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RESPIRATORY SYSTEM

Congenital diseases Infections Malignancy of the respiratory system

The respiratory system


Lungs Nasopharynx and trachea The diaphragm and muscle of the chest wall The regulatory neural circuits

Aetiological factors
Infection Smoking Air pollution Occupation genetic Influenza, measle, bacterial pneumonia, TB Lung cancer, chronic bronchitis, emphysema Chronic bronchitis Pneumoconiosis, asbestosis, lung cancer Cystic fibrosis, astma, 1-antitrypsin deficiency

Function of respiratory system


Gas exchange (O2 & CO2) Regulation of blood pH ( acid-base balance) Olfaction (smelling) Defense mechanism

Diseases
1. acute or chronic infection of URT or LRT e.g sinusitis, pharingitis, bronchitis, pneumonia, TB 2. Obstructive lung disease (COPD) in which there is a temporary or permanent obstruction of the airways e.g chronic bronchitis, asthma, emphesema. The FEV1/FVC ratio is < 80% (hallmark). These disease will reduce air flow through the lung and air trapping inside the lungs which affect tissue perfusion.

3. Restrictive lung diseases in which there is a restricted lung expansion. The FEV1/FVC ratio is >80% e.g. interstitial lung disease as NRDS or poor breathing mechanics (extrapulmonary) 4. Tumors: benign or malignant 5. Pleural cavity diseases 6. Pulmonary vascular disease : embolism

Atelectasis
Collapse Loss of lung volume caused by inadequate expansion of airspaces

Resorption- obstruction prevents air from reaching distal airways Compression- accumulation of fluid, blood or air within the pleural cavity Microatelectasis- loss of surfactant Contraction- fibrotic changes in the lung or pleura hamper expansion

OBSTRUCTION & RESTRICTIVE LUNG DISEASE


1) Obstructive limitation of airflow asthma, bronchitis, bronchiectasis, cystic fibrosis & bronchiolitis FVC- Normal or increased 2) Restrictive- FVC is reduced, expiratory flow rate Extrapulmonary disorders- neuromuscular disorders Acute or chronic interstitial lung disease sarcoidosis, idiopathic pulmonary fibrosis

Asthma
Episodic, reversible bronchospasm resulting from exaggerated bronchoconstrictor response to various stimuli. It is a wide spread disease nearly affecting 300 million people around the world It is a common chronic disorder of the airways characterized by recurring variable and reversible symptoms. Depending on the frequency and severity of symptoms it is either intermittent, mild moderate or severe

Patho physiology of asthma


3 hallmarks Inflammation (no infection) Hyperplasia of smooth muscles Excessive mucous secretion

Inflammation
Normal tissue response to pathogens or irritants Protective mechanism- remove the injurious agent and start healing process Signs- redness, swelling, pain, hotness Initiated by tissues cells e.g. mast cells that release chemical mediators e.g bradikynin As a result vasodilatation occurs and neutrophils and other WBC migrate to inflammatory site to remove the pathogen End result- tissue necrosis followed by healing

1) -

Extrinsic asthma Type 1 hypersensitivity rxn due to an extrinsic antigen IgE levels is high Allergic reaction to dust, pollens, foods, Family history of asthma

2) Intrinsic asthma - nonimmune, no history of allergic manifestation - No of stimuli that have little or no effect on normal subjects such as aspirin, exercise and pulmonary infection caused by virus

Causes of asthma
Allergen from nature e.g. pollen, dust, mites etc Medications e,g. aspirin Childhood infections Food allergies Exercise Hormonal changes e.g. adolescence Stress

Pathogenesis
Exaggerated bronchoconstrictor response Immediate Rxn by Ag induced mast cells Mediators released, Ag can enter the mucosa and activate the mast cells & eosinophils More mediators- bronchospasm, increased vascular permeability and mucous production

Hypersensitivity causes
Bronchial obstruction with distal overinflation or etelactasis (collapse) of lung Mucus plugging of bronchi Mucous gland hypertrophy Bronchial wall smooth muscle hypertrophy Thickening of bronchial basement membrane

Severe condition may lead to respiratory failure and death Over distended lungs

Clinical Course
Episodic dyspnea cough wheezing high mucus secretion

Diagnosis
Clinical picture and examination: cough, wheezing and dyspnea Pulmonary function test : decreases FEV1 more than 20% of the predicted value (FEV1/FVC ratio is 80%). Also the PEFR is used both as a diagnostic and to follow up the treatment.

Chronic Obstructive pulmonary


Irreversible airflow obstruction 2 common cond.- Emphysema & Cr. Bronchitis

Emphysema
Permanent enlargement of the airspaces distal to the terminal bronchioles accompanied by destruction of their walls Involve small airways (acinus)-respiratory bronchioles, alveolar ducts and alveoli

Pathogenesis
In smokers neutrophils and macrophages accumulates in alveoli 1-antitypsin is an inhibitor of protease secreted by neutrophils during inflammation High protease activity causes elastic tissue destruction Destruction of acinus wall and enlargement of airspace

Clinical features Progressive Dsypnea Weight loss hyperinflated lung Reduced FEV & ratio of FEV to FVC

Ch. Bronchitis
A persistent productive cough for at least 3 consecutive months in at least 2 consecutive years Middle aged men who are smokers Involves large (trachea & bronchi) and small (bronchioles) airways - inflammation, fibrosis and resultant narrowing of bronchioles - Coexistent emphysema

Aetiology Cause- smoking, air pollutant Recurrent, low grade bronchial inf. By Haemophilus influenza, Strept. Pneumonia RSV Local bronchial irritation causing chronic inflammation and bronchoconstriction.

Pathogenesis
Hyper secretion of mucous in bronchi Hypertrophy of mucous gland Metaplastic formation of mucin secreting goblet cells In addition they cause inflammation

Clinical course Prominent cough and production of sputum indefinitely without ventilatory dysfunction

Chronic bronchitis

Emphysema

Based on clinical features Morphology Eg. Chronic & recurrent cough with excess mucous secretion Affect both large (mucous secretion) & small (obstruction) airways Acinus Loss of elastic recoil

Bronchiectasis
The permanent dilation of bronchi and bronchioles caused by destruction of muscles and elastic supporting tissues associated with chronic infection Resulting from or associated with chronic necrotizing infections Secondary disease Dx- history & radiography

Aetiology
Ass with bronchial obstruction Foreign body, tumors, impaction of mucus Chronic bronchitis or atopic asthma Congenital or hereditary condition Cystic fibrosis due to viscid mucus Repeated bacterial infection in immunodeficiency state Kartagener syndrome ass with impair mucociliary clearance Complication of suppurative bronchopneumonia

Pathogenesis
2 critical processes: obstruction & ch. Persistent infection Normal clearance mechanism hampered by obstruction followed by 2ry infection Damage to bronchial wall weakening & permanent dilatation and fibrosis

Clinical course Persistent cough with expectoration of mucopurulent foul smelly sputum & may contain blood Clubbing of fingers Severe case
Pneumonia, lung abscess, emphysema, remote abscess (brain abscess) Obstructive ventilatory defects (hypoxemia, hypercapnia)

Adult respiratory distress syndrome


Aetiology
Shock, trauma, infection, gas inhalation (NO2, smoke, SO2), narcotic abuse, gastric aspiration, oxygen toxicity, DIVC.

Causes diffuse alveolar damage (unknown pathogenesis) Lungs are edematous, congested and hemorrhage. Poor prognosis

Defined by a) The acute onset of dyspnea b) Decreased arterial oxygen pressure c) Developmental of bilateral pulmonary infiltrates on radiograph d) Absence of clinical evidence of primary left sided heart failure

Respiratory infection
Primary with no underlying predisposing condition Secondary with predisposing factors
Loss or suppression of cough reflex Coma, anesthesia, neuromuscular disorder, post surgery Ciliary defects Immotile cilia syndromes Immunosuppressant HIV Macrophages fx inhibition Smoker, hypoxia Pulmonary edema Mucus disorder Excessive viscosity in cystic fibrosis or chr. bronchitis

Lung infection diseases


Bronchitis Bronchiolitis Pneumonia Pulm. Tuberculosis

Pneumonia
Alveolar inflammation Formation of protein rich exudate Clinical feature
Fever, cough, dyspnea, tachypnoea, sputum

Classification
Lobar pneumonia Bronchopneumonia

Brochopneumonia
Patchy consolidation Centered on bronchioles or bronchi More to infant, old age

Bronchopneumonia
Predisposing factors pre-existing dis such as acute bronchitis, chr obstructive airway dis and cystic fibrosis pts with debilitating dis. such as cancer, renal and heart failure, stroke Immunosuppressant pts failure to clear respiratory secretion in post operative pts Aetiology Staphylococi, streptococci, haemophilus influenza, fungi Affected area usually at basal and bilateral Histology- typical acute inflammation with exudates Complications septicemia, reduced consciousness, cyanosis, Heal with organization and scarring

bronchopnemonia

Lobar pneumonia

Lobar pneumonia

Lobar pneumonia
Affect a large part, or the entirely of a lobe Aetiology 90% peumococcal pneumonia- more to healthy adult Clinical feature Cough, fever, purulent sputum with flecks of blood Chest are dullness to percussion involving four stages Congestion--outpouring of exudate to alveolar spaces and venous congestion Red hepatisationmassive accumulation of polymorphs, lymphocytes and macrophages.Lung is red, solid and airless Grey hepatisation----further accumulation of fibrin, destruction of RBC & WBC Resolution8-10 days in untreated cases. Preservation of alveolar architecture

Pneumonia in immunosuppressed host


Known as opportunistic infection Aetiology Pneumocystic carinii Candida, aspergillus Cytomegalovirus, measles HIV lung disease for up to 70% of AIDS pts and cause of death in 1/3 of all AIDS pts

Aspiration pneumonia
Occurs in marked debilitated patients or those who aspirate gastric contents either while unconsciousness or during repeated vomiting Lung damaged due to gastric content and bacterial infection

Pulmonary Tuberculosis
Lung is the commonest site for tuberculosis Only occurs in about 10% of Mycobacterium tuberculosis (tubercle bacilli) infection. Majority cases due to M. tuberculosis hominis Risk factors Poverty, crowding, old age, malnutrition, alcoholism, , immunosuppressant, HIV chronic debilitating illness (eg; diabetes, chronic lung dis.) Clinical feature Weight loss Chronic cough with/without sputum Low grade fever Dyspnoea Hemoptysis Night sweat Early case of primary tuberculosis -asymptomatic

Stages of tuberculosis
Primary tuberculosis Secondary tuberculosis Miliary tuberculosis

Primary tuberculosis
Lung usually initial site of contact between tubercle bacilli Develop in unexposed and unsensitized person Asymptomatic focus of primary infection-Ghon focus 10mm size, at middle lobe of one lung Central zone of caseous necrosis surrounded by epitheloid histiocytes, Langerhans Giant cell and lymphocytes Ghon complex combination of primary infection and hilar node involvement Most cases heal with fibrocalcific (scar) nodule But tubercle bacilli present in the scar nodule Reactivation at later time when host defenses are compromised

Secondary tuberculosis
Mostly reactivation of primary infection Located at lung apices (high O2 tension) and always bilateral Histologically Typical granulomas with central zone of caseous necrosis Granuloma is an aggregate of epitheloid histiocytes (in lung tissue monocyte will change to specialized macrophage called histiocyte or epitheloid cell, have little phagocytic activity but have secretary fx). Some of histiocyte converted into multinucleated giant cell (Langhans giant cell) Giant cell form when foreign particle is too big to be ingested by one macrophages Two or more macrophages simultaneously try to engulf the tubercle bacilli, their membrane fuse and the cell unite Multinucleated giant cells may contain over 100 nuclei. Most lesion converted to fibrocalcific scar (fibrosis) and cavitations

primary

Primary TB

Secondary TB

Secondary TB

Miliary TB

granuloma

Langhans cell

Miliary tuberculosis
Consequences of primary or secondary Severe impairment of host resistance Lesion are common in lungs, meninges, kidney, bone marrow, liver but no organ exempt. Scattered small granulomas in lungs Mantoux test is frequently negative

Lung Cancer
90% is primary Aetiology
Smoking Occupational hazards-asbestos, dust, arsenic, nickel Pulmonary fibrosis

Clinical features
Weight loss, cough and hemoptysis

Most tumors arise from bronchi closed to hilum Usually upper lobe of main bronchus Ulceration is common Histological classification
Non small lung carcinoma (NSLC) (70-75%) Squamous cell carcinoma 20-30% Adenocarcinoma 30-40% Large cell undifferentiated carcinoma 10-15%

Small lung cell (oat cell) carcinoma 20-25%

Oat cell carcinoma produce


Adrenocorticotrophic hormone Antidiuretic hormone Calcitonin Gastric releasing peptide

NSLC produce
parathyroid hormone

adenocarcinoma

Pleura cavity disorder


Pneumothorax
Gas in plueral cavity Aetiology
spontaneous pneumothorax-mainly in healthy adult men without lung disease secondary pneumothorax-lung disorder such as emphysema, lung abscess, TB, or fractured ribs.

Hemothorax
Collection of blood in pleural cavity

Lung Cancer
90% is primary Aetiology
Smoking Occupational hazards-asbestos, dust, arsenic, nickel Pulmonary fibrosis

Clinical features
Weight loss, cough and hemoptysis

Most tumors arise from bronchi closed to hilum Usually upper lobe of main bronchus Ulceration is common Histological classification
Non small lung carcinoma (NSLC) (70-75%) Squamous cell carcinoma 20-30% Adenocarcinoma 30-40% Large cell undifferentiated carcinoma 10-15%

Small lung cell (oat cell) carcinoma 20-25%

Oat cell carcinoma produce


Adrenocorticotrophic hormone Antidiuretic hormone Calcitonin Gastric releasing peptide

NSLC produce
parathyroid hormone

adenocarcinoma

Pleura cavity disorder


Pneumothorax
Gas in plueral cavity Aetiology
spontaneous pneumothorax-mainly in healthy adult men without lung disease secondary pneumothorax-lung disorder such as emphysema, lung abscess, TB, or fractured ribs.

Hemothorax
Collection of blood in pleural cavity

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