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MINISTRY OF HEALTH OF UKRAINE

Vinnitsa national medical university of N.I.Pirogova

"Approved"
At methodical meeting of chair
Internal medicine №1
Head of the department
____________ prof. Stanislavchuk M. A.
«______» _______________ 20 ___

METHODICAL RECOMMENDATIONS
For students

Subject matter Principles of internal medicine

Module № 1 Principles of internal medicine (gastroenterology, pulmonology,
hematology)
Substantial module № 2 Principles of diagnosis, treatment and prevention of basis
diseases in Pulmonology
Subject of the lesson Chronic obstructive pulmonary disease. Chronic bronchitis.
Lung Emphysema.
Course 4
Faculty Medical № 1

Vinnytsia
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1. The subject of the lesson: COPD. Chronic bronchitis.

Study-hours: 4
The aim: The students must be able to diagnose COPD, determine the severity, and prescribe the
proper treatment.
Topicality: Chronic obstructive pulmonary disease (COPD) is a chronic, slowly progressive
disorder characterised by airways obstruction (FEV1 < 80% predicted and FEV1/FVC ratio < 70%)
which does not change markedly over several months. The impairment of lung function is largely
fixed but is partially reversible by bronchodilator or other. Historically, the term 'chronic bronchitis'
was used to define any patient who coughed up sputum on most days of at least 3 consecutive
months for more than 2 successive years (provided other causes of cough had been excluded) and
'emphysema' referred to the pathological process of a permanent destructive enlargement of the
airspaces distal to the terminal bronchioles. Although 'pure' forms of these two conditions do exist,
there is considerable overlap in the vast majority of patients. COPD is an important cause of activity
limitation in the population. In the United States, about 12 million people suffer from COPD. It is
second only to heart disease as a cause of disability that forces people to stop working. It is the
fourth most common cause of death, accounting for more than 120,000 deaths per year in the
United States. COPD affects men more often than women, but men and women die as a result of
COPD at about equal rates.

Educational goal:
1. Determine main aetiological factors of COPD.
2. Learn the modern classification of COPD.
3. Define the clinical symptoms of COPD.
4. Make the plan of additional investigation of the patient and analyze their results.
5. Make the clinical diagnosis of the patient with COPD.
6. Prescribe the proper treatment.

The student must know:

1. Aetiology and pathogenesis of COPD.
2. Clinical symptoms of COPD.
3. Modern classification of COPD.
4. Methods of diagnostics of COPD.
5. Methods of treatment of COPD.

The student must be able:

1.To choose the symptoms of COPD from the history data.
2. In examination of the patient to choose the symptoms of COPD.
3. To make the scheme of investigation.
4. To define the type and the severity of the COPD.
5. To determinate the treatment depending on the type and degree of COPD.
6. To prescribe the proper treatment for the patient with COPD.

2. Basic level of training

№п/п The names of previous courses The obtained skills

1. Normal anatomy To know the anatomical structure of the organs of
respiratory system, their topography, blood supply and
innervation.
2. Histology Aware of the cellular structure of the organs of respiratory
system.
3. Biochemistry To have an understanding of the mechanisms of gas
exchange through the alveolar-capillary membrane, the
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biochemical structure of the surfactant and the importance

of its structure for performing the functions; the
biochemical composition of bronchial mucus.
4. Normal physiology To know the basic functions of respiratory tract; have an
idea about the process of gas exchange, how respiratory
system take part in the elimination of metabolic products,
in thermoregulation, in maintaining acid-base balance;
know neuro-hormonal mechanisms of regulation of
respiration.
Understand the importance of protective elements of
respiratory system - mucocilliar clearance, surfactant,
immune mechanisms (alveolar macrophages, neutrophils,
lymphocytes, immunoglobulins, complement system,
lysozyme, lactoferrin).
5. Physiopathology To know etiological factors of development of COPD. To
know reversible and nonreversibe mechanism of
obstractive disorders in COPD. To have an understanding
pathogenic mechanisms of various disorders of the
respiratory tract in case of COPD: cough, shortness of
breath, respiratory discomfort.
6. Pharmacology To know the mechanism of action, indications and
contraindications of medicines, wyich is used in treating of
pneumonia and be able to write them in the form of
recipes.
8. Demonstrate skills in examination of patients with COPD
Propaedeutic therapy (collecting complaints, history of disease and life, doing an
objective examination, analyzing the results diagnostic
testing (chest X-ray, functional tests, CBC, general
analysis of sputum).

3. CONTENTS OF THE TRAINING MATERIALS

Subject of the lesson:
Aetiology
The single most important cause of COPD is cigarette smoking although in developing
countries exposure to smoke from biomass and solid fuel fires is also important. Smoking is thought
to have its effect by inducing persistent airway inflammation and causing a direct imbalance in
oxidant/antioxidant capacity and proteinase/antiproteinase load in the lungs. Individual
susceptibility to smoking is, however, very wide, with only 15% of smokers likely to develop
clinically significant COPD. Recent studies have also emphasised the strong familial risks
associated with the development of COPD, with the incidence of disease in an individual who
smokes and has an affected sibling being 4.7 times that of matched controls. A small additional
contribution to the severity of COPD has been reported in patients exposed to dusty or polluted air.
An association also exists between low birth weight, bronchial hyper-responsiveness and the
development of COPD. Alpha1-antitrypsin deficiency can cause emphysema in non-smokers but
this risk is increased dramatically in enzyme-deficient patients who smoke. Stopping smoking slows
the average rate of the decline in FEV1 from 50-70 ml/year to 30 ml/year (i.e. equal to non-
smokers). Interestingly, there is no evidence that acute exacerbations or drug therapy affect the rate
of decline of the FEV1
Pathogenesis of the disease.
COPD leads to chronic airflow obstruction, which is defined as a persistent decrease in the
rate of airflow from the lungs when the person breathes out (exhales). This airflow obstruction is
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partially reversible in most people, either spontaneously or with treatment. COPD includes the
diagnoses of chronic obstructive bronchitis and emphysema. Many people have both disorders.
Chronic bronchitis is defined as cough that produces sputum repeatedly during two successive
years. When chronic bronchitis involves airflow obstruction, it qualifies as chronic obstructive
bronchitis. Emphysema is defined as widespread and irreversible destruction of the alveolar walls
(the cells that support the air sacs, or alveoli, that make up the lungs) and enlargement of many of
the alveoli.
The small airways (bronchioles) of the lungs contain smooth muscles and are normally held
open by their attachments to alveolar walls. In emphysema, the destruction of alveolar wall
attachments results in collapse of the bronchioles, causing permanent airflow obstruction.
In emphysema, the destruction of alveolar wall attachments results in collapse of the
bronchioles, causing permanent airflow obstruction. In chronic bronchitis, the glands lining the
larger airways (bronchi) of the lungs enlarge and increase their secretion of mucus. Inflammation of
the bronchioles develops and causes smooth muscle to contract (spasm), further obstructing airflow.
Inflammation also causes airflow to be blocked by secretions. Asthma is also characterized by
airflow obstruction. However, in contrast with the airflow obstruction of COPD, the airflow
obstruction of asthma is completely reversible in most people, either spontaneously or with
treatment. The airflow obstruction of COPD causes air to become trapped in the lungs after a full
exhalation, increasing the effort required to breathe. Also in COPD, the number of capillaries in the
walls of the alveoli decreases. These abnormalities impair the exchange of oxygen and carbon
dioxide between the alveoli and the blood. In the earlier stages of COPD, oxygen levels in the blood
may be decreased, but carbon dioxide levels remain normal. In the later stages, carbon dioxide
levels increase and oxygen levels fall.
The decrease in oxygen levels in the blood stimulates the bone marrow to send more red
blood cells into the bloodstream, a condition known as secondary polycythemia. The decrease in
oxygen levels in the blood also increases the pressure in the artery through which blood flows from
the heart to the lungs (pulmonary artery). As a result of the increased pressure, pulmonary
hypertension and cor pulmonale can occur.
Role of inflammation in COPD
In contrast to the eosinophil, which is the most prominent inflammatory cell in asthma, the
cellular composition of the airway inflammation in COPD is predominantly mediated by the
neutrophils. Cigarette smoking induces macrophages to release neutrophil chemotactic factors and
elastases, thus unleashing tissue destruction. Severity of airflow obstruction has correlated with
greater induced sputum neutrophilia that is also more prevalent in patients with chronic cough and
sputum production and is associated with an accelerated decline in lung function.
Macrophages also play an important role through macrophage-derived matrix
metalloproteinases (MMPs). Cigarette smoke causes neutrophil influx and is required for the
secretion of MMPs, therefore suggesting that both neutrophils and macrophages are required for the
development of emphysema.
Clinical features
The clinical state is dictated largely by the severity of disease. The initial symptoms are
usually repeated attacks of productive cough, usually after colds during the winter months, which
show a steady increase in severity and duration with successive years until cough is present all the
year round. Thereafter, patients suffer recurrent respiratory infections, exertional breathlessness,
regular morning cough, wheeze and occasionally chest tightness. Sputum may be scanty, mucoid,
tenacious and occasionally streaked with blood during infective exacerbations. Frankly purulent
sputum is indicative of bacterial infection, which often occurs in these patients. Breathlessness is
aggravated by infection, excessive cigarette smoking and adverse atmospheric conditions.
In patients with mild to moderate disease the respiratory examination may be normal.
However, variable numbers of inspiratory and expiratory rhonchi, mainly low- and medium-
pitched, are audible in most patients. Crepitations (crackles) which usually, but not always,
disappear after coughing may be audible over the lower zones.
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Physical signs associated with severe disease reflect pulmonary hyperinflation, hypoxaemia,
the development of cor pulmonale (pulmonary hypertension and right heart failure) and
polycythaemia

Clinical classification
Stage I: Mild COPD - Characterized by mild airflow limitation (FEV1/FVC < 0.70; FEV1 . 80%
predicted). Symptoms of chronic cough and sputum production may be present, but not always. At
this stage, the individual is usually unaware that his or her lung function is abnormal.
Stage II: Moderate COPD - Characterized by worsening airflow limitation (FEV1/FVC < 0.70; 50%
. FEV1 < 80% predicted), with shortness of breath typically developing on exertion and cough and
sputum production sometimes also present. This is the stage at which patients typically seek
medical attention because of chronic respiratory symptoms or an exacerbation of their disease.
Stage III: Severe COPD - Characterized by further worsening of airflow limitation (FEV1/FVC <
0.70; 30% . FEV1 < 50% predicted), greater shortness of breath, reduced exercise capacity, fatigue,
and repeated exacerbations that almost always have an impact on patients’ quality of life.
Stage IV: Very Severe COPD - Characterized by severe airflow limitation (FEV1/FVC < 0.70;
FEV1 < 30% predicted or FEV1 < 50% predicted plus the presence of chronic respiratory failure).
Respiratory failure is defined as an arterial partial pressure of O2 (PaO2) less than 8.0 kPa (60 mm
Hg), with or without arterial partial pressure of CO2 (PaCO2) greater than 6.7 kPa (50 mm Hg)
while breathing air at sea level. Respiratory failure may also lead to effects on the heart such as cor
pulmonale (right heart failure). Clinical signs of cor pulmonale include elevation of the jugular
venous pressure and pitting ankle edema. Patients may have Stage IV: Very Severe COPD even if
the FEV1 is > 30% predicted, whenever these complications are present. At this stage, quality of
life is very appreciably impaired and exacerbations may be life threatening.
Complications
Pulmonary bullae are thin-walled airspaces created by rupture of alveolar walls. They may be
single or multiple, large or small, and tend to be situated subpleurally. Rupture of subpleural bullae
may cause pneumothorax, and occasionally bullae increase in size, compress functioning lung tissue
and further embarrass pulmonary ventilation. Respiratory failure and cor pulmonale are generally
late complications in COPD patients.
Investigations
Pulmonary function tests
The diagnosis and classification of COPD rest on objective demonstration of airways
obstruction by spirometric testing. An abnormal FEV1 (< 80% predicted), with an FEV1/VC ratio
of < 70% and little variation in serial PEF, strongly suggests COPD. A normal FEV1 excludes the
diagnosis. The relationship between FEV1 and PEF is poor in COPD, and PEF in particular may
under-estimate the degree of airflow obstruction in these patients.
Reversibility testing to salbutamol and ipratropium bromide is necessary to detect patients with
substantial increases in FEV1 who really have asthma, and to establish the post-bronchodilator
FEV1 which is the best predictor of long-term prognosis. Significant reversibility is defined as a
15% and at least 200 ml increase in FEV1. Evidence of a similar objective response to a course of
oral prednisolone (30 mg daily for 2 weeks) should also be performed in all patients with COPD.
Alveolar underventilation causes a fall in PaO2 and often a permanent increase in PaCO2,
especially in severe cases. Measurement of arterial blood gases should be performed in all patients
with severe COPD (FEV1 < 40% predicted).
Imaging
COPD cannot be diagnosed on a chest radiograph but this investigation is useful in excluding
other pathology. In moderate and severe COPD the chest radiograph typically shows
hypertranslucent lung fields with disorganisation of the vasculature, low flat diaphragms or
'terracing' of the hemidiaphragms and prominent pulmonary artery shadows at both hila. Bullae may
also be observed. CT can be used to quantify the extent and distribution of emphysema but its
clinical value is currently restricted to the assessment of bullous emphysema and the potential for
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lung volume reduction surgery or lung transplantation. Patients with α1-antitrypsin deficiency
typically display basal disease, compared with the predominantly apical disease seen in smokers
with normal α1-antitrypsin levels
Haematology
Polycythaemia may develop but should not be assumed to be secondary without measurement
of PaO2. Venesection may be considered if the haematocrit is above 0.55.

Management:
Reduction of bronchial irritation
It is of extreme importance that the patient who smokes should stop completely and permanently.
Participation in an active smoking cessation programme, together with the use of nicotine
replacement therapy, leads to a higher quit rate. In well-motivated patients bupropion (150 mg once
daily increasing to 150 mg 12-hourly on day 7) commenced 1-2 weeks prior to stopping smoking is
also a valuable adjunct to smoking cessation. Bupropion is contraindicated in those patients with a
history of epilepsy or known CNS tumour and should only be used for 7-9 weeks
Dusty and smoke-laden atmospheres should be avoided; this may involve a change of
occupation.
Treatment of respiratory infection
Respiratory infection should be treated promptly because it aggravates breathlessness and may
precipitate type II respiratory failure in patients with severe airflow obstruction. Purulent sputum is
treated with amoxicillin 250 mg 8-hourly (clarithromycin 250-500 mg 12-hourly if penicillin-
sensitive) pending sputum culture results. Co-amoxiclav 375 mg 8-hourly should be used if there is
no response or if a β-lactamase-producing organism is cultured. The usual causative organisms are
Streptococcus pneumoniae or Haemophilus influenzae. A 5-10-day course of treatment is usually
effective. Well-informed, reliable patients can be given a supply of one of these drugs and start a
course of treatment on their own initiative when the need arises.
Continuous suppressive antibiotic treatment is not advised as it is apt to promote the emergence
of drug-resistant organisms within the respiratory tract. Influenza immunisation should be offered to
all patients each year.
Bronchodilator and anti-inflammatory therapy
Bronchodilator therapy with regular inhaled anticholinergic agents and short-acting β2-agonists
taken as required provides useful symptomatic relief in the majority of patients. In moderate and
severe COPD these agents should be used regularly and in combination, and low-dose inhaled
steroids considered in patients with severe COPD and frequent exacerbations requiring hospital
admission. These latter agents should not be used routinely (see EBM panel). Theophyllines and
long-acting β2-adrenoceptor agonists are of limited value in COPD but may produce small
increases in exercise tolerance and quality of life. There is no role for other anti-inflammatory
drugs. It is vital to check inhaler use as many patients with COPD struggle to use metered-dose
inhalers (MDIs) effectively; dry powder inhalers or large-volume spacer devices are often
preferable. The use of home nebulisers to deliver high doses of bronchodilator drugs is
controversial. Treatment is expensive and may have important side-effects; however, a few patients
may show significant objective or subjective improvements with such treatment.
Long-term domiciliary oxygen therapy
Long-term low-concentration oxygen therapy (2 litres/min by nasal cannulae) decreases
pulmonary hypertension, reduces secondary polycythaemia, improves neuropsychological health
and, most importantly, prolongs life in hypoxaemic COPD patients. The most efficient method of
providing oxygen in this way is by an oxygen concentrator. Low-concentration oxygen should be
administered for 15 hours or more per 24 hours.
Surgical intervention
A very small group of patients are suitable for surgical intervention. Young patients, particularly
those with α1-antitrypsin deficiency and severe disease, should be considered for lung
transplantation (usually single-lung), and surgical removal of expanding or very large bullae may be
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indicated in some patients. Lung volume reduction surgery, in which the most severely affected
areas of emphysematous lung are removed in order to improve pulmonary mechanics, particularly
by enhancing diaphragmatic function, is currently under assessment.

Task №1.
Patient L. 54, smokes 20 years, complained of shortness of breathing that progresses over
several years, increasing during exacerbations of bronchitis, after exercise, inhalation of cold, moist
air, sharp odor. Condition worsened after hypothermia 3 days ago. There was marked general
weakness, fever to 38.50C, not enough effect of NSAIDs. Increased cough with yellow-green
sputum, palpitation.
Examination: The skin, mucous membranes pale, gray color. Chest is emphysematous,
additional muscles takes part in breathing. The RR 20/min. Heart rate 100/min, BP 135/80 mmHg.
Resistance of the chest is enlarged, vocal fremitus is weakened, percussion sound is tympanicus,
during auscultation - weakened vesicular breathing, diffused dry rales and wheezing.
The ECG: diffuse changes in the myocardium. overload of right heart. CBC: Er - 4,0 ∙
10 / l, Hb - 135 g / l, CI - 1,0, Leuk. - 12,0 ∙ 10 9 / L, eosinophils - 2%, segm. – 75%, lymph. -
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12%, mon. - 11%, platelets - 210 ∙ 10 9 / l, ESR - 25 mm/h. Total sputum analysis: sputum purulent,
yellow-green liquid; leukocytes: 52 in visual field, neutrophils: 45 in visual field Chest X-ray:
increased transparency of lung fields, enhanced pulmonary picture, the lower border of the lungs are
shifted down. Spirometry: FEV1 - 63%, daily fluctuations -5%, test Tyffno - 65%, a negative test
with bronchodilators.
1.Make the diagnosis.
2.What is the treatment should be prescribed for patient?

Recommended literature:
А. Main:
1. Davidson’s Principles and Practice of Medicine, 2006, P. pages 526 - 532.

Materials for self-control:

А. The questions for self-control:
1. Name the main aetiological factors of COPD.
2. Give the main principles of the modern classification of COPD.
3. What are the main clinical syndromes of COPD?
4. Make the plan of additional investigation of the patient with COPD.
6. Name the main drugs for the treatment of COPD.

Б. Tests for self-control:

Methodic chart made by M.D. Ostapchuk O.I.