PATHOLOGY OF LOWER RESPIRATORY TRACT
1. Bronchitis
(a) Acute bronchitis
Definition: A common condition caused by infection and inhalants.
Aetiology: infectious agents – allergens, viruses, bacteria
Pathogenesis: Inflammation of the mucosal lining of the tracheobronchial tree due to viral or bacterial
infection. Increased secretion of the mucus, bronchial swelling, and dysfunction of the cilia lead to
increased resistance to expiratory airflow, causing air trapping on expiration.
Clinical manifestations:
History -the patient may give a history of the following;
 Recent upper respiratory infection
 Chronic lung disease
 Smoking
 Exposure to respiratory irritants
 Mucopurulent productive congestion
Examination
 Fever
 Sputum; mucoid (viral), mucopulent (bacterial)
 Wheezing
(b) Chronic bronchitis
Definition: Continued bronchial inflammation with progressive increase in productive cough and
dyspnea not attributable to specific causes.
Pathogenesis: The bronchial mucosa becomes thickened and rigid due to vasodilatation, congestion,
and edema. Excessive secretion of mucus, together with narrowing of the passageways due to
inflammation, causes obstruction to maximal expiration and later to maximal inspiration.
Clinical manifestations
History: The client may give a history of the following;
 Cough (bronchial irritation) with copious sputum production
 Recurrent chest infections, initially in winter but becoming perennial
 Cigarette smoking
 Generally overweight
Examination
 Cyanosis and edema; 'blue bloaters'
 Percussion note resonant
 Wheezing
 Cardiac enlargement
 Peripheral edema
2. Bronchial asthma
Definition: An episodic disorder characterized by recurrent paroxysms of wheezing and dyspnea not
attributable to other disease.
Pathogenesis: Response is initiated by release of chemical mediators in an IgE mast cell interaction.
This results in increased bronchial secretion from goblet cells and in mucosal swelling and
bronchospasm. There is constriction of the air passages and air trapping.
Extrinsic asthma mainly affects children with a family history of allergies. Attacks usually disappear
or decrease in severity and frequency as the person matures.
Intrinsic asthma, mainly affects adults and attacks are usually related to a respiratory tract infection,
exercise, or emotion. Allergy can play a part.
Clinical manifestations
History; patients may give a history of the following;
 Childhood asthma
 Inhalation of irritants
 Respiratory infection
 Positive family history/childhood asthma
 Tightness in chest
 Psychogenic factors
 Dyspnea
 Fatigue due to increased work of breathing
Examination
Tachypnea
Wheeze
Cough
Production of sputum.
Prognosis: The lungs usually return to normal once the attack has subsided and the precipitating
factors have cleared.
3. Bacterial pneumonia: Pneumococcal pneumonia (streptococcus pneumoniae)
Definition: A common bacterial infection of the lung, responsible for 30 to 80 percent of community
acquired pneumonias.
Aetiology: Malnutrition, alcoholism, and aging are risk factors for its development.
Pathogenesis: An acute inflammatory response leads to consolidation of the affected part of the lung.
The involved alveoli become airless, causing perfusion with poor ventilation, but rarely cause severe
hypoxia.
The disease progresses in four stages:
 Hyperemia: Alveolar spaces become engorged with fluid and blood.
 Red hepatization: The involved lung becomes red and granular (liver like) from the influx of
red blood cells, fibrin, and polymorphonuclear leukocytes.
 Gray hepatization: The lung tissue becomes solid and grayish as leukocytes consolidate in the
alveoli.
 Resolution: Excudate is lysed and reaborded by neutrophilis and macrophages. Lung structure
and function are restored.
Clinical manifestations include fever, cough, pleuritic chest pain, and production of rusty-colored or
blood-streaked sputum.
Prognosis: On the elderly, bacterial pneumonia may be life threatening. Classic symptoms vary and
may manifest themselves as lethargy or confusion. Mycoplasmal pneumonia is a self-limiting disease
that is a common cause of respiratory tract infections (the mycoplasmal organism is smaller than
bacteria but is not classified as a virus). Viral pneumonia is usually mild and self-limiting in adults but
may be rapidly proliferative and be fatal in children (usually under age 2).
4. Pulmonary tuberculosis
Definition: A chronic inflammatory lung disease caused by Mycobacterium tuberculosis (an acid-fast
bacillus) and transmitted via droplets from persons with active tuberculosis. It is more common in
malnourished and aged persons.
Pathogenesis: Bacterial invasion leads to a chronic inflammatory response resulting in scarring,
reduced compliance, and reduced lung function. Pulmonary tuberculosis may be primary (in the
immune-competent) or secondary (re-activated).
Clinical manifestations may include evening fever with night sweat, cough with sputum production,
malaise, weight loss and hemoptysis. The disease may spread, involving other structures such as
meninges, kidneys, bones.
Diagnostic tests include sputum for AAFB, skin tests, chest radiographs.
5. Pulmonary Embolism
Definition: An occlusion of one or more pulmonary vessels due to a venous thrombus (usually from
the deep veins of the legs or pelvis). It may lead to infarction of lung tissue distal to the occlusion. The
severity depends on the following; the size of the embolus, the sensitivity of the tissue, the presence of
collateral or secondary circulation. Thrombus. An abnormal clot that develops in and remains attached
to the wall of a blood vessels.
Embolus. A clot that has broken from a thrombus and circulates in the vascular system and becomes
lodged in a new location.
Pathogenesis
Sequence of events: A venous thrombosis occurs on the vein wall, the clot dislodges, creating an
embolus, the embolus increases in sizes as it progresses toward the heart, the right ventricle pumps the
embolus into the lungs, the blood clot lodges in the pulmonary capillary bed, there is obstruction of
blood flow beyond the point of occlusion, perfusion of affected area of the pulmonary capillary bed
closes. Infarction of lung tissue may result, large obstructions may cause increased resistance to
pulmonary blood flow and right-sided heart failure (corpulmonale). Increases in venous pressure may
damage the vessels, causing hemorrhage into the pulmonary tissues.
Clot formation: Factors contributing to thrombosis include the following;
Venostasis: Sluggish blood flow, endothelial disruption of the vessel lining may provide a place for
clots to form.
Hypercoagulability: thrombi become dislodged and released into venous circulation. Factors that affect
this include the following; abrupt position change, exercise after a period of inactivity, straining at
stool (Valsalva maneuver).
Precipitating factors: Risk factors include the following; immobility and obesity, prior history of
embolus or thrombosis, the elderly, pelvic trauma or surgery, prior history of congestive heart failure,
use of birth control pills containing estrogen, blood dyscrasias
Resolution: The pulmonary embolus becomes dissolved by the fibrinolytic system. Fibrous
replacement converts infracted lung tissue to scar tissue.
Clinical manifestations
History: The client may give a history of the following;
 May be clinically silent
 Dyspnea of sudden onset
 Cough, with hemoptysis
 Chest pain: Pleuritic or deep and crushing
 Tachypnea, fever
 Anxiety, apprehension, restlessness
 Palpitations
 Diaphoresis and weakness
 Nausea and vomiting
Shock
Examination
 Cyanosis
 Distended neck veins
 Tachycardia
 Decreased breath sounds
 Localized wheezing
6. Tumors of the lung may be benign but are mainly malignant.
Malignant: Predisposing factors include cigarette smoking, air pollution, industrial chemicals or
certain occupations (e.g., asbestos workers). Chronic bronchitis may develop into bronchogenic
carcinoma.
Clinical manifestations
May be asymptomatic for a long time
Diagnosis by chest xray, sputum cytology, and bronchscopy.
Prognosis
Generally poor