How not to fail an Exam. Respiratory system

You have just taken a history of a middle aged patient who has a productive cough, wheezes with each breath and is breathless, may have chest pain on exertion. You have decided to present this case as a case of COPD. What questions do you expect to be asked?

What do you mean by COPD? What are the diseases included in the term COPD?

Some information that may help you answer well.

This term includes emphysema, chronic bronchitis and chronic obstructive asthma. It is a frequent cause of hospital and clinic visits and is one of the leading causes of mortality after putting the patient through much misery. COPD is preventable to a considerable degree and can be controlled to a considerable degree. Bronchiectasis is usually not included in COPD and needs to be excluded.

Why are these diseases grouped together as COPD?

All the diseases are grouped together as COPD  because they are characterized by persistent respiratory symptoms and airflow limitation (cough and/or breathlessness) that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases. Chronic airflow limitation  is caused by a mixture of small airways disease (eg, obstructive bronchiolitis) and parenchymal destruction (emphysema), the relative contributions of which vary from person to person. Chronic inflammation causes structural changes, small airways narrowing, and destruction of lung parenchyma. A loss of small airways may contribute to airflow limitation and mucociliary dysfunction, which is a characteristic feature of the disease. Remember Reid’s index.

To summarize this group includes damage to the lungs as follows:

  • small airway disease or bronchiolitis.
  • parenchymal loss or emphysema
  • chronic airway inflammation contributing to both of the above pathologies
  • exposure to gas, smoke or other noxious airborne particles.
  • mucociliary dysfunction.
  • based on the understanding of the above factors the diseases can be treated and prevented.

Which one of these do you think your patient has? You answer chronic bronchitis and the next question is why do you favor this diagnosis? Or define chronic bronchitis.

Chronic bronchitis is defined as a chronic productive cough for three months in each of two successive years in a patient in whom other causes of chronic cough (eg, bronchiectasis) have been excluded. It may precede or follow development of airflow limitation. This definition has been used in most studies on this disease and is WHO accepted. As the patient has productive cough and progressive breathlessness he is likely to fit into the chronic bronchitis diagnosis. I hope you remembered to ask about how many months the cough has persisted in the last 2 years,

What is the relationship between smoking and chronic bronchitis?

Smokers tend to develop this disease as early as 36 years of age and have more frequent exacerbations. Current and past smokers have increased airway mucin concentration (MUC5AC and MUC5B), compared with never smokers, this contributes to mucolytic dysfunction So remember that COPD can develop in non-smokers but is less severe and develops later and there are fewer exacerbations. These patients have been exposed to smoke from factories or wood fire or a noxious gas.

How can you objectively determine the severity of COPD? The short answer is by determining the FEV1/FVC ratio and counting the number of exacerbations each year with and without hospitalization.

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines.

In patients with FEV1/FVC <0.7:*
GOLD 1 Mild ≥80
GOLD 2 Moderate 50 to 79
GOLD 3 Severe 30 to 49
GOLD 4 Very severe <30
GOLD: Assessment of symptoms and risk of exacerbations
Exacerbation/hospitalizations Symptom assessment
mMRC 0 to 1; CAT <10Δ mMRC ≥2; CAT ≥10
0 or 1 exacerbations without hospitalization A B
≥2 exacerbations or ≥1 hospitalization C D

COPD: chronic obstructive pulmonary disease; FEV1: forced expiratory volume in one second; FVC: forced vital capacity; CAT: COPD Assessment Test; mMRC: modified Medical Research Council (mMRC) dyspnea scale.

Why doesn’t your patient have emphysema?
There is an overlap between emphysema and chronic bronchitis. Emphysema is a term which describes the pathology which causes structural changes leading to loss of lung tissue without its being replaced by fibrosis. These changes include abnormal and permanent enlargement of the airspaces distal to the terminal bronchioles that is accompanied by destruction of the airspace walls, without obvious fibrosis. When emphysema predominates the cough and expectoration are not prominent but dyspnea is a major feature. They tend not to have cyanosis hence are often called “pink puffers”
Is it important to detect clubbing to diagnose COPD?
Clubbing is not a feature of the diseases which comprise COPD. If clubbing is present then it is important to investigate for a lung malignancy.
Does this patient have pulmonary hypertension? To which group does his PH belong?
Here is some information to help you answer this question. The World Health Organization (WHO) classifies patients with pulmonary hypertension into five groups based upon etiology.
  • Group 1 are considered to have pulmonary arterial hypertension (PAH; also sometimes referred to as precapillary pulmonary hypertension).
  • Group 2 (due to left-sided heart disease).
  • Group 3 (due to lung disorders and hypoxemia).
  • Group 4 (due to pulmonary artery obstructions).
  • Group 5 (associated with different or mixed mechanisms).

How will you treat the PH?

Disease-specific therapies are assumed to result in improved alveolar hypoxia, which is thought to contribute to the pathogenesis of PH and to progression of pulmonary hypertension. While some strategies (eg, continuous positive airway pressure) modestly reduce pulmonary artery pressures (PAP), evidence to suggest significant reductions in PH or improved clinically impactful outcomes (eg, reduced mortality, improved exercise capacity, delayed progression) is lacking. For patients with high altitude PH, re-exposure to normal inspired oxygen tension is appropriate.

Why does this patient have exertional chest pain?
Answer: This patient has also developed pulmonary hypertension in which chest pain on exertion is a feature. He is also likely to have right heart failure or early cor pulmonale. I need to check for peripheral edema and other signs of fluid retention like ascites and pleural effusion although in early right heart failure an increase in the dyspnea on exertion and fatigue may be the only features.
Exertional chest pain (ie, angina) is usually due to subendocardial hypoperfusion caused by increased right ventricular wall stress and myocardial oxygen demand. However, it is occasionally caused by dynamic compression of the left main coronary artery by an enlarged pulmonary artery; this risk is greatest for patients with a pulmonary artery trunk at least 40 mm in diameter. I would like to request an echocardiogram to look particularly for the size of the root of the pulmonary artery and for the size of the right ventricle. 
Symptoms and signs of pulmonary hypertension (PH) may be difficult to recognize because they are nonspecific. PH may not be recognized for several years. Initially, patients present with exertional dyspnea and fatigue. Because PH is progressive, the presentation evolves over time so that patients may eventually develop the signs and symptoms of severe pulmonary hypertension with overt right ventricular failure (eg, exertional chest pain or syncope and congestion including peripheral edema, ascites, and pleural effusion).
What specific treatment will you give for PH?
This is a group 3 PH caused by the accompanying chronic bronchitis. There is no specific treatment and adequate management of the lung disease will take care of the PH. If there is fluid retention diuretics can be added and nitrates for the chest pain.
What auscultatory findings do you expect i a patient with PH when examining the heart?
I would expect to hear a prominent P wave which can be palpable or split if there is right bundle branch block. There may be a right sided 4th heart sound. The murmur of tricuspid regurgitation may be audible i.e. a holosystolic murmur.
What treatment will you prescribe for this patient? How will you manage this patient?
The patient’s prominent symptoms are productive cough and breathlessness and he appears to be in an acute exacerbation of the disease. The initial therapy is based on improving the air flow and reducing the bronchospasm.
Avalable choices: Beta agonists either short acting such as albuterol, salbutamol, or levalbuterol or long acting beta agonists (LABA) like salmeterol, formoterol, arformoterol, indacaterol, vilanterol, and olodaterol are useful.
The short acting beta agonists can be given as inhalers or in a nebuliser solution. They can be prescribed as “use when needed” or a fixed time dose. They need to be combined with a muscarinic agent like ipratropium bromide and inhaled steroids.
Risks of beta-agonist overuse are possible if an individual attempts to achieve maximal bronchodilation by using higher doses. These risks include tremor and reflex tachycardia due, in part, to peripheral arterial dilation. Hypokalemia can also occur in extreme cases and should be monitored in patients at risk. Oral beta-2 agonists are generally not prescribed because their incidence of side effects is particularly high.
Oral beta agonists are readily available and cheap. In a society where the patient cannot afford to buy the inhaled forms and does not have access to government funded medical care the oral forms may be life saving.
Long-acting muscarinic agents — The LAMAs (also known as long-acting anticholinergic medications) include tiotropium, aclidinium, umeclidinium, and glycopyrronium.
Combined bronchodilator therapy can be used in the inhaled form combining a beta agonist and a muscarinic agent ie. a LABA and a LAMA  instead of inhaled steroid.
Alternative choices. Occasional patients will prefer regular use of short-acting bronchodilators despite needing to use them several times a day to relieve symptoms. GOLD guidelines include theophylline as an inexpensive alternative to the above described long-acting inhaled bronchodilator therapy.
 

Alternative choices — For patients who have further COPD exacerbations despite regular use of a LAMA, the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines suggest regular treatment with one of these choices:

Both a LAMA and a long-acting beta agonist (LABA)

Both a LABA and an inhaled glucocorticoid (ICS)

Less preferred options include regular use of short-acting beta-agonist and/or short-acting muscarinic agent; a phosphodiesteras-4 inhibitor, or theophylline

Alternative choices — For patients who have further COPD exacerbations despite regular use of a LAMA, the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines suggest regular treatment with one of these choices:

Both a LAMA and a long-acting beta agonist (LABA)

Both a LABA and an inhaled glucocorticoid (ICS)

Less preferred options include regular use of short-acting beta-agonist and/or short-acting muscarinic agent; a phosphodiesteras-4 inhibitor, or theophylline.

Choose your therapy after assessing the patient’s financial capability.

Use of corticosteroids in COPD. The available data, suggest that inhaled glucocorticoids decrease exacerbations and modestly slow the progression of respiratory symptoms, but appear to have little impact on lung function and mortality. In COPD, inhaled glucocorticoids are used as part of a combined regimen, but should NOT be used as sole therapy for COPD. Oral glucocorticoid therapy. Systemic glucocorticoid therapy appears to have a small but beneficial effect in outpatients with exacerbations of COPD. Using a dose that is the equivalent of prednisone 40 mg per day for five days may be useful in an acute exacerbation of COPD. The patient may be treated in the OPD and not require hospitalization. So do not use inhaled steroid monotherapy but use inhaled steroids in combination with LABA and LAMA. Use oral therapy at the start of an acute episode. 

In the TRILOGY study, single-inhaler triple therapy with beclomethasone/formoterol/glycopyrrolate was compared to beclomethasone/formoterol in 1368 patients with severe-to-very severe COPD and increased exacerbation risk (TRILOGY). Triple therapy reduced exacerbation rates by 23 percent. 

How will you help clear up the secretions?

Secretion clearance. There is little evidence that routine thinning of secretions or increasing clearance induces clinical improvement in COPD. However, selected patients who have excessive secretions or an ineffective cough may benefit from techniques such as postural drainage, positive expiratory pressure therapy, forced expiratory technique, and flutter valve therapy. Using an expectorant or a cough suppressant agent is counterproductive so do not prescribe these medicines.

Will you use oxygen therapy?

Oxygen therapy. Many patients with stable severe COPD (especially GOLD Stage IV disease) have chronic hypoxemia. Long-term oxygen therapy (LTOT) should be prescribed for patients with chronic, severe hypoxemia at rest (arterial oxygen tension [PaO2] ≤55 mmHg or pulse oxygen saturation [SpO2] ≤88 percent), as LTOT has been shown to improve survival and quality of life in these patients.

What counselling will you give?

Stop smoking. Move out from the dusty environment that is causing the problem. Advise influenza and pneumococcal vaccination. Respiratory rehabilitation at a center with trained staff. There is no specific diet. Teach the patient the correct technique for using an inhaler.

When will you use antibiotics?

Viral and bacterial infections cause most exacerbations, whereas atypical bacteria are a relatively uncommon cause. The remaining 30 percent are due to environmental pollution, pulmonary embolism, or have an unknown etiology. Some COPD exacerbations of unknown etiology may be related to other medical conditions, such as myocardial ischemia, heart failure, aspiration, or pulmonary embolism.

I will use an appropriate antibiotic when the patient has an acute exacerbation as 70 % of acute exarcerbations are caused by respiratory infections whose cause are the bacteria given below.

Haemophilus influenzae 13 to 50 %
Moraxella catarrhalis 9 to 21 %
Streptococcus pneumoniae 7 to 26 %
Pseudomonas aeruginosa        1-13 %                    

How will you assess a patient with an acute exacerbation?

Initial assessment will include the following:

  • Assessment of pulse oxygen saturation
  • A chest radiograph to exclude pneumonia, pneumothorax, pulmonary edema, pleural effusion
  • Laboratory studies (eg, complete blood count and differential, serum electrolytes and glucose)
  • Arterial blood gas analysis, if acute or acute-on-chronic respiratory acidosis is suspected or if ventilatory support is anticipated.
  • ECG.
  • Troponin testing to exclude myocardial infarction.
  • Natriuretic peptide levels to check for heart failure.

Concern about acute-on-chronic hypercapnia might be prompted by a history of prior elevation in arterial tension of carbon dioxide (PaCO2), an elevated serum bicarbonate (perhaps reflecting compensation for chronic hypercapnia), or the presence of severe airflow obstruction eg, GOLD III or IV by checking the FEV1/FEV ratio.

Will you use antibiotics routinely in COPD?

Use of antibiotics in COPD.  To try to maximize the benefit of antibiotic therapy, many clinical practice guidelines recommend antibiotic therapy only for those patients who are most likely to have bacterial infection or are most ill.

In moderate or severe exacerbation of COPD, which is defined as having at least two of these three symptoms – increased dyspnea, increased sputum volume, or increased sputum purulence prescribe an antibiotic. Sputum culture and sputum Gram staining are of little use.

The initial antibiotic regimen should target likely bacterial pathogens (Haemophilus influenzaeMoraxella catarrhalis, and Streptococcus pneumoniae in most patients) and take into account local patterns of antibiotic resistance. In uncomplicated COPD use a macrolide like azithromycin or clarithromycin or use a third generation cephalosporin like ceforoxime or use doxycycline or trimethoprim/sulphamethoxazine. In more severe cases ie. if the patient has had a Pseudomonas infection in the past 1 year, has had frequent acute exacerbations in the past year or repeated hospital admission then get a sputum Gram stain and culture and start ciprofloxacin otherwise start amoxicillin/clavulonic acid or quinolone like levofloxacin  or moxafloxacin.

You should remember the dosages.

What are the methods of delivering oxygen?

There are numerous devices available to deliver supplemental oxygen during an exacerbation of COPD:

Venturi masks are the preferred means of oxygen delivery because they permit a precise delivered fraction of inspired oxygen (FiO2). Venturi masks can deliver an FiO2 of 24, 28, 31, 35, 40, or 60 percent.

Nasal cannula can provide flow rates up to 6 L per minute with an associated FiO2 of approximately 40 percent. They are more comfortable and convenient for the patient, especially during oral feedings.

When a higher FiO2 is needed, simple face masks can provide an FiO2up to 55 percent using flow rates of 6 to 10 L per minute. However, variations in minute ventilation and inconsistent entrainment of room air affect the FiO2 when simple face masks (or nasal cannula) are used.

Non-rebreathing masks with a reservoir, one-way valves, and a tight face seal can deliver an inspired oxygen concentration up to 90 percent, but are generally not needed in this setting.

High flow nasal cannula (HFNC) provide supplemental oxygen (adjustable FiO2) at a high flow rate (up to 60 L/min, resulting in a low level of continuous positive airway pressure.

A high FiO2 is not required to correct the hypoxemia associated with most exacerbations of COPD. Inability to correct hypoxemia with a relatively low FiO2 (eg, 4 L/min by nasal cannula or 35 percent by mask) should prompt consideration of pulmonary emboli, acute respiratory distress syndrome, pulmonary edema, or severe pneumonia as the cause of respiratory failure.

How will you deal with hypercapnia?

Adequate oxygenation (ie, to achieve an oxygen saturation of 88 to 92 percent) must be assured, even if it leads to acute hypercapnia. Hypercapnia is generally well tolerated in patients whose arterial carbon dioxide tension (PaCO2) is chronically elevated. However, mechanical ventilation may be required if hypercapnia is associated with depressed mental status, profound acidemia, or cardiac dysrhythmias. 

I have tried to cover all the commonly asked questions. Surprisingly students appear unprepared for them. My intention was to clarify the points that students seem to have missed  during their studies. Enjoy learning.

 

 

 

 

 

 

 

 

 

 

 

f the patient had a pseudomonas infection in the past

Published by

shaheenmoin

I am a Professor of Medicine and a Nephrologist. Having served in the Army Medical College, Pakistan Army for 27 years I eventually became the Dean and Principal of the Bahria University Medical and Dental College Karachi from where I retired in 2016. My passion is teaching and mentoring young doctors. I am associated with the College of Physicians and Surgeons Pakistan as a Fellow and an examiner. I find that many young doctors make mistakes because they do not understand how they should answer questions; basically they do not understand why a question is being asked. My aim is to help them process the information they acquire as part of their education to answer questions, pass examinations and to best take care of patients without supervision of a consultant. Read my blog, interact and ask questions so that I can help you more.

One thought on “How not to fail an Exam. Respiratory system”

  1. Madam thank you very much for sparing time for the blog and sharing experience. I am sure this is a source of continuous guidance for the candidates

    Like

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