Module 2 “Pulmonology, Haematology” icon

Module 2 “Pulmonology, Haematology”

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Sumy State University

Internal Medicine Department

Methodological Instructions

for the 4th course students, 8 semester

Module 2

Pulmonology, Haematology”

Prepared by Orlovsky A. V., assistant, c.m.s.,

Murenets N. A., assistant

Sumy - 2009

Methodological Instruction to Lesson № 1.

Propedeutics in pulmonology.

Hours: 5.

Working place: classroom, hospital wards.


  1. Structure of the bronchial tree.

  2. Determination of the lungs border.

  3. Structure of the respiratory segment (part) of the lung.

  4. Comparative percussion of the lungs.

  5. Blood supply of the lung.

  6. Cough, its characteristics.

  7. Structure of the bronchial mucous. Concept of bronchial clearance.

  8. Rales and their characteristics.

  9. Physiology of respiration.

  10. What is vocal fremites and method of its indication?

  11. Show the spirogram schematically. What is the purpose of the spirogram?

  12. Name kinds of dispnoea.

  13. What is forced expiration volume in 1 second (FEV1), forced vital capacity (FVC)?

  14. Comparative percussion of the lungs.

  15. What is this pneumotachometry?

  16. Name main symptoms of respiratory diseases.

  17. Name main groups of drugs in patients with respiratory diseases.


  1. Propedeutics to Internal medicine Part 1 Diagnostics/O. M. Kovalyova, T. V. Ashcheulova. – Vinnytsya. – 2006. – P.60 - 138.

  2. Davidson’s Principles and practice of medicine (nineteenth edition)/Christopher Haslett, Edvin R. Chilvers and others. – Edinburgh, 2002.

Prepared by Orlovsky A. V., assistant, c. m. s.,

Murenets N. A., postgraduate

Short theoretic material


When evaluating a patient with shortness of breath, one should first determine the time course over which the symptom has become manifest. Patients who were well previously and developed acute shortness of breath (over a period of minutes to days) may have acute disease affecting either the upper or the intrathoracic airways (e.g., laryngeal edema or acute asthma, respectively), the pulmonary parenchyma (acute cardiogenic or noncardiogenic pulmonary edema or an acute infectious process such as a bacterial pneumonia), the pleural space (a pneumothorax), or the pulmonary vasculature (a pulmonary embolus). A subacute presentation (over days to weeks) can suggest an exacerbation of preexisting airways disease (asthma or chronic bronchitis), an indolent parenchymal infection (Pneumocystis jiroveci pneumonia in a patient with AIDS, mycobacterial or fungal pneumonia), a noninfectious inflammatory process that proceeds at a relatively slow pace (Wegener's granulomatosis, eosinophilic pneumonia, cryptogenic organizing pneumonia, and many others), neuromuscular disease (Guillain-Barrй syndrome, myasthenia gravis), pleural disease (pleural effusion from a variety of possible causes), or chronic cardiac disease (congestive heart failure). A chronic presentation (over months to years) often indicates chronic obstructive lung disease, chronic interstitial lung disease, or chronic cardiac disease. Chronic diseases of airways (not only chronic obstructive lung disease but also asthma) are characterized by exacerbations and remissions. Patients often have periods when they are severely limited by shortness of breath, but these may be interspersed with periods in which symptoms are minimal or absent. In contrast, many of the diseases of the pulmonary parenchyma are characterized by slow but inexorable progression. Chronic respiratory symptoms may also be multifactorial in nature, as patients with chronic obstructive pulmonary disease may also have concomitant heart disease.

^ Other Respiratory Symptoms

Cough may indicate the presence of lung disease, but cough per se is not useful for the differential diagnosis. The presence of sputum accompanying the cough often suggests airway disease and may be seen in asthma, chronic bronchitis, or bronchiectasis.

Hemoptysis can originate from disease of the airways, the pulmonary parenchyma, or the vasculature. Diseases of the airways can be inflammatory (acute or chronic bronchitis, bronchiectasis, or cystic fibrosis) or neoplastic (bronchogenic carcinoma or bronchial carcinoid tumors). Parenchymal diseases causing hemoptysis may be either localized (pneumonia, lung abscess, tuberculosis, or infection with Aspergillus) or diffuse (Goodpasture's syndrome, idiopathic pulmonary hemosiderosis). Vascular diseases potentially associated with hemoptysis include pulmonary thromboembolic disease and pulmonary arteriovenous malformations.

Chest pain caused by diseases of the respiratory system usually originates from involvement of the parietal pleura. As a result, the pain is accentuated by respiratory motion and is often referred to as pleuritic. Common examples include primary pleural disorders, such as neoplasm or inflammatory disorders involving the pleura, or pulmonary parenchymal disorders that extend to the pleural surface, such as pneumonia or pulmonary infarction.

^ Additional Historic Information

Information about risk factors for lung disease should be explicitly explored to ensure a complete basis of historic data. A history of current and past smoking, especially of cigarettes, should be sought from all patients. The smoking history should include the number of years of smoking, the intensity (i.e., number of packs per day), and, if the patient no longer smokes, the interval since smoking cessation. The risk of lung cancer falls progressively in the decade following discontinuation of smoking, and loss of lung function above the expected age-related decline ceases with the discontinuation of smoking. Even though chronic obstructive lung disease and neoplasia are the two most important respiratory complications of smoking, other respiratory disorders (e.g., spontaneous pneumothorax, respiratory bronchiolitis–interstitial lung disease, pulmonary Langerhans cell histiocytosis, and pulmonary hemorrhage with Goodpasture's syndrome) are also associated with smoking. A history of significant secondhand (passive) exposure to smoke, whether in the home or at the workplace, should also be sought as it may be a risk factor for neoplasia or an exacerbating factor for airways disease.

The patient may have been exposed to other inhaled agents associated with lung disease, which act either via direct toxicity or through immune mechanisms. Such exposures can be either occupational or avocational, indicating the importance of detailed occupational and personal histories, the latter stressing exposures related to hobbies or the home environment. Important agents include the inorganic dusts associated with pneumoconiosis (especially asbestos and silica dusts) and organic antigens associated with hypersensitivity pneumonitis (especially antigens from molds and animal proteins). Asthma, which is more common in women than men, is often exacerbated by exposure to environmental allergens (dust mites, pet dander, or cockroach allergens in the home or allergens in the outdoor environment such as pollen and ragweed) or may be caused by occupational exposures (diisocyanates). Exposure to particular infectious agents can be suggested by contacts with individuals with known respiratory infections (especially tuberculosis) or by residence in an area with endemic pathogens (histoplasmosis, coccidioidomycosis, blastomycosis).

A history of coexisting nonrespiratory disease or of risk factors for or previous treatment of such diseases should be sought, as they may predispose a patient to both infectious and noninfectious respiratory system complications. Common examples include systemic rheumatic diseases that are associated with pleural or parenchymal lung disease, metastatic neoplastic disease in the lung, or impaired host defense mechanisms and secondary infection, which occur in the case of immunoglobulin deficiency or with hematologic and lymph node malignancies. Risk factors for AIDS should be sought, as the lungs are not only the most common site of AIDS-defining infection but can also be involved by noninfectious complications of AIDS. Treatment of nonrespiratory disease can be associated with respiratory complications, either because of effects on host defense mechanisms (immunosuppressive agents, cancer chemotherapy) with resulting infection or because of direct effects on the pulmonary parenchyma (cancer chemotherapy, radiation therapy, or treatment with other agents, such as amiodarone) or on the airways (beta-blocking agents causing airflow obstruction, angiotensin-converting enzyme inhibitors causing cough).

Family history is important for evaluating diseases that have a genetic component. These include disorders such as cystic fibrosis, 1-antitrypsin deficiency, pulmonary hypertension, pulmonary fibrosis, and asthma.

Physical Examination

The general principles of inspection, palpation, percussion, and auscultation apply to the examination of the respiratory system. However, the physical examination should be directed not only toward ascertaining abnormalities of the lungs and thorax but also toward recognizing other findings that may reflect underlying lung disease.

On inspection, the rate and pattern of breathing as well as the depth and symmetry of lung expansion are observed. Breathing that is unusually rapid, labored, or associated with the use of accessory muscles of respiration generally indicates either augmented respiratory demands or an increased work of breathing. Asymmetric expansion of the chest is usually due to an asymmetric process affecting the lungs, such as endobronchial obstruction of a large airway, unilateral parenchymal or pleural disease, or unilateral phrenic nerve paralysis. Visible abnormalities of the thoracic cage include kyphoscoliosis and ankylosing spondylitis, either of which can alter compliance of the thorax, increase the work of breathing, and cause dyspnea.

On palpation, the symmetry of lung expansion can be assessed, generally confirming the findings observed by inspection. Vibration produced by spoken sounds is transmitted to the chest wall and is assessed by the presence or absence and symmetry of tactile fremitus. Transmission of vibration is decreased or absent if pleural liquid is interposed between the lung and the chest wall or if an endobronchial obstruction alters sound transmission. In contrast, transmitted vibration may increase over an area of underlying pulmonary consolidation. Palpation may also reveal focal tenderness, as seen with costochondritis or rib fracture.

The relative resonance or dullness of the tissue underlying the chest wall is assessed by percussion. The normal sound of underlying air-containing lung is resonant. In contrast, consolidated lung or a pleural effusion sounds dull, while emphysema or air in the pleural space results in a hyperresonant percussion note.

On auscultation of the lungs, the examiner listens for both the quality and intensity of the breath sounds and for the presence of extra, or adventitious, sounds. Normal breath sounds heard through the stethoscope at the periphery of the lung are described as vesicular breath sounds, in which inspiration is louder and longer than expiration. If sound transmission is impaired by endobronchial obstruction or by air or liquid in the pleural space, breath sounds are diminished in intensity or absent. When sound transmission is improved through consolidated lung, the resulting bronchial breath sounds have a more tubular quality and a more pronounced expiratory phase. Sound transmission can also be assessed by listening to spoken or whispered sounds; when these are transmitted through consolidated lung, bronchophony and whispered pectoriloquy, respectively, are present. The sound of a spoken E becomes more like an A, although with a nasal or bleating quality, a finding that is termed egophony.

The primary adventitious (abnormal) sounds that can be heard include crackles (rales), wheezes, and rhonchi. Crackles are the discontinuous, typically inspiratory sound created when alveoli and small airways open and close with respiration. They are often associated with interstitial lung disease, microatelectasis, or filling of alveoli by liquid. Wheezes, which are generally more prominent during expiration than inspiration, reflect the oscillation of airway walls that occurs when there is airflow limitation, as may be produced by bronchospasm, airway edema or collapse, or intraluminal obstruction by neoplasm or secretions. Rhonchi is the term applied to the sounds created when there is free liquid or mucus in the airway lumen; the viscous interaction between the free liquid and the moving air creates a low-pitched vibratory sound. Other adventitious sounds include pleural friction rubs and stridor. The gritty sound of a pleural friction rub indicates inflamed pleural surfaces rubbing against each other, often during both inspiratory and expiratory phases of the respiratory cycle. Stridor, which occurs primarily during inspiration, represents flow through a narrowed upper airway, as occurs in an infant with croup.

A summary of the patterns of physical findings on pulmonary examination in common types of respiratory system disease is shown in Table 1.

Table 1 Typical Chest Examination Findings in Selected Clinical Conditions




Breath Sounds

Voice Transmission

^ Adventitious Sounds




Vesicular (at lung bases)



Consolidation or atelectasis (with patent airway)




Bronchophony, whispered pectoriloquy, egophony


Consolidation or atelectasis (with blocked airway)












Interstitial lung disease











Absent or wheezing







Pleural effusion





Absent or pleural friction rub

aMay be altered by collapse of underlying lung, which will increase transmission of sound.

Chest Radiography

Chest radiography is often the initial diagnostic study performed to evaluate patients with respiratory symptoms, but it can also provide the initial evidence of disease in patients who are free of symptoms. Perhaps the most common example of the latter situation is the finding of one or more nodules or masses when the radiograph is performed for a reason other than evaluation of respiratory symptoms.

A number of diagnostic possibilities are often suggested by the radiographic pattern. A localized region of opacification involving the pulmonary parenchyma can be described as a nodule (usually <3 cm in diameter), a mass (usually 3 cm in diameter), or an infiltrate. Diffuse disease with increased opacification is usually characterized as having an alveolar, an interstitial, or a nodular pattern. In contrast, increased radiolucency can be localized, as seen with a cyst or bulla, or generalized, as occurs with emphysema. The chest radiograph is also particularly useful for the detection of pleural disease, especially if manifested by the presence of air or liquid in the pleural space. An abnormal appearance of the hila and/or the mediastinum can suggest a mass or enlargement of lymph nodes.

Methodological Instruction to Lesson № 2.

Chronic obstructive pulmonary disease.

Hours: 5.

Working place: classroom, hospital wards.


  1. Give the definition of COPD.

  2. Etyology of COPD. Give external and internal risk factors of COPD.

  3. Pathogenesis of COPD. What reflects airflow limitation.

  4. Pathology of COPD.

  5. Clinical symptoms of COPD.

  6. Name co-morbidities in patients with COPD.

  7. Physical findings of patients with COPD.

  8. X-Ray findings of patients with COPD.

  9. Studing of external respiration functions. Spyrometry.

  10. Clinical and functional monitoring.

  11. Give the classification of COPD.

  12. Name main treatment principles of patients with COPD.

  13. Name drug, which are used in treatment of patients with COPD.

  14. Name the phaemacotherapy for patienta with COPD depending on the level of gravity of the disease.

  15. Role of glucocorticosteroids in treatment of patients with COPD.

  16. Name the other pharmacological treatment of patients with COPD.

  17. Rehabilitation of patients with COPD.

  18. Name the reasons exacerbations of COPD.

  19. Algorithm of managing exacerbation of COPD in the outpatient setting.

  20. Name the indications for hospitalisation in case of exacerbation of COPD.

  21. Name the indications to antibacterial therapy. What is influenced on choosing antibacterial therapy.

  22. Name antibacterial therapy of patients with COPD.

Examples of tests

  1. What is the most important cause of COPD?

    1. exposure to dusty or polluted air

    2. alpha1- antitrypsin deficiency

    3. cigarette smoking

    4. familial predisposition

    5. low birth weight

  1. Chronic cough, which characterised COPD, is:

    1. cough precedes dyspnea

    2. cough is parallel to dyspnea

    3. cough after marked dyspnea

    4. there are no defined law

    5. cough may be absent

  2. Inhalation ?2- agonists of short – term action are the following drugs, except:

    1. Salbutamol

    2. Fenoterol

    3. Terbutalin

    4. Salmeterol

  3. The main symptoms of the COPD are:

    1. abdominal pain and diarrhea,vomiting

    2. cough

    3. headache

    4. constipation

    5. sneezing

  4. Differential diagnosis of the COPD with:

    1. Asthma

    2. Peritonitis

    3. Piothorax

d .appendicitis

e.myocardial infarction

6. The Symptoms and Signs of the COPD are:

    1. constipation

    2. bloody vomiting

    3. frequent headache

    4. chronic cough and sputum production

    5. sneezing

Answers to the self-assessment:

1-c, 2-a, 3-d, 4-b, 5-a, 6-d


    1. Therapy: Manual. The course of lectures/V. M. Fedosyeyeva, A. A. Chrenov. – Simferopol, 2003. – 27 - 37 p.

    2. Davidson’s Principles and practice of medicine (nineteenth edition)/Christopher Haslett, Edvin R. Chilvers and others. – Edinburgh, 2002. – 508-513 p.

    3. Harrisons Principle if internal medicine (seventeenth Edition)/Fauci, Braunwald, Hasper and other. – Part 10, section 2, Chapter 254.

    4. The Merck Manual of Diagnosis and Therapy (seventeenth Edition)/ Robert Berkow, Andrew J. Fletcher and others. – published by Merck Research Laboratories, 1999.

Prepared by Orlovsky A. V., assistant, c. m. s.,

Murenets N. A., postgraduate

Short theoretic material


Chronic obstructive pulmonary disease is the internationally preferred term encompassing chronic bronchitis and emphysema.

By definition COPD is a chronic, slowly progressive disorder characterised by airflow obstruction (FEV1 < 80% predicted and FEV1/VC ratio <70%) which does not change markedly over several months. The impairment of lung function is largely fixed but may be partially reversible by bronchodilator therapy.

Historically, the term 'chronic ronchitis' 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.

The death rate from COPD currently exceeds 25 000/year (> 20-fold higher than asthma) in England and Wales and this condition accounts for over 10% of all hospital medical dmissions in the United Kingdom.


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. 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.


The pathologic findings include hypoplasia and hypertrophy of the submucosal bronchial mucous glands, hyperplasia of bronchiolar goblet cells, squamous metaplasia of bronchial mucosal cells, chronic and acute inflammatory infiltrates in the bronchial submucosa, profuse inflammatory exudates in the lumens of bronchi and bronchioles, and denudation of bronchial mucosa.

Airflow limitation reflects both mechanical obstruction in the small airways and loss of pulmonary elastic recoil. Loss of alveolar attachments around such airways makes them more liable to collapse during expiration.
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