Respiratory III (COPD; Acute asthma)

Question 2

Define COPD [1]

Answer 2

Chronic obstructive pulmonary disease (COPD) involves a long-term, progressive condition involving airway obstruction, chronic bronchitis and emphysema. It is almost always the result of smoking and is largely preventable.While it is not reversible, it is treatable.

Question 3

Define chronic bronchitis [1] and emphysema [1]

Answer 3

Chronic Bronchitis- the presence of chronic productive cough and sputum for at least 3 months in each of two successive years

Emphysema involves damage and dilatation of the alveolar sacs and alveoli,

Question 4

Describe the typical presentation of a COPD patient

Answer 4

A typical presentation of COPD is a long-term smoker with persistent symptoms of:

• Shortness of breath
• Cough
• Sputum production
• Wheeze
• Recurrent respiratory infections, particularly in winter
• Barrel chested

Question 5

Which symptoms does COPD not cause? [4]

Answer 5

Clubbing
Chest pain
Haemoptysis
Chest pain

If have these, investigate other diseases

Question 6

Describe the pathophysiology of COPD [5]

Answer 6

Inflammation
- Inhalation of noxious particles or gases, such as cigarette smoke or occupational irritants, triggers an inflammatory response in the airways and lung parenchyma.
- Causes infiltration of neutrophils, macrophages, and lymphocytes, leading to the release of pro-inflammatory cytokines and chemokines.

Protease-Antiprotease Imbalance
- Causes an imbalance between proteases (e.g., neutrophil elastase, matrix metalloproteinases) and antiproteases (e.g., alpha-1 antitrypsin, tissue inhibitors of metalloproteinases)
- The excess protease activity degrades extracellular matrix components, leading to the destruction of lung parenchyma and the development of emphysema.

Oxidative Stress:
- Toxins induce ROS
- ROS causes direct cellular damage, impair antiprotease activity, and promote inflammation

Airway Remodeling
- thickening of the airway wall
- increased mucus production
- goblet cell hyperplasia

Alveolar Destruction
- destruction of alveolar walls, leading to the formation of larger, less efficient airspaces and a reduction in the surface area available for gas exchange.

Question 7

Explain genetic disorder can lead to early onset COPD? [1]

Answer 7

Alpha-1 antitrypsin deficiency:
- reduced inhibition of neutrophil elastase, leading to uncontrolled protease activity and lung tissue destruction

Question 8

What are the 5 grades of the MRC dyspnoea scale? [5]

Answer 8

• Grade 1: Breathless on strenuous exercise
• Grade 2: Breathless on walking uphill
• Grade 3:Breathlessness that slows walking on the flat
• Grade 4: Breathlessness stops them from walking more than 100 meters on the flat
• Grade 5: Unable to leave the house due to breathlessness

mMRC ≥2

Question 9

What investigations would you conduct for COPD? [7]

Answer 9

Spirometry:
- FEV1/FVC < 70%

Pulse ox:
- low oxygen saturation
- In patients with chronic disease, an oxygen saturation of 88% to 90% may be acceptable.

CXR:
- hyperinflation
- bullae
- flat hemidiaphragm

COPD Assessment Test (CAT) or Modified British Medical Research Council (mMRC)
- mMRC ≥2 or CAT score ≥10 indicates higher symptoms burden

FBC
- polycythaemia (raised haemoglobin due to chronic hypoxia),
- anaemia
- infection & WBC count

BMI:
- weight loss occurs in severe disease

Serum alpha-1 antitrypsin
- look for alpha-1 antitrypsin deficiency

Question 10

What are common ECG changes might you see in COPD patients? [4]

Answer 10

• Rightward deviation of the P wave and QRS axis
• Low voltage QRS complexes, especially in the left precordial leads (V4-6)
• With development of cor pulmonale, right atrial enlargement (P pulmonale) and right ventricular hypertrophy
• Arrhythmias including multifocal atrial tachycardia

Question 11

State how the different severity scores for COPD are calculated [4]

Answer 11

The severity can be graded using the forced expiratory volume in 1 second (FEV1):

Stage 1 (mild):
- FEV1 more than 80% of predicted

Stage 2 (moderate):
- FEV1 50-79% of predicted

Stage 3 (severe):
- FEV1 30-49% of predicted

Stage 4 (very severe):
- FEV1 less than 30% of predicted

If the FEV1 is greater than 80% predicted but the post-bronchodilator FEV1/FVC is < 0.7 then this is classified as Stage 1 - mild. Symptoms should be present to diagnose COPD in these patients

Question 12

Describe the stepwise approach to treating COPD

Answer 12

First line treatment:
- SABA (salbutamol) or SAMA (e.g ipratropium bromide)

The next stage depends on whether the patient has asthmatic features / features suggesting steroid responsiveness

If NONE: use a combination:
- Add LABA AND LAMA regularly

If ASTHMATIC features:
- Add LABA & ICS regularly

Next stage for both:
- Use LABA AND LAMA AND ICS

Question 13

What are the determinants that decide if COPD is asthmatic or steroid responsive? [4]

Answer 13

• Previous diagnosis of asthma or atopy
• Variation in FEV1 of more than 400mls
• Diurnal variability in peak flow of more than 20%
• Raised blood eosinophil count

Question 14

Label A-E

Answer 14

Question 15

When is oral theophylline indicated for COPD treatment? [1]

Answer 15

NICE only recommends theophylline after trials of short and long-acting bronchodilators or to people who cannot used inhaled therapy

Question 16

Polypharmacy of which drug classes with oral theophylline would cause the dose of theophylline to decrease [2]

Answer 16

the dose should be reduced if macrolide or fluoroquinolone antibiotics are co-prescribed

Question 17

Which antibiotic is given as oral prophylactic antibiotic therapy in some COPD patients? [1]

Answer 17

azithromycin prophylaxis is recommended in select patients

Question 18

Explain which further tests would you need to conduct if giving azithromycin prophylaxis? [4]

Answer 18

ECG:
- can cause QT prolongation

LFTs:
- Can cause liver injury

CT scan:
- to exclude bronchiectasis

Sputum culture:
- exclude atypical infections and tuberculosis

Question 19

Name a long-term risk of azithromycin use [1]

Answer 19

Long-term azithromycin use is associated with clinically significant hearing loss

Question 20

What need to consider before prescribig azithromycin in COPD patients? [1]

Answer 20

. Little evidence of treatment benefit is seen in
current smokers

Question 21

When are mucolytics indicated in COPD patients? [1]

Answer 21

Consider if have a chronic productive cough

Question 22

Name an example and describe the MoA of phosphodiesterase-4 (PDE-4) inhibitors in COPD

Answer 22

roflumilast:
- antiinflammatory and immunomodulatory effects in the pulmonary system due to increased levels of intracellular cyclic AMP

Question 23

When are roflumilast / PDE-4 inhibitors indicated in COPD treatment? [2]

Answer 23

FEV1 < 50%
AND
Ptx has two or more exacerbations in previous twelve months despitre triple therapy (LAMA; LABA & ICS)

Question 24

A 62-year-old man presents to his general practitioner (GP) with symptoms of exertional breathlessness, wheeze and cough. He has a 30 pack-year smoking history.

As part of the patient’s work-up, spirometry is requested:

FEV1/FVC ratio 0.61

Given the likely diagnosis, which of the following would be an appropriate first-line treatment?

Ipratropium

Formoterol

Salmeterol

Tiotropium

Beclometasone

Answer 24

Ipratropium

SAMA or SABA is first line COPD

Question 25

Describe what is meant by the term cor pulmonale [2]

Answer 25

**RIght-sided heart failure caused by respiratory disease:** - The **increased pressure** and **resistance in the pulmonary arteries** (pulmonary hypertension) **limits** the **right** **ventricle** **pumping blood** into the **pulmonary** **arteries**. - This causes **back-pressure** into the **right atrium, vena cava and systemic venous system**.

Question 26

What are the most common causes of cor pulmonale? [5]

Answer 26

**COPD** (the most common cause) **Pulmonary embolism** **Interstitial lung disease** **Cystic fibrosis** **Primary pulmonary hypertension**

Question 27

State 6 examination findings of cor pulmonale [6]

Answer 27

* **Hypoxia** * **Cyanosis** * **Raised JVP** * **Peripheral oedema** * **Loud second heart sound** * **systolic parasternal heave** * **Hepatomegaly** due to back pressure in the hepatic vein (pulsatile in tricuspid regurgitation)

Question 28

Describe how you treat cor pulmonale? [2] Which drugs are not recommended? [3]

Answer 28

**Loop diuretics** for oedema **LTOT** **ACE-inhibitors, calcium channel blockers and alpha blockers** are not recommended by NICE

Question 29

Explain the physiological reasons of what can happen to CO2 levels when treated with oxygen in COPD patients? [2]

Answer 29

**Many patients retain CO2 when treated with oxygen (oxygen induced hypercapnia)** Due to: **Increased V/Q mismatch** (most important) - COPD ptx optimise **gas** **exchange** by **hypoxic vasoconstriction** leading to altered **Va/Q ratios** - **Excessive oxygen administration overcomes** this, leading to **increased blood flow to poorly ventilated alveoli**, and **thus increased Va/Q mismatch and increased physiological deadspace** **The Haldane effect**: - **deoxygenated Hb** binds **CO2** with **greater affinity** than **oxygenated Hb** - Thus: **oxygen** induces a **rightward shift of the CO2 dissociation curve** (Haldane effect)

Question 30

When should you assess patients for LTOT in COPD patients? [5] How often do you assess ABGs when deciding LTOT? [2]

Answer 30

* very severe airflow obstruction: **FEV1 < 30% predicted** * **cyanosis** * **polycythaemia** * **peripheral oedema** * **raised jugular venous pressure** * **oxygen saturations less than or equal to 92% on room air** **Assessment** is done by **measuring arterial blood gases on 2 occasions at least 3 weeks apart** in patients with stable COPD on optimal management.

Question 31

What pO2 level is LTOT therapy given to COPD without any other factors? [1] What pO2 levels [1] and other conditions [3] mean that LTOT is given to COPD factors?

Answer 31

Offer LTOT to patients with a **pO2 of < 7.3 kPa** OR To those with a **pO2 of 7.3 - 8 kPa** and one of the following: * **secondary polycythaemia** * **peripheral oedema** * **pulmonary hypertension**

Question 32

What's the rule with LTOT and smoking in COPD patients? [1]

Answer 32

**do not offer LTOT** to people **who continue to smoke** despite being offered smoking cessation advice and treatment, and referral to specialist stop smoking services **(fire risks)**

Question 33

Which of the following is not an indication for long-term oxygen therapy (LTOT) in patients with stable chronic obstructive pulmonary disease (COPD)? PaO2 = 7.3-8.0 kPa with secondary polycythaemia PaO2 = 7.3-8.0 kPa with anaemia PaO2 = 7.3-8.0 kPa with pulmonary hypertension PaO2 < 7.3 kPa PaO2 = 7.3-8.0 kPa with peripheral oedema

Answer 33

**PaO2 = 7.3-8.0 kPa with anaemia** NICE recommends that LTOT should be considered in patients with stable COPD who do not smoke and are on optimal medical therapy in the following circumstances: PaO2 < 7.3 kPa PaO2 7.3-8.0 kPa with secondary polycythaemia PaO2 7.3-8.0 kPa with peripheral oedema PaO2 7.3-8.0 kPa with pulmonary hypertension (eg. loud P2, RVH on ECG)

Question 34

What indicates COPD patients to start LTOT? [1]

Answer 34

LTOT if **2 measurements of pO2 < 7.3 kPa**

Question 35

A patient presents with COPD. They are currently on a SAMA but are having worsening symptoms. They show no signs of asthmatic involvement / eosinophilic involvement. What is the next step in their treatment? [1]

Answer 35

COPD: **Discontinue SAMA** (**switch** to **SABA**) **if commencing LAMA**

Question 36

What are three most common symptoms of worsening / acute exacerbation of COPD? [3]

Answer 36

Most commonly increasing **dyspnoea**, **sputum volume** and **sputum purulence.**

Question 37

Which bacterial [3] and viral infections [3] most commonly cause acute exacerbations of COPD?

Answer 37

**Bacterial infections:** - **Haemophilus influenzae** - **Moraxella** **catarrhalis**, - **Streptococcus pneumoniae** **Viral infections:** * **Rhinovirus** * **influenzae** * **respiratory syncytial virus**

Question 38

Describe the pathophysiological changes that occur in acute exacerbations of COPD [5]

Answer 38

* **Increased inflammation, mucosal oedema and bronchospasm** further **limit expiratory flow** * **Gas trapping worsens**, increasing **ventilation-perfusion mismatch** * The resulting **hypoxia** and **hypercapnia** **trigger** the **neural drive to increase ventilation** * **Respiratory muscles fatigue**, leading to a '**neuromechanical decoupling**' that **reduces the ventilatory drive** * **Existing cardiac dysfunction worsens** due to **increasing pulmonary vascular resistance**

Question 39

Describe in detail the signs of acute exacerbations of COPD? [4]

Answer 39

**Increased respiratory effort**: - tachypnoea - nasal flaring - use of accessory muscles - paradoxical chest wall movement **Tachycardia** (anxiety; hypoxia; increased resp effort) **Worsening airway obstruction on ascultation**" - Reduced breath sounds - Prolongation of the expiratory phase with wheezing - Crackles which could indicate an infective component **Indicators of hypoxia**: - New or worsening central cyanosis - Asterixis - Altered mentation e.g. confusion, drowsiness

Question 40

Describe which investigations do NICE recommend for all patients admitted with COPD acute exacerbations of COPD? [5]

Answer 40

**Blood tests to establish a baseline:** * Full blood count * Urea and electrolytes * Theophylline levels if the patient is on it **Serial arterial blood gases (ABGs) to monitor for the development of Type 2 respiratory failure** * A PaO2 of < 7 kPa and a pH level of < 7.35 are indications that the patient should continue to be managed in hospital **Chest X-ray** * overt changes such as opacification and oedema should prompt a reconsideration of the diagnosis **ECG** * helps to exclude acute ischaemia and/or comorbid cardiac dysfunction **Microbiological investigations:** * Sputum sample for microscopy and culture if sputum purulent * Blood cultures if pyrexia present

Question 41

What are the three key differential diagnoses for acute exacerbations of COPD? [3] Describe the findings that would indicate the differentials as opposed to COPD

Answer 41

**Pneumonia:** - Bronchial breathing - Increased VR - Opacification on CXR **PE** - Dysopnea and hypoxia predominate - Lower limb VTE **Pulmonary oedema** (due to MI or acute-on-chronic HF) - Frothy sputum - CXR: alveolar and intersitial oedema

Question 42

Treatment of acute exacerbations of COPD:

Answer 42

1 **Supplemental oxygen** titrated to achieve target saturations of **88-92%** 2 **Repeat ABG** measurements every 30-60 mins 3 **Pharmacological managment:** - **SABA** &/or **SAMA** initially via **inhaler or nebuliser** - **LABA**, **LAMA** & **ICS** continued - **5-day** course of **oral prednisolone** - **IV theophylline** if response inadequate - **Abx** (if evidence of infection) 4 Patients with persistent hypercapnia and respiratory acidosis despite optimal medical management need to be started on **NIV** 5 Escalate to **invasive mechanical ventilation**

Question 43

State three ways in which supplemental oxygen can be given in treatment of acute excaerbation of COPD [3]

Answer 43

A **24% Venturi** mask at **2-3 L/min** A **28% Venturi** mask at **4 L/min** **Nasal cannulae** at **1-2 L/min**

Question 44

BTS recommends that NIV is indicated if WHICH features are present 60 minutes after optimal supplemental oxygen and bronchodilation have been given in COPD? [3]

Answer 44

BTS recommends that NIV is indicated if the following features are present 60 minutes after optimal supplemental oxygen and bronchodilation have been given: Acidosis - **pH < 7.35** Hypercapnia - **pCO2 > 6.5** Respiratory rate **> 23**

Question 45

Which Abx [3] are commonly used in treating acute exacerbations of COPD and why [2]?

Answer 45

penicillin e.g. **amoxicillin** macrolides e.g. **clarithromycin** tetracyclines e.g. **doxycyclin** Due to their effectiveness against **Haemophilus influenzae** and **Streptococcus pneumoniae**

Question 46

# Acute exacerbation of COPD Which features of a decompensating a patient would indicate moivng to invasive mechanical ventilation? [5]

Answer 46

* **Imminent respiratory arrest** * **Severe respiratory distress** * **Failure of NIV** - persistent acidosis (pH < 7.25) and tachypnoea (RR > 35) * **Persistent or worsening acidosis** (pH < 7.15) * **Depressed consciousness** (GCS < 8)

Question 47

A 73-year-old man presents to the emergency department with a 3-day history of increased dyspnoea and cough. He has a past medical history of severe COPD and uses a Trimbow inhaler daily. He is admitted and treated for an acute exacerbation with prednisolone 30 mg daily for 5 days and nebulisers. This is his fourth exacerbation in the past 3 months. What option is most appropriate to reduce the risk of future exacerbations? Amoxicillin Carbocisteine Doxycycline Long-term oxygen therapy Roflumilast

Answer 47

**Roflumilast** **Oral PDE-4 inhibitors** such as roflumilast reduce the risk of COPD exacerbations in patients with severe COPD and a history of frequent COPD exacerbations

Question 48

When is NIV indicated in acute exacerbations of COPD? [1]

Answer 48

NIV should be considered in all patients with an acute exacerbation of COPD in whom a **respiratory acidosis (PaCO2>6kPa, pH < 7.35 ≥7.26) persists despite immediate maximum standard medical treatment**

Question 49

When are O2 sats targets in COPD patients: 88-92% and 94-98%? [2]

Answer 49

**pCO2 is known to be normal** the target oxygen saturations should be **94-98%.** **pCO2 is known to be high** the target oxygen saturations should be **88-92%.**

Question 50

What are the presenting features of an acute exacerbation of asthma? [5]

Answer 50

* Progressively shortness of breath * Use of accessory muscles * Raised respiratory rate (tachypnoea) * Symmetrical expiratory wheeze on auscultation * The chest can sound “tight” on auscultation, with reduced air entry throughout

Question 51

Describe what is meant by brittle asthma [2]

Answer 51

***Type 1**: - **wide PEF variability** (>40% diurnal variation for >50% of the time over a period >150 days) **despite intense therapy** ***Type 2**: - **sudden** **severe** **attacks** on a background of **apparentlywell-controlled asthma**

Question 52

Describe what is meant by moderate exacerbation of asthma [6]

Answer 52

* Increasing symptoms * Speech normal * PEF >50-75% best or predicted * No features of acute severe asthma * RR < 25 / min * Pulse < 110 bpm

Question 53

What is a pneumonic for life-threatening exacerbation of asthma?

Answer 53

33-92 CHEST: - PEF **< 33%** - sats **< 92%** - **C**yanosis or **c**onfusion - **H**ypotension - **E**xhaustion - **S**ilent chest - **Tachy or bradychardia**

Question 54

Describe what is meant by an acute severe exacerbation of asthma [4]

Answer 54

Any one of: * **PEF 33-50%** best or predicted * respiratory rate **>25/min** * HR **> 110bpm** * inability to complete sentences in one breath | Admit – if persisting symptoms

Question 55

Describe what is meant by a near fatal exacerbation of asthma [1]

Answer 55

**Raised PaCO₂ (>6kPa)** and/or **need for mechanical ventilation.** *It typically correlates with an FEV1 around 20% of predicted or less.*

Question 56

What PEF can you discharge if other needs are met? [1] State some reasons why might not be discharged [5]

Answer 56

**> 75% after 1hr**

Question 57

# D Describe the treament algorithm / management plan for acute asthma

Answer 57

**ABC** **Oxygen**: - High flow - Aim sats >92 **IV fluids** **Reassess** - Every 15mins with PEFR **Therapys**: **O**xygen **S**albutamol **H**ydrocortisone/Prednisolone **I**pratropium bromide **T**heophylline **!** Magnesium sulphate

Question 58

What dose salbutamol would you give? [1] How is it delivered? [1] How often? [1]

Answer 58

**2.5-5mg** every **10 minutes** **Nebulised with oxygen**

Question 59

Which ICS would you give in acute asthma? [2] What dose? [2] How is it delivered? [1] How often? [1]

Answer 59

**Hydrocortisone** -IV 100-200mg QDS **prednisolone** - PO 40mg OD

Question 60

# Acute asthma What dose ipratropium bromide would you give? [1] What is the MoA? [1] How is it delivered? [1] How often? [1]

Answer 60

**Ipratropium bromide** - Nebulised with oxygen - Muscarinic antagonist: Bronchodilator - 500 micrograms every 4-6 hours

Question 61

# Acute asthma What dose Magnesium sulphate would you give? [1] What is the MoA? [1] How is it delivered? [1] How often? [1]

Answer 61

**Magnesium sulphate** 1.2 – 2 grams over 20 minutes IV Bronchodilator

Question 62

What dose theophylline would you give? [1] What is the MoA? [1] How is it delivered? [1] How often? [1]

Answer 62

**Theophylline** **Inhibit phosphodiesterase** and **increase cAMP** – smooth muscle dilation Life-threatening Senior guidance

Question 63

What is the treatment plan for Mild asthma attacks? [5]

Answer 63

* Inhaled beta-2 agonists (e.g., salbutamol) via a spacer * Quadrupled dose of their inhaled corticosteroid (for up to 2 weeks) * Oral steroids (prednisolone) if the higher ICS is inadequate * Antibiotics only if there is convincing evidence of bacterial infection * Follow-up within 48 hours

Question 64

What is the treatment plan for moderate asthma attacks? [3]

Answer 64

* Consider hospital admission * **Nebulised beta-2 agonists** (e.g., salbutamol) * **Steroids** (e.g., oral prednisolone or IV hydrocortisone)

Question 65

What indications would be for intubation in life-threatening asthma? [5]

Answer 65

There are few indications apart from **coma** and **arrest**. However, findings such as **severe fatigue**, **cardiovascular compromise** and **pneumothorax** may be useful in decision making about mechanical ventilation

Question 66

Describe side effects of salbutamol tx [3]

Answer 66

Serum potassium needs monitoring with salbutamol treatment, which causes potassium to be absorbed from the blood into the cells, resulting in **hypokalaemia** - **tachycardia** (fast heart rate) - **lactic acidosis.**

Question 67

What might an ECG reveal when treating acute asthma? [1]

Answer 67

**Sinus tachycardia** (from Mg2+ and K)

Question 68

What is the follow up plan when discharing acute asthma exacerbations? [3]

Answer 68

o Follow up within 48 hrs o < 30 days post discharge by GP/nurse specialist o under specialist supervision indefinitely for near-fatal asthma and at least 1 yeat for severe asthma attack

Question 69

When a patient is presenting at hospital with acute asthma, how do you decide what ICS might be prescribed? [2]

Answer 69

All patients with **acute** asthma should receive **oral** **prednisolone** Only if **vomiting: give IV hydrocortisone**

Question 70

A 35-year-old lady with a history of asthma is brought to the Emergency Department with an acute asthma attack. She has previously been admitted to the intensive therapy unit (ITU) with the same problem. Treatment is commenced with high-flow oxygen and regular nebulisers. Which of the following is a feature of life-threatening asthma? Normal PaCO2 Peak expiratory flow rate < 50% of predicted or best Pulse rate 105 bpm Respiratory alkalosis Unable to complete full sentences

Answer 70

**Normal PaCO2**

Question 71

What indicates life-threatening asthma? [1] Why? [1]

Answer 71

**A normal PaCO2** in an acute asthma attack indicates exhaustion and should, therefore, be classified as life-threatening

Question 72

Explain why in acute asthma, a pH of < 7.35 is particularly alarming [1]

Answer 72

A pH less than **7.35 likely represents carbon dioxide retention** in a **tiring patient** and is an ominous sign in acute asthma.