The lung and the Upper Respiratory Tract -1 Atelectasis Obstructive Lung Disease

Thoracic Assessment Breath Sounds absent or decreased –Atelectasis: Pneumothorax: –Emphysema: Pleural Effusion. Tactile fremitus –Increased= consolidation of pneumonia –Decreased= pleural effusion, pleural thickening (fibrosis),Pneumothorax, bronchial obstruction, COPD/emphysema. Hyperresonant =COPD, hyperinflation.

Atelectasis (collapse) Definition: collapse of the lung. Major types of atelectasis: 1.Resorption atelectasis. obstruction of bronchus by mucous plug, peanut → absorption of air → collapse. 2.Compression atelectasis Accumulation of fluid, blood, and air in the plural cavity → Compression → collapse of lung.

Atelectasis Clinical: sudden respiratory distress, no breath sound at that part, mediastinal shift towards the effected area.

Atelectasis: morphology of lung Airless, Heavy Airless, Heavy Dark purple Dark purple wrinkled pleura wrinkled pleura Tracheal shifting Tracheal shifting Resp. distress Resp. distress

Obstructive Vs Restrictive lung disease Obstructive (COPD): increased resistance to airflow: due to obstruction in airway. Restrictive: decreased lung capacity and volume. Due to fibrosis.

Remember this Points Obstructive lung disease Restrictive lung disease Total lung capacity IncreasedDecreased FEV1 Decreased ( > FVC). Reduced Forced Vital capacity (FVC) Normal / Decreased Reduced FEV1: FVC Decreased. Ratio may be normal.

Chronic Obstructive Lung Diseases (COPD) Def : group of disorder characterized by airflow obstruction. Major obstructive disorders: 1.Asthma. 2.Emphysema. 3.Chronic bronchitis. 4.Bronchiectasis.

BRONCHIAL ASTHMA

Bronchial Asthma Definition : stimulation of hyperactive airways → episodic bronchospasm. Age: older people. Types: 1.Extrinsic asthma (immune asthma) Atopic. Atopic. Aspergeliosis Aspergeliosis 2.Intrinsic asthma (non-immune).

Extrinsic Asthma Mechanism: A Type I hypersensitivity reaction involve IgE bound to mast cell. Feature: begins in child hood with a family history of asthma. Atopic: (most common type of Extrinsic asthma) IgE and eosinophils are elevated in the serum. Caused by antigens like: pollen, fumes, animal dander, molds.

Pathogenesis of atopic asthma: 1 st exposure by antigen ( childhood with h/o allergic rhinitis, urticaria, or eczema ) Ag. presentation by APC ↓ CD4 activation ↓ Cytokine release ( IL4) ↓ Th2 cell activation →activating B cell ↓ IgE production ↓ Coating of the mast cell by IgE Recruitment of these cells in resp. Mucosa = Sensitization of patient.

Pathogenesis of atopic asthma: 2 nd exposure by that antigen ( adult or young age) Binding of the antigen to the IgE (to Fab part ) on Mast cell ↓ 1. Early 1. Early phage reaction = Release of histamine from mast cell ( duration: few hours) ↓ 2. Late phage reaction by Eosinophils (IL-5 fetch these cell) ↓ Release of major basic protein etc. (duration: hr)

Early phase Mediators : mast cells Mediators: –Histamine: Increased capillary permeability → mucous formation. –Prostaglandins D2, E2 and F2 alpha : smooth muscle contraction → bronchospasm ( asthma!! ) –Stimulation of subepithelial vagal receptors by antifgen.

Late phase mediators Major basic protein Similar function :: bronchospasm and mucous production

Intrinsic Asthma  Onset: adult life  Triggering mechanisms are non-immune:  Aspirin ( by inhibiting the cyclooxygenase pathway without affecting the lipoxygenase route ),  infection ( like virus- by stimulating sub epithelial vagal receptors ).  Cold, Psychological stress, Exercise  No personal or family history of allergy, & IgE levels are normal in the serum.

Morphology of airways in atopic asthma Inflated lung Eosinophil in mucosa Thick basement membrane Hypertrophy of smooth muscle in the bronchial wall.

Clinical Course of atopic Asthma Presentation of asthmatic attack: Severe dyspnea, coughing, and episodic wheezing. Severe case: Status asthmaticus: Severe paroxysm of broncho-constriction that last for days or weeks and does not respond to therapy. May be fatal &q=status+asthmaticus&total= 2&start=0&num=10&so=0&type=search&plindex=1

Lab findings : sputum Curschmann spiral : Inspissated sputum and epithelial cells.→ Charcot leyden crystal: developed from eosinophil.→

Chronic Bronchitis Definition  Persistent productive cough for at least 3 consecutive months in at least 2 consecutive years ( usually all winter). Etiology: –Smoking, Air pollution (Sulfur dioxide and Nitrogen). –Infection

Chronic Bronchitis: morphology of airways Following ratio ( Reid index) is increased Thickness of the mucous gland layer Thickness of the wall (epithelium to cartilage) Squamous metaplasia  dysplasia  cancer.

Clinical Course of Chronic Bronchitis Persistent cough productive of sputum. Others: –Hypercapnia. –Hypoxemia. May lead to infection, CorPulmonale and lung cancer.

Emphysema Definition: –Permanent abnormal dilatation of the distal airways and alveolar space (ACINI). Etiology: smoking ( strong association) Types: 4

Pathogenesis ↑ Protease (Elastase) and ↓ antiprotesase ( alpha- 1 anti trypsin – AAT) ↓ Loss of elastic tissue around the acini Dilatation of acini= Emphysema

Emphysema Types ( according to its anatomical distribution). 1.Centriacinar. 2.Panacinar. 3.Distal Acinar. 4.Irregular

Centriacinar (centrilobular) emphysema Seen in cigarette smokers. Seen in cigarette smokers. Involvement central or proximal parts of the acini. Involvement central or proximal parts of the acini. Location : Upper lobes (apical). Location : Upper lobes (apical).

Pathogenesis: Centrilobular emphysema Smoking↓ Attract Neutrophils Attract Neutrophils↓ Secret elastase ↓ Reduce AAT (acquired deficiency) ↓ Loss of elastic tissue around the acini ↓ Dilatation of acini = emphysema

Panacinar (panlobular) emphysema Etiology: congenital alpha 1- antitrypsin deficiency Involved respiratory bronchiole to the terminal alveoli. Location: lower lung zones.

Genetic factor Hereditary alpha 1 anti-trypsin deficiency. –lack of secretion of anti-trypsin from liver… accumulate in liver (PAS positive). Homozygous : piZZ gene Other organ effected: Cirrhosis of liver

Distal Acinar or paraseptal emphysema: AKA: bullous emphysema 1.Involvement of the distal potion of the acinus (close to pleura). 2.Location: upper part of the lungs. 3.Complication: may rupture and produce Pneumothorax. Collapse of lung, shifting of trachea to other side and acute resp. distress. Collapse of lung, shifting of trachea to other side and acute resp. distress.

Clinical Course of Emphysema Progressive dyspnea → barrel-chested individual, flat diaphragm. Increase AP length (diameter) of lung. Dyspnea, cyanosis and respiratory acidosis. Weight loss  patients are thin. hyperresonant lung. Respiratory acidosis.

Respiratory Acidosis ↑ pCO2. Compensation by: ↑ HCO3

Initial value / after Compensation Without Compensation pH (<7.35) PaCO2 (>47 mm Hg) HCO mmol/L After Compensation pH ( ~ 7.35) PaCO2 (>47 mm Hg) HCO3: 32mmol/L ( acute) HCO3: 44mmol/L ( chronic)

Bronchiectasis Definition: permanent abnormal dilation due to necrosis and chronic inflammation of the airways. Factor responsible: –Obstruction : Tumor, foreign body, mucous Tumor, foreign body, mucous Cystic fibrosis: increased sweat chloride and pancreas aciner atrophy. Kartagener syndrome

Conditions that predispose to bronchiectasis Kartagener syndrome: Defect in motility of the cilia of bronchus, ear and sperm cilia ( tail). Features: Sinusitis, bronchiectasis, male sterility and hearing loss.

Morphology of Bronchiectasis Location: Lower lobes (often bilateral). Dilated bronchiole take Dilated bronchiole take saccular appearance.

Complications Lung Abscess Septic emboli - Metastatic brain abscesses. Reactive amyloidosis- extra cellar deposit of Amyloid Associate type of Amyloid protein ( congored positive pink hyaline material).

Clinical 1. High Fever 2. Copious, purulent sputum ( may contain blood) 3. Clubbing of the fingers. 4. In severe wide-spread cases  hypoxia, hypercapnia, pulmonary hypertension, & cor pulmonale.

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