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Lung Ch. 12 p (459 – 512) Feb
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WEIGHT LOBES SEGMENTS BRONCHI ARTERIES, pulmonary VEINS
bronchial VEINS PLEURA, visceral parietal NERVES
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Histology Bronchioles
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The Alveolar – Capillary Membrane
TEM of the Alveolar – Capillary Membrane Pneumocyte Type I (P) – BM – Endothelium (E)
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Normal Lung
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Respiratory Pathology Outline
Congenital anomalies Atalectises Acute respiratory distress syndrome Obstructive lung diseases Restrictive lung diseases Vascular diseases Infections Carcinoma
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Most common 82% Esophageal atresia and Tracheoesophageal fistula.
A, Blind upper and lower esophageal segments. B, Blind upper segment with fistula between lower segment and trachea. C, Fistula between patent esophagus and trachea. Type B is the most common.
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CYSTIC FIBROSIS AR disease Defect is of chloride ion transport
The principal defect is of chloride ion transport, resulting in high salt concentrations in sweat and in viscous luminal secretions in respiratory and gastrointestinal tracts. • Cardiopulmonary complications constitute the most common cause of death; pulmonary infections, especially with resistant pseudomonads, are frequent. Bronchiectasis and right-sided heart failure are long-term sequelae. • Pancreatic insufficiency is extremely common; infertility caused by congenital bilateral absence of vas deferens is a characteristic finding in adult patients with CF Liver disease, including cirrhosis, is increasing in frequency due to improved survival.
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Respiratory Pathology Outline
Congenital anomalies Atalectises Acute respiratory distress syndrome Obstructive lung diseases Restrictive lung diseases Vascular diseases Infections Carcinoma
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Atelectasis Greek = incomplete stretching, or expansion Lung collapse
Reduced lung volume Inadequate O2 Hypoxia
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Atelectasis
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Atelectasis
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Respiratory Pathology Outline
Congenital anomalies Atalectises Acute respiratory distress syndrome Obstructive lung diseases Restrictive lung diseases Vascular diseases Infections Carcinoma
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Acute Respiratory Distress Syndrome (ARDS)
Diffuse alveolar damage: hyaline membranes
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ARDS (Adult & Infantile)
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Respiratory Pathology Outline
Congenital anomalies Atalectises Acute respiratory distress syndrome Obstructive lung diseases Restrictive lung diseases Vascular diseases Infections Carcinoma
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Bullous emphysema with large apical and subpleural bullae.
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Mic. Of Emphysema
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Pathology of emphysema
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Pathogenesis of emphysema
Pathogenesis of emphysema. Excessive protease activity and ROS are additive in their effects to tissue damage. α1-antitrypsin (α1-AT) deficiency can be either congenital or “functional” as a result of oxidative inactivation.
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Pathogenesis of emphysema
Pathogenesis of emphysema. Excessive protease activity and ROS are additive in their effects to tissue damage. α1-antitrypsin (α1-AT) deficiency can be either congenital or “functional” as a result of oxidative inactivation. Pathogenesis of emphysema Smoking α-1 antitrypsin deficiency 23
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Bullous
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Emphysema (Centriacinar)
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Panacinar
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Emphysema: dilated air spaces
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Chronic Bronchitis Definition: persistent, productive cough for ≥ 3 months in ≥ 2 consecutive years Pathogenesis: hypersecretion of mucous Cause: smoking (mostly) and pollution 28
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Chronic bronchitis. marked thickening of the mucous gland layer (twice-normal) and sq metaplasia of lung epithelium.
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Reid index= 0.4 normally
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Increase Ried index
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COPD Dyspnea & hyperventilation are prominent, so that until very late in the disease, gas exchange is adequate and blood gas values are relatively normal. Because of prominent dyspnea and adequate oxygenation of Hb, these patients are called “pink puffers.”
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“Pink puffer" versus “Blue bloater"
At the other extreme in emphysema is a patient who also has pronounced ch bronchitis & a history of recurrent infections with purulent sputum. Dyspnea usually is less, with diminished respiratory drive, so the patient retains CO2, becomes hypoxic, and often is cyanotic. Such patients tend to be obese—hence the designation “blue bloaters.” “Pink puffer" versus “Blue bloater"
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Asthma Chronic inflammatory disease of airways leading to bronchial constriction Symptoms: wheezing, breathlessness Hallmarks: intermittent, reversible airway obstruction, chronic inflammation, increased mucus. Atopic (allergic) vs. non-atopic Triggers: allergens, infection, smoke, cold, exercise 34
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How is asthma triggered?
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Then what happens?
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1 2 3 Bronchial biopsy from an asthmatic patient ; showing
1. sub BM fibrosis, 2. eosinophilic, & 3. SM hyperplasia (4. Mucous & goblet cells hyperplasa)
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Curshmann’s spiral A microscopic finding in the sputum of asthmatics which are spiral shaped mucus plugs. These may occur in several different lung diseases
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Charcot–Leyden crystals
Are microscopic crystals found in people who have allergic disease such as asthma or parasitic infections such as parasitic pneumonia or ascariasis Are microscopic crystals found in sputum in allergic disease (asthma or parasitic pneumonia or ascariasis) They consist of an enzyme synthesized by eosinophils, and are produced from the breakdown of these cells
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Bronchiectasis Permanent dilation of bronchi and bronchioles due to chronic inflammation Secondary to: obstruction (tumor) congenital conditions (cystic fibrosis) bad pneumonia 41
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Bronchiectasis In a patient with cystic fibrosis who underwent lung resection for transplantation. C/S of lung shows markedly dilated bronchi, filled with purulent mucus, extending to subpleural regions.
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Bronchiactasis
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Mic. Of Bronchiactasis
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