Respiratory System Lectures (PDF)

Upper respiratory tract and the lung Prof. Laila Elbarghati First lecture  Course objectives Students should emerge from the course with an understanding of the pathologic changes that occur in patients with a variety of respiratory diseases. They should understand...

Upper respiratory tract and the lung Prof. Laila Elbarghati First lecture  Course objectives Students should emerge from the course with an understanding of the pathologic changes that occur in patients with a variety of respiratory diseases. They should understand the role played by genetic, environmental & socioeconomic factors in diseases such as COPD, restrictive lung diseases, pneumonia & lung cancer. Finally, students should begin to learn to piece together the various features of a patient’s illness to arrive at a list of the most likely diagnostic possibilities. Respiratory tract  Lung diseases 1- Obstructive & Restrictive Diseases 2- Pulmonary Vascular Diseases 3- Pulmonary Infections 4- Pulmonary Neoplasia 5- Diseases of the pleura  Lesions of upper respiratory tract Acute infections: 1. Acute rhinitis 2. Acute sinusitis 3. Acute tonsillitis 4. Acute pharyngitis 5. Acute epiglottitis 6. Acute laryngitis Nasal polyps  Acute rhinitis Inflammation of the nasal mucosa 2 types 1. Common cold 2. Allergic rhinitis  Common cold (Coryza) Common disease caused by pathogens as corona virus, rhinoviruses, influenza viruses & RSV. 40% unknown cause. Cause fever, nasal congestion, watery discharge & sore throat. Self limited (week) or Complicated by otitis media & sinusitis.  This inflammation divided into 2 phases: 1. Viral phase: virus adheres to cell surface protein, enter the cell & replicate causing edema & congestion with no neutrophils exudation. 2. Bacterial phase: where bacteria invade the damaged tissue & cause features of acute inflammation.  Allergic rhinitis (hay fever) Type 1 allergic reaction. Atopic disease characterized by edema & eosinophils infiltrate. Patient present with itching, sneezing & watery discharge.  Acute sinusitis Inflammation of the mucosa lining the sinuses (maxillary sinus). It occurs as a complication of rhinitis or dental sepsis. Caused by S. pneumoniae or S. aureus. Excessive mucous obstructing the sinus cavities, that may become purulent & spread to the brain. Sinuses  Acute tonsillitis Common caused by streptococcus hemolyticus. 3 types: 1. Catarrhal: enlarged & hyperemic tonsils 2. Follicular: purulent exudate over lymph follicles. 3. Membranous: purulent exudate forms a membrane covers the tonsils. Follicular tonsillitis -Gross  It should be treated or cause: 1. Quinsy (peritonsillar abscess) 2. Direct spread of infection 3. Acute rheumatic fever 4. Post streptococcal glomerulonephritis  Acute pharyngitis Pharyngitis caused by EBV & adenovirus (70%) or by β-hemolytic streptococci (30%). It accompanies cold or tonsillitis. It may be complicated by: 1. Reteropharyngeal abscess 2. Adenoid: hyperplasia of the lymphoid tissue in the posterior pharyngeal wall results in adenoid face (open mouth, short upper lip & narrow nasal opening). Adenoid face  Acute epiglottitis Caused by H. influenza. Vaccination against H. influenza reduce the incidence. Acute onset, pain & airway obstruction (fatal).  Acute laryngitis Caused by inhalation of irritants gases (chlorine) or agents causing common cold. Rarely tuberculous form where infected sputum coughed up or diphtheric form in which exotoxin cause pseudomembrane formation.  Diphtheric laryngitits ▪ Affect children between 2-5 years. ▪ Rare due to vaccination (DPT). ▪ Caused by Corynebacterium diphtheriae. ▪ Exotoxin cause necrosis of the mucosa & pseudomembrane formation. Complications of diphtheric laryngitis: 1. *Sloughing & aspiration of this membrane result in asphyxia & death. 2. Toxic myocarditis. 3. Peripheral neuropathy. Diaphtheric laryngitis  Nasal polyps Recurrent infections of the nose lead to polypoid thickening of the mucosa. Bilateral rounded masses that arise in the middle turbinate. Gelatinous with smooth surface, consist of loose edematous connective tissue that covered by ciliated respiratory epithelium. Upper respiratory tract tumors Tumors of the nose Nasopharyngeal carcinoma Laryngeal tumors - Vocal cord polyps - Squamous papilloma - Carcinoma of the larynx  Tumors of the nose Rare but present at an advanced stage. Benign such as sinonasal papilloma that require surgical excision. Malignant such as squamous cell carcinoma & lymphomas.  Nasopharyngeal carcinoma Viral oncogene of genetic susceptibility (EBV in Chinese). More in children & old age. 3 types: 1. Keratinizing squamous cell carcinoma 2. Non keratinizing squamous cell carcinoma 3. Undifferentiated carcinoma: common, large neoplastic cells with reactive lymphocytes.  Undifferentiated nasopharyngeal carcinoma Lymphocytes Large cells  Spread to cervical lymph node, then to the blood. Radiosensitive tumor. 5 years survival rate is 50%.  Laryngeal tumors Benign lesions 1. Vocal cord polyps 2. Squamous papilloma  Vocal cord polyps Occur in heavy smokers or singers (Singer’s nodes). Smooth round mass (0.5 cm). Consist of fibrous tissue covered with stratified squamous epithelium.  Squamous papilloma Benign tumor, caused by human papilloma virus 6,11. Single in adult, multiple in children (Juvenile laryngeal papilloma) that regress at puberty. Soft finger like projections (1 cm) consist of fibrovascular tissue covered by stratified squamous epithelium. It is premalignant in adult not in children. Laryngeal squamous papilloma  Carcinoma larynx 2% of all cancer. More in men (7:1). Caused by asbestos, smoke & alcohol.  Morphology It is either Glottic tumor in 70% Supraglottic in 25% Subglottic in 5% Appear as gray wrinkled plaques on mucosal surface that ulcerate. 95% are squamous cell carcinoma. Laryngeal carcinoma Carcinoma larynx (squamous)  Clinical course Interfere with vocal cord mobility cause persistent hoarseness. The spread is rare in glottic tumor due to few lymphatics, unlike supraglottic & subglottic tumors that spread to cervical nodes. Treated by surgery & radiation.  Causes of epistaxis Local General Trauma Hypertension Tumors Leukemia Nasal polyps Haemorrhagic blood diseases Vitamin C & K deficiency Second lecture  Normal lung Right bronchus is more vertical in line with the trachea so, aspirated foreign bodies, vomitus & blood enter the right lung than the left. Pulmonary & bronchial arteries (of aortic origin) supply the lung. Exchange gases between inspired air and blood. Normal Lung Normal Lung N O C R X M A R L  Histology The respiratory tree till the bronchus is lined by pseudostratified columnar ciliated epithelial cells, cartilaginous airways with mucus secreting goblet cells. The bronchioles unlike bronchi have no cartilage & submucosal glands. With each division the epithelium become cubiodal to flat non ciliated epithelium.  Normal bronchus Stratified columnar epithelium Cartilage Mucous glands Normal bronchus Normal bronchiole Bronchi bronchioles terminal bronchioles (2mm) acinus (7mm). The acinus is composed of respiratory bronchioles which give rise to several alveoli (site of gas exchange). 3-5 terminal bronchioles with its acinus called pulmonary lobule. Terminal bronchiole Structure of acinus Terminal bronchiole  Alveolar wall consist of: 1. Capillary endothelium. 2. Type 1 pneumocytes: flattened cells cover 95% of the surface. 3. Type 2 pneumocytes: rounded granular cells secrets surfactant & undergo hyperplasia when type 1 cells are injured. 4. Pulmonary interstitum: separate the basement membrane of epithelium & endothelium. 5. Alveolar macrophages: attached to epithelial cells or lying free within the alveolar space. Alveolar wall Normal alveoli The alveolar walls are not solid but are perforated by numerous pores of kohn which permit the passage of bacteria & exudate between adjacent alveoli. Adjacent to alveolar cell membrane is the pulmonary surfactant layer.  Adequate respiration is maintained by: 1. Adequate intake of air. 2. Adequate perfusion of pulmonary circulation. 3. Rapid diffusion along alveolar walls.  Atelectasis (collapse) Loss of lung volume caused by inadequate expansion of air spaces. This result in shunting of inadequate oxygenated blood from pulmonary arteries into veins. Thus give rise to ventilation-perfusion imbalance & hypoxia.  Atelectasis divided into 3 categories: 1. Resorption atelectasis (obstruction). 2. Compression atelectasis (passive or relaxation). 3. Contraction atelectasis (cicatrization). Lung atelectasis can occur in premature infants due to weak respiratory action & lack of surfactant called microatelectasis  Types of atelectasis  Resorption atelectasis Occurs when an obstruction prevent air from reaching distal Airway (complete obstruction). Depending on the level of obstruction, an entire lung, a complete lobe, or one or more segment may be involved.  The causes of bronchus obstruction: 1. Mucous plug which occur in bronchial asthma, chronic bronchitis or bronchiectasis. 2. Foreign bodies in children. 3. Blood clots during oral surgery. 4. Bronchiogenic carcinoma. 5. Enlarged lymph node as from T.B.  Compression atelectasis Accumulation of fluid, blood or air into pleural cavity that mechanically collapse the adjacent lung. Basal atelectasis result from elevated diaphragm as in bedridden patients, during & after surgery, ascites.  Contraction atelectasis Occurs when either local or generalized fibrotic changes in the lung or pleural prevent expansion. Atelectasis except that caused by contraction is reversible & should be treated to prevent hypoxemia.  Morphology Macroscopic The affected area bluish, depressed with rubbery consistency. Microscopic: The alveolar walls are apposed to each other with narrow space.