Everything you need to know about ASTHMA and COPD

Summary

Join medical experts Emma McEwen, Harish Bava, and Aishwarya Baskar in an in-depth on-demand teaching session about Asthma and COPD. This tutorial is open to all and focuses on core presentations and diagnostic techniques. Learn about presenting symptoms, potential triggers, and detailed case studies. Benefit from revising disease pathophysiology, discover the intricacies of patient history taking, and delve into the latest insights on diagnostic methods including Peak Flow, FeNO, spirometry, and more. The session also reviews how to distinguish between COPD & asthma, and provides guidelines for effective patient management. Reviewed by doctors for accuracy, these tutorials are a must-attend for medical professionals looking to expand their knowledge in managing Asthma and COPD. Stay updated about upcoming sessions via email and group chats.

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Description

Welcome to Teaching Things!

We're excited to bring you this high-yield teaching series, designed to help you ace both your written and practical exams.

This tutorial will focus on Asthma and COPD to ensure you're well-prepared.

The session will be led by Emma and Harish, both medical students in their clinical years at UCL, who are passionate about delivering practical, exam-focused content.

Don’t forget to fill out the feedback form after the tutorial—we value your input! And remember, you can access recordings of all past tutorials on our page

Learning objectives

Understand the distinguishing characteristics and differences between Asthma and COPD, including the common symptoms and risk factors for both diseases.
Learn about the various diagnostic techniques used for Asthma and COPD, such as spirometry, peak flow meter, and FeNO tests.
Understand the physiology and pathophysiology of Asthma and COPD, including the underlying immunological and genetic factors that contribute to the development of these conditions.
Understand the key aspects of a patient's medical history relevant to Asthma and COPD and how these may factor into diagnosis and treatment planning.
Learn about the various management strategies for Asthma and COPD, including lifestyle changes, conservative measures, and medical treatment settings.

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EVERYTHING YOU NEED TO KNOW ABOUT ASTHMA AND COPD Tutor Names Emma McEwen and Harish Bava Aishwarya Baskar Here’s what we do: ■ Weekly tutorials open to all! ■ Focussed on core presentations and teaching diagnostic technique If you’re new here… ■ Bstudentsl students, for medical ■ Reviewed by doctors to ensure W elcome to accuracy T eaching ■ We’ll keep you updated about our Things! upcoming events via email and groupchats!ASTHMA Emma McEwenCase Study A 35-year-old woman presents to her GP with SOB and chest tightness. You go to take a history. What do you want to know?Case Study A 35-year-old woman presents to her GP with SOB and chest tightness. HPC: - Recurrent episodes of SOB for past few months - Feels difficult to breathe, struggling to get enough air, tightening of chest - Associated cough - Worse after going for run - Notices breathing is often worse in the morning and sometimes wakes from sleepCase Study A 35-year-old woman presents to her GP with SOB and chest tightness. PMH: - Hay fever: has had since childhood, treats with antihistamines DH: - NKDA FH: - Father has hypertension SH: - Non-smoker, no EtOH, no recreational drugs - Works as school teacherBackground: Asthma ■ Chronic condition ■ Recurrent episodes of: – Airﬂow obstruction (mostly reversible) – Bronchial hyperresponsiveness – Underlying inﬂammation ■ Signiﬁcant disease burden worldwide – 5-10% population (increasing prevalence) – 1000 people die every year in UKAetiology ■ Genetic factors – Heritability: 35-95% – Atopic triad: ■ Hay fever ■ Eczema ■ AsthmaAetiology ■ Genetic factors – Heritability: 35-95% ■ Environmental factors – Allergens – Respiratory infections – Tobacco smoke – Air pollution – Occupational exposures (chemicals / dust / etc)Aetiology ■ Genetic factors – Heritability: 35-95% ■ Environmental factors – Allergens – Respiratory infections – Tobacco smoke – Air pollution – Occupational exposures (chemicals / dust / etc) ■ Immunological factors – Imbalance of immune responsePathophysiology ■ Type 1 hypersensitivity reaction – Variable & recurringPathophysiology ■ Type 1 hypersensitivity reaction ■ Airway inﬂammation – Th2 cell-mediated – Other pro-inﬂammatory mediators: ■ Cytokines ■ Chemokines ■ Histamine ■ Leukotrienes – May lead to persistent airway inﬂammation & damagePathophysiology ■ Type 1 hypersensitivity reaction ■ Airway inﬂammation ■ Airway hyperresponsiveness – Excessive narrowing in response to stimuliPathophysiology ■ Type 1 hypersensitivity reaction ■ Airway inﬂammation ■ Airway hyperresponsiveness ■ Bronchoconstriction – Contraction of airway smooth muscle + impaired bronchodilator mechanisms – Narrowing of airways → obstruction of airﬂowPathophysiology ■ Type 1 hypersensitivity reaction ■ Airway inﬂammation ■ Airway hyperresponsiveness ■ Bronchoconstriction ■ Mucous production & airway remodelling – Structural changes in airway wall – May result in irreversible airﬂow obstruction→ progressive decline in lung function – Extent of remodelling is associated with disease severity & durationPathophysiologyPresentation ■ Mild intermittent → Severe persistentPresentation ■ Mild intermittent → Severe persistent ■ Wheeze – Widespread & bilateral – High-pitched whistling sound during expiration – Turbulent airﬂow passing through narrowed airways – Not speciﬁcPresentation ■ Mild intermittent → Severe persistent ■ Wheeze ■ Cough – Dry or productive – Often worse at night / early in morning (diurnal variation) ■ May disrupt sleep – May be in response to triggerPresentation ■ Mild intermittent → Severe persistent ■ Wheeze ■ Cough ■ Dyspnoea – Primarily due to bronchoconstriction – May be during exercise / at rest / result of trigger – May be worse in morningPresentation ■ Mild intermittent → Severe persistent ■ Wheeze ■ Cough ■ Dyspnoea ■ Chest tightness – May be due to airway obstruction & increased work of breathingCase Study Based on our history we are considering a diagnosis of asthma. Which investigations might we consider?Investigations ■ Peak ﬂow – Acute asthma – Peak ﬂow diary – Technique very importantInvestigations ■ Peak ﬂow ■ FeNO – NO produced by 3 types of nitric oxide synthases ■ Inducible nitric oxide (iNOS) tends to rise in inﬂammatory cells (eosinophils) ■ Levels of NO correlate with levels of inﬂammation ■ Smoking may give falsely low result – Adults: >40ppb – Children: >35ppbInvestigations ■ Peak ﬂow ■ FeNO ■ Spirometry – FEV1: forced expiratory volume ■ Volume exhaled at end of 1st second of forced expiration ■ Usually signiﬁcantly reduced in asthma – FVC: forced vital capacity ■ Volume exhaled after maximal expiration following full inspiration ■ Often normal in asthmaInvestigations ■ Peak ﬂow ■ FeNO ■ Spirometry – FEV1:FVC <70% (obstructive) – Cannot distinguish between COPD & asthmaInvestigations ■ Peak ﬂow ■ FeNO ■ Spirometry ■ Reversibility testing (BDR) – Use of bronchodilator → repeat spirometry – Helps distinguishing between asthma & COPD – Adults: >12% improvement in FEV1 or >200 mL increase in volume – Children: >12% improvement in FEV1Investigations ■ Peak ﬂow ■ FeNO ■ Spirometry ■ Reversibility testing (BDR) ■ Bronchial challenge – ‘Induction of asthma attack’ – Inhalation of irritating drug → determines sensitivity of airways – Risk: not done routinelyDiagnosis ■ Different for adults & children – All patients >5 years should have objective testsDiagnosis ■ Different for adults & children – All patients >5 years should have objective tests ■ Children <5 years – Diagnosis made on clinical judgmentDiagnosis ■ Different for adults & children – All patients >5 years should have objective tests ■ Children <5 years – Diagnosis made on clinical judgment ■ Children 5-16 years – Spirometry with bronchodilator reversibility (BDR) test – FeNO if normal / obstructive spirometry with negative BDR testDiagnosis ■ Different for adults & children – All patients >5 years should have objective tests ■ Children <5 years – Diagnosis made on clinical judgment ■ Children 5-16 years – Spirometry with bronchodilator reversibility (BDR) test – FeNO if normal / obstructive spirometry with negative BDR test ■ All patients >17 years – Spirometry with BDR + FeNO – Consider occupational asthma if better away from workCase Study The patient’s spirometry results have shown FEV1:FVC 67%, and a 12.7% improvement in FEV1 following bronchodilator use. What conservative measures may improve her outcomes?Management ■ Conservative – Vaccinations (ﬂu, COVID, pneumococcal) – Smoking cessation – Patient education ■ Asthma action plan ■ Attending regular asthma reviews (primary or secondary care) ■ Identiﬁcation & avoidance of triggers – Management of conditions that exacerbate asthma ■ Rhinitis / hay fever ■ Allergies ■ Acid reﬂuxManagement ■ Conservative ■ Medical What drugs are used in asthma management?Management ■ SABA (short-acting beta agonist) – E.g. Salbutamol – ‘Reliever’ / ‘Blue inhaler’ – Typically used if patient develops symptoms – Mechanism: relaxes smooth muscle of airways – Side effects: tremorManagement ■ SABA (short-acting beta agonist) ■ ICS (inhaled corticosteroid) – Eg. beclometasone dipropionate – ‘Preventer’ / ‘brown inhaler’ – Taken every day: regardless of symptoms – Mechanism: reduces inﬂammation – Side effects: oral candidiasis & stunted growthManagement ■ SABA (short-acting beta agonist) ■ ICS (inhaled corticosteroid) ■ LABA (long-acting beta agonist) – E.g. Salmeterol – Taken every day: regardless of symptomsManagement ■ SABA (short-acting beta agonist) ■ ICS (inhaled corticosteroid) ■ LABA (long-acting beta agonist) ■ LTRA (leukotriene receptor antagonist) – E.g. Montelukast – Taken orallyManagement ■ SABA (short-acting beta agonist) ■ ICS (inhaled corticosteroid) ■ LABA (long-acting beta agonist) ■ LTRA (leukotriene receptor antagonist) ■ AIR therapy (anti-inﬂammatory reliever therapy) – Low-dose ICS + formoterol combination inhaler – Taken for symptomatic reliefManagement ■ SABA (short-acting beta agonist) ■ ICS (inhaled corticosteroid) ■ LABA (long-acting beta agonist) ■ LTRA (leukotriene receptor antagonist) ■ AIR therapy (anti-inﬂammatory reliever therapy) ■ MART (maintenance and reliever therapy) – Combined ICS + LABA in single inhaler – Used for daily maintenance therapy & relief of symptoms as requiredManagement ■ SABA (short-acting beta agonist) ■ ICS (inhaled corticosteroid) ■ LABA (long-acting beta agonist) ■ LTRA (leukotriene receptor antagonist) ■ MART (maintenance and reliever therapy) ■ Biologics – Benralizumab – MepolizumabManagement ■ Conservative ■ Medical – NICE, BTS, SIGN (Nov 2024) – Previously different guidelinesManagement ■ Conservative ■ Medical – Step 1: newly-diagnosed asthma What should be given?Management ■ Conservative ■ Medical – Step 1 ■ Anti-inﬂammatory reliever (AIR) therapy – Low-dose ICS + formoterol combined inhaler – For symptom-relief onlyManagement ■ Conservative ■ Medical – Step 1 ■ AIR therapy – Step 2: not controlled on step 2 or newly-diagnosed asthma with symptoms >3x / week or night-time wakingManagement ■ Conservative ■ Medical – Step 1 ■ AIR therapy – Step 2 ■ Low-dose MARTManagement ■ Conservative ■ Medical – Step 1 ■ AIR therapy – Step 2 ■ Low-dose MART – Step 3 ■ Moderate-dose MARTManagement ■ Conservative ■ Medical – Step 1 ■ AIR therapy – Step 2 ■ Low-dose MART – Step 3 ■ Moderate-dose MART – Step 4 ■ Check FeNO & eosinophils – If raised: refer to asthma specialist – If normal: moderate-dose MART + LTRA or LAMAManagement ■ Conservative ■ Medical – Step 1 ■ AIR therapy – Step 2 ■ Low-dose MART – Step 3 ■ Moderate-dose MART – Step 4 ■ Check FeNO & eosinophils – If raised: refer to asthma specialist – If normal: moderate-dose MART + LTRA or LAMA – Step 5 ■ Refer to asthma specialist Management Previous treatment New treatment SABA only → AIR therapy SABA + low-dose ICS +/- LABA / LTRA → MART therapy SABA + moderate-dose ICS +/- LABA / LTRA / LAMA → Moderate-dose MART therapy Treatment regime with high-dose ICS → Refer to asthma specialistManagement ■ Complete control – Characterised by: ■ No daytime symptoms ■ No night-time awakening ■ No need for rescue medication – Aims to: ■ Improve functional status & quality of life ■ Reduce risk: death, acute attacks, emergency care, medication side effectsCase Study After having been started on AIR therapy several weeks ago, the patient presents to A&E with sudden-onset SOB, a widespread wheeze, and a cough. Her observations show: HR: 104 bpm BP: 110/65 mmHg RR: 26 / min SpO2: 94% on room air Temp: 37.7 C What diagnosis should we suspect?Acute Asthma ■ Progressive worsening of asthma symptoms over acute or subacute periodAcute Asthma ■ Progressive worsening of asthma symptoms over acute or subacute period ■ –stCan be fatalper yearAcute Asthma ■ Progressive worsening of asthma symptoms over acute or subacute period ■ Estimated 8.4% per year ■ Increased risks – Homelessness – Drug / alcohol use – Overuse of salbutamol – Lack of personalised asthma plan – Previous admissions / near-fatal attacksAcute Asthma ■ Progressive worsening of asthma symptoms over acute or subacute period ■ Estimated 8.4% per year ■ Increased risks ■ Presentation: onset <6 hours – Dyspnoea / cough / wheeze / chest tightness – Tachypnoea / tachycardia – Inability to speak in full sentences – Silent chest (rare)Acute Asthma Classiﬁcation ■ Based on: – Peak expiratory ﬂow rate (PEFR) – Arterial O2 saturation (SpO2) – Partial arterial pressure of O2 (PaO2) – Partial arterial pressure of CO2 (PaCO2)Acute Asthma Classiﬁcation ■ Based on: – PEFR – SpO2 – PaO2 – PaCO2 ■ Determines appropriate managementAcute Asthma Classiﬁcation ■ Moderate acute asthma exacerbation – Increasing symptoms – PEFR >50-75% of patient’s best or predicted score – No features of severe acute asthmaAcute Asthma Classiﬁcation ■ Moderate acute asthma exacerbation – Increasing symptoms – PEFR >50-75% of patient’s best or predicted score – No features of severe acute asthma ■ Severe acute asthma exacerbation – PEFR 33-50% of patient’s best or predicted score – RR: ≥ 25 / min – HR: ≥ 110 bpm – Inability to complete sentences in one breathAcute Asthma Classiﬁcation ■ Moderate acute asthma exacerbation – PEFR >50-75% ■ Severe acute asthma exacerbation – PEFR 33-50% ■ Life-threatening acute asthma exacerbation – PEFR <33% of patient’s best or predicted score – SpO2 <92% – PaO2 <8kPa – Silent chest: absence of audible breath sounds over chest – Cyanosis (usually of lips) – Exhaustion or reduced respiratory effort – New-onset arrhythmia – Reduced GCS – HypotensionAcute Asthma Classiﬁcation ■ Moderate acute asthma exacerbation – PEFR >50-75% ■ Severe acute asthma exacerbation – PEFR 33-50% ■ Life-threatening acute asthma exacerbation – PEFR <33% ■ Near-fatal acute asthma exacerbation – Raised PaCO2 >6kPa – Need for mechanical ventilationAcute Asthma Classiﬁcation PaCO2 ■ Moderate acute asthma exacerbation – PEFR >50-75% ● Moderate / severe asthma: low ■ Severe acute asthma exacerbation – PEFR 33-50% ● Life-threatening asthma: normal ● Near-fatal asthma: high ■ Life-threatening acute asthma exacerbation – PEFR <33% ■ Near-fatal acute asthma exacerbation – Raised PaCO2 >6kPa – Need for mechanical ventilationAcute Asthma Investigations ■ Peak ﬂow (PEFR) or FEV1 – PEFR often more appropriateAcute Asthma Investigations ■ Peak ﬂow (PEFR) or FEV1 ■ Observations – HR – BP – RR – SpO2 – TempAcute Asthma Investigations ■ Peak ﬂow (PEFR) or FEV1 ■ Observations ■ ABG: if SpO2 <92% or PEFR <30% – PaO2: lower = more severe – PaCO2: correlates with FEV1 ~20% predicted – Most patients: respiratory alkalosisAcute Asthma Investigations ■ Peak ﬂow (PEFR) or FEV1 ■ Observations ■ ABG: if SpO2 <92% or PEFR <30% – PaO2: lower = more severe – PaCO2: correlates with FEV1 ~20% predicted – Most patients: respiratory alkalosis Why do most patients have a respiratory alkalosis?Acute Asthma Investigations ■ Peak ﬂow (PEFR) or FEV1 ■ Observations ■ ABG: if SpO2 <92% or PEFR <30% – PaO2: lower = more severe – PaCO2: correlates with FEV1 ~20% predicted – Most patients: respiratory alkalosis ■ Will become acidotic in hypercapnia – VBG used if ABG not possibleAcute Asthma Investigations ■ Peak ﬂow (PEFR) or FEV1 ■ Observations ■ ABG: if SpO2 <92% or PEFR <30% – PaO2: lower = more severe – PaCO2: correlates with FEV1 ~20% predicted – Most patients: respiratory alkalosis ■ Will become acidotic in hypercapnia – VBG used if ABG not possible ■ Chest X-ray: only if underlying diagnosis suspectedAcute Asthma Management ■ Hospital admission: life-threatening or near-fatal acute asthma – Severe acute asthma should be admitted if failing to respond to treatmentAcute Asthma Management ■ Hospital admission: life-threatening or near-fatal acute asthma ■ O–ygIf acutely unwell or Spo2 <92%Acute Asthma Management ■ Hospital admission: life-threatening or near-fatal acute asthma ■ Oxygen therapy – If acutely unwell or Spo2 <92% What options of delivering oxygen do we have?Oxygen TherapyAcute Asthma Management ■ Hospital admission: life-threatening or near-fatal acute asthma ■ Oxygen therapy – If acutely unwell or Spo2 <92% Which option is most appropriate?Acute Asthma Management ■ Hospital admission: life-threatening or near-fatal acute asthma ■ Oxygen therapy ■ SABA – High-dose inhaled salbutamol – If already diagnosed: likely already taken prior to presentation – Standard pressurised MDI or nebuliser – Requires monitoring ■ Hypokalaemia ■ Tachycardia → lactic acidosisAcute Asthma Management ■ Hospital admission: life-threatening or near-fatal acute asthma ■ Oxygen therapy ■ SABA ■ Prednisolone 40-50mg >5 days – Continue normal medication (including ICS) – IV hydrocortisone 100mg every 6h if unable to swallow tabletsAcute Asthma Management ■ Hospital admission: life-threatening or near-fatal acute asthma ■ Oxygen therapy ■ SABA ■ Prednisolone 40-50mg >5 days ■ Ipratropium bromide (SAMA) – Severe / life-threatening asthma or not responding to SABAAcute Asthma Management ■ Hospital admission: life-threatening or near-fatal acute asthma ■ Oxygen therapy ■ SABA ■ Prednisolone 40-50mg >5 days ■ Ipratropium bromide (SAMA) ■ Magnesium sulphate – IV or nebulizer – Severe / life-threatening asthma or not responding to treatment ■ Aminophylline – IV – Severe / life-threatening asthma or not responding to treatmentAcute Asthma Management ■ Hospital admission: life-threatening or near-fatal acute asthma ■ Oxygen therapy ■ SABA ■ Prednisolone 40-50mg >5 days ■ Ipratropium bromide (SAMA) ■ Magnesium sulphate ■ Aminophylline ■ Mechanical ventilation – Clinical decision ■ Severe fatigue ■ Cardiovascular compromise ■ Coma ■ Cardiac arrest – High rate of complicationsAcute Asthma Management ■ Hospital admission: life-threatening or near-fatal acute asthma ■ Oxygen therapy ■ SABA ■ Prednisolone 40-50mg >5 days ■ Ipratropium bromide (SAMA) ■ Magnesium sulphate ■ Aminophylline Oh S*** I Hate My Asthma ■ Mechanical ventilation Oxygen Salbutamol Ipratropium bromide Hydrocortisone / prednisolone Magnesium sulphate AminophyllineAcute Asthma F ollow-Up comfortably and consistently maintaining her SpO2 >94%.eeling better, is breathing What should we do now?Acute Asthma F ollow-Up ■ Identifying triggers ■ Inhaler use & technique ■ Optimising treatmentAcute Asthma F ollow-Up ■ Identifying triggers ■ Inhaler use & technique ■ Optimising treatment SBA A 16-year-old presents for an asthma review. She demonstrates her inhaler technique and does the following steps when administering her salbutamol: Removes cap and shakes the puffer. Breathes out gently. Puts the mouthpiece in her mouth and presses the canister when she breathes in and inhales deeply. Holds her breath for 20 seconds. She then repeats this process immediately for the next administration. Are there any issues with the technique? A. Her technique is sound and requires no changes B. She must wait at least 30 secs before administering her next dose C. She must wait at least 1 min before administering her next dose D. She must hold her breath for 10 secs after administering the medication E. She must hold her breath for 30 secs after administering the medication SBA A 16-year-old presents for an asthma review. She demonstrates her inhaler technique and does the following steps when administering her salbutamol: Removes cap and shakes the puffer. Breathes out gently. Puts the mouthpiece in her mouth and presses the canister when she breathes in and inhales deeply. Holds her breath for 20 seconds. She then repeats this process immediately for the next administration. Are there any issues with the technique? A. Her technique is sound and requires no changes B. She must wait at least 30 secs before administering her next dose C. She must wait at least 1 min before administering her next dose D. She must hold her breath for 10 secs after administering the medication E. She must hold her breath for 30 secs after administering the medication COPD Chronic Obstructive Pulmonary Disease Harish BavaCase - 67 year old A 67 year old man has come in with dyspnoea (SOB). What more would you like to know? What differentials do you have at this point in time?Dyspnoea History - PC/HPC ■ S - N/A ■ O - when did it start? When does it come on? Is it with activity? – If activity, important to identify their baseline ■ I.e. previously could walk 1km with no issues, now SOB after 100m ■ C - N/A ■ R - N/A ■ A - any associated wheeze, cough, fever, tight chest, fatigue etc. ■ T - when is it worse in the day? Is there diurnal variation? How has the SOB changed? Has it worsened? ■ E - Does anything make it better or worse? Have you noticed any speciﬁc triggers? ■ S - How bad is the dyspnoea? Does it stop you from doing day to day activities?Dyspnoea History - associated symptoms Infective - fever, N/V, productive cough, wheeze, chest tightness/pain, pleuritic chest pain, night sweats, sudden weight loss, haemoptysis cough, wheeze, chest tightness/pain, fatigue, ﬁnger clubbing, cachexia, central cyanosis, tachypnoea, headache, myalgia Neoplastic - weight loss, fatigue, night sweats, hoarseness, chest wall pain, pain in shoulder, enlarged lymph nodes Pulmonary embolism - tachycardia, dry cough, haemoptysis, pleuritic chest pain, current/recent DVT Cardiac - leg oedema, orthopnoea, ﬁnger clubbing Traumatic - wheeze, pleuritic chest pain, fainting, tachycardiaSBA A 59 year-old patient comes to the GP with dyspnoea and cough. Upon further questioning, she says she has lost 7kg of weight over the last 2 months. She wakes up very sweaty at night and feels generally quite fatigued during the day. She is unable to go to the shops and do her daily activities of living. She tells you she is an ex-smoker with a 20 pack-year history. What should you do? A - Discharge with oral antibiotics B - Urgent referral to the emergency department C - Discharge with nebulisers and referral to COPD clinic D - 2-week-wait referral for suspected lung cancer E - Referral for chest x-raySBA A 59 year-old patient comes to the GP with dyspnoea and cough. Upon further questioning, she says she haslost 7kg of weight over the last 2 months. She wakes up very sweaty at night and feels generally quite fatigued during the day. she is an ex-smoker with a 20 pack-year history. What should you do?ng. She tells you A - Discharge with oral antibiotics B - Urgent referral to the emergency department C - Discharge with nebulisers and referral to COPD clinic D - 2-week-wait referral for suspected lung cancer - this history shows a number of red ﬂags which are concerning of lung cancer E - Referral for chest x-rayDyspnoea History - RED FLAGS Important red ﬂags: ■ Sudden, unexplained weight loss ■ Fatigue ■ Night sweats ■ Haemoptysis - unexplained ■ Chest pain If a patient complains of these, you will need to consider an urgent 2-week-wait referral for urgent chest X-ray and further investigation.Dyspnoea History - other important questions PMH - previous asthma, HTN, HF, DVT, HIV, autoimmune conditions etc. Drug history - some medications can precipitate cough and ILD Family history - any history of lung, cardiovascular, autoimmune or malignancy Travel history - any travel to endemic countries of TB, or atypical pneumoniae Social history ■ Occupation - do they work around asbestos? Occupational asthma? Exposure to allergens? ■ Smoking history - incredibly important - how many per day? How long for? ■ Alcoholey tried to stop before? How many pack-years? ■ Housing - type of accommodation, stairs, mould/dust ■ Support/independence - do they have carers? Do they need any assistance with AoDLCase - 67 year old man Hx reveals: ■ Dyspnoea has been on/off for the last 6 months and has been getting ■ He has reduced exercise tolerance. He used to walk to the shops every day which is 2km away. He now becomes SOB after a few hundred meters and ﬁnds himself feeling quite wheezy ■ He has no signiﬁcant PMH or DH and has NKDA ■ He is a smoker of 40 years, smoking 1 pack a day ■ He is a social drinker, and lives at home with his wife in a 2 storey house, and is a retired accountant What is your top differential?What is COPD? ■ Chronic Obstructive Pulmonary Disease ■ One of the most commonly seen respiratory diseases, especially in older adults ■ It is a combination of chronic bronchitis and emphysema – This is caused by chronic irritation of the lung parenchyma leading to inﬂammation and structural lung damage – This results in airway narrowing (bronchitis) and reduced lung elasticity (emphysema)Epidemiology and Etiology ■ Typically affects adults >40, with prevalence increasing with age ■ Currently third most common cause of morbidity and mortality in the world ■ Most common cause and risk factor is Tobacco smoking - causing 70% of cases in high-income countries ■ Other causes include: – Environmental and occupational exposures: ■ Air pollution, coal, cotton, cement, grain – Alpha-1 antitrypsin deﬁciencyPathophysiology ■ Chronic inﬂammation affecting central and peripheral airways, lung parenchyma and alveoli, and pulmonary vasculature ■ There is repeated injury and repair leading to structural/physiological changes – This involves oxidative stress and protease-antiprotease imbalances ■ Emphysema is destruction of alveolar air sacs – Irritation from smoking recruits neutrophils and macrophages and other inﬂammatory mediators ■ Excess proteases leads to destruction of alveoli, typically centriacinar, sparing distal alveoli ■ Destruction of elastin leads to loss of elastic recoil and airway collapse during exhalation ■ Chronic bronchitis is a narrowing of the airways – Irritation leads to hypertrophy and hyperplasia of mucus-secreting cells (goblet cells) – Smoke also damages cilia and are ineffective at removing excess mucus – Leads to narrowing of airways causing difficulty breathingPathophysiology Alpha-1 antitrypsin deﬁciency ■ Most common cause of COPD in the young (<40) or non-smokingpopulation ■ An autosomal recessive condition located on chromosome 14 ■ presents with associated liver injury ■ Alpha-1 antitrypsin is a protease inhibitor produced by the liver with the role of protecting cells from enzymes such as neutrophil elastase that are released in response to infection in the lungs ■ Deﬁciency therefore leads to panacinar emphysema, frequently of the lower ■ Build up of misfolded enzyme leads to cirrhosis and increased risk of hepatocellular carcinomaCase - 67 year old man O/E: ■ General inspection: increased WOB, coughing, accessory muscle use, pursed-lip breathing, nasal ﬂaring ■ Tar staining on hands ■ Reduced chest expansion, dynamic hyperinﬂation (barrel chest) ■ Hyper-resonance to percussion ■ Bilateral wheeze on auscultation What else might you ﬁnd on examination?Examination ﬁndings General inspection ■ Increased WOB ■ Cough - productive - due to excess mucus production ■ Accessory muscle use, tripod position - sign of respiratory distress, to inhale as much air as possible ■ Cyanosis - due to hypoxia ■ Flushed/pallor - in severe COPD due to cor pulmonale ■ Nasal ﬂaring - to increase volume of inhaled air ■ Pursed lip breathing – Slows down expiration to produce a small amount of positive end-expiratory pressure (PEEP) – This prolonged expiration to allow increased CO2 clearance by supporting patency of airways and alveoli and increasing surface area for gas exchangeExamination ﬁndings Hands ■ Tar staining - indicates smoking use ■ Peripheral cyanosis - hypoxia ■ Clubbing ■ Asterixis – CO2 retention – Negative myoclonus caused by toxicity at diencephalic motor centres in brain which are responsible for regulating innervation of muscles that are responsible for maintaining position ■ Temperature - cool suggesting poor perfusion ■ Pulses – Bounding pulse associated with CO2 retention – Measure RR whilst feeling pulses ■ Tachypnoea >20 /minExamination ﬁndings Face and Neck ■ Central cyanosis in mouth - hypoxaemia ■ Oral candidiasis - inhaled corticosteroid use ■ Raised JVP - severe COPD causing cor pulmonale Chest ■ Dynamic hyperinﬂation of the chest - barrel chest ■ Reduced chest expansionExamination ﬁndings Percussion and auscultation ■ Hyper-resonance to percussion – Due to hyperinﬂation of the chest because of emphysema and air trapping due to incomplete expiration ■ Wheezing – Airway inﬂammation and resistance on expiration ■ Dullness/crackles – Hyper secretion of mucus – Infective exacerbationsInvestigations 1st line: ■ Spirometry ■ CXR ■ Pulse oximetry ■ FBCSBA Our 67 year old patient undergoes spirometry. Which of the following best represents his likely results? A. FEV1/FVC = 0.82, FEV1 = 90% of predicted B. FEV1/FVC = 0.75, FEV1 = 80% of predicted C. FEV1/FVC = 0.53, FEV1 = 75% of predicted D. FEV1/FVC = 0.94, FEV1 = 90% of predictedSBA Our 67 year old patient undergoes spirometry with bronchodilator reversibility testing. Which of the following post-bronchodilator spirometry results is most applicable to our patient? A. FEV1/FVC = 0.82, FEV1 = 90% of predicted B. FEV1/FVC = 0.75, FEV1 = 80% of predicted C. FEV1/FVC = 0.53, FEV1 = 75% of predicted - a FEV1/FVC ratio of <0.7 post bronchodilator is diagnostic for COPD D. FEV1/FVC = 0.94, FEV1 = 90% of predictedInvestigations Spirometry ■ Obstructive picture: – FEV1/FVC ratio <0.7 – FEV1 is signiﬁcantly more reduced than FVC ■ Restrictive picture – FEV1/FVC >/= 0/7 – FVC is signiﬁcantly more reduced than FEV1 ■ COPD: – Post bronchodilator FEV1/FVC <0.7 is diagnostic – The FEV1 of predicted is very useful for staging and severity of disease – May also see a decreased DLCO (diffusing capacity of the lungs for carbon monoxide) ■ Signiﬁes impaired gas exchange due to emphysema Investigations Spirometry Post-bronchodilator FEV1/FVC FEV1 of predicted Severity <0.7 >80% Stage 1 - Mild - patient should be symptomatic for diagnosis <0.7 50-79% Stage 2 - Moderate <0.7 30-49% Stage 3 - Severe <0.7 <30% Stage 4 - Very severeInvestigations Chest X-ray ■ Will show hyperinﬂation of the chest – Flattened hemidiaphragms (red arrows) ■ Will see bullae (white arrows) – Air-ﬁlled spaces in lungs due to emphysema ■ Rule out lung cancer!Investigations Pulse oximetry ■ Reduced due to hypoxemia FBC ■ Exclude secondary polycythaemia – Chronic hypoxemia can trigger increased EPO production leading to increased RBCOther Investigations ■ Exercise testing – To determine new baseline and can direct management ■ Alpha-1 antitrypsin level – Important to rule out ■ Sleep study – COPD can commonly cause sleep apnea ■ ECG/echo – COPD risk factors similar to ischaemic heart disease so important to monitor – Check for cor pulmonale ■ ABG – Used more in acute exacerbations – To monitor levels of hypercapniaHypercapnia in COPD ■ The majority of people rely on a hypercapnic drive to drive respiration: – High CO2 levels drives an increase in respiratory rate to expel more CO2 ■ Due to emphysema, airway narrowing and a reduced ventilatory capacity, COPD patients retain more CO2 – Over time, this leads to hypercapnia and a respiratory acidosis – As time passes, COPD patients lose their hypercapnic drive and become “CO2 retainers”Hypercapnia in COPD ■ Instead, they rely on a hypoxic drive – Chemoreceptors in the aortic arch and carotid bodies detect changes in the O2 level in the blood – This drives an increase in respiratory rate and increased depth of ventilation – When given supplemental oxygen, the chemoreceptors detect a rise in O2 levels, therefore diminishing respiratory effort, leading to a build of CO2 and a respiratory acidosis ■ You can determine this by ABG – Shows hypercapnia – If increased HCO3-, shows metabolic compensation→ CO2 retainer – If normal HCO3-, shows no compensation → not a retainer ■ This is because it takes a while for the body to adaptCase - 67 year old man ■ Investigations show a FEV1/FVC ratio <0.7 ■ CXR shows hyperinﬂation of the chest How do we manage this patient?SBA Your patient has been newly diagnosed with COPD. What management options beneﬁcial to reduce disease progression and risk of complications.e very A - Salbutamol inhalers and vaccinations B - Corticosteroid therapy and smoking cessation C - Smoking cessation, vaccinations and pulmonary rehabilitation D - Smoking cessation and prophylactic antibioticsSBA Your patient has been newly diagnosed with COPD. What management options beneﬁcial to reduce disease progression and risk of complications.e very A - Salbutamol inhalers and vaccinations B - Corticosteroid therapy and smoking cessation C - Smoking cessation, vaccinations and pulmonary rehabilitation D - Smoking cessation and prophylactic antibioticsStable Management Conservative management ■ Smoking cessation advice – The most important to reduce risk of progression – Offering NRT, varenicline or bupropion ■ Annual inﬂuenza vaccination and one-off pneumococcal vaccination to reduce risk of infections ■ Pulmonary rehabilitation – For functionally disabled – Involves exercises in a group to improve ventilationStable Management Medical management ■ SABA or SAMA is ﬁrst-line ■ Check for asthmatic/steroid responsive features – Previous asthma or atopy – High eosinophil count – Substantial diurnal variation in PEF – Substantial variation in FEV1 over timeStable Management Medical management ■ No asthmatic features/steroid responsiveness – ADD LABA + LAMA ■ Switch SAMA to SABA if necessary ■ Asthmatic features/steroid responsiveness – ADD LABA + ICS – If breathlessness remains → TRIPLE THERAPY ■ LAMA + LABA + ICS – Switch SAMA to SABA if necessaryStable Management Medical management ■ Oral theophylline – After trials of bronchodilators ■ Oral prophylactic antibiotic therapy – Azithromycin is used as prophylaxis in selected patients ■ Patients must not smoke, have optimised standard treatments, continue to have exacerbations ■ Must exclude QT prolongationStable Management Medical management ■ Standby short course of oral corticosteroids and antibiotics – If recent exacerbation in last year – Counselled and understands medications including risks/beneﬁts – Well safety-netted ■ Phosphodiesterase-4 (PDE-4) inhibitors – E.g. Roﬂumilast to reduce risk of exacerbationsCase - 67 year old man Our patient returns 6 months later with an increase in dyspnoea, cough and wheeze. He is BIBA with increased sputum production and also seems slightly confused. What is happening here and what do you want to do ﬁrst?Case - 67 year old man Our patient returns 6 months later with an increase in dyspnoea, cough and confused.e is BIBA with increased sputum production and also seems slightly He is having an acute exacerbation of COPD. This is one of the most common reasons why people present to hospital in developed countries. First step is always A-E examination.Case - 67 year old man A-E examination: R - responds to voice A - patent airway, some sputum seen in mouth which is suctioned B - increased WOB, accessory muscle use, reduced chest expansion, dullness to percussion, bilateral wheeze and crackles heard at right lower zone. O2 sats: 84% RR: 34 /min C - Sweating, CRT 3s, dry mucous membranes. HR: 120/min, BP: 85/45 D - Responds to Voice, PEARL, CBG: 5.2 E - no DVT, no oedema How should you acutely manage this patient?SBA What should be your ﬁrst step in the management of this patient? A - Call ITU and get a bed ready B - Chest X-ray C - Give a ﬂuid bolus of 1L normal saline D - Give a ﬂuid bolus of 500ml normal saline E - Start supplemental oxygenSBA What should be your ﬁrst step in the management of this patient? becomes more stablet a bed ready - you may want to do this after the patient B - Chest X-ray - though valuable, not the ﬁrst step C - Give a ﬂuid bolus of 1L normal saline - this is not a bolus D - Give a ﬂuid bolus of 500ml normal saline - this is an important step but you must treat the hypoxia ﬁrst E - Start supplemental oxygen -correct! This is your ﬁrst step as hypoxia kills ﬁrstCase - 67 year old man 1. Breathing a. Oxygen. 15L NRB mask with targets of 94-98% i. Guidance varies on this, and always follow your trust guidelines/ask for immediate senior support ii. When you are unsure of whether a patient is a CO2 retainer or not, start the patient on high-ﬂow oxygen, HYPOXIA KILLS! iii. If you then conﬁrm that the patient is hypercapnic/is a CO2 retainer, reduce O2 to 4l/min via 28% venturi mask with targets of 88-92% b. Bronchodilator therapy i. You can hear a wheeze ii. Start nebulised salbutamol and ipratropium bromide (SABA and SAMA) c. Antibiotic therapy i. You can hear crackles ii. Start antibiotic therapy with amoxicillin or clarithromycin or 2. Circulationycycline a. They are hypotensive - give a ﬂuid bolus b. You are seeing signs of sepsis - START SEPSIS 6 c. CALL FOR HELP! - you may even do this before!Acute exacerbation of COPD Most common infective causes: ■ Bacteria – Haemophilus inﬂuenzae (most common bacterial cause) – Streptococcus pneumoniae – Moraxella catarrhalis ■ Respiratory viruses – Account for 30% of exacerbations – Human rhinovirus is most important pathogenAcute exacerbation of COPD ■ Patients present with increased symptoms, sputum production, hypoxia and confusion ■ Management without admission: – Increased frequency of bronchodilator therapy - consider nebuliser – Oral prednisolone 30mg daily for 5 days – Common practice to give oral antibiotics ■ Amoxicillin OR ■ Clarithromycin OR ■ DoxycyclineAcute exacerbation of COPD Admission criteria ■ Severe breathlessness ■ Acute confusion or impaired consciousness ■ Cyanosis ■ O2 sats <90% ■ Social reasons e.g. living alone ■ Signiﬁcant comorbidity e.g. cardiac diseaseAcute exacerbation of COPD Management in secondary care ■ Oxygen therapy ■ Nebulised salbutamol and ipratropium bromide ■ Steroid therapy – IV hydrocortisone 100mg may be used instead ■ IV theophylline – With senior support if not responding to nebulised bronchodilators ■ NIV using BiPaP (better for removal of CO2) – If type 2 respiratory failure develops – Respiratory acidosis of pH 7.25-7.35 ■ <7.25 would require HDU or ITU admission and has lower threshold for intubation and ventilationComplications ■ Cor pulmonale - right sided heart failure – Increased pressure causes pulmonary hypertension which increases strain on right side of heart – Symptoms: raised JVP, hepatomegaly, loud P2, peripheral oedema – Treat with furosemide to reduce oedema and optimise COPD treatment, consider long-term oxygen therapy ■ Lung cancer – COPD is a risk factor for lung cancer ■ Depression – Common consequence of COPD – May need psychiatric evaluation ■ Recurrent pneumonia ■ PneumothoraxLong T erm Oxygen Therapy ■ Patients on LTOT will be breathing supplemental oxygen forat least 15 hours a day ■ Patients are assessed for LTOT if they have: – Very severe airﬂow obstruction (FEV1 <30%) – Cyanosis – Polycythaemia – Peripheral oedema – Raised JVP – Oxygen sats =< 92% ■ Must NOT be offered to patients who continue to smoke despite being offered smoking cessation advice, treatment and referral to specialist smoking cessation servicesLong T erm Oxygen Therapy ■ Assessment is done by looking at 2 ABGs at least 3 weeks apart. Patients must be stable on optimal management ■ Criteria for LTOT – pO2 < 7.3 kPa OR – pO2 7.3-8 kPa AND one of: ■ Secondary polycythaemia ■ Peripheral oedema ■ Pulmonary hypertension ■ A risk assessment should be carried out for: – Falls from tripping over equipment – Burns and ﬁres - especially if there is someone at home who smokes (including e-cigarettes) THANKS FOR W ATCHING! TTutor 2: Harish Bava Please ﬁll out the feedback form on Medall and see you next week!