § It follows a sequence of events beginning with a left to right cardiac shunt, due to, for example, a ventricular and/or atrial septal defect, patent ductus arteriosus. Over time this causes progressive pulmonary hypertension as the delicate pulmonary vasculature is subjected to blood emerging from the left ventricle, via the shunt, at greater pressures than normal pulmonary pressures. Eventually the pulmonary hypertension provides enough resistance to REVERSE the direction of the shunt. § Ultimately it leads to heart failure and can only be cured by heart-lung transplant. Women of childbearing age must be warned about the increased mortality in pregnancy (over 50%) and strongly advised against it. § This condition has become relatively rare in the UK due to early surgical correction of cardiac defects (indeed this is the rationale behind early correction of such defects). **Overall: Where L-R cardiac shunt becomes R-L - In ASD and PDA - Results in PHT - Increased MR in pregnant women

Characteristics of empyema aspirate

§ Empyema: Turbid effusion with pH<7.2, Low glucose, High LDH § Following a pneumonia, some patients develop a free-flowing exudate (parapneumonic effusion) that may become infected when there is bacterial invasion across the damaged lung epithelium. § In the presence of pus, this effusion is termed an empyema, and is characterised as having a pH <7.2, a low glucose (<3.4 mmol/L), and a high LDH (>200 IU/L or 2-3 times above upper limit of normal range for serum).

Which drugs are used in the management of chronic pulmonary oedema?

§ Furosemide (loop diuretic) § Spironolactone (aldosterone receptor antagonist)

Genetic predisposition in sarcoidosis

§ HLA alleles: note susceptibility and protective alleles § Also other non HLA genes. • Familial clustering in several populations • More common in monozygotic than dizygotic twins • Many studies showing associations with major histocompatibility complex region (MHC) class II alleles a) susceptibility alleles: HLA DR 11, 12, 14, 15, 17 b) protective alleles: HLA DR1, DR4 • Other non HLA genes: BTNL2, IL-23R, NOTCH4, 11q13 locus in common with other immune mediated diseases (ulcerative colitis, ank spond, RA)

What are the most common bacterial organisms that cause infective exacerbations of COPD?

§ Haemophilus influenzae (most common cause) § Streptococcus pneumoniae § Moraxella catarrhalis *§ if acute exacerbation of COPD without signs of purulent symptoms - then 5 day course of pred, no ABx

Why should you worry particularly about haemoptysis?

§ Haemoptysis should always be investigated thoroughly for two reasons: 1) It may be the presenting symptom for life-threatening lung disease. 2) Massive haemoptysis, variably defined as anything from >100 mL to >1000 mL over 24 hours, may be life-threatening itself, usually through asphyxiation but potentially also shock. Haemoptysis is thus a 'red flag' symptom and any patient with haemoptysis requires a full diagnostic work-up.

There has been a large decrease in the incidence of epiglottitis in recent years, particularly in children. How can you explain this?

§ Historically, epiglottitis primarily affected children and was a severe, sometimes fatal, condition. § It is nearly always due to bacterial infection by Haemophilus influenzae B (HiB). The development and introduction of a HiB vaccine into the UK vaccination schedule in the mid-1990s has led to a decrease in both meningitis (another condition often caused by HiB) and epiglottitis.

Which metabolic imbalance is important to watch out for in patients with potential lung cancer?

§ Hypercalcaemia of malignancy § This is due to spread of the cancer to bone or PTHrp ** NOTE: keep and eye out for signs of hypercalcaemia (e.g. hypotonia, Hyporeflexia, weak arms)

Which of the following are associated with Sarcoidosis? § Hypercalcaemia § Hypokalaemia § Lung fibrosis § Hepatosplenomegaly § Uveitis § Mesothelioma on histological analysis § Caseating granulomas

§ Hypercalcaemia§ Lung fibrosis § Hepatosplenomegaly § Uveitis *Hypercalcaemia is commonly associated with sarcoidosis. *Hypokalaemia is not a feature of sarcoidosis. *Pulmonary fibrosis is a feature of sarcoidosis and may improve with oral steroids for 6 months. *Anterior uveitis is seen in 3-12% of patients with sarcoidosis and later the disease may include posterior uveitis which, if unresponsive to treatment, may lead to blindness. *Mesothelioma is associated with asbestos exposure. *Sarcoid granulomata are characteristically non-caseating.

If risk factors for cancer are present and chest radiograph doesn't show anything, what further investigations might you consider?

§ If risk factors for cancer are present, e.g. male, over 40 years of age, significant smoking history, you may wish to consider a CT SCAN. § If this is still inconclusive, you may also consider further tests including PET and fibreoptic bronchoscopy.

Pathophysiology of a pneumothorax

§ In a normal lung, the lung tissue has a natural tendency to recoil inwards whereas the ribcage naturally recoils outwards. § The pleural space has a fixed volume and is at negative pressure - it acts as the link between the lung and chest wall. § During a full inspiration, the chest wall expands and hence needs to pull the lungs with it. The negative pressure of the pleural cavity allows the chest wall to do this. § If you puncture either the chest wall or the lungs, then the fixed volume pleural cavity is compromised. § Air will fill the pleural cavity, elastic recoil will take over and the lung will collapse § A tension pneumothorax occurs when a functional valve is created which allows air to be drawn in on inspiration in to the pleural cavity but does not let the air out. The mediastinum is pushed over in to the contralateral mediastinum, compressing the great veins. Unless air is rapidly removed, cardiorespiratory arrest will occur.

OSA: who to treat?

§ In the UK we have carried out many treatment trials in patients with OSA. The UK Respiratory Sleep Network: Researching The Best Ways To Treat OSA § We use brompton treatment algorithm for OSA treatment. § we treat Mild OSA (5-15 events/hour) + symptoms

Which diseases can cause an inability to fully inflate the lungs?

§ Increased work - due to obesity and stiffness due to interstitial lung disease § Weak respiratory muscles - Guillain-Barre syndrome, myasthenia gravis § Hyperinflated lungs - COPD

Summarise the prognosis for patients with asthma

● Many children improve as they grow older ● Adult-onset asthma is usually chronic

Criteria for diagnosing chronic asthma

§ Inspect FEV1: FVC ratio § PEFR = Peak Expiratory Flow Rate § FeNO: fractional exhaled nitric oxide Criteria for diagnosing asthma •FEV1% (FEV1/FVC) <70% •PEFR varies by at least 20% for 3 days in a week over several weeks or PEFR increases by at least 20% •Reversibility: 12% pre- and post-bronchodilator spirometry •FeNO ≥40 parts per billion (always done in adults; only done in 5-16yo if the spirometry is inconclusive)

What is associated with superior sulcus tumours?

§ Invasion of the brachial plexus § Invasion of the sympathetic chain § Cord compression § Invasion of the recurrent laryngeal nerve § A hoarse voice **When Pancoast tumours compress or invade surrounding structures the resulting symptoms are known collectively as Pancoast syndrome. **Invasion tends to involve the brachial plexus first leading to shoulder and arm pain. There may be compression of the spinal cord which occurs in 10-25% of people with Pancoast. **Recurrent laryngeal nerve invasion may cause vocal cord palsy and a hoarse voice.

How does reversibility of condition affect diagnosis?

§ It can be useful to assess reversibility with a bronchodilator if considering asthma as a cause of obstructive airway disease. § Patients should be asked to stop bronchodilator therapy prior to spirometry, to ensure previous treatments do not affect the results (if the patient has severe disease, this would not be advisable): a) Short-acting beta-2-agonists should be stopped 6 hours prior to testing. b) Long-acting beta-2-agonists should be stopped 12 hours prior to testing. **To assess reversibility, administer 400 micrograms of salbutamol and repeat spirometry after 15 minutes: § The presence of reversibility is suggestive of a diagnosis of ASTHMA. § The absence of reversibility suggests fixed obstructive respiratory pathology such as chronic obstructive pulmonary disease (COPD). § Partial reversibility may suggest a COEXISTING diagnosis of asthma and another obstructive airway disease (e.g. COPD).

Aminophylline is a drug which may be administered as an IV infusion in severe asthma. Which of the following 3 statements relating to Aminophylline are true? § It is a phosphodiesterase inhibitor § It is associated with hyperkalaemia § It is associated with cardiac arrhythmias § Increased doses are needed in the presence of cardiac or liver failure § Infusion dose should be tailored to levels in the plasma § A loading dose for the infusion is also needed in patients already on oral preparations

§ It is a phosphodiesterase inhibitor § It is associated with cardiac arrhythmias § Infusion dose should be tailored to levels in the plasma *Aminophylline may cause hypokalaemia and cardiac arthythmias - heart monitoring needed. *Reduce dose in cardiac or liver failure and in patients on certain drugs e.g. Ciprofloxacin, Cimetidine *Omit loading-dose for IV infusion in patients already on oral treatment and, in all cases, monitor drug levels carefully whilst the infusion is ongoing.

Mrs Finnegan told you that she was concerned she may have lung cancer, because she used to smoke and her sister died of lung cancer. Can you reassure Mrs Finnegan that she does not have lung cancer?

§ It is important to address a patient's concerns and expectations. If these issues are not addressed, patients will go away unsatisfied and worried. This is not only unethical, as you could prevent the unnecessary agitation, but potentially uneconomical, as they may seek a second opinion. § Mrs Finnegan does not give a history suggesting any warning signs for lung cancer (dry cough, haemoptysis, hoarse voice, loss of weight, poor appetite, night sweats). § Head and neck examination revealed no lymphadenopathy or Horner's syndrome. Her chest radiograph showed no 'coin lesions' that could indicate a tumour. But despite all this, it would be unwise to categorically inform the patient that 'she does not have lung cancer' because one cannot be 100% sure that she doesn't have a small tumour which we simply haven't picked up. Given her 20-pack-year smoking history, it is probably wiser to explain that although she is at an increased risk of lung cancer because of her previous smoking, you could not see any tumours on her current chest radiograph nor were there any signs in her history or examination that are suggestive of cancer. Explain that you cannot rule out cancer 100% with any tests, but that you have found no evidence of it at the moment and her current symptoms are much more likely to be due to heart failure.

You see a patient in clinic with lung cancer who has a bovine cough. Can you explain this symptom?

§ It is likely that this patient has a recurrent laryngeal nerve (RLN) palsy. § Such a palsy is more common on the left than the right. § The left branch of the RLN loops around the arch of the aorta and thus has a longer intrathoracic course (and hence is more likely to be aff ected by chest pathology) than the right branch - which loops around the right subclavian artery. § Damage to the recurrent laryngeal nerve is most commonly due to malignancy (e.g. a Pancoast apical lung tumour) or surgery (e.g. neck surgery).

The notes of a patient you are asked to see state that his past medical history is of 'asthma/COPD'. Is such a diagnosis possible?

§ It is obviously possible to have both COPD and asthma at the same time, but it is much more likely that a clear diagnosis has simply not been made. § Asthma and COPD are very different diseases and should not be confused: • Asthma is a reversible and transient obstruction of the airways caused by excessive mucus production, airway inflammation, and constriction of the bronchi. Flow spirometry shows only obstructive changes (i.e. drop in FEV1 <70% but normal FVC, that is, a reduced rate of air flow but a normal lung capacity). It is usually accompanied by a cough and is often worse at night. It is often linked to triggers such as pollen, dust mites, or cold air and is common in patients who are atopic (i.e. who suffer from multiple diseases caused by excessive IgE-mediated hypersensitivity, such as eczema, hayfever, or urticaria). § COPD is an irreversible and progressive obstruction of the airways. There is a history of chronic bronchitis and/or emphysema. Flow spirometry shows obstructive changes (i.e. drop in FEV1 <70%) but often also a degree of restrictive change (i.e. FVC <70%). Patients are usually older and have a smoking history of >20 pack years.

Mr Marley (COPD patient from the previous case) is admitted to hospital 5 months after he is diagnosed with COPD by the respiratory physicians. He has become very short of breath, confused, and unable to complete full sentences. His daughter explains that he has been deteriorating gradually over the past week and was due to see the respiratory physicians again next week. He is immediately given high-flow 100% oxygen. An arterial blood gas (ABG) is performed and shows PaO2 = 6.2 kPa, PaCO2 = 7.3 kPa, pH = 7.28, bicarbonate = 33 mM, base excess = -1 (on 15 L of O2). The emergency physicians request a chest radiograph, which shows no signs of consolidation (pneumonia) or pulmonary oedema. His ECG, FBC, and serum biochemistry are normal. What is the problem? How would you proceed?

§ Mr Marley's arterial blood gas shows type II respiratory failure (PaO2 <8 kPa and PaCO2 >6.5 kPa). With his history and ABG results (indicating a degree of metabolic compensation but with an acute acidosis), this is an acute-on-chronic picture. § Type II respiratory failure is a MEDICAL EMERGENCY. § Untreated, the rising CO2 will narcose the patient, who will fall into an irreversible coma and die. **Treatment involves: 1) Controlled oxygen therapy. The high CO2 that defines type II respiratory failure often means that patients no longer rely on CO2 levels to stimulate breathing. If you give 100% oxygen, you risk causing a respiratory arrest so this must be stopped in Mr Marley's case. Instead, give controlled oxygen (24-28% using a special connector on the oxygen mask) aiming for oxygen saturations of 80-90%. Perform repeated arterial blood gases, looking for a drop in PaCO2. 2) Improve ventilation. If the CO2 does not drop with controlled oxygen therapy, ensure the airway is fully patent and involve the intensive therapy unit (ITU) physicians as the patient will need assisted ventilation (e.g. non-invasive ventilation) and/or respiratory stimulants (e.g. doxapram). 3) Treat the underlying cause. Assess for reversible causes of reduced gas exchange (e.g. pneumothorax, pneumonia, pulmonary oedema, PE) and reversible causes of reduced ventilation (e.g. airway obstruction due to reduced consciousness, opiate medication).

A 78-year-old woman presents with increasing shortness of breath and a productive cough. Nursing home staff are concerned as she has been having fevers today and the sputum appears red and jelly-like. She has a background of previous alcohol dependence, type 2 diabetes mellitus and a recent ischaemic stroke. She is currently risk feeding and awaiting follow up with speech and language therapy in the community.Chest x-ray demonstrates right upper zone consolidation.What is the most likely cause of the pneumonia?

§ Klebsiella pneumonia-> commonly due to aspiration § Klebsiella pneumonia is more common in diabetics and patients with a history of alcohol excess. § It is also frequently caused by aspiration. § In this scenario, the recent stroke has caused problematic dysphagia. § Klebsiella commonly affects the upper lobes of the lungs. GET RED CURRANT JELLY SPUTUM § Haemophilus influenzae is common in older patients with chronic obstructive pulmonary disease (COPD) and can present as a hospital-acquired pneumonia. It does not cause 'red-currant jelly' sputum. § Mycoplasma is an atypical pneumonia which classically presents with a gradual onset dry cough and occasionally other features, such as autoimmune haemolytic anaemia and erythema multiforme. § Staphylococcus aureus pneumonia commonly occurs after influenza and can also be a complication of measles infection. On chest x-ray, multi-lobar consolidation, cavitation or a pneumothorax might be seen. § Streptococcus pneumoniae is the most common cause of pneumonia and characteristically presents with a high fever and pleuritic chest pain.

What is pneumonia- URTI or LRTI?

§ LRTI § HAP - catching it after being in hospital >48 hours § Aspiration pneumonia (usually from anaerobes from gut flora) e.g. in stroke § chlamydia psittaci - pet birds § klebsiella - alcoholics **General risk factors •Smoking •Travel •Immunocompromised

Lung collapse vs pneumothorax CXR

§ Lung collapse --> 'white-out' from fluid § but pneumothorax

Atelectasis and lung cancer

§ Lung collapse can be a consequence of lung cancer (often SqCC) § if cancer obstructs airway, and not getting air into it --> atelectasis § sail sign (triangular side)- highly suggestive or left lower lobe collapse)

Explain why heart failure causes orthopnoea

§ Lying down leads to increased venous return to a failing heart § This leads to congestion in the pulmonary vasculature, forcing more fluid into the alveoli § This leads to breathlessness

Maggie is a 16-year-old student referred to the respiratory physicians for her recurrent shortness of breath. She describes how she has found herself getting short of breath over the last few months. This mainly occurs in the evenings, and is often associated with a dry cough. In between these episodes, she describes herself as being fine, although she admits that she feels 'a bit unfit because I'm breathless when I go for even a gentle run with my dad'. She denies any weight loss, fevers, dark faeces, or changes in menstruation. She thinks her father suffers with eczema, and is sure that her brother and father have mild hayfever, as does she. She lives at home with her family, none of whom smoke, and a pet dog. What is the most likely cause of shortness of breath in Maggie? How can this be confirmed? What long-term management will Maggie require?

§ Maggie has intermittent episodes of shortness of breath that are worse in the evenings and on exercising. § Some episodes are associated with a dry cough but in between episodes she is apparently fine. § She also has a family history of atopic individuals, with several members including herself having hayfever and/or eczema. § The picture of reversible, intermittent shortness of breath and cough in someone with a family history of atopy is strongly suggestive of ASTHMA. § Asthma is a disease caused by a hypersensitive immune reaction in the bronchi, which leads to excessive mucus production and bronchoconstriction. The combination leads to an obstructive airways disease which can be confirmed on SPIROMETRY. Th is should show a relatively normal FVC but a significantly reduced forced expiratory ratio (FER) - as the problem is not lung capacity but obstruction affecting the speed at which air can get out of the lungs. **Management of asthma is based on three different mechanisms: 1) Avoidance of trigger(s). These can include smoke, allergens (e.g. dust mites, pollen, pets), or exercising in cold air, but often no obvious trigger is known. 2) Bronchodilation. Dilatation of the bronchi can be achieved by either increasing sympathetic stimulation to the lungs (e.g. β2-agonists or phosphodiesterase inhibitors = theophyllines) or decreasing parasympathetic stimulation to the lungs (e.g. antimuscarinics). These compounds can be inhaled in short-acting forms for acute attacks, or in long-acting forms for prophylaxis. β2-Agonists can also be given intravenously (IV) if needed. 3) Reduction of immune response in lungs. This can be achieved using inhaled or, in severe cases, oral corticosteroids.

DDx for nodule in lung on CXR

§ Malignancy - primary or secondary § Abscess § Granuloma § Carcinoid tumour § Pulmonary hamartoma (rare, benign) § AV malformation § Cyst § Foreign body § Skin tumour

What signs would you be looking for on chest radiograph for haemoptysis?

§ Mass lesion/nodule: carcinoma, TB, granuloma, abscess, vasculitides, e.g. Wegener's granulomatosis § Diff use alveolar infiltrates: pulmonary oedema § Hilar lymphadenopathy: carcinoma, infection (if accompanying infi ltrates), TB § Lobar or segmental infiltrates: pneumonia, PE, obstructing carcinoma, TB § Patchy alveolar infiltrates: bleeding disorders, Goodpasture's syndrome, idiopathic pulmonary haemosiderosis

The patient has already had a chest radiograph (image below) and ECG performed by the casualty officer. Which four of the following signs does it show?

§ Mediastinal shift to the left. § Normal heart size. § Large right-sided pneumothorax. § Collapse left lower lobe. This patient is not compromised and has already had a chest radiograph. This confirms a large right pneumothorax with mediastinal shift to the left. No causative rib fractures, are evident (there is no history of trauma). Note collapse of left lower lobe also, probably due to mediastinal shift - this appears as a triangular area of increased density behind the heart.

List some drugs that are associated with interstitial lung disease.

§ Methotrexate § Amiodarone § Nitrofurantoin

Miss Bonprat is a 31-year-old primary school teacher referred to the medical admissions unit of her local hospital because of sudden haemoptysis. She describes feeling unwell and lethargic for the past few weeks and thinking she had 'caught something off the children'. She developed a cough that morning but was alarmed when she noticed she had coughed up some specks of blood onto her handkerchief. She smokes a pack of 'light cigarettes' every day and has not travelled abroad recently. Systems enquiry is unrevealing. Her past medical history is remarkable for hypothyroidism, for which she takes levothyroxine every day. Examination of Miss Bonprat reveals only that her blood pressure is 160/110 mmHg and that her urinalysis is positive for protein (+) and blood (+++). A mid-stream urine sample is sent off to the laboratories, who later that day confi rm the presence of red cell casts on urine microscopy. What diagnosis should you be concerned about?

§ Miss Bonprat has presented with haemoptysis. She also has hypertension, haematuria, and proteinuria on urinalysis suggesting infl ammation of her kidneys (glomerulonephritis) that is manifesting as a nephritic syndrome. § The presence of red cell casts (clumps of red cells that have squeezed through the glomeruli) is indicative of glomerular damage. § The combination of haemoptysis and glomerulonephritis should alert you to the possibility of a pulmonary-renal syndrome

What is defined as moderate, severe, life-threatening and near-fatal asthma?

§ Moderate: PEF = 50-75% § Acute-severe: PEF = 33-50% § Life threatening: PEF <33% § Near fatal: pCO2 is raised **Other info: § previous ITU § other medical conditions § allergies § any infective symptoms

The chest radiograph is shown below. What is shown?

§ heart size is within normal limits § There is abnormal soft tissue density at the right lung apex § The left lung is clear § Rib destruction is evident at the right lung apex **A magnification view is shown below of the soft tissue mass at the right apex - note destruction of posterior right 2nd rib (arrows). The heart size is within normal limits whether AP or PA x-ray.

Mr Andreyov is a 42-year-old investment banker who presents to your clinic complaining of shortness of breath. He says the sensation of breathlessness is always present. He doesn't think it is connected, but mentions that he has found it increasingly difficult to type at his computer recently and he has noticed some twitching of his thighs that he initially put down to stress. He has no relevant past medical history and is not on any medication. He has never smoked and drinks approximately 10 units of wine a week with evening meals. He sleeps well and has not noticed any change in his appetite nor any bloody or dark faeces or urine. He is worried he may be developing heart problems because he admits his diet is not very healthy and he doesn't exercise enough. Cardiovascular, respiratory, and abdominal examination is unremarkable. Neurological examination reveals that the first dorsal interossei on both hands are wasted. In addition, you note fasciculations over both his thighs, reduced power (4/5) on knee flexion, and an upgoing plantar reflex. Flow spirometry reveals FVC = 60% and FER = 80%. What important diagnosis should you consider in this patient?

§ Mr Andreyov has presented with shortness of breath and a history suggestive of weakness/poor coordination in distal muscle groups of his upper limbs. § He has wasting of his hand muscles (suggesting a lower motor neuron or muscular pathology). He also has fasciculations in his right leg (suggesting a lower motor neuron pathology) but an upgoing plantar reflex (suggesting an upper motor neuron pathology). § The combination of upper and lower motor neuron pathology signs in any patient should always arouse the suspicion of MOTOR NEURON DISEASE and warrants referral to a neurologist. § The shortness of breath is likely to be due to diaphragmatic weakness, usually a late sign of this disease.

Mr Frick is a 28-year-old gentleman who is attending the Respiratory Clinic at his hospital. He has recently had several episodes of haemoptysis. He is well known to the respiratory physicians, who have managed him since he was a child. He has chronic rhinitis and has suffered for most of his life from a rattly cough which is frequently productive of green sputum. He suffered from many episodes of serous otitis media as a child. He still suffers from frequent episodes of sinusitis and has recently been referred to a fertility clinic by his GP because he and his wife have not been able to conceive a child after 18 months of trying. A recent chest CT showed dilated bronchi with thick walls extending to the peripheries of both lungs. What diagnosis could explain the constellation of symptoms that Mr Frick has suffered during his life? How would you confirm such a diagnosis? How do you think Mr Frick is being managed?

§ Mr Frick has a history of recurrent cough productive of green sputum and occasional haemoptysis that is highly suggestive of bronchiectasis (bronchos = airway; ektasis = stretched out). § His chest CT does indeed reveal dilated bronchi. In bronchiectasis, the bronchi are chronically inflamed as the lungs struggle to clear irritant mucus for any of a variety of reasons, e.g. obstruction, thickened mucus, poor ciliary function of the epithelia. § The consequence of chronic inflammation is the laying down of scar tissue in the interstitial tissue. Remember that scars shrink, therefore the airway walls are pulled back and the airways expand. § The mucus is often green due to the constant presence of neutrophils and macrophages fighting pathogens growing in the retained mucus. As neutrophils and macrophages die, they release an enzyme called MYELOPEROXIDASE which is green (and closely related to enzymes which give the spicy wasabi sauce favoured in Japanese cuisine its green colour). § In addition, Mr Frick has suffered from many episodes of sinusitis and serous otitis media (glue ear), both of which suggest an inability to clear mucus. § The inability to clear mucus in various organs of the body is highly suggestive of primary ciliary dyskinesia (PCD). § This is an autosomal RECESSIVE disorder that affects the protein machinery used by epithelial cells to rhythmically beat their cilia and by spermatozoa to rhythmically beat their tails. **The typical consequences of PCD are: § Bronchiectasis, due to an inability to clear mucus from the lungs. § Rhinitis and sinusitis, due to an inability to clear mucus from the nasal sinuses. § Otitis media (both secretory and acutely infective) due to an inability to clear mucus from the middle ear, down the Eustachian tube. § Male infertility, due to sperm immotility. Females are usually fertile because passage of the oocyte along the Fallopian tubes is more dependent on peristalsis of the Fallopian tubes than on the movement of the ciliae that line these tubes. § Situs inversus. The rhythmical beating of cilia is thought to play an important part in setting up the usual pattern of body asymmetry during embryogenesis. Many patients with PCD have their organs on the 'other side' (e.g. dextrocardia). ***Patients with PCD who show the clinical triad of bronchiectasis, sinusitis, and situs inversus may be said to have Kartagener's syndrome or Kartagener's triad.

§ Mr Hughes is a 48-year-old office worker who comes to his GP complaining of a chronic dry cough. He has had it for the last few months and thought it was a cold, but has come in as it hasn't resolved and is annoying his work colleagues and wife. His coughing spells occur throughout the day and night, with no predictable triggers. On questioning, he comments that he often has heartburn and wakes up with a sore throat. He is a non-smoker, drinks about 15 pints of lager a week, and has a high body mass index. His past medical history includes an inguinal hernia repair and childhood asthma, although he has not had to use an inhaler since he was a teenager. He also suffers from hayfever in the summer but has no other allergies. He has no new pets or other recent changes to his environment (new job or house). He does not have a history of diagnosed GORD despite his heartburn. His only recent travel was to Spain, and he has had no fevers, night sweats, rigors, or weight loss. His examination is unremarkable and spirometry is normal. What diagnosis is most likely? How would you test your hypothesis?

§ Mr Hughes' cough is dry and chronic, and he is a non-smoker. § Normal spirometry is not inconsistent with intermittent asthma, but his high BMI and heartburn should make you suspicious that his cough is caused by gastro-oesophageal reflux IRRITATING HIS LARYNX, despite the lack of a formal diagnosis. § You could start a therapeutic trial with a proton-pump inhibitor for GORD and arrange a follow-up appointment in clinic. § You should also advise weight loss, as this may bring symptomatic relief. Mr Hughes was started on such a trial and after 3 months his cough had resolved

Mr Johnson is a 55-year-old engineer who presents to A&E with haemoptysis. He has coughed up a teaspoonful of blood, which was a dark red colour, on each of the last 3 days. He has not had fever, weight loss, or breathlessness. However, he has had some chest pain on deep inspiration over the last day, which is not reproduced by pressing on his ribs. He does not recall any trauma to his ribs. He is a nonsmoker, has had no exposure to industrial antigens, or previous lung disease. He grew up in Scotland and has never been outside Europe. He recalls having a sore, swollen calf a few days ago but it resolved on its own so he did not go to the GP. His only risk factor for venous thromboembolism is stasis on the long bus journeys he is making every week back home to Scotland. On examination, his pulse is 94 bpm and regular, his blood pressure 122/64 mmHg, his respiratory rate 12/min and his temperature 35.9°C. His oxygen saturations, however, are 91% on room air. There are no other signs of cyanosis or stigmata of respiratory disease. His bloods show a haemoglobin concentration of 15.2 g/dL, a white cell count of 5.2 × 109 cells/L, a CRP of <2 mg/L, a urea of 6.1 mM, a creatinine of 58 µM, and a calcium of 2.45 mM. Urinalysis and an ECG are unremarkable. In light of the above, what diagnoses would you like to exclude? Is there a clinical algorithm or scoring system that would help?

§ Mr Johnson's history and examination do not clearly point to any diagnosis, but the long bus journeys may have predisposed to a DVT (which would explain the swollen calf) and the chest pain and low oxygen saturations suggest lung pathology, such as a PE. § You therefore should exclude a PE. When you suspect PE based on the history (the clinical examination will rarely show anything more than a tachycardia and/or mild fever), you should refer to the Wells' criteria to determine, based on your clinical findings, the best investigation. Th e criteria are listed in Table 8.1 with their scores. § A score of ≥4 merits a CTPA (or perfusion scan) to investigate further; a score of <4 only justifies a D-Dimer test to exclude a PE. It is worth noting that the Wells' criteria have been criticized because one of the weightier elements is subjective: whether PE is the most likely diagnosis. This can be the difference between low and moderate risk. An alternative clinical prediction tool has been recently developed, the revised Geneva score (2006), which does not rely on the clinician's judgement. It may come to replace the Wells' criteria if it is validated. Mr Johnson has a Wells' score of 4 (symptoms of a DVT and haemoptysis). His D-dimer was >500ng/mL so he had a CTPA, which confirmed a PE. § He was prescribed a prolonged course of anticoagulants and discharged.

§ Mr Marley is a 67-year-old retired musician. He has been referred to the respiratory physicians by his GP because of persistent shortness of breath and recurrent chest infections. § You enter the room to find him standing, with his arms propped against the edge of the table. His breathing is laboured and he has a rattling cough. He finally sits down and explains that he always feels short of breath, and his wife has noticed that he often wheezes. § He coughs up phlegm every day, and says he has been doing so for at least 2 years almost non-stop, although it is worse in winter. § He knows this is all because of his lifetime habit of smoking - he has smoked about 30 cigarettes a day for over 40 years. § On examination, you find there is peripheral and central cyanosis. His breathing is laboured, with intercostal recession and an audible wheeze. § His chest appears slightly hyperinflated and chest percussion fails to reveal the usual dullness over the liver and heart. § The rest of the examination is normal. Spirometry in the clinic reveals FVC = 70% of expected and FER = 60% of expected. What is the likely diagnosis? How should this be managed?

§ Mr Marley is a patient with >20 pack years of smoking who has had a productive cough every day for >3 consecutive months a year for at least 2 years (chronic bronchitis) and hyperinflated lungs (suggesting emphysema). § The combination of chronic bronchitis and emphysema in a lifelong smoker is highly suggestive of COPD. § This is a disease caused by the persistent toxicity of smoke, which leads to goblet cell hyperplasia (and thus excessive mucus production), damaged ciliated epithelial cells (which usually clear mucus), and inhibition of α1-antitrypsin (and thus active trypsin, which degrades the interstitial matrix proteins, leading to loss of elasticity of the lungs and alveoli merging into bullae). § The result is lungs with decreased compliance (hence the decreased FER), less surface area (hence the decreased FVC), and lots of mucus that cannot be cleared. As a consequence, patients suffer chronically from poor gas exchange in their lungs and recurrent infections. § According to British Thoracic Society (BTS) guidelines, COPD can only be diagnosed if spirometry shows FEV1 <80% predicted and FEV1:FVC (FER) ratio <70% predicted. § Notice that spirometry in COPD patients often shows both a reduced FER (due to obstructed airways) and a reduced FVC (although the lungs are hyperinflated, their lack of elasticity means they shift a smaller volume of air as much remains trapped in the lungs). This is not the case in asthma, where usually only the FER is affected. § Notice also that the shortness of breath in COPD is PERSISTENT and largely IRreversible. Again, this is not the case in asthma, where patients are not short of breath between attacks. **The management of COPD (as per the NICE 2004 guidelines) involves: a) Smoking cessation. Th is is the single most important factor in limiting the progression of the disease. b) Effective inhaled therapy. As in asthma, short- and long-acting β2-agonists and/or antimuscarinics can be used to control symptoms and improve exercise tolerance in patients. Inhaled corticosteroids should be added to long-acting bronchodilators to decrease exacerbation frequency in patients with an FEV1 less than or equal to 50% predicted who have had two or more exacerbations requiring treatment with antibiotics or oral corticosteroids in a 12-month period. c) Pulmonary rehabilitation (for all patients who need it). A programme of physiotherapy, exercise, education, etc. This increases exercise tolerance and quality of life. d) Non-invasive ventilation (NIV). This is the treatment of choice when medical therapy fails to control persistent hypercapnic ventilatory failure during exacerbations. e) Long-term oxygen. Patients who are hypoxic with an arterial partial pressure of oxygen (PaO2) <7.3 kPa on air, or <8.0 kPa and pulmonary hypertension, should use long-term oxygen for 15 hours each day. This prevents progression to cor pulmonale but does not improve symptoms. Ambulatory oxygen can be given to those who desaturate whilst walking, whilst short-burst oxygen is for psychological benefi t only. f) Manage exacerbations. Appropriate use of inhaled steroids, bronchodilators, and vaccines should be used to reduce the incidence of exacerbations. Th e impact of exacerbations should be minimized by: i) Giving self-management advice on responding promptly to the symptoms of an exacerbation ii) Starting appropriate treatment with oral corticosteroids and/or antibiotics iii) Use of non-invasive ventilation when indicated iv) Use of hospital-at-home or assisted-discharge schemes.

How can ITU/HDU help in severe asthma attack

§ higher level oxygen - optiflow - can deliver up to 60L/min). on ward can only do max of 15L/min. § ventilation

Mr Morris is a 78-year-old retired man who presented at his GP's surgery with a persistent cough. He says he has had a smoker's cough for 40 years, but that in the last few months it has got worse. He had gone to his GP because his wife was being kept awake by his coughing at night. The cough is non-productive and he has had no fever, chest pain, night sweats, or any significant weight loss that he is aware of - although he admits that he is thin anyway and never weighs himself. He is not known to be asthmatic, has no known allergies, and does not suff er from reflux. He is on no medications and jokes that 'the cigarettes keep me healthy'. He has smoked 20 a day since he joined the army for national service in 1949. He is partial to a beer or two but rarely goes to the pub these days (less than once a week). Mr Morris' pulse is 80 bpm, blood pressure 130/82 mmHg, respiratory rate 13/min, temperature 37.3ÅãC. On examination, he is thin but does not appear cachectic, and is comfortable at rest. He appears well perfused with a capillary refill time of <2 seconds. There is no cervical lymphadenopathy or any other peripheral stigmata of respiratory disease, although there is heavy tar staining of the fingers of his right hand. Chest expansion, percussion, and auscultation are all unremarkable. The GP refers Mr Morris to the hospital for a chest radiograph and respiratory opinion. The chest radiograph shows a large mass at the right hilum. What is the most likely diagnosis?

§ Mr Morris most likely has lung cancer. Although he has had a (smoker's) cough for a long time, the recent change should alert you to possible pathology. § Given that the cough is non-productive and that on examination he is afebrile and has no respiratory signs, an infective process appears unlikely. § In light of his history of lifelong smoking, lung cancer is a definite possibility. § This is made even more likely by the chest radiograph. § Assuming a diagnosis of lung cancer is confirmed by biopsy, it will most likely be a SQUAMOUS cell carcinoma because of the HILAR location. § This will be investigated in more detail by the specialist team. Th e GP was right to be suspicious and order a chest radiograph.

Mr O'Hara is a 62-year-old retired paratrooper who presents to your clinic complaining of shortness of breath. He first noticed this a month ago when he was jogging, but says he now feels breathless with minimal exertion. He has not had a cough and has never smoked. He drinks a few pints of ale every weekend. His only past medical history is a fractured right tibia 20 years ago and hypertension for which he takes a thiazide diuretic and an ACE inhibitor. He has not noticed any changes in his bowel habit or urine, but admits that he has probably lost weight over the past few months. On examination, you can feel several enlarged lymph nodes in the right anterior cervical chain of his neck. His right lung shows decreased expansion and is dull to percussion in the bases. Vocal fremitus is markedly reduced on the right. His cardiovascular, abdominal, and neurological examinations are all normal. What diagnosis should you consider for Mr O'Hara? What are your next steps?

§ Mr O'Hara gives a history of worsening shortness of breath and weight loss. § His respiratory examination reveals lymphadenopathy of the neck and signs consistent with a right-sided pleural effusion. § Th e combination of weight loss, lymphadenopathy, and pleural effusion should make you think of a MALIGNANT PLEURAL EFFUSION caused by infiltration of the pleural space by metastatic cancer cells. § Your next step should be to arrange a CHEST RADIOGRAPH. § If this confirms a rightsided pleural effusion, the effusion should be sampled (THORACOCENTESIS) to determine if the fluid in the pleural space is due to changes in osmotic forces (transudate, with protein <25 g/L) or due to infiltration of the pleural space by metastatic cancer cells, infectious agents or inflammatory proteins (exudate, with protein >35 g/L). A finding of protein between 25 and 35 g/L is considered indeterminate and you should then use Light's criteria. § You should also arrange for a lymph node fine needle aspiration (FNA), as Mr O'Hara's history of weight loss should alert you to the possibility of a malignancy. § Mr O'Hara's chest radiograph showed a massive pleural effusion in his right lung. Thoracocentesis showed it to be an exudate, with low glucose and abnormal-looking lymphocytes. § A lymph node biopsy confirmed the presence of binucleated lymphocytes (Reed-Sternberg cells), which are diagnostic of Hodgkin's lymphoma.

Mrs Aurelie is a 52-year-old lady who complains of a cough during a follow-up visit to her GP. Her GP has recently diagnosed her with hypertension. She has had the cough for a few weeks, but has had no sputum or haemoptysis, fever, breathlessness, chest pain, or wheeze. She has never smoked and does not have a history of asthma or GORD. She has no allergies. She takes enalapril for her hypertension and alendronate, calcium, and vitamin D for osteoporosis prevention because she had a hysterectomy and bilateral salpingo-oopherectomy when she was aged 43. Examination of her respiratory system is entirely normal. What is the most likely cause of Mrs Aurelie's cough?

§ Mrs Aurelie has had a non-productive cough for the past few weeks. § She has also recently been diagnosed with hypertension and started on enalapril. § In the absence of any clues in the history or examination to suggest an alternative diagnosis, it is most likely that her cough is due to the ACE inhibitor (enalapril) that she is taking, as ACE inhibitors can cause a dry cough in 10-20% of patients. § This is because ACE is also responsible for breaking down the inflammatory bradykinins in the lungs. § Thus, inhibition of ACE leads to a build up of bradykinins and lung inflammation, triggering cough. § Her GP changed her prescription from enalapril to an angiotensin II receptor blocker (e.g. losartan, candesartan, valsartan), which offer the same renal protection but do not cause a dry cough. Mrs Aurelie's cough had disappeared by the time she was next seen by her GP a few weeks later.

Mrs Betty is a 48-year-old magistrate who attends your clinic complaining of persistent breathlessness that has been getting worse over the last year. It is worst when she takes her dog for a brisk walk, but is always present, even at rest. She denies any cough, weight loss, or night sweats. She smokes 'the odd cigarette' at social events, but never more than five cigarettes a month. A recent blood test ordered by her referring GP shows: § RBC 4.7 Å~ 1012 cells/L § WCC 8 Å~ 109 cells/L § Hb 11.5 g/dL § ESR 72 mm/h § HbA1c 5% § Blood glucose 4.8 mM § Total cholesterol 4.3 mM § LDL 2.2 mM § HDL 2.1 mM Her past medical history includes rheumatoid arthritis, for which she takes methotrexate. On examination, you notice swelling of the metacarpophalangeal joints (MCPJs) and ulnar deviation of her fingers on both hands. Her pulse is 80 bpm and regular, her blood pressure is 120/80 mmHg and she is apyrexial. There are no signs of peripheral or central cyanosis, anaemia, or lymphadenopathy. Her trachea is central and her apex beat undisplaced. Heart sounds I and II are present with no added sounds, and no carotid bruits. Her lungs expand symmetrically and show normal resonance to percussion. However, very fine crackles can be heard all over her lung fields. She has no peripheral oedema and her abdominal and neurological examinations are entirely normal. Flow spirometry reveals FVC = 65% and FEV1 = 88%. An ECG shows sinus rhythm with no abnormalities. What is the most likely cause of Mrs Betty's shortness of breath? How would you confirm this?

§ Mrs Betty does not have any features that are strongly suggestive of the 'most likely' or 'must exclude' diagnoses listed earlier. § Her flow spirometry suggests a restrictive lung pathology as her expiratory rate is normal (FEV1 >70%) but her lung capacity is reduced (FVC <70% predicted value) - in other words, the problem is not getting air out but how much air her lungs can hold. § The fine crackles heard all over her lungs, combined with her flow spirometry and absence of another obvious diagnosis, suggest that Mrs Betty has PULMONARY FIBROSIS. § Pulmonary fibrosis can be caused by CONGENITAL diseases (e.g. neurofibromatosis, Gaucher disease), SYSTEMIC INFLAMMATORY diseases (e.g. rheumatoid arthritis, ankylosing spondylitis, sarcoidosis), CHEMICAL irritation (e.g. silica, asbestos, coal dust, chlorine), DRUGS (e.g. methotrexate, ALLERGIC reations (e.g. bird-funcier's lung), RADIATION or the cause may not be known (e.g. cryptogenic fibrosing alveolitis/usual interstitial pneumonitis). **The best way to confirm Mrs Betty's postulated diagnosis of pulmonary fibrosis is a high-resolution chest computed tomography (CT) scan. Radiologists can diagnose pulmonary fibrosis with high sensitivity and specificity by looking for characteristic linear reticular opacities and a ground-glass appearance of the lung. **Mrs Betty should switch from methotrexate to another immunosuppresive agent in order to control her rheumatoid arthritis. Whilst this is unlikely to improve her condition significantly, it will at least prevent further deterioration, particularly if the fibrosis was mainly due to the methotrexate rather than the rheumatoid arthritis (which explains her elevated ESR).

Mrs Virginia's (78 y/0) CRP and white cell count are raised, with a neutrophilia. Her saturations are 95% (on 28% oxygen) and her ABG shows PaO2 (arterial partial pressure of oxygen) = 12.4 kPa, PaCO2 (arterial partial pressure of carbon dioxide) = 6.2 kPa, pH 7.42, HCO3 - = 32 mM. Her U&Es show Na 142 mM, K 4.7 mM, Cl 103 mM, urea 9.2, creatinine 122 μM. An ECG showed sinus tachycardia but no other changes. In light of the history, examination, and investigations, what is the diagnosis? What is the CURB-65 score, what is it used for, and how is it calculated? How should she be managed?

§ Mrs Virginia has a pneumonia exacerbating her COPD. § Her mild hypercapnia should not be a cause of concern as her pH is within the normal range, suggesting the CO2 retention is chronic and therefore unlikely to be clinically significant. § The CURB-65 score can be used to calculate severity of pneumonia and therefore determine the need for hospitalization. § CURB-65 is an acronym for the constituent prognostic factors; the presence of any one scores 1 point, up to a maximum of 5. Patients with a score of 2 or more need to be admitted to hospital. § C onfusion (new to the patient), defined as an AMTS of ≤8/10 § U rea >7 mM §R espiratory rate >30/minute § B lood pressure <90 systolic and/or <60 diastolic § >65 years old **Mrs Virginia's CURB-65 score is 2. She should therefore be admitted, partly because of the CURB-65 score and partly because elderly patients with pneumonia can deteriorate rapidly. § She should be given a broad-spectrum antibiotic in line with local protocol, which should take into account: a) Severity, a • s assessed by the CURB-65 score b) Comorbidity with COPD c) Hospital-acquired (nosocomial) infection versus community-acquired infection d) Suspicion of unusual organism (e.g. Pneumocystis jirovecii in HIV-positive patients, Pseudomonas in cystic fibrosis patients) e) Whether she has had any pneumonia treated by antibiotics in the past few weeks (this would suggest the antibiotics did not work properly, so you may need to use different ones) f) Whether or not a particular antibiotic is deemed to predispose to infections such as Clostridium difficile colitis.

With regard to anti-tuberculous chemotherapy which five of the following statements are true? § Multiagent (3-4 drugs) therapy is initiated for 8 weeks § Optic neuritis is a side-effect of ethambutol § Hepatitis is a side effect of rifampicin § Pyridoxine supplementation is recommended routinely § Drug therapy ceases at 8 weeks in light of a good response § Directly observed treatment should be continued following hospital discharge in the patient in this case

§ Multiagent (3-4 drugs) therapy is initiated for 8 weeks § Optic neuritis is a side-effect of ethambutol § Hepatitis is a side effect of rifampicin § Pyridoxine supplementation is recommended routinely § Directly observed treatment should be continued following hospital discharge in the patient in this case **Following 8 weeks multiagent therapy, treatment is continued usually with 2 drugs e.g. rifampicin and isoniazid for a further 4 months. **Vitamin supplementation is required to prevent peripheral neuropathy which may occur with certain agents e.g. isoniazid. **This patient is at high risk of non-compliance and his treatment will need to be observed (if possible).

Which differentials would you consider if a patient complains of shortness of breath and muscle weakness/fatigue?

§ Myasthenia gravis § Lambert-Eaton syndrome § Motor neurone disease § Guillain-Barre syndrome § Polymyositis

Specifc Tx for COVID

§ NIV and invasive § proning § dexamethasone and remdesivir § anticoagulation § dialysis

List some drugs that exacerbate the symptoms of asthma

§ NSAIDs § Beta-blockers § Aspirin

Which of the following statements are true regarding pneumothorax? § In severely compromised patients it is important to confirm the diagnosis with a chest radiograph prior to treatment § Mediastinal shift toward the pneumothorax is to be expected for large pneumothoraces § Needle aspiration of large pneumothoraces is helpful to relieve symptoms prior to insertion of a chest-drain § Small pneumothoraces may only be apparent on expiratory chest radiographs § Failure of lung expansion following drainage is an indication for discussion with a thoracic surgical unit

§ Needle aspiration of large pneumothoraces is helpful to relieve symptoms prior to insertion of a chest-drain § Small pneumothoraces may only be apparent on expiratory chest radiographs § Failure of lung expansion following drainage is an indication for discussion with a thoracic surgical unit. If you suspect a tension pneumothorax do not wait for results of a chest radiograph - get on with treatment. If you are unsure and patient condition allows, wait to review radiograph. Recurrent pneumothoraces require surgical review and surgical treatment may be needed. Mediastinal shift occurs away from large pnuemothoraxes. If there is volume loss e.g. lobar collapse, mediastinal shift occurs towards the affected side.

What is the difference between a 'pink puffer' and a 'blue bloater'?

§ Note that these terms are NOT synonymous with type I and type II respiratory failure! § They are outdated terms but still used on the wards sometimes to describe two distinct clinical pictures that arise in chronic lung disease (e.g. COPD), although this is of course a simplification and every patient will be different: § 'Pink puffers' respond to hypercapnia and hypoxaemia by increasing their respiratory rate, resulting in normal PaO2 levels and a 'pink' appearance. As a result of the hard work to maintain their oxygenation, they often have a barrel-shaped, hyperinflated chest and may breathe through pursed lips. They nonetheless complain of shortness of breath on mild exertion. Broadly speaking, their prognosis is BETTER than that of 'blue bloaters'. § In 'blue bloaters' the presence of chronically high PaCO2 levels results in desensitization of the respiratory centre to PaCO2 and chronic cyanosis, giving them a 'blue' appearance. They are chronic CO2 retainers, becoming reliant on their hypoxic (rather than hypercapnic) drive. They are often bloated because of widespread peripheral oedema caused by right heart failure secondary to the lung problems (cor pulmonale). In general, their prognosis is poor.

What features of sarcoidosis suggest infectious etiology

§ Other granulomatous diseases have infectious etiology § Epidemiological evidence suggesting clusters of disease in environments linked with bioaerosol production § Sarcoidosis can be transmitted via transplanted organs § also get more microbial lineages in sarcoidosis. but couldn't find consistent bacteria/fungi across tissues

A 16-year-old female presents to hospital with drowsiness and dehydration. They have no previous past medical history and are on no regular medication. An ABG is performed on room air reveals the following: PaO2: 14 (11 - 13 kPa) ||105 mmHg (82.5 - 97.5 mmHg) pH: 7.33 (7.35 - 7.45) PaCO2: 3.0 (4.7 - 6.0 kPa) || 22.5 mmHg (35.2 - 45 mmHg) HCO3-: 17 (22 - 26 mEq/L)

§ Oxygenation (PaO2): A PaO2 of 14 on room air is at the upper limit of normal, so the patient is not hypoxic. § pH: A pH of 7.33 is lower than normal and therefore the patient is acidotic. The next step is to figure out whether the respiratory system is contributing the acidosis (i.e. ↑ CO2). § PaCO2: The CO2 is low, which rules out the respiratory system as the cause of the acidosis (as we would expect it to be raised if this was the case). So we now know the respiratory system is NOT contributing to the acidosis and this is, therefore, a metabolic acidosis. The next step is to look at the HCO3- to confirm this. § HCO3-: HCO3- is low, which is in keeping with a metabolic acidosis. § Compensation: We now know that the patient has a metabolic acidosis and therefore we can look back at the CO2 to see if the respiratory system is attempting to compensate for the metabolic derangement. In this case, there is evidence of respiratory compensation as the CO2 has been lowered in an attempt to normalise the pH. An important point to recognise here is that although the derangement in pH seems relatively minor this should not lead to the assumption that the metabolic acidosis is also minor. The severity of the metabolic acidosis is masked by the respiratory system's attempt at compensating via reduced CO2 levels. § Interpretation: Metabolic acidosis with respiratory compensation. The underlying cause of the metabolic acidosis, in this case, is diabetic ketoacidosis.

Sleep apnoea mechanism

§ PCO2 goes up and O2 stays same when breathing. § central sleep apnoea (top LHS) - reduced absent efferent activity from brainstem respiratory control neurones in medulla e.g. in stroke/ CCHS/ pulmonary oedema in CCF (causes hyperventilation --> brings CO2 --> central sleep apnoea). § top RHS obstructive - partial or complete occlusion or upper airway with paradox breathing (increased breathing effort and inadequate ventilation). pharyngeal airway is soft tissue with tongue in front and pharyngeal constrictor muscle round back. this airway can collapse when go to sleep due to negative pressure generated in lungs --> pull on flexible airway --> OSA. § apnoea - stop breathing. hypopnea - pause breathing. § if someone does this >15 times in an hours, is v bad. Prevalence is increasing due to obesity and aging population

List some causes of sudden-onset haemoptysis.

§ PE § Erosion of cancer into a blood vessel

What is definition of respiratory failure?

§ PO2 <8kPa • Two types - Differentiated by PCO2 (normal range 4.6-6kPa): 1) Type I Respiratory failure - PCO2 Normal or Low: § Arises due to a ventilation, perfusion mismatch 2) Type II Respiratory failure - PCO2 High (>6kPa): § Arises due to alveolar hypoventilation +/- Ventilation perfusion mismatch

Which features of an ECG might indicate that the patient has previously suffered an MI?

§ Pathological Q waves § Bundle branch block

Patients diagnosed with pneumonia who have COPD should be given...

§ Patients diagnosed with pneumonia who have COPD should be given corticosteroids even if no evidence of the COPD being exacerbated

What extra-pulmonary sites does TB most commonly affect? What does it cause in each?

§ TB can affect virtually any organ. § Some of the more common manifestations include: A) Bone: osteomyelitis, septic arthritis, Pott's disease (in the spine) B) Neurological: meningitis, intracranial granulomas C) Renal: granuloma TB less commonly affects the heart, skeletal muscles, pancreas, thyroid, or adrenals (causing Addison's disease). Indeed, TB was found on autopsy in 70-90% of Dr Addison's patients in his original description of the eponymous syndrome (this figure is in fact lower in larger, more recent studies)

Which patients should not necessarily be given 100% oxygen and why?

§ Patients with COPD are at risk of becoming hypoxaemic for a number of reasons: a) The airways contain significant amounts of mucus that impairs ventilation. b) The lungs are hyperinflated, making them less efficient at moving air. c) The hypoxic vasoconstriction mechanism is blunted. This usually ensures that areas of lung that are poorly ventilated are supplied with less blood, so that gas exchange only occurs in well-ventilated areas. If this mechanism no longer works well, blood travels through poorly ventilated areas of the lung and is not well oxygenated. § When COPD patients become hypoxic, it is tempting to administer 100% oxygen. However, in a minority of COPD patients, it has been observed that administration of 100% oxygen to combat hypoxaemia can be detrimental, leading to patients developing hypercapnia (high CO2) which obtunds them and can eventually make them comatose. Traditional teaching states that this is because some COPD patients no longer rely on detecting high CO2 levels to stimulate breathing (as is normally the case in people without COPD) but rather rely on low O2 levels ('hypoxic drive'). Giving too much oxygen in these cases can actually remove the stimulus to breathe. However, experiments suggest this is not the case, as hypercapnia develops in COPD patients given O2 without any signifi cant drop in ventilation rate, so clearly their stimulus to drive is not reduced. The current hypothesis is that too much oxygen further diminishes the hypoxic vasoconstriction eff ect that usually prevents poorly ventilated areas of lung being perfused with blood. In other words, it is believed that giving too much oxygen results in blood being diverted ('shunted') to areas of the lungs that in COPD patients are incapable of effi cient gas exchange, thus diverting blood from the areas of lung that are still able to exchange gas effi ciently. For this reason, COPD patients who become hypoxaemic are administered oxygen using 'Venturi' masks, which allow oxygen to be delivered at safer, smaller, fi xed ratios (from 24% to 40%) such that the lungs are better ventilated, but not so much so that the COPD patient can become hypercapnic. **Overall, it diminishes the hypoxic drive to breathe - this results in the patient becoming very hypercapnic It also diminishes hypoxic vasoconstriction leading to VQ mismatch. USE Venturi mask used instead.

Mr Thomas is a 27-year-old retail manager who is referred to the respiratory clinic for investigation of his persistent cough. His referral letter documents an episode of pneumonia 9 weeks ago, which was treated by the GP with antibiotics. He made a good recovery, but the cough became dry and persisted. The cough does not vary with time of day and is not associated with exercise or any other triggers. There is no history of asthma, allergies, or gastro-oesophageal reflux. He has never smoked and takes no regular medications. Mr Thomas' pulse is 64 bpm, blood pressure 120/72 mmHg, oxygen saturations 98% on room air, respiratory rate 11/min, temperature 36.8ÅãC. There are no peripheral stigmata of respiratory disease and chest expansion, percussion, and auscultation are all unremarkable. Lung function tests performed in the respiratory clinic are normal. What is the most likely cause of his persistent cough? What are the treatment options?

§ Patients with pneumonia, particularly viral pneumonia, can have a persistent post-infectious cough some time after the infection has subsided. § Judging from the history and the negative findings on examination and lung function testing, this looks to be the most likely cause. § There are a number of treatment options available: a) Antitussives (cough suppressants)? If an underlying cause cannot be identified, these may offer symptomatic relief (e.g. if sleep is being disrupted). These operate via two mechanisms: (1) depressing the brainstem 'cough centre', e.g. codeine, pholcodine; (2) reducing peripheral receptor sensitivity, e.g. benzocaine (a local anaesthetic). Unfortunately, there is currently no high-quality evidence to suggest that cough suppressants actually work, despite their widespread use. Furthermore, the opiate cough suppressants are associated with side-effects such as constipation, particularly with codeine but less so with pholcodine, and may be associated with dependence. b) Inhaled corticosteroids? The evidence is mixed on the efficacy of corticosteroids. It is thought that in some patients chronic cough is associated with airway inflammation, even in the absence of asthma, and that corticosteroids suppress this inflammation. c) Inhaled ipratropium bromide? This is an anticholinergic that blocks the efferent limb of the cough reflex, and may also decrease stimulation of cough receptors. This has been shown to be of benefit in patients with persistent cough after an upper respiratory tract infection.

State two investigations that you would perform to investigate a respiratory cause of shortness of breath.

§ Peak expiratory flow rate § Spirometry

Causes of transudate and exudate pleural effusion

§ Pleural effusions may be classified as being either a transudate or exudate according to the protein concentration. 1) Transudate (< 30g/L protein) a) heart failure (most common transudate cause) b) hypoalbuminaemia (liver disease, nephrotic syndrome, malabsorption) c) hypothyroidism d) Meigs' syndrome 2) Exudate (> 30g/L protein) infection: a) pneumonia (most common exudate cause), TB, subphrenic abscess b) connective tissue disease: RA, SLE c) neoplasia: lung cancer, mesothelioma, metastases d) pancreatitis e) pulmonary embolism f) Dressler's syndrome g) yellow nail syndrome **Features: dyspnoea, non-productive cough or chest pain are possible presenting symptoms classic examination findings include dullness to percussion, reduced breath sounds and reduced chest expansion

List some differentials for shortness of breath that occurs over hours/days.

§ Pneumonia § Heart failure § Pleural effusion § ARDS § Post-operative atelectasis

what is precision medicine?

§ Precision medicine is an emerging approach for disease treatment and prevention that takes into account individual variability in genes, environment, and lifestyle for each person. § Personalised medicine is an older term for precision medicine. § 4P Medicine: Predictive, Preventive, Personalised, Participatory

Well's score for PE

§ Previous DVT/PE- 1.5 § Evidence of DVT- 3 § Stasis- 1.5 § Cancer- 1 § Opinion is PE- 3 § Rate Raised (>100)- 1.5 § Exsanguination (Haemoptysis)- 1

Non-acute management flowchart of a pneumothorax

§ Primary <2cm --> discharge and repeat CXR. >2cm --> aspiration (chest drain if unsuccessful) § Secondary <2cm --> aspiration. >2cm --> chest drain

Cost effectiveness of CPAP therapy

§ Probability CPAP was cost-effective (NHS threshold £20,000/QALY gained): 0.61. So is cost-effective, but only if they use it correctly. NICE will only say a treatment can be used if it is both clinically effective and cost effective § In UK, we treat patients with mild OSA (5-15 AHI) + symptoms

What does pulse oximetry meausre?

§ Pulse oximetry measures the amount of oxygenated haemoglobin circulating in the peripheral arterial circulation, presenting this as a percentage of the total haemoglobin present. § A low SpO2 indicates that either oxygen is not reaching the alveoli, or it is not being uploaded onto haemoglobin molecules and transported to the peripheral arterial circulation. § Pulse oximetry is not a perfect tool and its readings can be adversely affected by a number of clinical and environmental factors. § Pulse oximetry can be used to assess and monitor patients with known respiratory conditions, or with respiratory symptoms to determine the severity of the illness and also as a screening tool in acutely unwell patients to detect conditions that can give rise to hypoxia. § Pulse oximetry can be used to decide how to manage a patient, in terms of whether or not oxygen therapy is required and whether the patient should be admitted to hospital or not. SpO2 levels feature in many of the risk assessment and clinical decision-making tools in various NICE/BTS/SIGN guidelines.

Typical spirometry findings in restrictive lung disease

§ Reduced FEV1 (<80% of the predicted normal) § Reduced FVC (<80% of the predicted normal) § FEV1/FVC ratio normal (>0.7)

Causes of a low SpO2

§ Reduced atmospheric oxygen (e.g. high altitude, carbon monoxide-rich environment) § Respiratory depression (e.g. head injury, drug overdose) § Upper airway obstruction (e.g. epiglottitis, croup, inhaled foreign body) § Lower airway obstruction (e.g. bronchospasm, lung collapse/consolidation) § Restriction to chest/diaphragmatic expansion (e.g. pain from rib fractures, neurological conditions) § Restriction to lung expansion (haemothorax, large pleural effusion) § Inability to create negative intrathoracic pressure (flail chest, tension pneumothorax) § Obstruction to oxygen transfer across the alveolar wall (e.g. pulmonary oedema)

Subjective measurement of sleep

§ difficult is getting the right terminology e.g . nodding off, snoozing. § People find it hard to assess sleepiness § hence we use the epworth sleepiness scale

Resp vs metabolic compensation

§ Respiratory acidosis/alkalosis (changes in CO2) can be metabolically compensated by increasing or decreasing the levels of HCO3- in an attempt to move the pH closer to the normal range. § Metabolic acidosis/alkalosis (changes in HCO3-) can be compensated by the respiratory system retaining or blowing off CO2 in an attempt to move the pH closer to the normal range. **Rate of compensation: § Respiratory compensation for a metabolic disorder can occur quickly by either increasing or decreasing alveolar ventilation to blow off more CO2 (↑ pH) or retain more CO2 (↓ pH). § Metabolic compensation for a respiratory disorder, however, takes at least a few days to occur as it requires the kidneys to either reduce HCO3- production (to decrease pH) or increase HCO3- production (to increase pH). As a result, if you see evidence of metabolic compensation for a respiratory disorder (e.g. increased HCO3-/base excess in a patient with COPD and CO2 retention) you can assume that the respiratory derangement has been ongoing for at least a few days, if not more. **It's important to note that 'over-compensation' should never occur and, therefore, if you see something that resembles this you should consider other pathologies driving the change (e.g. a mixed acid/base disorder).

List some autoimmune diseases that are associated with interstitial lung disease.

§ Rheumatoid arthritis § Sarcoidosis § SLE

When to suspect PE

§ S1Q3T3 is sign of right ventricular strain § CXR can show Westermark's signs ---> translucency in some parts of lungs 1) Acute Massive PE § Sudden complete occlusion of pulmonary artery §Collapse §Central crushing pain §Severe Dyspnoea **On ECG: §S1Q3T3 pattern §RAD §RBBB 2) Acute Submassive & Small PE: § Sudden incomplete occlusion of pulmonary artery or distal §Pleuritic chest pain §Haemoptysis §Dyspnoea **On ECG §Sinus tachycardia 3) Chronic PE: § Chronic occlusion of pulmonary microvasculature §Exertional Dyspnoea **Note: CXR can show Westermark's Sign (high +ve pred. value)

List some presenting symptoms of heart failure

§ SOBOE Orthopnoea (=SOB when lying flat) § Paroxysmal nocturnal dyspnea § Swollen ankles

Identifying patients at risk of progression of lung fibrosis in sarcoidosis

§ Severity of pulmonary fibrosis: • Irreversible changes present • Integration of symptoms, lung function and imaging § Which lung function thresholds ? Lung function: • FVC <60% • DLCO <50% • Major airflow obstruction § Longitudinal behaviour

Mrs Finnegan is a 78-year-old widow who presents to your clinic complaining of increasing shortness of breath. She describes that for the past 4 months she has gradually become increasingly short of breath when she walks back up the hill to her bungalow after going to the shops. She is finally seeking medical help because she now finds herself short of breath when she does her gardening. Her sister (a lifelong smoker) died of lung cancer aged 73, and given that Mrs Finnegan used to smoke, she is especially concerned that she may have lung cancer. In broad terms, what pathological processes could cause shortness of breath?

§ Shortness of breath essentially means either that not enough oxygen is getting around the body or that there is a cause for increased respiratory drive. Th is could be due to: 1) Insufficient oxygen getting into the lungs: a) Obstructed airways (obstructive lung disease impairing airflow, e.g. asthma, chronic obstructive pulmonary disease (COPD), lung cancer, or upper airway obstruction, e.g. anaphylaxis) b) Decreased lung compliance (restrictive lung disease limiting inspiratory volumes, e.g. pulmonary fibrosis) c) Decreased lung space (e.g. pneumothorax, lung collapse) d) Weak diaphragm (e.g. Guillain-Barr. syndrome, myasthenia gravis) e) Chest wall that cannot inflate properly (e.g. obesity, kyphoscoliotic spine) 2) Insufficient oxygen getting from the air into the blood (ventilation-perfusion mismatch): a) Pulmonary oedema (e.g. heart failure, liver failure, nephrotic syndrome) b) Pneumonia c) Pulmonary embolism (PE; area of lung is not perfused, so no exchange can occur) d) Pulmonary fibrosis 3) Insufficient oxygen getting around the body: a) Reduced cardiac output (e.g. heart failure, aortic stenosis) b) Anaemia c) Shock (i.e. blood pressure <90/60 mmHg from any cause, e.g. sepsis, haemorrhage) 4) Increased respiratory drive per se: a) Hysterical hyperventilation b) Acidaemia (e.g. diabetic ketoacidosis)

Describe how acute pulmonary oedema caused by heart failure is managed

§ Sit up § Oxygen § Venodilators (e.g. diamorphine, furosemide, GTN)

What ectopic endocrine secretions are associated with which lung cancers? What symptoms do they cause?

§ Small cell lung carcinomas are derived from endocrine cells in the lung and therefore have the potential to synthesize and secrete hormones or hormone-like substances. The substances secreted by small cell lung cancers are antidiuretic hormone (ADH), resulting in hyponatraemia, and ACTH, resulting in Cushing's syndrome. § Squamous cell carcinomas may not have the cell machinery to produce cholesterol-based steroids, but they can produce peptides including PTHrP. This causes hypercalcaemia.

List some key features of the past medical history for haemoptysis

§ Smoking § Exposure to asbestos and other inhaled substances § Prior lung disease (e.g. TB) § Growing up abroad and recent travel § Risk factors for DVT/PE § Anticoagulant use or bleeding diathesis

Which of the following are the likely pathogens for suspected community acquired pneumonia? § Streptococcus pneumoniae § Pseudomonas aeruginosa § Klebsiellla § Haemophilius influenzae § Mycoplasma pneumoniae § Proteus spp 2) He is commenced on Co-Amoxiclav 625mg TDS and Erythromycin 500mg QDS by the admitting doctor. Is the chosen antibiotic regime appropriate? 3) After 3 days of treatment on the ward, he is feeling no better and he continues to spike high temperatures of up to 39.5°C. Which of the following blood parameters would you use to monitor response to treatment?

§ Streptococcus pneumoniae § Haemophilius influenzae § Mycoplasma pneumoniae **The most common cause of community acquired pneumonia (CAP) leading to hospital admission is Strep pneumoniae (39%), followed by viral and C. pneumoniae (both 13%), mycoplasma (11%), H.influenzae (5%). Other bacteria sometimes isolated are Legionella, S. aureus, Moraxella catarrhalis, C. psittici. Treatment is nearly always initiated on an empirical basis, and therefore must always include cover against strep pneumoniae. It is very common for blood cultures to be non-diagnostic in CAP, particularly after prior antibiotic treatment, and sputum cultures (it is actually unusual to expectorate in CAP) are often unhelpful/misleading. 2) Yes. The chosen antibiotic regimen is very reasonable, providing cover against all the common bacterial pathogens likely to have caused this episode of CAP. In someone who has severe pneumonia (as judged by CURB65 criteria) an intravenous route is essential. For patients with non-severe CAP not previously treated with Amoxicillin prior to admission, the combination of Amoxicillin and Erythromycin is acceptable, but in this case the non-response to Amoxicillin meant that a step up in treatment was appropriate. 3) Renal function (if impaired at presentation), CRP, White cell count. **Total white cell and neutrophil count and CRP improve quickly as the pneumonia improves. In patients with sepsis and renal impairment, renal function should be monitored regularly until at baseline. Procalcitonin may be a useful test if it is not clear whether the infection is caused by bacteria. However, this is not a first line test and should not be done at this stage.

Which pathogens that cause pneumonia produce antigens that can be detected in the urine?

§ Streptococcus pneumoniae § Legionella pneumophila

TAC from UBIOPRED sputum analysis

§ TAC1 - severe eosinophilic asthma

Which 3 of these other conditions can be associated with erythema nodosum? § TB § Graves Disease § Oral contraceptives § Rheumatoid arthritis § Cushing's disease § Crohn's disease

§ TB § Oral contraceptives § Crohn's disease **Erythema nodosum can be associated with a number of systematic diseases and drug reactions. It is not associated with rheumatoid disease, Cushing's or Grave's

What is aim of treatment in fibrotic sarcoidosis

§ don't want to treat so much that leads to toxicity • Is the fibrotic disease stable or progressive? • Aim of treatment is to prevent progression of fibrosis, but avoid toxicity in stable fibrosis • Ongoing active inflammation likely to lead to further progression of fibrosis

Objective measurement of sleep

§ electroencephalogram § in-ear sleep monitor

Mr Morris' oxygen saturations are 95% on room air. His FBC shows a haemoglobin concentration of 14.5 g/dL, a white cell count of 4.6 × 109 cells/L, a CRP of <2 mg/L, a urea of 5.8 mM, a creatinine of 68 µM, and a corrected calcium of 2.54 mM. Urinalysis is unremarkable. In light of his history and examination, computed tomography pulmonary angiogram (CTPA) and a skin test for TB are not requested. His chest radiograph is shown here. What is the most likely diagnosis? What should your next step be?

§ The chest radiograph shows a mass lesion sometimes called a 'coin lesion' in the patient's left hilum. § This, in combination with his history (smoker, haemoptysis, and weight loss) and examination (hepatomegaly), is strongly suggestive of lung cancer (although there is a broader differential diagnosis for a coin lesion; see the Viva questions). § You need to confirm and classify the diagnosis with cytology of sputum and bronchoscopic washings. If the lesion is peripheral, one might opt for a CT-guided percutaneous fine needle biopsy. § The reason is that cancer is ultimately a pathological diagnosis: clinical features can make you strongly suspect malignancy, but only a pathological sample will confirm it. You also need to STAGE the cancer with a CT scan, looking for local spread and lymph node involvement, and a BONE SCAN, looking for bone metastases.

Miss Chanda is a 27-year-old factory worker from Zambia who has been referred to the medical admissions unit of her hospital because of severe shortness of breath, which has been present for the last few days. She finds she is always breathless but it is worse with even mild exertion such as walking. She has felt very weak for the last few days and has had a dry cough and fever. On hindsight, she thinks she has probably been losing weight for the past few months. Her past medical history is unremarkable and she takes no regular medications. On examination, Miss Chanda has a temperature of 37.6C and a respiratory rate of 25/min. Her JVP is not raised, there is no peripheral oedema, and both heart sounds are present without any added sounds. There are fine crackles heard over the entirety of both lung fields. The rest of the examination is entirely normal. Her oxygen saturations are 90% on air but the attending nurse comments that when Miss Chanda came back from walking to the toilet, her saturations had dropped to 82%. A chest radiograph shows diffuse interstitial shadowing throughout both lung fields. What is the likely diagnosis? What tests will you arrange?

§ The clinical picture of dry cough, shortness of breath, low oxygen saturation/ desaturation on exercise, and diffuse interstitial shadowing throughout the lungs on a chest radiograph in a young patient from Africa should always make you suspicious of Pneumocystis jiroveci pneumonia (previously known as Pneumocystis carinii pneumonia, or PCP). § Pneumocystis is an opportunistic organism that rarely causes problems in healthy adults but commonly causes pneumonia in IMMUNOSUPPRESSED patients. Indeed, Pneumocystis pneumonia is a common complication of patients with AIDS. § It is diagnosed by performing microscopy (+ silver staining) and culture on sputum and broncho-alveolar lavage samples. § If you suspect Pneumocystis pneumonia, you should arrange to test for two other infections: a) HIV testing. Offer Miss Chanda an HIV test. If this is positive, you will need to check her CD4+ lymphocyte levels, as these dictate the need for antiretroviral therapy. b) Tuberculosis testing, as this is a frequent cause of pulmonary pathology in HIV-positive patients. Testing is by microscopy (+ Ziehl-Neelsen staining) and culture of sputum and broncho-alveolar lavage samples.

What is the doctrine of double effect? How is this relevant to a lung cancer patient being treated with opiates for pain relief?

§ The doctrine of double effect applies when a treatment has two (or more) effects. The primary (intended) effect is to relieve the symptoms. But a secondary effect, which is foreseen but not intended, in some way hastens death. § In legal terms, although the treatment is bringing about mortality, as its primary (intended) effect is beneficial it is viewed as distinct from euthanasia. § This applies directly to the lung cancer patient being treated with opiates. As well as providing analgesia and suppressing the cough reflex (and hence the likelihood of haemoptysis), opiates can cause respiratory depression if given in sufficiently large doses. § However, the benefits are considered to outweigh the drawbacks, particularly given that the doses are usually insufficient to cause respiratory depression (making this a somewhat theoretical point). § Thus, opiates are commonly used in terminally ill patients suffering with chronic pain.

In the context of a pleural diffusion, what is the difference between a transudate and an exudate? What are the causes of each?

§ The fluid from a pleural effusion can be defi ned as a transudate or an exudate depending on the protein content. § A transudate is defined as having <25 g/L of protein. Transudates are low in protein because they are the result of fluid alone squeezing into the pleural space, either due to increased hydrostatic pressure in the lung vasculature (heart failure, fluid overload, constrictive pericarditis) or due to reduction in the oncotic pressure which usually keeps fluid in the vasculature (reduced serum protein due to liver failure, malabsorption/malnutrition, nephrotic syndrome). § An exudate is defined as having >35 g/L of protein. Exudates are rich in protein because they are the result of cells in the pleural space: either pathogens (infection), inflammatory cells, or malignant cells. **• If the pleural fluid protein is between 25 and 35 g/L, Light's criteria should be used to differentiate exudates from transudates. These state that the fluid is an exudate if any of the following applies: − Pleural fluid protein divided by serum protein >0.5 − Pleural fluid lactate dehydrogenase (LDH) divided by serum LDH >0.6 − Pleural fluid LDH more than two-thirds the upper limit of normal serum LDH

Explain why heart failure causes bibasal crackles

§ The increase in fluid in the lungs dilutes surfactant meaning that it is less able to keep the alveoli open § Alveoli collapse § Breathing in deeply makes these alveoli pop open causing the crackling sound

Miss Wilson is a 33-year-old nurse who has been referred to the respiratory clinic by her GP with a 3-month history of a dry cough. The GP's letter notes that she has never smoked and has no previous history of respiratory illness, reflux, or any allergies, but has a high body mass index (BMI). You take a history in which Miss Wilson confirms all of this. She adds that her cough got worse in the spring, but can think of no other exacerbating factors. She says that sometimes she wakes up at night coughing. She has not had a fever, night sweats, or rigors. She has had no chest pain. She does not have a wheeze, is no more breathless than usual on exertion, and is not breathless at rest. What diagnoses are most likely? If you are the registrar seeing her in outpatients, what investigations would you conduct and what would you be looking for?

§ The three most common causes of chronic cough in a non-smoker are ASTHMA, POST-NASAL DRIP AND GORD. § Asthma is a likely cause in this lady, despite the lack of allergies or atopy (e.g. eczema) and her age (asthma is most common in children and the elderly). § As such, in addition to listening to her lungs, you should perform SPIROMETRY or PEAK FLOW measurement to assess her lung function. § The BTS guidelines for diagnosing asthma suggest using measurements of either peak expiratory fl ow (PEF) or forced expiratory volume in 1 second (FEV1) - both of these are reduced in obstructive airways disease such as asthma and COPD. § However, asthma is characterized by variability in PEF and FEV1, either in response to treatment (e.g. with an inhaled short-acting bronchodilator) or spontaneously (e.g. diurnal variation). § Demonstrating the following variations can be used to diagnose asthma: • PEF: ≥20% and 60 L/min variation on ≥3 days a week over a fortnight ( recorded in a PEF diary). • FEV 1: ≥15% and 200 mL increase after a short-acting bronchodilator (e.g. salbutamol) or trial of steroid tablets (e.g. prednisolone 30 mg/day for 14 days), or ≥15% decrease after 6 minutes of exercise. These can be compared with predicted normal values for someone of a given gender, height, and age. § It is important to request a chest radiograph as well, to exclude any unusual but more serious causes such as lung cancer, but we would not expect to see any abnormality indicating asthma. § On examination, Miss Wilson's lungs sound clear, with no added sounds. § However, her FEV1 is 2500 mL and improves to 3600 mL after salbutamol. Th is 44% (and greater than 200 mL) increase following administration of a β2-agonist together with the history strongly suggests asthma, and she is started on a trial of salbutamol inhalers. **Post-nasal drip is still a possibility but is largely a diagnosis of exclusion. If inhalers do not work after a trial period, you may wish to try antihistamines and/or nasal decongestants. **Finally, reflux (GORD) is still also a possibility, particularly given her high BMI, although she does not give any history of heartburn or regurgitation. In your letter to her GP you may want to add that if treatment for asthma and post-nasal drip do not work, Miss Wilson could try antacids, histamine H2 antagonists, or proton-pump inhibitors.

Mr Humbolt is a 52-year-old gentleman who underwent a partial hepatectomy for primary hepatic carcinoma 24 hours ago. On the ward round, Mr Humbolt complains of a 'painful, rattling cough'. His pulse is 105 bpm regular, blood pressure 125/75 mmHg, respiratory rate 18/min and temperature 37.1.C. Chest expansion is reduced bilaterally and there are crackles in both lung bases. The base of the right lung is dull to percussion and has reduced breath sounds on auscultation. What reasons can you think of for this patient's breathlessness? What is the most likely diagnosis in this patient?

§ There are many reasons for breathlessness post-operatively: a) Atelectasis (alveolar collapse). Pain sometimes prevents patients from breathing adequately and expectorating any mucus in their lungs. The mucus eventually plugs the bronchioles, preventing air entry, and areas of lung collapse as the trapped air is gradually absorbed into the surrounding tissues. In some countries this is prevented by having post-operative patients blow bubbles though a straw placed in a bottle of water, which encourages forceful expiration. b) Pneumonia. Th is is fairly common post-operatively for a combination of factors: poor clearance of mucus due to pain, aspiration of gastric contents, infection from operative intubation, and a somewhat weakened immune response from the physiological stress of surgery. c) Pulmonary oedema. This can be due to heart failure and/or excessive fluids peri-operatively. d) PE. DVT is very common after surgery due to the combination of trauma and immobility, and classically occurs 10 days post-operation. Large DVTs can be prevented by using compression stockings on the legs, mobilizing patients as early as possible, and using low-molecular weight heparin. e) Anaemia. Patients may be anaemic if there was significant blood loss during surgery. f) Pneumothorax. This should always be considered if the patient has had any interventions near the chest either during the surgery or around the time of surgery (e.g. insertion of central venous line, intercostal anaesthetic block). ***The 'rattling cough' is highly suggestive of mucus trapped in the lungs. The reduced chest expansion, crackles, and dull percussion all suggest a collapse of a segment of lung, most notably on the right. This picture would fit with post-operative atelectasis, caused by the patient not breathing out deeply enough to clear his lungs of mucus. This can be prevented with adequate analgesia. Nonetheless, it is important to confirm this diagnosis and exclude the others listed above so this patient would require a: i) chest radiograph (looking for collapse, consolidation from pneumonia, oedema, or a pneumothorax) iii) FBC (looking for anaemia or a raised white cell count (WCC) from infection such as pneumonia) iii) and C-reactive protein (CRP) levels (which will be raised in infection or tissue damage but is useful to monitor as a sign of improvement or deterioration). Th e most important treatment for post-operative atelectasis is physiotherapy, analgesia and oxygen.

Type of inflammation in eosinophilic asthma

§ eosinophils part of type 2 inflammation which drives asthma (this is driven by IL-4, 5 and 13) § innate and adaptive cells produce these cytokines

Gram negative vs gram positive

§ gram negative more difficult to treat due to outer cell membrane e.g. macrolides, amoxicillin, piperacillin

What are the signs of typical causes of pneumonia

§ green suggests bacterial infection § bronchial breathing - high-pitched loud size

Which of the following statements concerning Aspergillus species and the lung are true? § They cause a type I hypersensitivity reaction § They are a cause of bronchiectasis § Recurrent exposure is associated with a type III hypersensitivity reaction. § They are a cause of eosinophilia § They are a risk factor for carcinoma of the lung

§ They cause a type I hypersensitivity reaction § They are a cause of bronchiectasis § Recurrent exposure is associated with a type III hypersensitivity reaction. § They are a cause of eosinophilia Although type I (IgE-mediated) hypersensitivity is common, type III (IgG-mediated immune complex) and type IV (cell-mediated) reactions have also been observed with Aspergillus species in the lung. Damage caused by persistent inflammation caused by ABPA can lead to bronchiectasis. Eosinophilia is associated with ABPA (type I IgE-mediated hypersensitivity).

Claire is a 15-year-old student who presents to her GP complaining of general fatigue and shortness of breath when she exercises. She has recently found herself feeling unusually tired towards the end of the day and complains that she is more breathless than usual during her netball training. She does not smoke, denies any cough, and is never woken at night feeling short of breath. She has never travelled further than Italy, and is otherwise fi t and well. She has no family history of respiratory disease. When specifically asked, she reveals with some embarrassment that her periods are 'a bit heavy' but she denies her faeces ever being dark or bloody. Physical examination is unremarkable. Spirometry reveals an FVC = 90% and FER = 88%. What tests should the GP arrange? What is the most likely diagnosis?

§ This patient does not have any features of heart failure (no clinical features and a bit young), aortic stenosis (no murmur), asthma (no cough, no wheeze, normal spirometry), COPD (young with no family history to suggest α1-antitrypsin, non-smoker, no cough), Guillain-Barr. syndrome (no recent infection, normal spirometry), lung collapse (no physical signs), or pneumothorax (no physical signs). § However, she does complain of fatigue and admits to having menorrhagia (heavy menstrual periods). It is therefore very likely that this patient is ANAEMIC, as the most common cause for anaemia in menstruating women is menorrhagia. § The GP should order an FBC (which will probably reveal a microcytic hypochromic anaemia, compatible with an iron-deficiency anaemia) and clotting studies (to rule out a clotting disorder that may be causing or exacerbating her menorrhagia). § If a gynaecologist referral does not reveal any abnormality causing the menorrhagia, the patient will probably benefit from pharmacological treatment. § NICE guidelines recommend a levonorgestrel-releasing intrauterine device (LNG-IUD) or the combined oral contraceptive pill

How can MI lead to acidosis?

§ This patient had a cardiac arrest which meant there was a period of impaired ventilation and end-organ perfusion. § This has ultimately led to hypercapnia causing a respiratory acidosis, in addition to the accumulation of products of anaerobic respiration (as a result of hypoxia and reduced end-organ perfusion) causing metabolic acidosis.

How can urosepsis lead to metabolic acidosis?

§ This patient has presented profoundly septic, with fever, hypotension and evidence of reduced end-organ perfusion (reduced urine output). § Reduced end-organ perfusion causes tissue hypoxia resulting in cells resorting to anaerobic respiration to generate energy. § Anaerobic respiration produces lactic acid as a byproduct, which has resulted in the addition of acid to the patient's serum causing lactic acidosis. **Urosepsis - likely given the clinical presentation and history of recent catheter change

Which of the following statements about the diagnosis and treatment of mesotheliomas are correct? § Cytology of pleural fluid at initial presentation almost always is diagnostic § Thoracoscopy with biopsy and histology of pleura may be required § Instillation of sclerosant substances may be used to prevent re-accumulation of pleural effusions § Chemotherapy is highly effective

§ Thoracoscopy with biopsy and histology of pleura may be required § Instillation of sclerosant substances may be used to prevent re-accumulation of pleural effusions. **Cytology of pleural fluid is often non diagnostic particularly in the early stages and thoracoscopic biopsy may be necessary to obtain a tissue diagnosis. There are no effective treatments though instillation of sclerosants into the pleural space can prevent or reduce re-accumulation of pleural effusions and accompanying breathlessness.

What are two important features of the history of presenting complaint of a patient presenting with shortness of breath?

§ Time of onset § Alleviating/exacerbating factors

Type 1 respiratory failure

§ Type 1 respiratory failure involves hypoxaemia (PaO2 <8 kPa) with normocapnia (PaCO2 <6.0 kPa). It occurs as a result of ventilation/perfusion (V/Q) mismatch; the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lung tissue. As a result of the VQ mismatch, PaO2 falls and PaCO2 rises. The rise in PaCO2 rapidly triggers an increase in a patient's overall alveolar ventilation, which corrects the PaCO2 but not the PaO2 due to the different shape of the CO2 and O2 dissociation curves. The end result is hypoxaemia (PaO2 < 8 kPa) with normocapnia (PaCO2 < 6.0 kPa).¹ Examples of VQ mismatch include: § Reduced ventilation and normal perfusion (e.g. pulmonary oedema, bronchoconstriction) § Reduced perfusion with normal ventilation (e.g. pulmonary embolism)

Type 2 vs non-type inflammation asthma types

§ Type 2: eosinophilic, allergic, exercise-indued § Non-type 2: (late onset) obesity, smoking, smooth muscle mediatied

Pulmonary vasculature

§ VC --> RV --> PArtery --> lungs --> gas exchange

Why get thrombus in DVT

§ VTE likely in deep veins in calf as large compliance and low pressure § embolus --> pulmonary artery lungs

List the main causes of pulmonary-renal syndrome

§ Vasculitides (e.g. Granulomatosis with polyangiitis) § SLE § Goodpasture's syndrome

What do the following types of cough indicate: Wheezy cough Bovine cough Dry cough Gurgling/wet cough Whooping cough

§ Wheezy cough: Airway obstruction due to asthma or COPD § Bovine cough: Due to vocal cord paralysis (left recurrent laryngeal nerve) usually due to a Pancoast lung tumour § Dry cough: Bronchitis, Interstitial lung disease § Gurgling/Wet cough: Bronchiectasis § Whooping cough: Infection caused by Bordatella pertussis

When using an inhaler, for a second dose you should wait for approximately HOW LONG before repeating

§ When using an inhaler, for a second dose you should wait for approximately 30 seconds before repeating **The following inhaler technique guideline is for metered-dose inhalers (source: Asthma.org.uk, a resource recommended to patients by the British Thoracic Society) 1. Remove cap and shake 2. Breathe out gently 3. Put mouthpiece in mouth and as you begin to breathe in, which should be slow and deep, press canister down and continue to inhale steadily and deeply 4. Hold breath for 10 seconds, or as long as is comfortable 5. For a second dose wait for approximately 30 seconds before repeating steps 1-4. Only use the device for the number of doses on the label, then start a new inhaler.

Miss Gautam is a 19-year-old woman who presents with haemoptysis. She tells you she suffered from a lot of chest infections when she was growing up in Bangladesh. However, she has come to you because in the last week her sputum has become stained with bright red blood. There has been no more than an eggcup of blood at most. She has not had coryzal symptoms or felt feverish, but has felt 'not 100%' and had night sweats. She has also lost around a stone [about 6.5 kilos] in weight in the last 6 months, although she says she has been dieting and exercising. She denies any chest pain or shortness of breath. She is a non-smoker, has no history of exposure to industrial agents, or diagnosed lung disease. She grew up in Bangladesh until the age of 16, when she moved to the UK with her family. She has not been vaccinated against TB. She is on the combined oral contraceptive pill but is taking no other medications, and has no other risk factors for venous thromboembolism. On examination, she has a temperature of 39.2°C, a pulse of 89 bpm, blood pressure of 109/66 mmHg, respiratory rate of 12/min, and oxygen saturations of 96% on room air. There are no peripheral stigmata of respiratory disease. Her chest expansion is slightly reduced on the right hemithorax, and percussion over the right lower hemithorax is dull. Auscultation of the right lower lung field reveals reduced breath sounds, some crackles, and increased vocal resonance. Her bloods come back with a haemoglobin concentration of 10.3 g/dL, a white cell count of 7.2 × 109 cells/L, a CRP of 11 mg/L, a urea of 5.6 mM, a creatinine of 47 µM, and a Ca of 2.38 mM. Urinalysis and an ECG are unremarkable. You send off blood cultures and request a chest radiograph. While you are waiting for radiology to do this, your Consultant asks you to present the case with your working differential diagnosis and management plan. What is the diagnosis you are most concerned about? Given this, what specific actions should your management plan consider?

§ With her history of growing up in the Indian subcontinent and chronic cough (in the absence of smoking), haemoptysis, night sweats, and weight loss, you should be most concerned about pulmonary TB, although pneumonia is also a possibility. § The suspicion of TB is reinforced by examination and investigation findings consistent with an infection (temperature, raised white cell count, and CRP) and consolidation (reduced expansion, dullness to percussion, reduced breath sounds, crackles, increased vocal resonance). § The mild anaemia suggests a chronic disease process. Th is is likely a reactivation of the TB or post-primary infection. § Reactivation of TB typically (although not always) affects the upper lobes because Mycobacterium tuberculosis is a highly aerobic bacterium and the apices are the most oxygenated part of the lungs. **In addition to reviewing her need for resuscitation (ABC), you need to: 1) Ensure that microbiology know to look for acid-fast bacilli (i.e. using a Ziehl- Nielson or silver stain). Bear in mind that M. tuberculosis is a very slow-growing bacterium and it can therefore take many WEEKS before a positive result is obtained on culture. 2) TB is a notifiable disease so you must notify the authorities for CONTACT TRACING. They may vaccinate contacts with Bacille Calmette-Guérin (BCG) and, rarely, provide prophylactic therapy. 3) Place the patient in isolation to prevent further spread. 4) Test her for HIV, as although she most likely acquired TB during her childhood she may have acquired it more recently secondary to HIV infection which has implications for prognosis and management. 5) Look for signs of spread to other organs. Check particularly for meningeal irritation, bone or joint pain particularly in weight-bearing joints (e.g. Pott's fracture in the spinal column), dysuria or pelvic pain (genitourinary infection), or abdominal pain. 6) If the diagnosis is confirmed, refer the patient to the TB service, which offers specialized care for such patients. First-line treatment for TB will depend on the likelihood of a drug-resistant strain and the longer-term results of culture and sensitivities. However, the initial approach (as per the National Institute for Health and Clinical Excellence (NICE) guidelines on TB) is with a long-term regimen of FOUR antibiotics (RIPE): rifampicin and isoniazid for the first 4 months, pyrazinamide and ethambutol for the first 2 months. Note that long treatment leads to poor compliance. This is a problem that is leading to multidrug-resistant TB, and explains why in some jurisidictions (e.g. New York City, USA) social workers may come and check that patients are taking their medications.

A to E assessment

§ gross neuro score is making sure can move all 4 limbs. AVPU score too

Management of an acute PE

§ haemodynamic unstable - low BP, high HR (Evidence of cardiopulmonary compromise) § if unstable --> thrombolysis § if stable --> risk stratification (hestia/ PESI/sPESI) --> if low risk (discharge with high-dose LMWH, DOAC and warfarin for 3months), if high-risk (admit + LMWH + (oxygen))

Mr Philip Morris is a 72-year-old retired electrician who presents to his general practitioner (GP) after coughing up blood. He is not coughing up any blood at present, appears well, and is able to talk calmly about what has happened. The fi rst step should be to establish if this is truly haemoptysis. What might haemoptysis be confused with by the patient? How will you tell if it really is haemoptysis?

§ You need to ensure that you are not mistaking haemoptysis with: a) Haematemesis: brownish-red blood that is vomited from the gastrointestinal (GI) tract. b) Epistaxis (nosebleed): particularly posterior nosebleeds. c) Bleeding gums: combined with a cough, this may be confused with true haemoptysis. **To tell if it is really haemoptysis, you can ask the patient WHERE they think the blood is coming from (they may say it initially dripped from their nose), its COLOUR (darker, coff ee-ground appearance suggests partially digested blood), any HISTORY of nosebleeds, nausea, vomiting, gastric disease, or alcoholism. § For the latter, asking if he is an alcoholic is unlikely to yield a valid response. Instead, you can try the CAGE questions to detect alcohol dependence. An answer of 'yes' to two or more of the following questions is a fairly accurate detector of alcohol abuse and dependence: 1) H ave you ever felt you need to Cut down on your drinking? 2) H ave people Annoyed you by criticizing your drinking? 3) H ave you ever felt Guilty about your drinking? 4) H ave you ever needed an Eye-opener to steady your nerves in the morning?

Eosinophil activation in asthma

§ activated by IL-5 --> IL-4, IL-13, IL-5a

What is ARDS?

§ acute respiratory distress syndrome § alveolar membranes are destroyed by inflammation § they are no longer elastic § they collapse easily § they can fill with pus or fluid and get loss of surfactant § blood vessels become inflamed and leaky *hence get high chance of clots

Predictors of mortality in pulmonary sarcoidosis

§ age § fibrosis § pulmonary hypertension

Upper and lower airways

§ airways divided into upper: nasopharynx, oropharynx and laryngopharynx § once past vocal cords into lower airways, starting with trachea --> brochi --> bronchioles --> alveoli

Specific risk factor for klebsiella

§ alcoholic § cavitating lesions - air fluid level with pus § transverse myelitis with mycoplasma

What needs to be there for ventilation to occur

§ all airways need to be open § need functioning muscles § brain needs to tell body to breathe § lungs/alveoli need to be elastic enough

Celia is a 35 year old female who underwent a recent salpingectomy for an ectopic pregnancy. Today she awoke breathless, with pleuritic chest pain and haemoptysis. She has been taking the OCP for 5 years. A pulmonary embolism was suspected. CTPA identified filling defects within the pulmonary vasculature with pulmonary emboli. Her recent observations are: Temp: 37.4°C HR: 122 bpm BP: 105/78 RR: 22 SaO2: 93% on RA What is the next step in Celia's management? a)Apixaban b)Alteplase c)Embolectomy d)CPAP e) TED stockings

§ apixaban (DOAC) as is haemodynamically stable.

Classification of asthma - level of control

§ asthma does not necessarily remain in the same category permanently, but may change over months or years § patients may move up and down based on factors such as: a) presence of allergens b) incorrect/ correct use of medications and treatment c) lack of adherence to the treatment regimen § effective treatment should lead to better asthma control and allow the patient to move to a less severe category § therefore, for ongoing management of asthma, classification by level of control may be more relevant and useful

When might hear wheeze?

§ asthma, emphysema and chronic bronchitis

Clinical Effectiveness of CPAP on Diastolic BP and Sleepiness (ESS) in Patients with OSA

§ at bottom is 5 studies which shows left to orange bar --> so shows sleepiness improves § at top: shown if use CPAP correctly for over 4 hours is acc successful in lowering BP

Mechanism of ARDS

§ body responds with profound inflammatory response --> fluid overload due to increased vascular permeability § is not a cardiac problem § get alveolar oedema from fluid --> then collapse --> increases space between capillary and alveolus --> decreased diffusion --> V/Q mismatch --> SHUNT in upto 50% of alveoli § ARDS is a non-cardiogenic pulmonary oedema - T1RF

Common sites of lungs metastases

§ brain, bone, liver

Where does metastasised lung cancer generally come from?

§ breast , colorectal § lung cancer is most COMMON and most DEADLY in world § small cell (potentially from endocrine cells, SIADH) vs non-small (adeno -goblet, periperhal lung; sqcc - squamous epithelial cells ,PTHrp; large cell - epith) **smoking is less associated with adenocarcinoma than others

Triad in primary ciliary dyskinesia

§ bronchiectasis § sinusitis § situs invertus

Total left lung collapse CXR

§ can see tracheal and mediastinal shift towards collapse

Histopathology of TB

§ caseating (cheeselike) granulomata

What is one big complication of sarcoidosis

§ chronic pulmonary aspegillosis § haemoptysis is what you're worried about with cavitating lesions.

What occupation seen with pneumoconiosis?

§ coal worker (silicosis), builder (asbestosis) **Aetiology: •Inhalation of dust particles of coal dust, silica or asbestos (white/blue asbestos; latter more toxic) •Pathophysiology: large nodules of dust particles, surrounded by collagen and dying macrophages. •Damage by: •Direct cytotoxicity of particles •Particle ingestion by macrophages => free radical production •Proinflammatory cytokines from macrophages N.B. chronic asbestos exposure can lead to asbestosis (a pneumoconiosis) but eventually also mesothelioma (most common cancer from asbestos exposure) which may present with pleuritic chest pain (as the cancer is a cancer of the mesothelium)

Coarse vs Fine Crackles

§ coarse - pulmonary oedema and bronchitis § fine - CHF and pulmonary fibrosis

Alveolus anatomy

§ deoxygenated blood (high ppCO2) from RHS of heart --> from capillary into alveolus § oxygenated blood we breathe in has high ppO2 so diffuses down conc gradient into capillary

Targets in severe asthma

§ depends whether T2 or not T2 inflammation

Variability by geography and ethnicity in sarcoidosis

§ highest in northern europe, USA and India § x4 more common in african-americans than caucasians and get more severe disease § different lung involvement in different ethnicities: a) Acute uveitis and erythema nodosum in Scandinavians, Irish, Puerto Ricans b) in Japanese, eye and heart frequent, no Lofgren c) Lupus pernio more frequent in African-American

In normal lung tissue appearance

§ hilar lymph nodes are small § is spongy (full of air) § anthracotic pigment

Presentation of TB

§ history of chronic productive cough, fevers, or night sweats. § unintentionally lost weight. § travelled abroad for years (although he may have latent TB). § On examination, patient is pyrexic. § evidence of consolidation or a pleural effusion. § White cell count and CRP elevated § chest radiography suggesting TB (e.g. calcification).

Pneumothorax treatment algorithm

§ if symptomatic SOB changes Tx

Opacities on CXR

§ interstitial/alveolar - pneumonia/fluid § reticulo-nodular - fibrosis § homogenous - effusion § mass/cavitation - infection/ malignancy/inflammation **everything is either: infection/inflammation/malignancy

35 y/o man with SOB and dry cough. Has muscle aches and fever. Eczema, steroid medication and lives at home with dogs and pet parrots. What is most likely causative organism?

§ is not typical as dry cough and myalgia. § immunocompromised from steroids § pet parrots (bird) - RF for chlamydia psitacci

Assessing reversibility of sarcoidosis with HRCT

§ large granules --> more reversible § ground glass --> often irreversible § honeycomb, keeps in with UIP - usual interstitial pneumonia which is seen also in idiopathic pulmonary fibrosis § but CT cannot distinguish everything so can use FDG-PET

Definition of tension pneumothorax

§ life-threatening condition where air trapped in pleural cavity under a positive pressure, causing cardiopulmonary compromise § when air gets into pleural space (can occur spontaneously)

Pneumonia CXR types

§ lobar (often strep pneumonia) or bronchopneumonia (patchy) **Left image shows consolidation in middle zone of right lung (i.e. lobar pneumonia), left lung **Right image shows patchy consolidation in middle and lower zones of right lung (i.e. bronchopneumonia), left lung is clear. Remember - there's no middle lobe in left lung

How many samples take in TB? What stain?

§ lymph node biopsy -caseating granuloma (necrosis in middle of activated macrophages) § mantoux/ tuberculin test (TST) . Acid-fast bacilli - culture does not decolourise with acid TST injects purified protein derivative intradermally into skin. If you have TB, you will form a larger radius of induration due to T-cell activity. TST hardly done in UK (IGRA is preferred) IGRA = interferon gamma release assay (it is a blood test) - more specific but more expensive § IGRA test - blood test ( last two tests cannot distinguish between active and latent TB)

What do bloods look like in COVID?

§ lymphopaenia § elevated CRP § elevated D-Dimer (breakdown product of clots/sign of inflammation) § elevated Troponin (as COVID can cause myocarditis/cardiomyopathy; also make sure they not having active MI) § abnormal kidney function test (can cause acute tubular necrosis/ overall sepsis + hypotension --> pre-renal AKI) § ABG

Treatment options for Q of L reasons in sarcoidosis

§ mainly for severe fatigue, joint pains (especially ANKLE), skin disease • Discussion with the patient key • Decision not to treat, using NSAIDs for joint pains as needed • If a decision to treat is reached, consider: a)• Low dose prednisolone b)• Hydroxycloroquine c) Less likely to use methotrexate or azathioprine, except for particular cases

Management of sarcoidosis based on a key dichotomy

§ major loss of Qof L § danger from disease

Tension pneumothorax

§ medical emergency § one-way valve § air can only go into that part of pneumothorax so with each breath it goes bigger § when gets really big presses of vena cava, lose venous return, nothing to pump and cardiovascular collapse. Get mediastinal shift --> hypotension and tachycardia **Lung compression: § severe dyspnoea § tracheal deviation (away from lesion) § silent chest § HYPERresonance § reduced expansion on lesioned side

How many litres in nasal cannula

§ nasal cannula (24 or 28% FiO2) upto 4 L § simple face mask: 4-8 L § non-rebreather mask (85% FiO2) upto 15L

For biologic therapy for severe asthma, what conditions needed

§ need to be at step 5 (so is severe asthma) § need to meet type 2 inflammation criteria (high eosinophils, exhaled NO, sputum eosinophils, clinically allergen-driven, need for maintenace oral CS)

What are the commonest sites to which a mesothelioma is likely to spread from the pleural cavity?

§ other pleural cavity § Lung § Hilar lymph nodes Mesotheliomas usually spread through one pleural cavity then invade into the contiguous lung and chest wall. They can also spread to the other pleural cavity and pericardial cavity as well as the peritoneal cavity. Hilar nodes are involved by lymphatic spread. Death is usually due to lung/pleural involvement.

42 y/o with cough haemoptysis and fever. Recently returned from bangladesh. Losing weight. Sats of 91% RR of 22. What is next best step?

§ oxygen 15L via non-rebreather mask (target sats 94-98%)

When to give long term O2 to COPD patients

§ pO2 of < 7.3 kPa § pO2 of 7.3 - 8 kPa and one of the following... •Secondary polycythaemia •Nocturnal hypoxaemia •Peripheral oedema •Pulmonary hypertension

Alternative Treatments for OSA?

§ pillow § neck brace § mandibular advancement splint (pull bottom mandible forward to stop airway collapsing) **There are alternative treatments for OSA, but they do not work as well as CPAP

Extra-pulmonary diseases caused by TB?

§ pleural effusion § Pott's disease - infection in spine causes it to collapse § meningitis § addison's § erythema nodosum § clubbing

What might hear in mesothelioma?

§ pleural rub - crunching snow sound

5 P's of pleuritic chest pain

§ pneumonia § pneumothorax § PE § pleural effusion § pericarditis

PCWP (pulmonary capillary wedge pressure)

§ provides an indirect estimate of left atrial pressure (LAP). Although left ventricular pressure can be directly measured by placing a catheter within the left ventricle, it is not feasible to advance this catheter back into the left atrium § It is measured by inserting a balloon-tipped, multi-lumen catheter (Swan-Ganz catheter) into a central vein, and advancing the catheter into a branch of the pulmonary artery. The balloon is then inflated, which occludes the branch of the pulmonary artery and then provides a pressure reading that is equivalent to the pressure of the left atrium. § The normal pulmonary capillary wedge pressure is between 4 to 12 mm Hg. § Elevated levels of PCWP might indicate severe left ventricular failure or severe mitral stenosis.

Give 6 examples of T1RF

§ pulmonary oedema - alveoli w/ fluid § pneumonia - alveoli w/ pus § ARDS § pulmonary embolus § emphysema § Interstitial lung disease (alveolar wall dama **we improve oxygenation by increasing amount of oxygen available or keeping alveoli open

PE in CTPA

§ pulmonary trunk is white § the black mass next to it is PE

How to improve ventilation?

§ push more air into lungs during inspiration using positive pressure (CPAP) § if pt is unconscious can also take control of breathing rate and timing

The history of polyarthralgia, erythema nodosum and hilar lymphadenopathy on chest x-ray suggest the diagnosis o

§ sarcoidosis. § Hypercalcaemia is an indication for corticosteroid treatment. § Indications for corticosteroid treatment for sarcoidosis are: parenchymal lung disease, uveitis, hypercalcaemia and neurological or cardiac involvement **Sarcoidosis is a multisystem disorder of unknown aetiology characterised by non-caseating granulomas. It is more common in young adults and in people of African descent. § Indications for steroids: o patients with chest x-ray stage 2 or 3 disease who are symptomatic. Patients with asymptomatic and stable stage 2 or 3 disease who have only mildly abnormal lung function do not require treatment o hypercalcaemia o eye, heart or neuro involvement

Screening for cardiac sarcoidosis

§ should screen all patients § if abnormality found --> imaging **•Symptoms: palpitations, disproportionate breathlessness, syncope/presyncope ** ECG abnormalities: AV block, frequent premature ventricular ectopics, non-sustained/sustained ventricular tachycardia, LBBx or RBBx, Q waves, axis deviation ** Echo: reduced LVEF, regional wall abnormalities, wall thinning or thickening, ventricular aneurysms Further imaging needed

s1q3t3

§ sign of right heart strain against an occluded pulmonary circulation in PE

FDG-PET assessing severity of sarcoidosis

§ some which look irreversible in CT can, after treatment with infliximab (anti-TNF) then resolve

Diagnosis: bronchoscopy and biopsy for sarcoidosis

§ stage 1/2 --> biopsy (EBUS-TBNA: endobronchial ultrasound-guided transbronchial needle aspiration) § stage 3/4 --> lavage (would see lymphocytosis in active disease)

assessing symptoms of Asthma control

§ stmptoms § nighttime awakenings § interference with normal activity § use of medication § FEV1 or peak flow § validated questionnaire (ATAQ) **Risk: progressive loss of lung function, treatment related adverse effects

What is the most common bacterial cause of CAP? Which atypical organism is associated with faulty air conditioning systems? What scoring system is used to assess CAP severity? What non-invasive test(s) can be used to identify the causative organism?

§ streptococcus pneumoniae § legionella § CURB-65 § sputum culture (MC&S) and urinary testing

Eosinophils in asthma

§ this usually responds very well to steroids § eosinophils release toxic chemicals and biomarkers that increase the inflammation further and tissue damage occurs; the inflammation causes bronchial smooth muscle spasm; vascular congestion, oedema, a thickening of the mucus and impaired ciliary function, increased bronchial hyperresponsiveness

Dockyard worker with cancer. What is definitive way to diagnose pt?

§ thoracoscopy and histology for mesothelioma

Clinical phenotypes of asthma

§ treat asthma based on degree of asthma severity § we don't really consider the type of asthma they have § there is allergic asthma (e.g. cat) - more childhood-onset), occupational asthma (sensitiser-induced), pollution § eosinophilic vs non-eosinophilic. eosinophilic becoming more important

Complications of continuous positive airway pressure treatment in OSA

§ treatment include sleep disturbance, rhinitis, dermatitis, conjunctivitis, aerophagia, and dyspnoea. § Complications of oral appliance therapy include occlusal changes and facial pain. § Complications of surgery include bleeding, haematoma, velopharyngeal insufficiency, pharyngeal stenosis, dysphagia, airway obstruction, and, very rarely, death.

Chest X-ray in TB

§ typically TB affects upper lobe: •Consolidation (patchy/heterogenous) •Bi-hilar lymphadenopathy •Upper lobe scarring •(Cavitating lesions) •(Pleural effusions) § in miliary TB see lots of little dots (nodular shadowing) - bad prognosis

What does UIP mean?

§ typically seen on CT § Usual interstitial pneumonia (UIP) refers to a morphologic entity defined by a combination of (1) patchy interstitial fibrosis with alternating areas of normal lung (reticular opacities), (2) temporal heterogeneity of fibrosis characterized by scattered fibroblastic foci in the background of dense acellular collagen, and (3) architectural alteration due to chronic scarring or honeycomb change. **UIP pattern of ILD can be seen in idiopathic pulmonary fibrosis or secondary to underlying systemic diseases. These would include: § connective tissue disorders (CTD associated UIP) § rheumatoid arthritis: UIP is considered to be the dominant pattern in those with rheumatoid arthritis who have concurrent interstitial lung disease § systemic sclerosis (scleroderma): either a UIP or NSIP (commoner) pattern § polymyositis/dermatomyositis: a UIP, NSIP, or COP pattern § mixed connective tissue disease: either a UIP or NSIP pattern § asbestos-related interstitial lung disease: asbestosis § chronic hypersensitivity pneumonitis § radiation § medications/drug toxicity: amiodarone lung § ANCA associated vasculitides § Hermansky-Pudlak syndrome (very rare)

Monitoring pulmonary sarcoidosis: a multidisciplinary exercise

§ use symptoms + tests § Change in symptoms of breathlessness/cough § Lung function: change in FVC, FEV1 by ≥10%; DLCO ≥15% (ATS/ERS criteria)- (isolated drop in DLCO suggesting pulmonary vascular involvement) § Imaging changes: • chest Xray • chest HRCT better correlated with lung function changes • (FDG-PET to assess ongoing activity when disease not responding to treatment) ** (Serum biomarker changes) **Worsening in more than one domain will increase the likelihood of the change being real

What is aminophylline?

§ used in asthma management § metabolised to theophylline § Acts by inhibiting phosphodiesterase thus reducing bronchoconstriction by inc cAMP levels **OTHER MEDICATIONS: § B2-adrenoreceptor agonists- Relax bronchial smooth muscle, act within minutes. SEs: tachyarrhythmias, low K+, tremor, anxiety § Corticosteroids- Best inhaled to minimise systemic effects. Act over DAYS to reduce bronchial mucosal inflammation. RINSE mouth after inhaled steroids to prevent oral candidiasis. § Anticholinergics - May reduce muscle spasm synergistically with b2-agonists but NOT recommended in current guidelines for chronic asthma § Leukotriene receptor antagonists- Block effects of leukotrienes in airways Anti-IgE monoclonal antibody. May be of use in patients with persistent allergic asthma

Features of small cell lung cancer

§ usually central arise from APUD* cells associated with ectopic ADH, ACTH secretion § ADH → hyponatraemia § ACTH → Cushing's syndrome § ACTH secretion can cause bilateral adrenal hyperplasia, the high levels of cortisol can lead to hypokalaemic alkalosis § Lambert-Eaton syndrome: antibodies to voltage gated calcium channels causing myasthenic like syndrome

Respiratory innervation

§ ventral and dorsal respiratory groups at medulla § join and innervate the phrenic nerve --> diaphragm (C3,4,5) § at thoracic levels --> intercostal muscles

How to get lung biopsy in cancer?

§ via bronchoscopy. But if have peripheral lung cancer like adenocarinoma is better by transthoracic § Stage 1: Cancer is found in the lung, but it has not spread outside the lung. § Stage 2: Cancer is found in the lung and nearby lymph nodes. § Stage 3: Cancer is in the lung and lymph nodes in the middle of the chest. § Stage 3A: Cancer is found in lymph nodes, but only on the same side of the chest where cancer first started growing. § Stage 3B: Cancer has spread to lymph nodes on the opposite side of the chest or to lymph nodes above the collarbone. § Stage 4: Cancer has spread to both lungs, into the area around the lungs, or to distant organs.

What resp symptoms in asthma?

§ wheeze § chest tightness § SOB § cough Asthma is a heterogeneous disease, usually characterized by chronic airway inflammation. It is defined by the history of respiratory symptoms such as wheeze, shortness of breath, chest tightness and cough that vary over time and in intensity, together with variable expiratory airflow limitation.

Type 2 resp failure list examples

§ when VENTILATION fails (so not getting oxygen in or co2 out) o chest wall deformities o resp muscle weakening e.g. MND or MG o CNS depression e.g. drug overdose

Asbestosis

§Asbestosis onset occurs ≥10 years following the initial exposure to asbestos. § Patients may be asymptomatic or have progressive shortness of breath. § A chest x-ray is the preferred initial test. § There is no definitive treatment. § Cigarette smoking cessation is important to reduce risk of lung cancer. § Prognosis is related to extent of fibrosis noted at diagnosis and past cumulative exposure to asbestos. **Asbestosis is diffuse interstitial fibrosis of the lung as a consequence of exposure to asbestos fibres.[1][2] Pleural abnormalities, which are also caused by the inhalation of asbestos fibres, include plaques that may or may not be calcified, diffuse pleural thickening, benign pleural effusions or rounded atelectasis ( atypical form of lung collapse that usually occurs adjacent to scarred pleura and can be mistaken for lung cancer). These pleural abnormalities may occur either in concordance with or in the absence of parenchymal fibrosis

What is the most common causes of death in sarcoidosis patients?

• <10% of patients have a shortened life expectancy due to sarcoidosis • Respiratory failure and cardiac failure/arrhythmias the most common cause of death in sarcoidosis patients

Diagnostic algorithms for pulmonary sarcoidosis

• Compatible clinical/Xray/HRCT findings • Histology: non caseating granulomas • Exclusion of alternative diagnoses • Large series a mixture of histological and clinical diagnosis • Series of personal diagnostic algorithms • Aim for diagnostic probability >95% § need non-caseating granulomas and compatible clinical/Xray/JRCT finding § is quite non-specific symptoms § erythema nodosum on shin, CT - calcified lymph nodes egg shell around bilateral mediastinal lymph nodes (make sure don't confuse with TB (also get calcified lymph node here) /lymphoma) - would do TB elispot to exclude; also see caseating granulomas in TB - type of necrosis, which occurs in the centre of the granuloma) § X-ray - bilateral shadowing

What second-line investigations should be arranged for Mrs Finnegan (CHF patient)?

• Echocardiography to assess ventricular function and confi rm low cardiac output and heart failure, assess valve patency, and look for areas of dyskinesia. • Coronary angiography if you suspect this lady's heart is failing because of coronary artery disease. Th is is quite likely in Mrs Finnegan's case given her history of previous MI and risk factors for atherosclerotic disease.

FDG PET for assessing stable vs progressive fibrosis in sarcoidosis

• FDG-PET/CT signal correlates with other markers of disease activity: BAL Serum inflammatory markers

FDG-PET can help assess stable versus progressive fibrosis in sarcoidosis

• FDG-PET/CT signal correlates with other markers of disease activity: BAL Serum inflammatory markers

Risk stratification in sarcoidosis

• Integration of clinical, functional and imaging features to assess likelihood of progression of pulmonary sarcoidosis • In cardiac disease, we need markers of accurate early diagnosis to prevent loss of function and fatal arrhythmias

Progressive lung fibrosis in sarcoidosis

• Majority of patients with sarcoidosis have a benign course, with/without period of treatment • However, significant minority have progressive pulmonary fibrosis • Approximately 8-10% of sarcoidosis patients will have shortened life expectancy; of these roughly 70% due to pulmonary involvement

Overall, what used to determine pulmonary and cardiac sarcoidosis severity

• Risk stratification essential (for progression of pulmonary sarcoidosis and also cardiac disease) • In pulmonary disease, integration of lung function with HRCT findings +/- PET in selected cases and longitudinal behaviour • In cardiac disease, advanced imaging techniques (MRI and PET); studies on prognostic implications are ongoing • Pro-active management needed in cases with severe disease and/or high risk of progression

Limitation of sarcoid staging by X-ray

• Scadding stages useful for broad statements on prognosis • Cannot distinguish between active inflammation, fibrosis and inactive disease • Large variability within scorers on stage IV; trivial vs end stage lung fibrosis

How does Mrs Finnegan's diagnosis of CHF explain her symptoms (shortness of breath on exertion, orthopnoea) and signs (displaced apex beat, crackles in the lungs, peripheral oedema, raised JVP)?

• Shortness of breath. The failing heart can't pump enough blood out. This is especially true if venous return to the heart is increased (e.g. exercise, lying down) and the heart is forced to work harder (e.g. exercise). Back pressure forces fluid out from the pulmonary vasculature into the alveoli, causing 'wet lungs' and a feeling of shortness of breath (some patients will say it feels like drowning). A combination of decreased lung compliance, decreased gas exchange, and airways obstruction are the important drivers of dyspnoea in most left ventricular failure patients. • Orthopnoea. Lying down increases venous return to the heart, which is already struggling to pump out all the blood reaching it. This makes congestion of blood in the pulmonary vessels even worse, forcing more fl uid out into the lungs and therefore causing shortness of breath. Th is is why patients with heart failure often sleep propped up with pillows. • Displaced apex beat. Th e failing heart can't pump out all of the blood reaching it, so it gradually but inexorably dilates, leading to a displaced (and weak) apex beat. Th is can be thought of as a volume-overloaded heart. Do not confuse this with hypertrophy, which is caused by hypertension or aortic stenosis. Here, the heart has to pump harder and thus grows concentrically, leading to Mrs Finnegan's ECG shows pathological Q waves in leads V1-V4. Her FBC is normal. Her glucose is 6.2 mM and her HbA1c is 6.8%. Her total cholesterol = 6.2 mM, LDL = 3.1 mM and HDL = 1.1 mM. What is the diagnosis for Mrs Finnegan? Can you identify any risk factors for this diagnosis in her history and investigations? an undisplaced but forceful or heaving apex beat. Th is can be thought of as a pressure-overloaded heart. Ultimately, a pressure-overloaded heart can also dilate and fail, but this occurs later in the disease process. • Crackles in the lungs. Th e build-up of blood in the pulmonary vessels forces fl uid out of the vasculature into the alveoli. Th e alveoli are usually kept open by surfactant, but the interstitial fl uid dilutes this and results in increased alveolar surface tension, leading to collapse of the alveoli. As the patient breathes in deeply, the alveoli eventually 'pop open' - the crackles you can hear with the stethoscope. • Peripheral oedema. Th is is caused mainly because the failing heart cannot pump all of the blood reaching it (venous return), so one gets back pressure in the venous system. Th is is further compounded by salt and water retention due to activation of the renin-angiotensin-aldosterone system by a low cardiac output. Th e resultant pressure in the venous system often manifests as a raised JVP and/or a tender, enlarged liver. Th e increased blood pressure in the venous system also forces fl uid out into the surrounding tissues, particularly in places where the venous pressure is highest, i.e. the dependent parts of the body (ankles in someone who has been standing, sacrum in someone who has been in bed). A raised JVP and hepatomegaly are not always clinically apparent.

What is gold standard for asthma diagnosis?

•**Spirometry** - is the gold standard (pre and post bronchodilator) •Peak Expiratory Flow Rate (PEFR) - PEF monitoring for at least 3 days a week for several weeks which will show diurnal variation (>20%) •Blood tests -(FBC - infective causes/triggers, eosinophilia, IgE levels and CRP + U&E's) •CXR, ABG: -ABG (if raised pCO2 then very unwell and requires ventilation as cannot remove CO2). Normally should be low/normal O2 and low CO2, a normal CO2 shows patient is fatiguing (bad sign) and then raised is very critical!! - CXR - rule out other DDx such as pneumonia etc Criteria for Asthma Dx: 1.FEV1:FVC <70% 2.Reversibility as seen through a difference of at least 12% pre- and post-bronchodilator spirometry 3.PEFR varies by at least 20% for 3+ days/week over several weeks (diary is helpful)

2020 BTS guidelines for asthma management

•1 SABA (e.g. Salbutamol) •2 SABA + low-dose ICS (e.g. Salbutamol + Beclometasone) •3 SABA + low-dose ICS + LTRA (e.g.. Salbutamol, Beclometasone and Monteleukast) •4 LABA + low-dose ICS +/- LTRA (e.g. Symbicort (Budesonide+Formoterol) •5 LABA + high-dose ICS (+/- LTRA) •6 Trials such as Theophylline (long-acting muscarinic antagonist) •7 Oral Corticosteroids e.g. Prednisolone

BTS 2020 asthma guidance stepwise

List 5 complications of COPD

•Acute respiratory failure •Infections e.g. Pneumonia •Pulmonary hypertension (--> RHF/Cor Pulmonale) •Pneumothorax (secondary to bullae (air-space) rupture) •Secondary polycythemia • •COPD has a high morbidity

Investigations for mesothelioma

•Basic observations § Bedside tests •Sputum cytology •Pleural fluid cytology (via thoracentesis) § Bloods •FBC •Calcium (bone mets or PTHrp) •ALP (bone mets) •LFTs (liver mets) § Imaging •CXR •CT CAP, PET (staging) § Biopsy •Pleural lining biopsy (via thoracoscopy)

Pneumonia investigations

•Basic observations •Bedside tests: •Sputum MCS •Bloods: •FBC •CRP •ABG •Blood culture •Pleural fluid MCS (via thoracentesis) •Imaging: •CXR **Atypicals •Serology (all) •Urinary antigens (legionella) •Blood film (mycoplasma - cold agglutins) •LFTs (legionella)

Emphysema and chronic bronchitis

•COPD can be defined as "a chronic progressive lung disease characterised by airflow obstruction that is not fully reversible. It encompasses both emphysema and chronic bronchitis" •Emphysema --> Histological Dx, where there are enlarged air spaces distal to the terminal bronchus, with alveolar wall destruction •Chronic Bronchitis --> Clinical Dx of productive cough (sputum) for 3 months in 2 successive years. Sx improve after smoking cessation. •Epidemiology - Very common (8%) **Cause: Exposure to irritants i.e. tobacco smoke, dust, NO2 causes bronchial and alveolar damage. the pathological changes increase resistance to airflow in the small conducting airways. Therefore, the lungs are not emptying properly (causing trapped air/RV) thus reducing the - FVC (maximum volume breathed out in 1 breath) - FEV1 even lower - Thus, causing the FEV1/FVC ratio to be very low (<70%) as seen in obstructive disease -TLC increased due to air trapping - Both emphysema and CB often co-exist as same common RF - smoking

Suport for patients on CPAP therapy

•Centralised sleep therapy •Engagement •Goal setting •Expectation management § ResMed, AirView

List 5 complications of asthma

•Growth retardation •Recurrent infections •Pneumothorax •Respiratory failure (and death) •Lobar collapse due to mucus plug

Bronchiectasis - Complications

•Life-threatening haemoptysis •Pneumonia •Pneumothorax •Empyema (+ multi-organ abscesses) •Respiratory failure •Cor pulmonale

2020 Management for COPD

•MILD: SABA or SAMA (e.g. Salbutamol or Ipratropium Bromide) •MODERATE: SABA + LABA or SAMA + LAMA (e.g. + Salmeterol or Tiotropium) •SEVERE: LABA + LAMA or LABA + ICS (e.g. Salmeterol + Tiotropium or Symbicort) •V SEVERE: LABA + LAMA + ICS

Complications of pneumonia

•Pleural effusion •Lung abscess (often Staph aureus): Swinging fevers, Persistent pneumonia, Foul-smelling sputum. •Empyema •Sepsis

Ix for PE

•Well's score <4 --> D-dimer; >4 --> CTPA

● Diaphragm

⇒ Covered by parietal pleura above and peritoneum below ⇒ Motor and sensory nerve fibres go to each half of the diaphragm via the phrenic nerves (C3-5)

● Lungs

⇒ Divided into lobes by invaginations of the pleura ⇒ Right lung: upper, middle and lower lobe ⇒ Left lung: upper and middle lobe ⇒ The upper lobe lies mainly in front of the lower lobe ⇒ Each lobe is further subdivided into bronchopulmonary segments by fibrous septa ⇒ Each bronchopulmonary segment is further subdivided into individual lobules. Within each lobule a terminal bronchus supplies an acinus, and within this structure further divisions of the bronchioles eventually give rise to the alveoli.

● Pleura

⇒ Layer of connective tissue covered by a simple squamous epithelium ⇒ Split into visceral and parietal pleura ⇒ The visceral pleura covers the lung, lines the interlobar fissures and is continuous at the hilum with the parietal pleura which lines the inside of the hemithorax In between the visceral and parietal pleura, is the intrapleural space/pleural cavity containing pleural fluid

Lung vasculature

⇒ Lung has dual blood supply: deoxygenated blood from right ventricle via pulmonary artery and oxygenated blood via the bronchial circulation, arising from the descending aorta.

● Alveoli

⇒ There are approx. 300 million alveoli in each lung ⇒ The epithelial lining consists mainly of type I pneumocytes - these have an extremely thin layer of cytoplasm - thin barrier for gas exchange. Each cell is connected by a tight junction to limit movement of fluid in and out of alveoli. ⇒ Type II pneumocytes are more numerous but cover less of the lining. They have microvilli and can divide to form type I or II pneumocytes. These produce surfactant - substance that prevents alveoli from collapsing. ⇒ Large alveolar macrophages are also present

Recurrent laryngeal nerve palsy

● o Causes bovine cough o Associated with lung cancer

Summarise the prognosis for patients with pulmonary embolism

● 30% mortality in those left untreated ● 8% mortality with treatment ● Increased risk of future thromboembolic disease

Summarise the epidemiology of pneumonia

● 5-11/1000 ● Community-acquired pneumonia is responsible for > 60,000 deaths per year in the UK ● High in very young or old ● Mortality: 21% in hospital

Define arterial blood gas

● A blood test in which heparinised blood is usually taken from the radial or femoral artery to measure pH, PaO2 and PaCO2 ● Measured using an automated analyser

Recognise the signs of extrinsic allergic alveolitis on physical examination

● ACUTE o Rapid shallow breathing o Pyrexia o Inspiratory crackles ● CHRONIC o Fine inspiratory crackles (from fibrosis) o Clubbing (rare)

Recognise the presenting symptoms of extrinsic allergic alveolitis

● ACUTE: o Present 4-12 HOURS after exposure o REVERSIBLE episodes of: ▪ Dry cough ▪ Dyspnoea ▪ Malaise ▪ Fever/ chills ▪ Myalgia o Wheeze and productive cough may develop if repeat high-level exposure ● CHRONIC o Slowly increasing breathlessness o Decreased exercise tolerance o Weight loss o Exposure is usually chronic, low-level and there may be no history of previous acute episodes ● IMPORTANT: make sure you get a full occupational history and enquire about hobbies and pets

Define ARDS

● ARDS = non-cardiogenic pulmonary oedema and diffuse lung inflammation syndrome that often complicates chronic illness. ● A syndrome of acute and persistent lung inflammation with increased vascular permeability - may be caused by direct lung injury or occur secondary to severe systemic illness. ● Lung damage and release of inflammatory mediators cause increased capillary permeability and non-cardiogenic pulmonary oedema, often accompanied by multiorgan failure. **The diagnosis of ARDS is based on fulfilling three criteria: 1) Acute onset (within 1 week) 2) Bilateral opacities on chest x-ray 3) PaO₂/FiO₂ (arterial to inspired oxygen) ratio of ≤300 on positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) ≥5 cm H₂O

Identify the possible complications of COPD

● Acute respiratory failure ● Infections ● Pulmonary hypertension ● Right heart failure ● Pneumothorax (secondary to bullae rupture) ● Secondary polycythaemia

Summarise the epidemiology of asthma

● Affects 10% of children ● Affects 5% of adults ● Prevalence appears to be increasing

Summarise the prognosis for patients with pneumothorax

● After having one pneumothorax, at least 20% will have another ● Frequency increases with repeated pneumothoraces

Structure of the Respiratory System

● Air which enters the nose enters the nasal cavity. The epithelial cells of the nasal cavity act to warm, moisturise and filter air entering the body. Hairs and mucus lining the nasal cavity help trap any environmental contaminants. ● The air then travels to the pharynx (split in to the nasopharynx, oropharynx and laryngopharynx) ● The epiglottis then ensures that the air passes into the trachea by covering the opening to the oesophagus ● The trachea is a 10-12cm long tube made up of C-shaped hyaline cartilage rings lined with pseudostratified ciliated columnar epithelium. ● The trachea divides at the carina in to the right and left main bronchi. The carina lies under the junction of the manubrium sterni and second right costal cartilage. ● The right bronchus is more vertical than the left, hence, inhaled material is more likely to end up in the right lung. ● The bronchi split to form the upper and lower (and middle) lobe bronchi. These further split to form bronchioles. ● The bronchi and bronchioles are lined with ciliated epithelium and Goblet cells which act as a key defence mechanism ● The bronchioles finally divide into smaller respiratory bronchioles that have alveoli arising from the surface. Each respiratory bronchiole supplies approx. 200 alveoli.

Summarise the epidemiology of pneumothorax

● Annual incidence: 9/100,000 ● Mainly in 20-40 yr olds ● 4 x more common in MALES

Summarise the epidemiology of tuberculosis

● Annual mortality = 2 million (95% in developing countries) ● Annual UK incidence = 8200 ● Asian immigrants are the highest risk group in the UK

Recognise the signs of asbestos-related lung disease (incl. asbestosis and mesothelioma) on physical examination

● Asbestosis: o Clubbing, o Fine end-inspiratory crackles ● Mesothelioma: o Occasional palpable chest wall mass o Finger clubbing - due to underlying asbestosis (pulmonary fibrosis) o Recurrent pleural effusions (dullness to percussion and diminished breath sounds) o Signs of metastases: Lymphadenopathy, Hepatomegaly, bone tenderness o Abdominal pain/obstruction (peritoneal malignant mesothelioma) o Can rarely cause pneumothorax

Recognise the presenting symptoms of asbestos-related lung disease (incl. asbestosis and mesothelioma)

● Asbestosis: o Progressive dyspnoea o cough (dry, non-productive, frequency increases with progression. can be absent in patients with early asbestosis and is usually absent in patients with pleural changes alone. A productive cough may be seen if the patient has also developed COPD ● Mesothelioma: o Most common symptoms: SOB, Chest pain (dull, diffuse, developing), weight loss o Cough o Constitutional symptoms o Fatigue o Fever o Night sweats o Bone pain o Abdominal pain o Sometimes, bloody sputum - if tumour invades blood vessel

Identify appropriate investigations for asbestos-related lung disease (incl. asbestosis and mesothelioma) and interpret the results

● Asbestosis: history and exam 1) CXR (PA and lateral): reticular-nodular shadowing +/- pleural plaques. The presence of interstitial fibrosis in the lower zones and bilateral pleural thickening is highly specific 2) Pulmonary function tests - non-specific. restrictive changes; may have obstructive picture (especially if history of asbestos exposure and smoking). reduced lung diffusion capacity testing (DLCO) is the most sensitive pulmonary function change. ● Mesothelioma: 1) CXR - unilateral pleural effusion, irregular pleural thickening, reduced lung volumes, and/or parenchymal changes related to asbestos exposure (e.g., lower zone linear interstitial fibrosis). However, chest x-ray visualises the pleura poorly and will miss subtle abnormalities. Furthermore, it does not assess the mediastinal lymph nodes. 2) CT scan of chest and upper abdo with IV contrast: more sensitive. pleural thickening/effusion. BLOODY pleural fluid. May show pleural mass and rib destruction 3) MRI and PET 4) Pleural fluid: can be sent for cytological analysis and may be blood stained 5) Pleural biopsy 6) Diagnosis is made on histology, usually following a thoracoscopy (pleural biopsy) - often done post-mortem Biopsy of the tumour can be immunostained with a stain that reacts with CALRETININ

Recognise the presenting symptoms of Aspergillus lung disease

● Aspergilloma o ASYMPTOMATIC o May cause cough, haemoptysis (potentially massive), lethargy, weight loss ● ABPA o Difficult to control asthma o Recurrent episodes of pneumonia with wheeze, cough, sputum, dyspnoea, fever and malaise ● Invasive Aspergillosis o Dyspnoea o Rapid deterioration o Septic picture o fever o cough o pleuritic chest pain

Identify appropriate investigations for extrinsic allergic alveolitis

● Bloods o immunological response to causative antigen- Blood is checked to determine whether there is antibody to the putative antigen o FBC - neutrophilia, lymphopenia, ESR raised, o ABG - reduced PO2 + PCO2 ● Serology o Test for IgG to fungal or avian antigens o NOTE: these are not diagnostic because you may find these in normal individuals ● CXR o Often NORMAL in acute episodes o Acute: fibrosis may be seen in chronic cases - upper zone mottling/consolidation. Hilar lymphadenopathy in rare cases o Chronic: upper zone fibrosis, honeycomb lung ● High Resolution CT-Thorax o Detects early changes o Chronic: May show patchy 'ground glass' shadowing and nodules, extensive fibrosis ● Pulmonary Function Tests o Reversible restrictive defect (low FEV1, low FVC) o Preserved or increased FEV1/FVC ratio o Reduced total lung capacity o Reduced gas transfer during acute attacks ● Bronchoalveolar Lavage o Increased lymphocytes and mast cells ● Lung biopsy can also be performed

Define asbestos-related lung disease (incl. asbestosis and mesothelioma)

● Both are industrial dust diseases ● Asbestosis: long-term inflammation and scarring of the lungs caused by inhalation of asbestos fibres. Asbestosis onset occurs ≥10 years following the initial exposure to asbestos. Patients may be asymptomatic or have progressive shortness of breath. A chest x-ray is the preferred initial test. There is no definitive treatment. Cigarette smoking cessation is important to reduce risk of lung cancer. Prognosis is related to extent of fibrosis noted at diagnosis and past cumulative exposure to asbestos ● Mesothelioma: aggressive tumour of mesothelial cells that usually occurs in the pleura (90%), and sometimes in peritoneum, pericardium or testes. Largely caused by exposure to asbestos, with a 20- to 40-year latency period between exposure and development of malignancy; consequently the typical patient is in the sixth to ninth decade of life. Most patients present with shortness of breath and chest pain, which on investigation is often found to be associated with unilateral pleural effusion and pleural thickening. Despite advances in treatment, malignant pleural mesothelioma remains a highly lethal malignancy with few long-term survivors. **Note - the mesothelium is a thin epithelium that lines several body cavities including the pleura, peritoneum, mediastinum and pericardium, POOR PROGNOSIS

Management of chronic therapy for asthma

● CHRONIC THERAPY o Start on the step that matches the severity of the patient's asthma, moving up if needed or down if control is good for >3 months 1) STEP 1 ● Inhaled short-acting beta-2 agonist e.g. salbutamol used as needed for symptom relief, AND regular inhaled low-dose steroids e.g. beclometasome ● If needed > 1/day or night-time symptoms, then move onto step 2 2) STEP 2 ● Step 1 + inhaled long-acting beta-2 agonist (LABA) e.g. salmeterol 50ug/12h by inhaler ● If benefit but inadequate control with LABA, increase step 1 steroid dose (800 mcg/day) OR add a 4th drugg ● If no response to LABA, stop LABA and increase steroid dose (800 mcg/day) 3) STEP 3 - refer to specialist at this point ● Increase inhaled steroid dose (2000 mcg/day) ● Add 4th drug (e.g. leukotriene antagonist, slow-release theophylline or beta-2 agonist tablet) 4) STEP 4 ● Add regular oral steroids - prednisolone 1 dose daily, at lowest possible dose ● Refer to specialist asthma care **● Advice 1) Teach proper inhaler technique 2) Explain important of PEFR monitoring - twice a day, keep diary 3) Help quit smoking 4) Avoid provoking factors

Summarise the epidemiology of obstructive sleep apnoea

● COMMON ● 5-20% of men > 35 yrs ● 2-5% of women > 35 yrs ● Prevalence increases with age

Identify appropriate investigations for pneumoconiosis

● CXR o Simple: micronodular mottling o Complicated: ▪ Nodular opacities in upper lobes ▪ Micronodular shadowing ▪ Eggshell calcification of hilar lymph nodes (characteristic of silicosis) ▪ Bilateral lower zone reticulonodular shadowing and pleural plaques (in asbestosis) ● CT Scan - fibrotic changes can be visualised early ● Bronchoscopy - allows visualisation and bronchoalveolar lavage ● Lung Function Tests (spirometry) - restrictive pattern ● Beryllium lymphocyte proliferation test (BeLPT) - Essential component of the diagnosis of chronic beryllium disease. Sensitive test that identifies individuals sensitised to beryllium.

Explain the aetiology/risk factors of pneumoconiosis

● Caused by inhalation of particles of: o Coal dust o Silica o Asbestos o Beryllium ● Often co-exists with chronic bronchitis ● Factors o Occupational exposure (coal mining, quarrying, iron and steel foundries, stone cutting, sandblasting, insulation industry, plumbers, ship builders) o Risk is dependent on extent of exposure and the size/shape of particles o Individual susceptibility is also important o Co-factors such as smoking and TB also contribute

Recognise the presenting symptoms of COPD

● Chronic cough ● Sputum production ● Progressive Breathlessness ● Wheeze ● Reduced exercise tolerance ● Can have haemoptysis

Define Asthma

● Chronic inflammatory airway disease characterised by REVERSIBLE airway obstruction ● Type 1 hypersensitivity ● Three factors contribute to airway narrowing A) Bronchial muscle contraction, triggered by a variety of stimuli B) Mucosal swelling/inflammation, caused by mast cell and basophil degranulation leading to inflammatory mediators C) Increased mucus production **can see in pic - asthmatic aitwaythicker layer of smooth muscle, mucus hypersecretion due to goblet cell hyperplasia

Explain the aetiology/risk factors of bronchiectasis

● Chronic lung inflammation leads to fibrosis and permanent dilation of the bronchi due to destruction of the elastic and muscular components of the bronchial wall ● This leads to pooling of mucus, which predisposes to further cycles of infection, damage and fibrosis of bronchial walls ● Causes of bronchiectasis: o Idiopathic (50%) o Congenital: cystic fibrosis (most COMMON cause), Young's syndrome, primary ciliary dyskinesia, Kartagener's syndrome, alpha-1 antitrypsin deficiency (check for history of lung/liver disease) o Post-infectious (e.g. pneumonia, whooping cough, TB, measles, pertussis, bronchiolitis) o Host immunodeficiency: hypogammaglobulinaemia, HIV o Obstruction of bronchi (e.g. foreign body, tumour, enlarged lymph nodes) o GORD o Inflammatory disorders (e.g. rheumatoid arthritis, UC) o Allergic bronchopulmonary aspergillosis (ABPA)

Recognise the signs of bronchiectasis on physical examination

● Clubbing ● Coarse inspiratory crackles (usually at lung bases) o These shift with coughing ● Wheeze - high-pitched inspiratory squeaks ● rhonchi

Recognise the signs of idiopathic pulmonary fibrosis on physical examination

● Clubbing (50%) ● Bibasal FINE late inspiratory crackles ● Cyanosis ● Signs of right heart failure in advanced stages of disease

Explain the aetiology/risk factors of pneumonia

● Community-Acquired: o Most common: Streptococcus pneumoniae (70%) o Haemophilus influenzae o Mycoplasma pneumonia o Moraxella catarrhalis (occurs in COPD patients) o Chlamydia pneumonia o Chlamydia psittaci (causes psittacosis) o Legionella (can occur anywhere with air conditioning) o Staphylococcus aureus o Coxiella burnetii (causes Q fever) o TB o Viruses (15%) ● Hospital-Acquired - >48h after hospital admission: o Most common: Gram-negative enterobacteria (Pseudomonas, Klebsiella) or S aureus ● Aspiration pneumonia: o Those with stroke, myasthenia, bulbar palsies, reduced consciousness, oesophageal disease or poor dental hygiene risk aspirating oropharyngeal anaerobes ● Immunocompromised patients: o Strep pneumoniae o H influenza o S aureus o M catarrhalis o M pneumoniae o Gram -ve bacilli o Pneumocystis jiroveci ● Risk Factors o Age o Smoking o Alcohol o Pre-existing lung disease (e.g. COPD) o Immunodeficiency o Contact with patients with pneumonia

Croup: laryngotracheobronchitis

● Croup: laryngotracheobronchitis: o Type of respiratory infection caused by virus o Causes cough like barking seal, stridor and hoarse voice ● Recurrent laryngeal nerve palsy o Causes bovine cough o Associated with lung cancer

Recognise the signs of ARDS on physical examination

● Cyanosis ● Tachypnoea ● Tachycardia ● Bilateral widespread fine inspiratory crackles ● Hypoxia refractory to oxygen treatment ● Signs usually bilateral but may be asymmetrical in early stages ● Peripheral vasodilation

Define tuberculosis

● DEFINITION: Granulomatous disease caused by Mycobacterium tuberculosis ● Primary TB: initial infection may be pulmonary or (more rarely) gastrointestinal ● Miliary TB: results from haematogenous dissemination of TB ● Post-Primary TB: caused by reinfection or reactivation

Define obstructive sleep apnoea

● DEFINITION: a disease characterised by recurrent prolapse of the pharyngeal airway and apnoea (cessation of airflow for > 10 s) during sleep, followed by partial arousal from sleep. ● Also known as Pickwickian Syndrome ● Different to central sleep apnoea - defect in CNS

Define pneumothorax

● DEFINITION: air in the pleural space - the potential space between visceral and parietal pleura ● There are some other variants in which other substances are found in the pleural space: o Haemothorax - blood Chylothorax - lymph

Define idiopathic pulmonary fibrosis

● DEFINITION: chronic inflammatory condition of the lung resulting in fibrosis of the alveoli and interstitium. Previously known as cryptogenic fibrosing alveolitis. ● Idiopathic = unknown cause/mechanism ● Fibrosis = excess collagen in connective and interstitial tissue causing thickening § It is the most common interstitial lung disease among the idiopathic interstitial pneumonias, which share clinical features of shortness of breath, diffuse pulmonary infiltrates on imaging, and varying degrees of inflammation, fibrosis, or both on lung biopsy. § Initial therapy is with an antifibrotic agent. Important supportive measures include smoking cessation, pulmonary rehabilitation, and supplemental oxygen when appropriate. Some patients may be eligible for lung transplantation.

Define COPD

● DEFINITION: chronic, preventable, progressive lung disorder characterised by airflow obstruction, with little/no reversibility. Is treatable. It encompasses both emphysema and chronic bronchitis. ● FEV1 <80% predicted, FEV1/FVC ratio <0.7 ● It includes a) Chronic Bronchitis: ▪ Defined CLINICALLY as chronic cough and sputum production on most days for at least 3 months per year over 2 consecutive years ▪ Symptoms improve if they stop smoking b) Emphysema ▪ Defined HISTOLOGICALLY as permanent enlarged air spaces distal to the terminal bronchioles, with destruction of alveolar walls o These two often co-exist as they both have the same common risk factor of SMOKING

Define pneumonia

● DEFINITION: infection of distal lung parenchyma (acute lower respiratory tract illness) ● It can be categorised in many ways: o Community-acquired (CAP) o Hospital-acquired/nosocomial (HAP) o Aspiration pneumonia o Pneumonia in the immunocompromised o Typical o Atypical (Mycoplasma, Chlamydia, Legionella)

Define bronchiectasis

● DEFINITION: lung airway disease characterised by chronic bronchial dilation (bronchi and bronchioles) as well as impaired mucociliary clearance and frequent bacterial infections § Patients often present with recurrent pulmonary infections, including a chronic daily productive cough with mucopurulent sputum production. § Diagnostic testing for a potential aetiology of unexplained bronchiectasis should be performed. § A sputum sample should be obtained when the patient is in a stable state and during acute exacerbations. § Systemic antibiotics directed towards prior culture results should be administered. § Daily airway clearance is essential for treatment success. § Maintenance aerosolised antibiotics may be used for treatment of severe bronchiectasis or recurrent Pseudomonas aeruginosa infections. § Surgical therapy, including lung transplantation, should be considered for patients who continue to deteriorate despite optimal medical management.

Define pulmonary embolism

● DEFINITION: occlusion of pulmonary vessels, most commonly by a thrombus that has travelled to the pulmonary vascular system from another site ● Clots break off and pass through the veins and the right side of the heart before lodging in the pulmonary circulation.

Identify appropriate investigations for ARDS and interpret the results

● DIAGNOSTIC CRITERIA ⇒ Acute onset ⇒ CXR: bilateral infiltrates (fluffy represents pulmonary oedema) ⇒ Pulmonary capillary wedge pressure <19mmHg or lack of clinical congestive heart failure, PCWP is an indirect measure of the left atrial pressure ⇒ Refractory hypoxaemia (resistant to O2 treatment) with PaO2:FiO2 <200 1) CXR: bilateral alveolar and interstitial shadowing 2) Blood: ABG!!, FBC, U&E, ESR/CRP, amylase, clotting, BLOOD CULTURE, SPUTUM CULTURE 3) Echocardiography: severe aortic or mitral valve dysfunction 4) Pulmonary artery catheterisation: PWCP less than or equal to 18mmHg 5) Bronchoscopy: if cause cannot be determined from history, and to exclude differentials

Identify the possible complications of pulmonary embolism

● Death ● Pulmonary infarction -death of lung tissue ● Pulmonary hypertension -elevated pulmonary pressure resulting from an increase in pulmonary vascular resistance to blood flow through small arteries and arterioles. ● Right heart failure

Identify appropriate investigations for lung cancer

● Diagnosis o CXR - peripheral nodule, hilar enlargement, consolidation, lung collapse, pleural effusion, bony secondaries o Sputum and pleural fluid cytology o Bronchoscopy with brushings or biopsy - to give histology o CT/US-guided percutaneous biopsy o Lymph node biopsy ● Staging - requires CT/MRI of head, chest and abdomen. PET scans may also be useful Staging = TNM ● Radionuclide bone scan if suspected mets ● Lung function tests to assess suitability for lobectomy ● Bloods o FBC o U&Es o Calcium (hypercalcaemia is a common feature) o ALP (raised with bone metastases) o LFTs ● Pre-Op - ABG and pulmonary function tests

Explain the aetiology/risk factors of ARDS

● Direct lung injury or secondary to systemic illness --> lung damage --> release of inflammatory mediators --> increased capillary permeability due to endothelial dysfunction --> fluid leakage in to alveoli as well as reduced surfactant production --> impaired gas exchange and reduced lung compliance ● Common causes: Pulmonary ⇒ PNEUMONIA ⇒ Gastric ASPIRATION ⇒ Smoke inhalation ⇒ Injury ⇒ Vasculitis ⇒ Contusion Other ⇒ Shock ⇒ SEPSIS ⇒ Haemorrhage ⇒ Multiple transfusions ⇒ DIC ⇒ Pancreatitis ⇒ Acute liver failures ⇒ SEVERE TRAUMA ⇒ Head injury ⇒ Malaria ⇒ Fat embolism ⇒ Burns ⇒ Obstetric events: eclampsia, amniotic fluid embolus ⇒ Drugs/toxins: aspirin, heroin, paraquat

Recognise the presenting symptoms of asthma

● Episodic history - intermittent dyspnoea, wheeze, cough (worse in morning and at night) and sputum ● Precipitating Factors o Cold air o Viral infection o Drugs (e.g. beta-blockers, NSAIDs) o Exercise - quantify exercise tolerance! o Emotions o Allergens - house dust mite, pollen, fur, pets - ask about these at home o Smoking/passive smoking o Pollution o Ask if symptoms remit at weekend - may be trigger at work ● Check for history of atopic disease (e.g. allergic rhinitis, urticaria, eczema) ● Diurnal variation in symptoms or peak flow Marked morning dip in peak flow ● IMPORTANT: ask about previous hospitalisation due to acute attacks - this gives an indication of the severity of the asthma ● 40-60% of asthmatics have acid reflux

Recognise the signs of pneumoconiosis on physical examination

● Examination may be NORMAL ● Coalworker's pneumoconiosis and silicosis: o Decreased breath sounds ● Asbestosis: o End-inspiratory crackles o Clubbing ● Signs of pleural effusion or right heart failure (cor pulmonale due to pulmonary hypertension)

Recognise the presenting symptoms of obstructive sleep apnoea

● Excessive daytime sleepiness ● Unrefreshing or restless sleep ● Morning headaches ● Dry mouth ● Difficulty concentration ● Irritability and mood changes, decreased libido and cognitive performance ● Partner reporting loud snoring, nocturnal apnoeic episodes or nocturnal choking

Recognise the presenting symptoms of pneumonia

● Fever ● Rigors ● Sweating ● Malaise ● Dyspnoea ● Cough ● Purulent Sputum ● Haemoptysis ● Pleuritic chest pain ● Weight loss ● Confusion (in severe cases or in the elderly) ● Atypical Pneumonia Symptoms: o Headache o Myalgia o Diarrhoea/abdominal pain o DRY cough

Define pneumoconiosis

● Fibrosing interstitial lung disease caused by chronic inhalation of mineral dusts ● Types: a) Simple: Coalworker's pneumoconiosis or silicosis (symptom-free) - due to inhalation of coal dust particles over 15-20 yrs. They are ingested by macrophages which die, releasing their enzymes and causing fibrosis. b) Complicated: pneumoconiosis results in loss of lung function c) Asbestosis: a pneumoconiosis in which diffuse parenchymal lung fibrosis occurs as a result of prolonged exposure to asbestos

Recognise the presenting symptoms of lung cancer

● May be ASYMPTOMATIC ● Symptoms due to primary: o Cough o Haemoptysis o Chest pain o Dyspnoea o Recurrent pneumonia ● Symptoms due to local invasion: o Brachial plexus invasion --> shoulder/arm pain o Left recurrent laryngeal nerve invasion --> hoarse voice and bovine cough o Dysphagia o Arrhythmias o Sympathetic chain invasion --> Horner's syndrome ● Symptoms due to metastatic disease or paraneoplastic: phenomenon o Weight loss o Fatigue o Fractures o Bone pain

Recognise the presenting symptoms of pneumothorax

● May be ASYMPTOMATIC if the pneumothorax is small ● Sudden-onset breathlessness ● Pleuritic chest pain ● Distress with rapid shallow breathing in tension pneumothorax ● Patients on ventilation may present with hypoxia or increase in ventilation pressures

Identify appropriate investigations for COPD

● GOLD STANDARD: Spirometry and Pulmonary Function Tests o Shows obstructive picture o Reduced PEFR o Reduced FEV1/FVC o Increased lung volumes ● Decreased carbon monoxide gas transfer coefficient ● CXR: o May appear NORMAL o Hyperinflation (> 6 anterior ribs, flattened hemidiaphragm) o Reduced peripheral lung markings o Large central pulmonary arteries o Elongated cardiac silhouette ● Bloods: o FBC - increased Hb and haematocrit due to secondary polycythaemia ● ABG - may show hypoxia, normal/raised PCO2 ● ECG and Echocardiogram - check for cor pulmonale - right atrial and ventricular hypertrophy ● Sputum and Blood Cultures - useful in acute infective exacerbations ● a1 antitrypsin levels - useful in young patients who have never smoked **BMJ Best practice: 1st investigations to order: 1) Spirometry - FEV1/FVC ratio <0.70; total absence of reversibility is neither required nor the most typical result 2) Pulse oximetry - low O2 sat 3) ABG - acutely unwell, especially if they have an abnormal pulse oximetry reading. PaCO₂ >50 mmHg and/or PaO₂ of <60 mmHg suggests respiratory insufficiency and may need intubation. 4) CXR - rule out other pathologies and see hyperinflated lungs 5) FBC - raised haematocrit, possible increased WBC count 6) ECG - often comorbidity with IHD is seen - signs of right ventricular hypertrophy, arrhythmia, ischaemia. **Other ones can be considered - e.g. sputum culture for frequent exacerbations and a1 antitrypsin levels - useful in young patients who have never smoked

Systemic effects of sarcoidosis

● General Symptoms: o Fever o Malaise o Weight loss o Bilateral parotid swelling o Lymphadenopathy o Hepatosplenomegaly o Hypercalcaemia o Hypercalciuria o Renal stones ● Pulmonary Symptoms: o Breathlessness o Dry cough o Chest discomfort o Minimal clinical signs ● Musculoskeletal Symptoms: o Bone cysts - terminal phalangeal (e.g. dactylitis) o Polyarthralgia o Myopathy ● Eye Symptoms: o Keratoconjunctivitis sicca (inflammation of the conjunctivitis and surrounding tissues due to the eyes being dry) o Glaucoma o Uveitis o Papilloedema ● Skin Symptoms: o Lupus pernio (red-blue infiltrations of the nose, cheeks, ears and terminal phalanges) o Erythema nodosum o Maculopapular eruptions ● Neurological Symptoms: o Lymphocytic meningitis o Space-occupying lesions o Pituitary infiltration o Cerebellar ataxia o Cranial nerve palsies o Peripheral neuropathy o Meningitis ● Cardiac Symptoms: o Arrhythmia o Bundle branch block o Pericarditis o Cardiomyopathy o Congestive cardiac failure

Recognise the presenting symptoms of idiopathic pulmonary fibrosis

● Gradual-onset, progressive dyspnoea on exertion ● Dry irritating cough ● NO wheeze ● Symptoms may be preceded by a viral-type illness ● Fatigue and weight loss are common ● IMPORTANT: take a full occupational and drug history

Identify the possible complications of asthma

● Growth retardation ● Chest wall deformity (e.g. pigeon chest) ● Recurrent infections ● Pneumothorax ● Respiratory failure ● Death

Summarise the prognosis for patients with COPD

● High morbidity ● 3-year survival of 90% if < 60 yrs, FEV1 > 50% predicted ● 3-year survival of 75% if > 60 yrs, FEV1: 40-49% predicted

Explain the aetiology/risk factors for extrinsic allergic alveolitis

● In sensitised individuals, repetitive inhalation of allergens provokes a hypersensitivity reaction which varies in intensity and clinical course depending on the antigen. ● In the acute phase, the alveoli are infiltrated with acute inflammatory cells. ● Antigenic dusts include microbes and animal proteins ● Early diagnosis and prompt allergen removal can halt and reverse disease progression, so prognosis can be GOOD. ● With chronic exposure, granuloma formation and obliterative bronchiolitis. ● Examples: a) Farmer's Lung - caused by mouldy hay containing thermophilic actinomycetes b) Pigeon Fancier's Lung - caused by blood on bird feathers and excreta c) Maltworker's Lung - caused by barley or maltlings containing Aspergillus clavatus d) Bagassosis or sugar worker's lung (Thermoactinomyces sacchari)

Summarise the epidemiology of pneumoconiosis

● Incidence is increasing in developing countries ● Disability and mortality from asbestosis will continue to increase for the next 20-30 yrs

Recognise the signs of COPD on physical examination

● Inspection: o Respiratory distress o Use of accessory muscles - tripod position o Pursed lip breathing o Barrel-shaped over-inflated chest o Decreased cricosternal distance (distance <3 fingers = lung hyperinflation (e.g. asthma, COPD). o Cyanosis ● Palpation: o Reduced expansion ● Percussion: o Hyper-resonant chest o Loss of liver and cardiac dullness ● Auscultation: o Quiet breath sounds o Poor air movement o Prolonged expiration o Wheeze o Rhonchi - rattling, continuous and low-pitched breath sounds that sounds a bit like snoring. They are often caused by secretions in larger airways or obstructions o Sometimes crepitations ● Signs of CO2 Retention: o Bounding pulse o Warm peripheries o Asterixis ● LATE STAGES: signs of right heart failure (cor pulmonale) o Right ventricular heave o Raised JVP o Ankle oedema

Recognise the presenting symptoms of bronchiectasis

● KEY: Persistent cough with copious purulent sputum - may be worsened by lying flat ● Intermittent haemoptysis ● Breathlessness ● Chest pain ● Malaise ● Fever - recurrent episodes ● Weight loss ● rhinosinusitis ● Symptoms usually begin after an acute respiratory illness ● All symptoms worsen during acute exacerbations

Recognise the signs of obstructive sleep apnoea on physical examination

● Large tongue (macroglossia)/ micrognathia (maxillomandibular anomalies) ● Enlarged tonsils ● Long or thick uvula ● Retrognathia (pulled back jaws) ● Neck circumference o More than 42 cm in males o More than 40 cm in females ● Obesity ● Hypertension

Identify the possible complications of bronchiectasis

● Life-threatening haemoptysis ● Pneumonia ● Pneumothorax ● Persistent infections ● Empyema ● Respiratory failure ● Cor pulmonale ● Multi-organ abscesses ● Amyloidosis

Identify the possible complications of an ABG

● Local haematoma ● Artery vasospasm ● Arterial occlusion ● Air embolism ● Infection

Define Aspergillus Lung Disease

● Lung disease associated with Aspergillus fungal infection ● There are five different ways this group of fungi can affect the lungs 1) Asthma: type I hypersensitivity (atopic) reaction to fungal spores 2) Allergic bronchopulmonary aspergillosis (ABPA): type I and type III hypersensitivity reactions to Aspergillus fumigatus mould, typically affecting patients with asthma or cystic fibrosis. 3) Aspergilloma (mycetoma): a fungus ball within a pre-existing cavity (often caused by TB or sarcoidosis) 4) Invasive aspergillosis 5) Extrinsic allergic alveolitis (EAA): due to sensitivity to Aspergillus clavatus ('malt worker's lungs')

Recognise the signs of lung cancer on physical examination

● May be NO SIGNS ● Fixed monophonic wheeze (suggesting that there is a single obstruction) ● Signs of lobar collapse or pleural effusion ● Signs of metastases (e.g. supraclavicular lymphadenopathy or hepatomegaly, bone tenderness, confusion, fits, cerebellar syndrome, proximal myopathy, peripheral neuropathy) ● Cachexia ● Anaemia ● Clubbing ● Hypertrophic pulmonary osteoarthropathy causing wrist pain ● Lymphadenopathy - supraclavicular or axillary nodes

Summarise the epidemiology of asbestos-related lung disease (incl. asbestosis and mesothelioma)

● Mesothelioma is rare - more common in elderly (60-85 y/o males) ● Asbestos exposure is documented in 90% of cases ● Latent period between exposure and mesothelioma = up to 50 yrs

Summarise the epidemiology of lung cancer

● Most common FATAL cancer in the west (18% of cancer mortality worldwide) ● 3 x more common in MALES

Summarise the epidemiology of sarcoidosis

● Most common in AFRICANS and SCANDINAVIANS ● Can occur at any age but tends to be in adults 20-40 yrs ● More common in women

Summarise the epidemiology of bronchiectasis

● Most often arises initially in CHILDHOOD (also from CF) ● Incidence has decreased with the use of antibiotics ● 1/1000 per year ● Tall, thin, white females aged 60 or over are at greater risk of pulmonary non-tuberculous mycobacteria related bronchiectasis

Summarise the prognosis for patients with bronchiectasis

● Most patients continue to have symptoms after 10 years

Summarise the prognosis for patients with pneumonia

● Most resolve within treatment within 1-3 weeks ● Severe pneumonia has a high mortality ● The CURB-65 score is used to assess the severity of pneumonia: o Confusion < 8 AMTS o Urea > 7 mmol/L o Respiratory rate > 30/min o Blood pressure: systolic < 90 mm Hg or diastolic < 60 mm Hg o Age > 65 yrs **NICE recommend that the following information is given to patients with pneumonia in terms of how quickly their symptoms should symptoms should resolve: § 1 week- Fever should have resolved § 4 weeks- Chest pain and sputum production should have substantially reduced § 6 weeks- Cough and breathlessness should have substantially reduced § 3 months - Most symptoms should have resolved but fatigue may still be present § 6 months - Most people will feel back to normal.

Define sarcoidosis

● Multisystem granulomatous inflammatory disorder of unknown cause ● NOTE: granulomatous = a granuloma is a collection of histiocytes (macrophages) ● Non-caseating = caseation refers to a form of necrosis that appears cheese-like whereas non-caseating means there has been no necrosis. Caseating granulomas are typically seen in tuberculosis.

Explain the aetiology/risk factors of tuberculosis

● Mycobacterium tuberculosis is an intracellular organism ● It survives after being phagocytosed by macrophages ● When TB is first taken in via air droplets in to lungs, it leads to primary TB which is when you get signs of infection after exposure, although this does not always cause major symptoms. ● 3 weeks after this, there is cell-mediated immunity which leads to granuloma formation around the infected area of the alveoli. Inside the granuloma, there is cell necrosis called caseous necrosis. This usually occurs in the sub-pleural, lower lobe area. ● In some cases, although some scarring occurs, the TB is killed off by the immune system. But, in other cases, the TB may remain viable but latent. ● In these cases, when the person's immune system is weakened i.e. due to HIV or age, the TB is reactivated and spreads to the upper lobes where oxygenation is optimal (TB = aerobe). ● Here, there are more caseous regions formed and then cavities. This leads to dissemination throughout the lungs and via the vascular system leading to miliary TB. ● Military TB involves spread to multi-organs ◦ Kidneys causing sterile pyuria ◦ Meningitis ◦ Lumbar vertebrae causing Pott disease ◦ Adrenals causing Addison's ◦ Liver causing hepatitis ◦ Cervical lymph nodes ● Risk factors: 1) Immunocompromised, esp HIV 2) Low CD4 3) High ESR 4) Co-infections 5) Poor nutrition 6) High viraemia 7) having lived in Asia, Latin America, Eastern Europe, or Africa for years 8) exposure to someone with infectious tuberculosis (TB) 9) residence in an institutional setting and homelessness.

Recognise the presenting symptoms of pneumoconiosis

● OCCUPATIONAL HISTORY is very important ● Asymptomatic - picked up on routine CXR ● Symptomatic o Insidious onset shortness of breath o Dry cough o BLACK SPUTUM (melanoptysis) - produced occasionally in coalworker's pneumoconiosis o Pleuritic chest pain (due to acute asbestos pleurisy) - in patients exposed to asbestos

Normal vs Obstructive vs Restrictive

● Obstructive disease: the flow of air into and out of the lung is obstructed. Lungs operate at higher volumes ⇒ TLC increases ⇒ RV increases ⇒ VC decreases ⇒ FEV1/FVC ratio < 75% ⇒ FEV1 is reduced more than FVC ⇒ E.g. asthma, COPD ● Restrictive disease: inflation/deflation of the lung or chest wall is restricted ⇒ TLC decreases ⇒ RV decreases ⇒ VC decreases ⇒ FEV1/FVC 75% or > due to reduced FVC ⇒ E.g. lung fibrosis

Explain the aetiology/risk factors of obstructive sleep apnoea

● Occurs due to narrowing of the upper airways because of the collapse of soft tissues of the pharynx ● This is due to decreased tone of the pharyngeal dilators during sleep ● Typically affects obese, middle-aged men presenting with snoring or daytime somnolence with partner describing apnoeic episodes during sleep ● Associated with: o Weight gain - soft tissue in neck area o Surgical swelling o Smoking o Alcohol o Sedative use o Enlarged tonsils and adenoids in children o Macroglossia o Marfan's syndrome o Craniofacial abnormalities **RFs: § obesity § male sex § post-menopause (women) § large neck circumference § maxillomandibular anomalies (e.g., narrowing, retrognathia, and high, arched palate) § increased volume of soft tissues (includes tonsils, adenoids, and tongue) § family history of OSA § chronic snoring § polycystic ovary syndrome § hypothyroidism § Down's syndrome § mucopolysaccharidoses § increasing age § black, Hispanic, and Asian ethnicity § tobacco smoking

Explain the aetiology/risk factors of lung cancer

● Smoking ● Asbestos exposure ● Other occupational exposure: polycyclic hydrocarbons, nickel, radon gas, chromium, arsenic, iron oxides ● Atmospheric pollution

Explain the aetiology/risk factors of idiopathic pulmonary fibrosis

● Occurs in genetically predisposed individuals ● Recurrent injury to alveolar epithelial cells results in secretion of cytokines and growth factors by the pnuemocytes, in particular TGFb1 ● Usually there is interstitial tissue in between alveoli and capillaries containing fibroblasts and macrophages. The cytokines released causes fibroblast activation, recruitment, proliferation, differentiations into myofibroblasts and increased collagen synthesis and deposition ● Over time, this leads to a thickened interstitial layer causing problems with ventilation and oxygenation. The alveoli are also stiffer. ● This is a RESTRICTIVE disease as there is restricted lung expansion due to fibrosis of the interstitium. ● There is also loss of alveoli leading to fluid filled cysts surrounded by a thick wall - known as HONEYCOMBING ● Certain drugs can produce similar illness (e.g. methotrexate, amiodarone) ● Histological Patterns o Interstitial pneumonia ● Risk Factors o Age o Male o Smoking o Occupational exposure to metal or wood o Chronic microaspiration o Animal and vegetable dusts o family history

Identify the possible complications of pneumonia

● Pleural effusion ● Empyema ● Localised suppuration (e.g. abscess) o Symptoms of abscesses: ▪ Swinging fever ▪ Persistent pneumonia ▪ Copious/foul-smelling sputum ● Septic shock ● ARDS ● Acute renal failure ● Pericarditis ● Myocarditis ● Extra complications of Mycoplasma pneumonia: o Erythema multiforme o Myocarditis o Haemolytic anaemia o Meningoencephalitis o Transverse myelitis o Guillain-Barre syndrome

Generate a management plan for bronchiectasis

● Postural drainage should be performed twice daily for sputum and mucus clearance - chest physiotherapy may aid this. Can reduce frequency of acute exacerbations and aid recovery ● Treat acute exacerbations with IV ANTIBIOTICS, according to bacterial sensitivities. Patients known to culture Pseudomonas aeruginosa require either oral ciprofloxacin or IV antibiotics. ● Prophylactic antibiotics should be considered in patients with frequent exacerbations (> 3/year) ● Bronchodilators e.g. nebulised salbutamol - considered in patients with responsive disease e.g. asthma, COPS ● Inhaled Corticosteroids (e.g. fluticasone) - reduces inflammation and volume of sputum but does NOT affect the frequency of exacerbations or lung function - useful for ABPA ● Maintain hydration ● Flu vaccination ● Surgical - localised resection, lung or heart-lung transplantation - may be indicated in localised disease or to control severe haemoptysis ● Bronchial artery embolisation - if life-threatening haemoptysis due to bronchiectasis

Recognise the symptoms and signs of tuberculosis

● Primary TB: o Mostly ASYMPTOMATIC o Fever o Malaise o Cough o Anorexia o Wheeze o Erythema nodosum o Phlyctenular conjunctivitis ● Miliary TB: o Fever o Weight loss o Meningitis o Yellow caseous tubercles spread to other organs ● Post-Primary TB: o Fever/night sweats o Malaise o Weight loss o Breathlessness o Cough o Sputum o Haemoptysis o Pleuritic chest pain o Signs of pleural effusion o Collapse o Consolidation o Fibrosis ● Non-Pulmonary: TB - occurs mainly in the immunocompromised ● Lymph Nodes o Suppuration of cervical lymph nodes leading to abscesses or sinuses ● CNS - meningitis, tuberculoma ● Skin - lupus vulgaris (jellylike reddish-brown glistening plaques) ● Heart - pericardial effusion, constrictive pericarditis ● GI: o Subacute obstruction o Change in bowel habit o Weight loss o Peritonitis o Ascites ● Genitourinary: o UTI symptoms o Renal failure o Epididymitis o Endometrial or tubal involvement o Infertility ● Adrenal insufficiency ● Bone/Joint - osteomyelitis, arthritis, vertebral collapse (Pott's disease), spinal cord compression from an abscess

Define lung cancer

● Primary malignant neoplasm of the lung o WHO classification of bronchocarcinoma: ▪ Small Cell Lung Cancer - 20% ▪ Non-Small Cell Lung Cancer - 80% ● Note: small cell has much worse prognosis with 3 month medial survival ● Small cell - made up of small cells that divide and spread rapidly ● Non-small cell: divide and spread slowly

Recognise the signs of pneumonia on physical examination

● Pyrexia ● Respiratory distress ● Tachypnoea ● Tachycardia ● Hypotension ● Cyanosis ● Signs of consolidation: o Decreased chest expansion o Dull to percuss over affected area o Increased tactile vocal fremitus/vocal resonance over affected area o Bronchial breathing over affected area o Coarse crackles on affected side ● Chronic suppurative lung disease (empyema, abscess) --> clubbing ● Confusion and may be hypothermic - elderly

What does recurrent laryngeal nerve palsy cause?

● Recurrent laryngeal nerve palsy: o Causes bovine cough o Associated with lung cancer ** ● Croup: laryngotracheobronchitis o Type of respiratory infection caused by virus o Causes cough like barking seal, stridor and hoarse voice

Identify the possible complications of pneumothorax

● Recurrent pneumothoraces ● Bronchopleural fistula

Summarise the epidemiology of pulmonary embolism

● Relatively COMMON (especially in hospitalised patients) ● Occur in 10-20% of patients with confirmed proximal DVT **1st investigations to order: § computed tomographic pulmonary angiography (CTPA) - definitive diagnostic investigation. § echocardiography - for haemodynamically unstable patients who cannot have CTPA. § D-dimer § full blood count

Summarise the indications for an arterial blood gas

● Respiratory failure ● Identification of respiratory, metabolic and mixed acid-base disorders ● Any severe illness which may lead to metabolic acidosis, e.g. cardiac failure, liver failure, renal failure ● Ventilated patients ● Sleep studies ● Severely unwell patients

Identify appropriate investigations for obstructive sleep apnoea

● Simple studies: pulse oximetry, video recording ● Sleep Study (polysomnography) o Monitor overnight with polysomnogram o Monitor airflow, respiratory effort, pulse oximetry and heart rate and snoring and movement o Occurrence of 15 or more episodes of apnoea or hypopnoea during 1 hour of sleep indicates significant sleep apnoea ● Bloods o TFTs o ABG **Diagnosis is established using clinical evaluation plus polysomnography or portable sleep tests. **The diagnosis of OSA may be confirmed if the Apnoea-Hypopnoea Index (the sum per hour of episodes of apnoeas and hypopnoeas) or Respiratory Distress Index (the sum per hour of episodes of apnoea, hypopnoea, and respiratory effort-related arousals) established with polysomnography or portable sleep test is ≥15 episodes/hour. However, 5 episodes/hour is considered sufficient for diagnosis if additional symptoms or comorbidities are present. **may do endoscopy to look for polyps/obstructions in patients not responding to CPAP treatment

Identify appropriate investigations for bronchiectasis

● Sputum: o Culture and sensitivity o Common organisms: ▪ Pseudomonas aeruginosa ▪ Haemophilus influenzae ▪ Staphylococcus aureus ▪ Streptococcus pneumoniae ▪ Klebsiella ▪ Mycobacteria ● CXR: o Dilated bronchi (may be seen as parallel lines going from the hilum to the diaphragm (TRAMLINE shadows)) o Fibrosis o Atelectasis (collapse/closure of lung) o Pneumonic consolidations o May be NORMAL ● High-Resolution CT: o BEST DIAGNOSTIC METHOD FOR BRONCHIECTASIS o Helps assess extent and distribution of disease o Shows dilated bronchi with thickened walls ● FBC - WBC differential may reveal high eosinophil count in bronchopulmonary aspergillosis; neutrophilia suggests superimposed infection or exacerbation ● Bronchography - rarely used ● Spirometry usually shows obstructive image - should assess reversibility ● Others: sweat electrolytes (for cystic fibrosis), serum Ig, mucociliary clearance study, Aspergillus precipitins or skin-prick test

Recognise the signs of asthma on physical examination

● Tachypnoea ● Use of accessory muscles ● Prolonged expiratory phase ● Polyphonic wheeze - widespread narrowing of airways of differing calibre e.g. asthma, COPD ● Hyperinflated chest ● Hyper-resonant percussion note ● Reduced air entry ● On inspection -may be normal or have nasal polyposis (COUGH, WHEEZE, SOB) **Moderate Attack: o PEFR: >50-75% predicted ** Severe Attack o PEFR 33-50% predicted o Pulse > 110/min o RR > 25/min o Inability to complete sentences **Life-Threatening Attack: o PEFR < 33% predicted o Silent chest o Cyanosis - PaO2 <8kPa, normal/high PaCO2 >4.6kPa, low pH <7.35 o Bradycardia o Hypotension o Confusion o Coma **Near fatal: RAISED PaCO2 +/- require mechanical ventilation

Identify appropriate investigations for pulmonary embolism

● The Well's Score is used to determine the best investigation for PE ● If Well's 4 or less (1 or less if used simplified Well's score) o Do D-dimer ▪ If D-dimer negative: PE excluded ▪ If D-dimer raised: do CTPA ● If Well's >4 (>1 if using simplified score): do CTPA and start on LMWH ● Note: if CT is contraindicated (e.g. pregnancy): use V/Q scanning ● Additional investigations: a) Bloods - ABG (low PaO2 and PaCO2), thrombophilia screen b) ECG: ● May be normal ● May show tachycardia, right axis deviation or RBBB or right ventricular strain (inverted T in V1-V4) c) May show S1Q3T3 pattern (S waves in lead I, Q waves in III, Inverted T waves in III) d) CXR - often NORMAL but helps exclude other diagnoses. May show oligaemia of affected segment, dilated pulmonary artery, linear atelectasis, small pleural effusion, wedge shaped opacities e) Spiral CT Pulmonary Angiogram - GOLD STANDARD o Poor sensitivity for small emboli o VERY sensitive for medium to large emboli f) Ventilation-Perfusion (VQ) Scan: o Identifies areas of ventilation and perfusion mismatch, which would indicate an area of infarcted lung o Increasingly used if CTPA can't be done g) Pulmonary Angiography o Invasive o Rarely necessary h) Doppler US of Lower Limb - allows assessment of venous thromboembolism i) Echocardiography - may show right heart strain

The Mechanical Process of Breathing

● The lungs have an inherent elastic property giving them a tendency to collapse away from the thoracic wall generating a negative pressure within the pleural space. ● The strength of the retractive force is related to the volume of the lung with higher lung volumes stretching more and causing greater negative intrapleural pressure. This relationship is called lung compliance. ● At the end of a quiet expiration: the retractive force exerted by the lungs is balanced by the tendency of the thoracic wall to spring outwards. The volume of air remaining in the lung at this point is called the FUNCTIONAL RESIDUAL CAPACITY (FRC) ● Inspiration from FRC: The diaphragm moves down and ribs move up and outwards via contraction of the intercostal muscles. This creates a negative pressure driving air into the lungs More vigorous inspiration would involve accessory muscles as well as diaphragm ● Expiration is passive resulting from the natural tendency of the lung to collapse ● As lung volume decreases during expiration, the elastic recoil pressure of the lungs decreases and the 'collapse point' moves upstream towards the smaller airways. ● When there is pathological loss of recoil pressure e.g. in COPD, the 'collapse point' is located even higher causing expiratory flow limitation. To compensate, these patients purse their lips to increase airway pressure so that peripheral airways do not collapse. ● Forced expiration involves the accessory muscles of the abdominal wall pushing the diaphragm moving up.

Recognise the signs of pneumothorax on physical examination

● There may be NO signs if the pneumothorax is small ● Signs of respiratory distress (HIGH RR, PR) ● Reduced expansion on affected side ● Hyper-resonance to percussion on affected side ● Reduced breath sounds on affected side ● Tension Pneumothorax: o Severe respiratory distress o Tachycardia o Hypotension o Cyanosis o Distended neck veins o Tracheal deviation away from the side of the pneumothorax o Increased percussion note, reduced air entry/breath sounds on affected side **To assess the size of a pneumothorax you have to measure the interpleural distance. This is the distance between lung margin (visceral pleura) and the chest wall (parietal pleura). A 2cm pneumothorax equates to a 50% pneumothorax, which is a large pneumothora

Explain the aetiology/risk factors of pulmonary embolism

● Thrombus o 95% arise from DVT in the lower limbs o Rarely arises in the right atrium (in AF patients) ● Other causes of embolus: o Amniotic fluid o Air o Fat o Tumour o Mycotic o Parasites o Right ventricular thrombus (post MI) o Septic emboli (right sided endocarditis) ● Risk Factors: o Surgical patients o Immobility o Obesity o OCP o Heart failure o Malignancy o Thrombophilia o Pregnancy o Previous PE

Explain the aetiology/risk factors of sarcoidosis

● UNKNOWN ● Transmissible agents (e.g. viruses), environmental triggers and genetic factors have all been suggested ● Associated with HLA-DRB1 and DQB1 alleles ● Pathogenesis o An UNKNOWN antigen is presented on MHC class 2 complexes on macrophages to CD4+ T-lymphocytes o These accumulate and release cytokines o This leads to the formation of non-caseating granulomas in organs

Triggers for asthma

◼ Asthma is a common and potentially serious chronic disease that can be controlled but not cured ◼ Asthma causes symptoms such as wheezing, shortness of breath, chest tightness and cough that vary over time in their occurrence, frequency and intensity ◼ Symptoms are associated with variable expiratory airflow, i.e. difficulty breathing air out of the lungs due to ▪ Bronchoconstriction (airway narrowing) ▪ Airway wall thickening ▪ Increased mucus ◼ Symptoms may be triggered or worsened by factors such as viral infections, allergens, tobacco smoke, exercise and stress

How to diagnose asthma

◼ The diagnosis of asthma should be based on: ▪ A history of characteristic symptom patterns ▪ Evidence of variable airflow limitation, from bronchodilator reversibility testing or other tests ◼ Document evidence for the diagnosis in the patient's notes, preferably before starting controller treatment ▪ It is often more difficult to confirm the diagnosis after treatment has been started ◼ Asthma is usually characterized by airway inflammation and airway hyperresponsiveness, but these are not necessary or sufficient to make the diagnosis of asthma.

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