Seminars for the 5th year students
Seminar 10
Prof. Jiří Horák
LUNG DISEASES (2)
BRONCHIAL ASTHMA, CHRONIC OBSTRUCTIVE LUNG DISEASE,
BRONCHOGENIC CARCINOMA
Pulmonary gas exchange
Hypoventilation
= ventilation that (for a given metabolic demand) is inadequate to keep the
arterial PCO2 in the normal range
Causes of hypoventilation: pharmacologic depression or structural damage to
the respiratory center, neuromuscular disease, or chest wall abnormalities
Abnormal diffusion
The diffusing capacity of the lung must fall to less than 10% of normal before it
affects PaO2 at rest.
Factors interfering with complete equilibration: ↑ diffusion distance (thickening
of the alveolar capillary membrane); ↑ rate of blood flow or ↓ in the number of
open capillaries; ↓ driving pressure from alveolus to blood (as in extreme
altitudes)
Ventilation-perfusion inequality
If Va/Q inequality develops, the PaO2 will fall and the PaCO2 will rise. This is an
inevitable consequence of OLD. Desaturation and hypercapnia may develop at
night owing to ↓ in minute ventilation.
Asthma
Basic characteristics:
airway inflammation
airway hyperresponsiveness to a variety of stimuli
airway obstruction
Mucosal infiltration: eosinophils, activated T-lymphocytes, mast cells etc. →
production of cytokines, arachidonic acid metabolites, bradykinins
Types of asthma
Classification
Extrinsic
Intrinsic
Adult onset
Exercise induced
Aspirin-sensitive
assoc. with nasal polyps
Allergic bronchopulmonary
aspergillosis
Initiating factors
IgE – mediated external allergens
?
?
alteration in airway temperature and humidity;
mediator release
aspirin and other NSAIDs
hypersensitivity to Aspergillus species
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Seminars for the 5th year students
Seminar 10
Prof. Jiří Horák
Dg: episodic dyspnea with wheezing, intermittent cough; symptoms are worse at
night
Lab.: decreased FEV1 (improvement with bronchodilator); portable peak-flow
measurements; skin tests – demonstrate atopy; blood tests – eosinophilia and
IgE increase
Status asthmaticus – an attack of increased severity that is unresponsive to
routine therapy. The degree of severity is best appreciated by a measure of
expiratory flow rates. Hypoxemia is usually present. PaCO2 is typically ↓ early in
an attack. With increasing severity, PaO2 falls and PaCO2 returns to normal and
then rises.
Chronic obstructive pulmonary disease (COPD)
= slowly progressive airway obstruction with periodic exacerbations (↑ in
dyspnea and sputum production).
Clin: dyspnea, exercise intolerance, cough, sputum production.
Phys: lung overinflation, prominent use of accessory respiratory muscles,
diminished breath sounds, expiratory wheezing; pink puffer, blue bloater.
Dg: in early stages the physical examination may be normal → diagnosis
depends on ↓ expiratory flow rates.
Spirometry: ↓ VC and expiratory flow rates, ↑ RV, FRC and TLC.
Bronchodilators can often ↑ expiratory flow.
Arterial blood gases: hypoxemia of varying severity; hypercapnia is seen in
advenced stages only.
Severe hypoxemia → anatomic remodeling of pulmonary arteries → pulmonary
hypertension and subsequent right heart failure (cor pulmonale). Secondary
polyglobulia.
Emphysema
Def: abnormal enlargement of the air spaces distal to the terminal bronchioles
due to destructive changes in the alveolar walls. The degree of airway
obstruction in patients with COPD correlates closely with the severity of
emphysema.
Pathol: imbalance of proteases and antiproteases in the lung → lung destruction
Dg: physical examination, X-ray, ↓ diffusing lung capacity
Small airway disease
Inflammation of the terminal and respiratory bronchioles, fibrosis of the airway
leading to narrowing, goblet cell metaplasia → airway obstruction
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Seminars for the 5th year students
Seminar 10
Prof. Jiří Horák
Chronic bronchitis
Def: persistent cough with sputum production for › 3 months in each year over
three years
Th: symptomatic, reduction of the abnormal airway tone, treatment of
inflammation and specific complications (infection, excessive bronchial
secretions, hypoxemia, cor pulmonale)
Smoking cessation
Pharmacologic therapy
Sympathomimetics
- beta2-specific agents: metaproterenol, terbutaline, albuterol
- epinephrine
Methylxanthines
- theophylline
- aminophylline
Anticholinergics
- atropine
- ipratropium bromide
Anti-inflammatory drugs
- corticosteroids
- cromolyn sodium
Oxygen
Antibiotics
Lung cancer
-
the leading cause of death
causative factors: cigarette smoking – responsible for up to 90% of cases
4% of those who have smoked for 40 years develop cancer
2% of new lung cancer cases are due to passive smoking exposure
all types except bronchoalveolar carcinoma are associated with smoking
asbestos (esp. + smoking) – 14% of smokers with asbestosis develop lung
cancer
- small-cell and non-small cell carcinoma
secondary tumours:
- metastatic spread of neoplasma to the lung: lung parenchyma, bronchial
mucosa, chest wall, pleural space, mediastinum
- direct extension (the least common): breast, liver, pancreas
- hematogenous: renal, thyroid, testicular tumours, bone sarcomas
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Seminars for the 5th year students
Seminar 10
Prof. Jiří Horák
Clin: cough, weight loss, hemoptysis, dyspnea, chest pain
Pancoast‘s syndrome
Horner‘s syndrome
superior vena cave syndrome
postobstructive pneumonia
hoarseness (paresis of left n. recurrens)
pleural or pericardial effusion
paraneoplastic syndromes in 10 – 50% of patients:
- hypertrophic pulmonary osteoarthropathy
- gynecomastia
- syndrome of inappropriate ADH secretion
- hypercalcemia
- Cushing‘s syndrome
- Eaton-Lambert myasthenic syndrome
- thrombophlebitis
metastases: brain, liver, bone, lymph nodes
Dg: laboratory tests, X-ray, CT scan, bronchoscopy, biopsy
Th: surgery – for non-small cell carcinoma
radiation therapy – not beneficial in non-small cell carcinoma
chemotherapy in small cell carcinoma limited to the thorax prolongs survival
from 3 to 16 months
The 5-year survival rate for all patients with bronchogenic carcinoma is about
10%
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