syndrome
Broncho-obstructive
syndrome
Broncho-obstructive
syndrome is the
collective term including a symptomcomplex of specificly outlined clinical
implications of disturbance of bronchial
passableness, having in the basis
narrowing or an occlusion of respiratory
tracts.
Occurrence and its development are
influenced by various factors and, first of
all, a respiratory virus infection
contamination
Causes of Bronchial
obstruction
Pulmonary secretions
Foreign body
Bronchogenic carcinoma
Aspiration
Extrinsic compression by a
mass
Metastatic tumour
Asthma
COPD
Emphysema
Bronchiectasis
Fibrosing alveolitis
Lung collapse
Lung fibrosis
Tracheomalacia
Tracheal stenosis
Bronchial stenosis
Endobronchial tumors
Enlarged lymph nodes
Tuberculosis
Histoplasmosis
Enlarged pulmonary
arteries
Enlarged atrium from any
causes
Bronchial oedema
Asthma
COPD
BRONCHITIS
Bronchitis is characterized by
inflammation of the bronchial tubes (or
bronchi), which are the air passages that
extend from the trachea into the small
airways and and alveoli.
ETIOLOGY
Viral
ETIOLOGY (con---d)
Bacterial
Pneumococcus,
streptococcus, Haemofiulus
influenzae, Moraxella catarralis.
Mycoplasma pneumoniae and
clamydii also can be causative agent
in 10-20% of all acute bronchitis,
predominantly at young persons.
Chemical aerosols, smoke, dusts.
CLASSIFICATION
Catarrhal
Ulcerative
Hemorrhagic
Pseudomembranous
Capillary
CLASSIFICATION
Acute (Acute bronchitis is manifested
by cough and, occasionally, sputum
production that last for no more than
3 weeks)
Chronic (Chronic bronchitis is defined
clinically as cough with sputum
expectoration for at least 3 months
during a period of 2 consecutive
years)
PATHOGENESIS
Respiratory
PATHOGENESIS (con---d)
PATHOGENESIS (con---d)
Acute
COMPLAINS
COMPLAINS
Complains
Dyspnea
due to obstruction of
bronchial airways or inflammation of
upper respiratory tract.
Dyspnea and cyanosis: These are not
observed in adults unless the patient
has underlying COPD or another
condition that impairs lung function.
Complains
Raw
Complains
Muscle
aches
Extreme fatigue
Fever: This is a relatively unusual sign
and, when accompanied by cough,
suggests either influenza or pneumonia.
Nausea, vomiting, and diarrhea: These
are rare. Severe cases may cause general
malaise and chest pain. With severe
tracheal involvement, burning, substernal
chest pain associated with respiration,
and coughing may occur.
Clinical examination
The
CLINICAL EXAMINATION
Hiperemia of the skin if fever is present
Vocal fremitus and percussion sound
unchanged
Auscultation sharp vesicular breathing,
ronflant crackles if pathologic process is
in the big and medium bronchis and
sibilant crackles if pathological process
is in the small bronchis. This crackles
are changed after the coughing.
LABORATORY FINDINGS
Chest X-ray remains unchanged
General blood test leucocytosis
with neutrophillia
Sputum analysis leucocytosis,
bacteria
Complications
EVOLUTION
Usually
7-10 days
Prognosis
Patients
Chronic bronchitis
Chronic
bronchitis is defined
clinically as cough with sputum
expectoration for at least 3 months
during a period of 2 consecutive
years.
Chronic bronchitis
Chronic
Chronic bronchitis
As
Chronic bronchitis
When
Chronic bronchitis
Chronic
bronchitis is a condition
associated with excessive
tracheobronchial mucus production
sufficient to cause cough with
expectoration for at least 3
monthsfor more than 2 consecutive
years. The alveolar epithelium is both
the target and the initiator of
inflammation in chronic bronchitis.
Chronic bronchitis
Chronic bronchitis
Chronic
as:
simple chronic bronchitis,
chronic mucopurulent bronchitis, or
chronic bronchitis with obstruction.
Chronic bronchitis
Mucoid
sputum production
characterizes simple chronic
bronchitis.
Persistent or recurrent purulent
sputum production in the absence of
localized suppurative disease, such
asbronchiectasis, characterizes
chronic mucopurulent bronchitis.
Chronic bronchitis with obstruction
must be distinguished from chronic
infectiveasthma.
Chronic bronchitis
The
Chronic bronchitis
Chronic bronchitis
Chronic bronchitis
bronchitis cannot be
diagnosed radiologically. Although
findings such as increased lung
markings or tubular opacities,
bronchial wall cuffing (thickening)
can be seen with bronchitis, they are
nonspecific.
Emphysema
Emphysema
is
chronic obstructive pulmonary disease (
COPD)
.
Emphysema
Emphysema
is defined pathologically
as an abnormal permanent
enlargement of air spaces distal to
the terminal bronchioles,
accompanied by the destruction of
alveolar walls and without obvious
fibrosis.
Emphysema
Emphysema
frequently occurs in
association withchronic bronchitis.
These 2 entities have been
traditionally grouped under the
umbrella term COPD. Patients have
been classified as having COPD with
either emphysema or chronic
bronchitis predominance.
Emphysema
The
Classification
The
Centriacinar
Panacinar
Paraseptal
Causes
Cigarette
Causes
AAT
(alpha1-antitrypsin) deficiency
syndrome: This syndrome leads to
protease-antiprotease imbalance and
unopposed action of neutrophil
elastases.
Causes
Causes
Causes
Vasculitis syndrome, as follows:
Hypocomplementemic vasculitis
urticaria syndrome (HVUS) may be
associated with obstructive lung
disease.
Other symptoms include angioedema,
nondeforming arthritis, sinusitis,
conjunctivitis, and pericarditis.
Causes
Connective-tissue
disorders, as follows:
Cutis laxais a disorder of elastin that is
characterized most prominently by the
appearance of premature aging. The
disease usually is congenital, with various
forms of inheritance (ie, dominant,
recessive). Precocious emphysema has been
described in association with cutis laxa as
early as the neonatal period or infancy. The
pathogenesis of this disorder includes a
defect in the synthesis of elastin or
tropoelastin.
Causes
Marfan
syndromeis an autosomal
dominant inherited disease of type I
collagen characterized by abnormal
length of the extremities, subluxation
of the lenses, and cardiovascular
abnormality. Pulmonary
abnormalities, including emphysema,
have been described in
approximately 10% of patients.
Causes
Ehlers-Danlos
syndromerefers to a
group of inherited connective-tissue
disorders with manifestations that
include hyperextensibility of the skin
and joints, easy bruisability, and
pseudotumors.
Causes
Pathophysiology
Pathophysiology
Pathogenesis
Alpha1-antitrypsin
deficiency
Alpha1-antitrypsin
deficiency
Complains
Cough:
intermittent or daily
present throughout day- seldom only nocturnal
Sputum:
Any pattern of chronic sputum production
cough and sputum production due to Increased
mucus production and reduced mucociliary clearance
Dyspnea:
Progressive and Persistent
"increased effort to breathe" "heaviness" "air hunger"
or "gasping"
Worse on exercise
Worse during respiratory infections
History
Most
History (con---d)
Commonly,
History (con---d)
Breathlessness,
History (con---d)
Wheezing
History (con---d)
Clinical examination
Barrel chest
Clinical examination
The sensitivity of the physical evaluation in mild-tomoderate disease is relatively poor. However, the physical
signs are quite sensitive and specific for severe disease.
Patients with severe disease experience tachypnea and
respiratory distress with simple activities.
The respiratory rate increases in proportion to disease
severity. The use of accessory respiratory muscles and
paradoxical indrawing of lower intercostal spaces are
evident.
In advanced disease, cyanosis, elevated jugular venous
pressure, and peripheral edema can be observed.
Measurement of the forced expiratory time maneuver is a
simple bedside test; a forced expiratory time greater than
6 seconds indicates severe expiratory airflow obstruction.
Emphysema:ChronicBronchitis
Emphysema = pink puffer
Age
60+y
50y
Rest dyspnea
mild-mod
none
Exer dyspnea
severe
moderate
Cough
prominent
Sputum
scanty,mucoid
largevolume,purulent
Resp infect
lessoften
often
Resp failure
terminal
repeatedly
Cor pulmonale
terminal
common
PHT (rest)
0-mild
Mild-moderate
(exertion)
moderate
severe
Build
Asthenic,cachectic
obese,cyanosed
Hematocrit
35-45
50-55
Breath pattern
useaccessorymusclesofrespiration
donotuseaccessorymusclesofrespiration
Normal
sleepapnea
Hyperinflation;Bullae
Increasedbronchovascularmarkings
Sleep pattern
XRC
Diagnosis
Spirometry to Diagnose
Spirometry
FEV1 Forced expired volume in the first
second
FVC Total volume of air that can be exhaled
from maximal inhalation to maximal
exhalation
FEV1/FVC% - The ratio of FEV1 to FVC,
expressed as a percentage.
FEV1/FVC <70% and a postbronchodilator
FEV1 <80% predicted confirms the presence
of airflow limitation that is not fully reversible.
Spirometry
Classification by Severity
Laboratory Studies
Arterial
Laboratory Studies
Hematocrit
Laboratory Studies
Bicarbonate
value:
Chronicrespiratory acidosisleads to
compensatory metabolic alkalosis. In
the absence of blood gas
measurements, bicarbonate levels
are useful for following disease
progression.
Laboratory Studies
Laboratory Studies
Sputum
Imaging Studies
CXR shows hyperinflation, flattened diaphragms, increased
CT scanning
A
CT scanning
A
BRONCHIAL ASTHMA
Asthma
BRONCHIAL ASTHMA
Asthma
Causes
Causes
Occupational exposure
Irritants (eg, household sprays, paint fumes)
Various high and low molecular weight
compounds: A variety of high and low
molecular weight compounds are associated
with the development of occupational asthma,
such as insects, plants, latex, gums,
diisocyanates, anhydrides, wood dust, and
fluxes.
Emotional factors or stress
Perinatal factors: Prematurity and increased
maternal age increase the risk for asthma;
breastfeeding has not been definitely shown
to be protective. Both maternal smoking and
prenatal exposure to tobacco smoke also
increase the risk of developing asthma.
Frequency
Age
Asthma
Age
The
Pathophysiology
The
pathophysiology of asthma is
complex and involves the following
components:
Airway
inflammation
Intermittent airflow obstruction
Bronchial hyperresponsiveness
Pathophysiology
The
Pathophysiology
Some of the principal cells identified in airway
inflammation include mast cells, eosinophils,
epithelial cells, macrophages, and activated T
lymphocytes. T lymphocytes play an important
role in the regulation of airway inflammation
through the release of numerous cytokines. Other
constituent airway cells, such as fibroblasts,
endothelial cells, and epithelial cells, contribute
to the chronicity of the disease. Other factors,
such as adhesion molecules (eg, selectins,
integrins), are critical in directing the
inflammatory changes in the airway. Finally, cellderived mediators influence smooth muscle tone
Pathophysiology
The
Pathophysiology
Physical examination
General
Physical examination
Pulsus
paradoxus: This is an
exaggerated fall in systolic blood
pressure during inspiration and
may occur during an acute
asthma exacerbation.
Depressed sensorium: This
finding suggests a more severe
asthma exacerbation with
impending respiratory failure.
Physical examination
Chest examination
End-expiratory wheezing or a prolonged
expiratory phase is found most commonly,
although inspiratory wheezing can be heard.
Diminished breath sounds and chest
hyperinflation (especially in children)may be
observed during acute asthma exacerbations.
The presence of inspiratory wheezing or
stridor may prompt an evaluation for an upper
airway obstruction such as vocal cord
dysfunction, vocal cord paralysis, thyroid
enlargement, or a soft tissue mass (eg,
malignant tumor).
Physical examination
Upper
airway
Look for evidence of erythematous or
boggy turbinates or the presence of
polyps from sinusitis, allergic rhinitis, or
upper respiratory tract infection.
Any type of nasal obstruction may result
in worsening of asthma or symptoms of
exercise-induced bronchospasm.
Skin: Observe for the presence of atopic
dermatitis, eczema, or other
manifestations of allergic skin conditions.
Laboratory Studies
Imaging Studies
Imaging Studies
Sinus
Other Tests
Exercise testing
Exercise testing
Eucapnic hyperventilation
Eucapnic
Peak-flow monitoring
Peak-flow monitoring
Inform
Complications
The
Complications
Prognosis