Ministry of health of ukraine 


Мы поможем в написании ваших работ!



ЗНАЕТЕ ЛИ ВЫ?

Ministry of health of ukraine



MINISTRY OF HEALTH OF UKRAINE

Vinnitsa national medical university of N.I.Pirogova

 

"IS CONFIRMED"

At methodical meeting of chair

Internal medicine №1

                                                                   Head of the department               

____________ prof. Stanislavchuk M. A.

«______» _______________ 200 ___

 

METHODICAL RECOMMENDATIONS

For students

Subject matter Foundation of Internal medicine
Module № 1
Substantial module № 2
Subject of the lesson Symptoms and syndromes in pulmonology
Course 4
Faculty Medical № 1

 

 

Vinnytsya 2012

 

1. The subject of the lesson: SYMPTOMS AND SYNDROMES IN PULMONOLOGY

Study-hours: 4

The aim: The students must be able to find symptoms of lung disease, group them into syndromes, using additional methods of examination, make diagnosis.

Educational goal:  

1. Know the basic symptoms of respiratory diseases, the mechanisms of their development and causes.

2. Learn to group symptoms of diseases of the respiratory system in syndromes.

3. Understand which additional research methods can help to differentiate syndromes and to determine their origin.

4. Make the plan of additional investigation of the patient and analyze their results.

5. Using the results of additional research methods to make diagnose.

The student must know:

1. The main symptoms and syndromes that occur in the pathology of the respiratory system.

2. Pathogenetic ways of development main syndromes.
3. Modern classification and basic characteristics of the respiratory system disease syndrome.
4. Laboratory and instrumental methods used to differentiate the origin of syndromes and make diagnosis.

5. The main approaches to the treatment of respiratory diseases.

The student must be able:

1. Select the symptoms that occur in the pathology of the respiratory tract and group them into syndromes in collecting history, complaints and objectively examined.

2. To make the scheme of investigation.

3. Be able to interpret the results of the results of additional research methods

4. Formulate a diagnosis according to the current classification of disease and make treatment plan.

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 biochemical structure of the surfactant and the importance of its structure for performing 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 Know about the pathogenic mechanisms of various disorders of the respiratory tract: cough, shortness of breath, respiratory discomfort, chest pain, haemoptysis. Know about the pathogenic mechanisms of obstructive and restrictive disorders of ventilator functions of lung. 
6. Pharmacology To know the mechanism of action, indications and contraindications of medicines, which is used in treating of respiratory system diseases and be able to write them in the form of recipes.
8. Propaedeutic therapy Demonstrate skills in examination of patients with respiratory system diseases (collecting complaints, history of disease and life, doing an objective examination, analyzing the results diagnostic testing (chest X-ray, CTscan, functional tests, CBC, general analysis of sputum).  

COUGH

Cough is the most frequent symptom of respiratory disease. It is caused by stimulation of sensory nerves in the mucosa of the pharynx, larynx, trachea and bronchi.

The explosive quality of a normal cough is lost in patients with respiratory muscle paralysis or vocal cord palsy. Paralysis of a single vocal cord gives rise to a prolonged, low-pitched, inefficient 'bovine' cough accompanied by hoarseness. Coexistence of an inspiratory noise (stridor) indicates partial obstruction of a major airway (e.g. laryngeal oedema, tracheal tumour, scarring or compression or an inhaled foreign body) and requires urgent investigation and treatment. Sputum production is common in patients with acute or chronic cough, and its nature and appearance can provide valuable clues as to the aetiology.

 

Causes of cough

 

Origin

Common causes

Clinical features

Pharynx

Post-nasal drip

History of chronic rhinitis

Larynx

Laryngitis, tumour, croup

Voice or swallowing altered, harsh or painful cough
Paroxysms of cough, often associated with stridor

Trachea

Tracheitis

retrosternal pain with cough

Bronchi

Bronchitis (acute) and COPD

Dry or productive, worse in mornings

Asthma

Usually dry, worse at night

Bronchial carcinoma

Persistent (often with haemoptysis)

Lung parenchyma

Tuberculosis

Productive, often with haemoptysis

Pneumonia

Dry initially, productive later

Bronchiectasis

Productive, changes in posture induce sputum production

Pulmonary oedema

Often at night

Interstitial fibrosis

Dry, irritant

 

Patients with chronic cough present more of a diagnostic challenge, especially those individuals with a normal examination, chest X-ray and lung function studies. In this context, cough can be explained by post-nasal drip secondary to nasal or sinus disease; cough-variant asthma (where cough may be the principal or exclusive clinical manifestation) or gastro-oesophageal reflux with aspiration. Ten to fifteen per cent of patients (particularly women) taking angiotensin-converting enzyme (ACE) inhibitors develop drug-induced chronic cough.

DYSPNOEA

Breathlessness or dyspnoea can be defined as the feeling of an uncomfortable need to breathe.

CAUSES OF DYSPNOEA

System

Acute dyspnoea at rest

Chronic exertional dyspnoea

Cardio -vascular

Acute pulmonary oedema

Chronic heart failure

Myocardial ischaemia

Respi -ratory

Acute severe asthma
Acute exacerbation of COPD
Pneumothorax
Pneumonia
* Pulmonary embolus
Acute respiratory distress syndrome
Inhaled foreign body
Lobar collapse
Laryngeal oedema (e.g. anaphylaxis)

COPD
Chronic asthma
Bronchial carcinoma
Interstitial lung disease (sarcoidosis, fibrosing alveolitis, pneumoconiosis)
Chronic pulmonary thromboembolism
Lymphatic carcinomatosis
Large pleural effusion(s)

Others

Metabolic acidosis (e.g. diabetic ketoacidosis, lactic acidosis, uraemia, overdose of salicylates,
Psychogenic hyperventilation

Severe anaemia
Obesity

 

CHRONIC EXERTIONAL DYSPNOEA

 

Chronic obstructive pulmonary disease (COPD)

 

The exertional dyspnoea in COPD typically varies little day to day, but exercise capacity falls over months or years. Patients usually report relief of dyspnoea at rest and overnight, a useful distinction from asthma. If bronchitis is present, chronic cough and sputum is usual, particularly in the mornings, but sputum may be absent when emphysema predominates. There is often a history of recurrent acute exacerbations of breathlessness, usually in winter. Most of the patients have a smoking history. In advanced disease may develop cor pulmonale

 

Asthma

 

Dyspnoea in asthma is associated with episodes of wheeze or chest tightness, usually worse in the morning. There may be a history of childhood wheeze, or of wheeze or rhinitis provoked by allergens. In exercise-induced asthma, wheeze and chest tightness typically come on immediately after exercise.

 

Heart disease

 

Left ventricular function can cause exertional dyspnoea. Orthopnoea, cough and wheeze may also be present, as in lung disease. A history of angina or hypertension may be useful in implicating a cardiac cause. On examination, an increase in heart size. The chest X-ray may show cardiomegaly and an ECG may provide evidence of left ventricular disease.

 

Pulmonary thromboembolism

 

Pulmonary thromboembolism often presents with acute breathlessness with or without chest pain. However, chronic pulmonary thromboembolic disease should be suspected in patients who present with more gradual onset of breathlessness.

 

Condition

History

Signs

Chest radiography

Arterial blood gases ECG

Other tests

Pulmonary oedema

Chest pain
Orthopnoea
Palpitations
A previous cardiac history*

Central cyanosis JVP (→ or ↑) Sweating* Cool extremities Dullness and crepitations at bases*

Cardiomegaly
Upper zone vessel enlargement*
Overt oedema/pleural effusions*

Pa O2Pa CO2 Sinus tachycardia Signs of myocardial infarction/ ischaemia* Arrhythmia

ECG* (↓ left ventricular function)

Massive pulmonary embolus

Recent surgery or other risk factors
Chest pain
Previous pleurisy
Syncope*
Dizziness*

Severe central cyanosis Elevated JVP* Absence of signs in the lung (unless previous pulmonary infarction)* Shock (tachycardia, reduced blood pressure)

May be subtle changes only
Prominent hilar vessels
Oligaemic lung fields*

Pa O2Pa CO2 Sinus tachycardia S1Q3T3 pattern ↓ T (V1-V4) Right bundle-branch block

ECG*
V/Q scan*
CT pulmonary angiography*

Acute severe asthma

History of previous episodes, asthma medications, wheeze*

Tachycardia and pulsus paradoxus yanosis (late) JVP →* ⇓ peak flow, rhonchi*

Hyperinflation only (unless complicated by pneumothorax)*

Pa O2Pa CO2 (Pa CO2 rises in extremis) Sinus tachycardia (bradycardia with severe hypoxaemia-late)

 

Acute exacerbation of COPD

Previous episodes (admissions)* If in type II respiratory failure may not be distressed

Cyanosis Signs of COPD* Signs of CO2 retention (warm periphery, flapping tremor, bounding pulses)*

Hyperinflation*
Signs of emphysema
Signs of events precipitating exacerbation

↓ or ⇓ Pa O2 Pa CO2 ↑ in type II failure, with ↑ [H+] and ↑ bicarbonate Nil, or signs of right ventricular strain

 

Pneumonia

Prodromal illness*
Fever*
Rigors*
Pleurisy*

Fever, confusion Pleural rub* Consolidation* Cyanosis (only if severe)

Pneumonic consolidation*

Pa CO2Pa O2 Tachycardia

↑ CRP
↑ White cell count
Sputum and blood culture

Metabolic acidosis

Evidence of diabetes/renal disease*
Overdose of aspirin or ethylene glycol*

Fetor (ketones) Hyperventilation without physical signs in heart or lungs* Dehydration* Air hunger (Kussmaul's respiration)

Normal

Pa O2 normal* ⇓ Pa CO2 ⇓ pH (↑ H+)  

 

CHEST PAIN

 

Centra l Cardiac · Myocardial ischaemia (angina) · Myocardial infarction · Myocarditis · Pericarditis · Mitral valve prolapse syndrome Aortic · Aortic dissection · Aortic aneurysm Oesophageal · Oesophagitis · Oesophageal spasm · Mallory-Weiss syndrome · Massive pulmonary embolus Mediastinal · Tracheitis Malignancy Peripheral Lungs/pleura · Pulmonary infarct · Pneumonia · Pneumothorax · Malignancy · Tuberculosis · Connective tissue disorders Musculoskeletal · Osteoarthritis · Costochondritis (Tietze's · Rib fracture/injury syndrome) · Intercostal muscle injury · Epidemic myalgia (Bornholm disease) Neurological · Prolapsed intervertebral disc · Herpes zoster · Thoracic outlet syndrome  

 

 

HAEMOPTYSIS

Coughing up blood, irrespective of the amount, is an alarming symptom and nearly always brings the patient to the doctor.

 CAUSES OF HAEMOPTYSIS  

Bronchial disease

· Carcinoma

· Bronchiectasis

· Acute bronchitis

· Bronchial adenoma

· Foreign body

Parenchymal disease

· Tuberculosis

· Suppurative pneumonia

· Lung abscess

· Parasites (e.g. hydatid disease, flukes)

· Trauma

· Actinomycosis

· Mycetoma

Lung vascular disease

· Pulmonary infarction

· Polyarteritis nodosa

· Goodpasture's syndrome

· Idiopathic pulmonary haemosiderosis

 

 

 

Common causes

· Bronchial carcinoma

· Single metastasis

· Localised pneumonia

· Lung abscess

· Tuberculoma

· Pulmonary infarct

Uncommon causes

· Benign tumours

· Lymphoma

· Arteriovenous malformation

· Hydatid cyst

· Bronchogenic cyst

· Rheumatoid nodule

· Pulmonary sequestration

· Pulmonary haematoma

· Wegener's granuloma

· 'Pseudotumour'-fluid collection in a fissure

· Aspergilloma (usually surrounded by air 'halo')

     

 

 
 

PLEURAL EFFUSION

The accumulation of serous fluid within the pleural space is termed pleural effusion. Accumulations of frank pus (empyema) or blood (haemothorax) represent separate conditions. In general, pleural fluid accumulates as a result of either increased hydrostatic pressure or decreased osmotic pressure ('transudative effusion' as seen in cardiac, liver or renal failure), or from increased microvascular pressure due to disease of the pleural surface itself, or injury in the adjacent lung ('exudative effusion').

PLEURAL EFFUSION: MAIN CAUSES AND FEATURES

Cause Appearance of fluid Type of fluid Predominant cells in fluid

Other diagnostic features

Tuberculosis Serous, usually amber-coloured Exudate Lymphocytes (occasionally polymorphs)

Positive tuberculin test Isolation of M. tuberculosis from pleural fluid (20%)
Positive pleural biopsy (80%)

Malignant disease Serous, often blood-stained Exudate Serosal cells and lymphocytes Often clumps of malignant cells

Positive pleural biopsy (40%)
Evidence of malignant disease elsewhere

Cardiac failure* Serous, straw-coloured Transudate Few serosal cells

Other evidence of left ventricular failure
Response to diuretics

Pulmonary infarction* Serous or blood-stained Exudate (rarely transudate) Red blood cells Eosinophils

Evidence of pulmonary infarction
Source of embolism
Factors predisposing to venous thrombosis

Rheumatoid disease* Serous Turbid if chronic Exudate Lymphocytes (occasionally polymorphs)

Rheumatoid arthritis; rheumatoid factor in serum
Cholesterol in chronic effusion; very low glucose in pleural fluid

Systemic lupus erythematosus (SLE)* Serous Exudate Lymphocytes and serosal cells

Other manifestations of SLE
Antinuclear factor or anti-DNA in serum

Acute pancreatitis Serous or blood-stained Exudate No cells predominate

High amylase in pleural fluid (greater than in serum)

Obstruction of thoracic duct   Milky Chyle None

Chylomicrons

RESPIRATORY FAILURE

The term respiratory failure is used when pulmonary gas exchange fails to maintain normal arterial oxygen and carbon dioxide levels. Its classification into type I and type II relates to the absence or presence of hypercapnia Prompt diagnosis and management of the underlying cause is crucial to the management of patients with respiratory failure. Occasionally, rapid reversal of the precipitating event-e.g. tracheostomy for laryngeal obstruction, fixation of ribs in a flail chest injury, reversal of narcotic poisons, nebulised bronchodilators in acute severe asthma or tube drainage of a tension pneumothorax-will restore good gas exchange. In acute left ventricular failure, in massive pulmonary embolism and when pulmonary infarction or pneumonia is the cause of pleural pain, treatment with opiates is entirely appropriate, but these drugs depress respiratory drive and should never be used in asthma or COPD, except immediately prior to and during assisted mechanical ventilation.

 

RESPIRATORY FAILURE: UNDERLYING CAUSES AND BLOOD GAS ABNORMALITIES

 
 

Type I

Type II

 

Hypoxia (Pa O2 < 8.0 kPa (60 mmHg)) Normal or low Pa CO2 (<6.6kPa(50mmHg))

Hypoxia (Pa O2 < 8.0 kPa (60 mmHg)) Raised Pa CO2 (> 6.6 kPa (50 mmHg))

  Acute Chronic Acute

Chronic

H+ → or ↑

→ or ↑

Bicarbonate

Causes Acute asthma Emphysema Acute severe asthma

COPD

  Pulmonary oedema Lung fibrosis Acute exacerbation COPD

Sleep apnoea

  Pneumonia Lymphangitis carcinomatosa Upper airway obstruction

Kyphoscoliosis

  Lobar collapse Right-to-left shunts Acute neuropathies/paralysis

Myopathies/muscular dystrophy

  Pneumothorax Brain-stem lesion Narcotic drugs

Ankylosing spondylitis

  Pulmonary embolus   Primary alveolar hypoventilation

 

  ARDS   Flail chest injury

 

Common to all cases is the need to restore adequate arterial oxygen levels, for which oxygen therapy with or without mechanically assisted ventilation is important. The consequences of untreated severe hypoxaemia include systemic hypotension, pulmonary hypertension, polycythaemia, tachycardia, and cerebral dysfunction ranging from confusion to coma.

 

           

 

                                     

SYNDROMES

1. Syndrome of the pulmonary tissue consolidation.

2. Syndrome of increased airiness of the pulmonary tissue.

3. Syndrome of bronchium obstruction (bronchospastic syndrome).

4. Syndrome of fluid accumulation in pleural cavity (hydrothorax).

5. Syndrome of air accumulation in pleural cavity (pneumothorax).

6. Syndrome of the cavity in the lung.

 

Computed tomography (CT)

 
INVESTIGATION OF RESPIRATORY DISEASE
The 'plain' chest X-ray
Chest radiography is performed on the majority of patients suspected of having chest disease. A postero-anterior (PA) film provides information on the lung fields, heart, mediastinum, vascular structures and the thoracic cage. Additional information may be obtained from a lateral film, particularly if pathology is suspected behind the heart shadow or deep in the diaphragmatic sulci.
Increased shadowing may represent accumulation of fluid, lobar collapse or consolidation. Uncomplicated consolidation should not change the position of the mediastinum and the presence of an air bronchogram provides reassurance that proximal bronchi are patent. Collapse (implying obstruction of the proximal bronchus) is accompanied by loss of volume and displacement of the mediastinum towards the affected side.
The presence of ring shadows (diseased bronchi seen end-on), tramline shadows (diseased bronchi side-on) or tubular shadows (bronchi filled with secretions) suggests bronchiectasis. Nodular, reticular or honeycomb patterns are characteristic of diffuse parenchymal lung diseases. The presence of pleural fluid is suggested by a dense basal shadow which, in the erect patient, ascends towards the axilla. The assessment of a solitary pulmonary nodule is discussed below.  
COMMON CHEST X-RAY APPEARANCES
Increased lucency
· Consolidation: infection, infarction, inflammation, and rarely bronchoalveolar cell carcinoma · Lobar collapse: mucus plugging, tumour, compression by lymph nodes · Solitary nodule: see text · Multiple nodules: miliary TB, dust inhalation, metastatic malignancy, healed varicella pneumonia, rheumatoid disease · Ring shadows, tramlines and tubular shadows: bronchiectasis · Cavitating lesions: tumour, abscess, infarct, pneumonia (Staphylococcus/Klebsiella), Wegener's granulomatosis · Reticular, nodular and reticulonodular shadows: diffuse parenchymal lung disease, infection · Pleural abnormalities: fluid, plaques, tumour Increased translucency · Bullae · Pneumothorax · Oligaemia Hilar abnormalities · Unilateral hilar enlargement: TB, bronchial carcinoma, lymphoma · Bilateral hilar enlargement: sarcoid, lymphoma, TB, silicosis Other abnormalities · Hiatus hernia · Surgical emphysema  

 

 
 

CT scanning provides detailed images of the pulmonary parenchyma, mediastinum, pleura and bony structures. The contrast can be altered to highlight different structures such as the lung parenchyma, the mediastinal vascular structures or bone. Sophisticated software facilitates 3D reconstruction of the thorax and virtual bronchoscopy.

 

CT scanning is superior to chest radiography in determining the position and size of a pulmonary lesion and whether calcification or cavitation is present. It is now routinely used in the assessment of patients with suspected lung cancer and facilitates guided percutaneous needle biopsy. Information on tumour stage may be gained by examining the mediastinum, liver and adrenal glands.

 

High-resolution CT (HRCT) scanning uses thin sections to provide a detailed assessment of the pulmonary parenchyma and is particularly useful in assessing diffuse parenchymal lung disease, identifying bronchiectasis, and assessing the type and extent of emphysema.

 

CT pulmonary angiography (CTPA) is increasingly used in the diagnosis of pulmonary thromboembolism, where it may either confirm the suspected embolism or highlight an alternative diagnosis.

 

Ultrasound

 

Ultrasound is sensitive at detecting pleural fluid and may also be used to direct and improve the diagnostic yield from pleural biopsy. Information may also be provided on the anatomy of an empyema cavity and facilitate directed drainage.

 

Pulmonary angiography

 

Conventional pulmonary angiography is performed by passing contrast medium down a catheter inserted via the femoral vein into the main pulmonary artery. The technique represents the gold standard for the diagnosis of pulmonary embolism but is rarely used, particularly now that CTPA is widely available. It is essential in the investigation of patients with pulmonary hypertension, providing information on pulmonary and right heart pressures.

 

 

ENDOSCOPIC EXAMINATION

 

Laryngoscopy

 

The larynx may be inspected indirectly with a mirror or directly with a laryngoscope. Fibreoptic instruments allow a magnified view to be obtained.

 

Bronchoscopy

 

The trachea and larger bronchi may be inspected by either a flexible or a rigid bronchoscope. Flexible bronchoscopy may be performed under local anaesthesia with sedation as an outpatient. Structural changes, such as distortion or obstruction, can be seen. Abnormal tissue in the bronchial lumen or wall can be biopsied, and bronchial brushings, washings or aspirates can be taken for cytological or bacteriological examination. Small biopsy specimens of lung tissue taken by forceps passed through the bronchial wall (transbronchial biopsies) may reveal sarcoid granulomas or malignant diseases and may be helpful in diagnosing certain bronchocentric disorders (e.g. hypersensitivity pneumonitis, cryptogenic organising pneumonia), but are generally too small to be of diagnostic value in other diffuse parenchymal pulmonary disease. Transbronchial needle aspiration (TBNA) may sample mediastinal lymph nodes and assist with staging of lung cancer. Endobronchial ultrasound is currently undergoing assessment as a method of directing and enhancing the diagnostic yield of TBNA.

 

Rigid bronchoscopy requires general anaesthesia but is more advantageous in certain situations e.g. evaluating massive haemoptysis or removing foreign bodies. In addition, endobronchial laser therapy and endobronchial stenting may be more easily performed with rigid bronchoscopy.

 

SKIN TESTS

 

The tuberculin test may be of value in the diagnosis of tuberculosis. Skin hypersensitivity tests are useful in the investigation of allergic diseases.

 

Abbreviation

Stands for  

FEV1

Forced expiratory volume in 1 second  

FVC

Forced vital capacity  

VC

Vital capacity (relaxed)  

PEF

Peak (maximum) expiratory flow  

TLC

Total lung capacity  

FRC

Functional residual capacity  

RV

Residual volume  

TLCO

Gas transfer factor for carbon monoxide  

KCO

Gas transfer per unit lung volume  

In diseases characterised by airway narrowing (e.g. asthma, bronchitis and emphysema) maximum expiratory flow is limited by dynamic compression of small intrathoracic airways, some of which close completely during expiration, limiting the volume which can be expired. Hyperinflation of the chest results, and can become extreme if elastic recoil is also lost due to parenchymal destruction, as in emphysema. In contrast, diseases which cause lung inflammation and/or scarring and fibrosis are characterised by progressive loss of lung volume with normal expiratory flow rates. Gas exchange is impaired by both parenchymal destruction (emphysema) and by interstitial disease, which disrupts the local matching of ventilation and perfusion.

 

In respiratory function testing, airway narrowing, lung volume and gas exchange capacity are quantified and compared with normal values adjusted for age, gender, height and ethnic origin.

 

Airway narrowing is assessed by forced expiration into a peak flow meter or a spirometer. Peak flow meters are cheap and convenient for home monitoring (e.g. detection and monitoring of asthma) but values are effort-dependent. The forced expiratory volume in 1 second (FEV1) and vital capacity (VC) are obtained from maximal forced and relaxed expirations into a spirometer. FEV1 is disproportionately reduced in airflow obstruction resulting in FEV1/VC ratios of less than 70%. When airflow obstruction is seen, spirometry should be repeated following inhaled short-acting β2-adrenoceptor agonists (e.g. salbutamol); reversibility to normal is suggestive of asthma. To distinguish large airway narrowing (e.g. tracheal stenosis or compression) from small airway narrowing, flow-volume loops are recorded during maximum expiratory and inspiratory efforts.

 

Lung volume can be measured by dilution of an inhaled inert gas (usually helium) or by determining the pressure/volume relationship of the thorax by body plethysmography. The former method measures the volume of intrathoracic gas which mixes quickly with tidal breaths, while the latter measures total intrathoracic gas volume, including poorly ventilated areas such as bullae.

 

       

 

PATTERNS OF RESPIRATORY FUNCTION ABNORMALITIES IN DISEASE

 

 

Asthma Chronic bronchitis Emphysema Pulmonary fibrosis

FEV1

↓↓ ↓↓ ↓↓

VC

↓↓

FEV1/VC

→/↑

TLCO

↓↓ ↓ ↓

KCO

→/↓

TLC

→/↑ ↑↑

RV

→/↑ ↑↑

To measure the capacity of the lungs to exchange gas, patients inhale a test mixture of 0.3% carbon monoxide, which is avidly bound to haemoglobin in pulmonary capillaries. After a short breath-hold, the rate of disappearance of CO into the circulation is calculated from a sample of expirate, and expressed as the TLco or carbon monoxide transfer factor. Helium is also included in the test breath to allow calculation of the volume of lung examined by the test breath. Transfer factor expressed per unit lung volume is termed Kco.

 

Exercise tests

 

Resting measurements are sometimes unhelpful in early disease or in patients complaining only of exercise-induced symptoms. Exercise testing with spirometry before and after can be helpful in demonstrating exercise-induced asthma. Walk tests include the self-paced 6 minute walk and the externally paced incremental 'shuttle' test. These can provide simple, repeatable assessments of disability and response to treatment. Finally, cardiopulmonary exercise testing using cycle or treadmill exercise with measurement of metabolic gas exchange, ventilation and cardiac responses is useful in distinguishing cardiac limitation from respiratory limitation in the breathless patient.

 

           

The main stage

At this stage the student will continue to build professional skills. Particularly at the bedside student demonstrates the ability to collect complaints, history of disease and life, to make an objective examination of the patient by different systems and organs and on the basis of the data to the differential diagnosis to establish a preliminary diagnosis. To support his opinion, the student makes the plan an additional examination of the patient. Synthesizing all the data obtained during examination of the patient, the student formulates a final clinical diagnosis according to modern classification and diagnostic criteria.
Analysis of the results allows the student to prescribe appropriate treatment of the patient depending on clinical variant and degree of activity, complications, comorbidities and give recommendations for further treatment and lifestyle.

The final stage

Assessment of action of each student during class and standardized end control. It conducted the analysis of student achievement, announced rating of each student and put in the book of visits and student achievement. Parish groups simultaneously puts rating in accounting performance and attendance of students. The teacher assures them his signature.

Brief information for students on the theme of the next lesson and instructional techniques to prepare for it.

 

Task № 1.

Patient N., 54 entered to the hospital, complained of chest pain on the right side, fever to 38.5, overall weakness, sweating, headache, loss of appetite. In history - hypothermia 2 days ago. On examination: pale, clear skin. Temperature is 38,7 ° C. Heart rate 100/min, BP 125/80 mmHg. Respiratory rate is 28/min, increased vocal fremitus, dull percussion note, bronchial breathing, and wet rales over the lower part of the right half of the chest.

The ECG: overload right heart. CBC: Er – 4,2∙ 1012 / l, Hb - 135 g / l, CI – 0,96, Leuk. - 15,0 ∙ 109 / L, segm. - 75, lymph. - 12%, mon. - 13%, platelets - 196 ∙ 109 / l, ESR - 25 mm / h. Common sputum analysis: leukocytes: 56 in visual field, neutrophils: 41 in visual field, alveolar macrophages: 15 in visual field. X-ray chest: enhanced pulmonary image, increasing the size of the root of the right lung, infiltrative shadow in the projection of 10 and 9 segments of the right lung.

What are the syndromes can be identified in this patient?

What are the signs of symptoms of consolidation of lung tissue in the present opinion the patient?

 

Task № 2.

Patient L. 60, smokes 20 years, complained of marked general weakness, fever to 38.50C, cough with yellow-green sputum, palpitation, shortness of breathing that progresses over several years, increasing during exacerbations of bronchitis, after exercise, inhalation of cold, moist air, sharp odor.

Examination: The skin, mucous membranes pale, gray color. Chest is emphysematous, additional muscles takes part in breathing. The RR 28/min. Heart rate 110/min, BP 130/80 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: overload of right atrium. CBC: Er - 4,0 ∙ 1012 / l, Hb – 4,3∙1012/ l, CI – 0,91, Leuk. - 12,0 ∙ 109 / L, eosinophils - 2%, segm. – 77%, lymph. - 10%, mon. - 11%, platelets - 212 ∙ 109 / l, ESR - 31 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.

What are the syndromes can be identified in this patient?

What are the mechanisms of dyspnea in this patient?

Recommended literature:

   А. Main:

1. Davidson’s Principles and Practice of Medicine, 2006. 

 

  Materials for self-control:

А. The questions for self-control:

1. What are the symptoms and syndromes of respiratory diseases do you know?
2. In which diseases can occur dyspnea and what mechanisms of its occurrence?
3. What diseases are accompanied by the development of hemoptysis?
4. What are the main causes of cough?

5.What laboratory methods for diagnosis of respiratory diseases used?
6.What do you know instrumental methods of diagnosing diseases of respiratory tract?

     

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

 

 

MINISTRY OF HEALTH OF UKRAINE



Поделиться:


Читайте также:




Последнее изменение этой страницы: 2020-12-09; просмотров: 71; Нарушение авторского права страницы; Мы поможем в написании вашей работы!

infopedia.su Все материалы представленные на сайте исключительно с целью ознакомления читателями и не преследуют коммерческих целей или нарушение авторских прав. Обратная связь - 18.219.215.75 (0.249 с.)