Download
biomedicine review of the respiratory system n.
Skip this Video
Loading SlideShow in 5 Seconds..
Biomedicine Review of the Respiratory System PowerPoint Presentation
Download Presentation
Biomedicine Review of the Respiratory System

Biomedicine Review of the Respiratory System

88 Vues Download Presentation
Télécharger la présentation

Biomedicine Review of the Respiratory System

- - - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript

  1. Biomedicine Review of the Respiratory System • Felix Hernandez, M.D.

  2. Facts about the Respiratory System • 1. open-ended and in direct contact with the environment • Allows for a high number of URI • 2. exposed to many allergens inhaled in air • Allows for a high number of immunologic diseases • 3. Inhaled air contains pollutants, airborne particles, and gases that may cause disease • 4. The heart and the lungs for a functional unit • Pathology in one leads to pathology in the other • 5. inhaled air contains many potential carcinogens

  3. Locating Findings on the Chest • To locate findings around the circumference of the chest, imagine a series of vertical lines

  4. Lungs, Fissures, and Lobes • Each lung is divided roughly in half by an oblique (major) fissure • The right lung is further divided by the horizontal (minor) fissure • These fissures divide the lungs into lobes • The right lung is divided into upper, middle, and lower lobes • The left lung is divided into upper and lower lobes

  5. The Trachea and Major Bronchi • The trachea bifurcates into its mainstem bronchi at the levels of the sternal angle anteriorly and the T4 spinous process posteriorly • The Pleurae • The pleurae are serous membranes that cover the outer surface of each lung (visceral pleura), and also the inner rib cage and upper surface of the diaphragm (parietal pleura)

  6. Figure 17-4: Branching of the airways

  7. Inspiration: • Contraction of diaphragm / intercostal muscles  • Expansion of thorax  expansion of lungs  • Pressure in lungs ↓ • Air inflow • Expiration: • Relaxation of muscles  • Thorax / lung recoil back  • Pressure in lungs ↑ • Air outflow

  8. Hypothalamus (emotions / pain) • Cortex (voluntary control) • Chemoreceptors: • Central (in medulla oblongata): responds to CO2 ↑ • CO2 passes blood brain barrier • CO2 + H2O H2CO3 H+ + HCO3- • H+ stimulates receptors  breathing depth ↑ + rate ↑ • Peripheral (in aortic / carotid bodies): • responds when O2 < 60 mm Hg  increase ventilation • Responds to pH ↓ increase ventilation

  9. Marieb, Human Anatomy & Physiology, 7th edition

  10. Diaphragm & rib cage are pumps for inspiration • Alveolar surface exchanges O2 & CO2 with blood • The gasses in air act independently & move down a pressure gradient • Airway resistance can limit ventilation efficiency • Typically ventilation matches blood perfusion via local regulators of vasodilation & bronchodilation

  11. URI Etiology • Recognized as common colds • Acute inflammation of the nose, sinuses, throat or larynx • Most are caused by viruses • Most commonly influenza virus, parainfluenza virus, and rhinovirus • Predisposing factors include physical exhaustion, old age, and general poor health

  12. URI Clinical Presentation • Rhinorrhea • Throat pain, discomfort in swallowing, sneezing and a hacking cough • Lasts from a few days to 1 to 2 weeks • Heal spontaneously • Signs of purulent discharge indicates a bacterial superinfection

  13. Intranasal Steroids • Drugs: • Budesonide (Rhinocort) • Triamcinolone (Nasacort) • Fluticasone (Flonase) • Mometasone (Nasonex) • MOA: inhibit inflammatory cells in the nasal mucosa thus reducing the symptoms of rhinitis • Side effects: may increase the risk of thrush and prevent healing of damaged nasal mucosa

  14. Lobar Pneumonia Widespread/diffuse alveolar pneumonia Figure 8-07B

  15. Common Causes of Pneumonia • Bacteria- 75% of cases • Streptococcus pneumoniae #1 • Viruses • influenza virus • Fungi • Pneumocystis carinii • Bacteria-like organisms • Mycoplasma pneumoniae

  16. Bronchopneumonia • Bacterial invasion of the bronchial mucosa • PMN move into the lumen of the airways and starts an inflammatory response • The inflammation spreads form the bronchi into the adjacent alveoli • Lobular  single lobules • Lobar  large portions of entire lobes • Intra-alveolar exudate accumulates and replaces the air causing the lung parenchyma to become consolidated

  17. Bronchopneumonia Limited to the segmental bronchi and surrounding lung parenchyma Figure 8-07A

  18. Interstitial Pneumonia • Inflammation primarily affects the alveolar septa and does not result in exudation of PMNs into the alveolar lumen • Caused by viruses or M. pneumoniae that attach to the surface of respiratory epithelial cells • Cause cell necrosis and induce an infiltrate in the alveolar septa

  19. Interstitial Pneumonia Diffuse and bilateral Infection caused by Mycoplasma pneumiae or viruses Figure 8-07C

  20. Clinical Features of Pneumonia • Systemic signs of infection—fever, chills, prostration • Local signs of irritation—cough • Airway obstruction—shortness of breath (dyspnea), rapid breathing (tachypnea) • Inflammation and tissue destruction—expectoration of rusty sputum, hemoptysis

  21. Common Antibiotics Used to Treat Pneumonia • Amoxicillin • DOC for: empiric therapy in otitis media, sinusitis and pneumonia • Side Effects: Diarrhea • 2nd generation Cephs • moderate gram + and gram - coverage • Vancomycin • MOA: prevents transfer of cell wall precursors from plasma membrane to cell wall • Clinical Use: DOC for penicillin or methicilliin resistant staph and strep • Side Effects: thrombophlebitis, Red Man Syndrome

  22. Common Antibiotics Used to Treat Pneumonia • Erythromycin • MOA: Inhibits protein synthesis • DOC for Mycoplasma pneumonia

  23. Pulmonary Tuberculosis • Key feature is the formation of granulomas which are composed of lymphocytes, macs and giant cells. • The central portion of the granuloma is necrotic and consists of caseous necrosis • Primary infection • Hasn’t been exposed and results in localized lung inflammation • The lession is called the Ghon complex and it consists of granulomas in the lung parenchyma and enlarged regional lymph nodes. • 95% of the times the complex heals spontaneously and undergoes calcification

  24. Pulmonary Tuberculosis • Secondary infection • Develops as a result of reactivation of a dormant primary infection or reinfection • most are due to reactivation • Bacteria spread to the apex of the lung and cause a granulomatous lobular pneumonia • Confluent granulomas can form cavities which become a source of hemoptysis

  25. Ghon Complex Figure 8-10

  26. Drugs Used to TreatTuberculosis • Isoniazid • MOA: inhibits mycolic acid synthesis in the wall • Side Effects: peripheral neuropathies (prevent with treatment with pyridoxine) • Rifampin • MOA: stopping bacterial RNA synthesis • Side Effects: urine and sweat turn red • Pyrazinamide • Side Effects: hepatitis, hyperuricemia with gouty arthritis. • Ethambutol • MOA: inhibits mycolic acid synthesis in bacterial cell wall

  27. Chronic Obstructive Pulmonary Disease • A group of diseases characterized by chronic airway obstruction • Includes the following diseases: • Chronic bronchitis • Emphysema • Bronchiectasis

  28. Bronchiectasis • A permanent dilatation of the bronchi • Occurs as a result of persistent inflammation inside the airways • Larger bronchi show saccular dilatation, smaller bronchi show cylindrical dilatation • Dilated bronchi are filled with mucopurulent material which cannot be cleared by coughing • Infection spreads to adjacent alveoli causing recurrent pneumonias

  29. Bronchiectasis Figure 8-12

  30. Chronic Bronchitis • Excessive production of tracheobronchial mucus causing cough and expectoration for at least three months during 2 consecutive years • Smoking is the cause in more than 90% of cases • Non-specific pathology • The walls of the bronchi are thickened and the lumen contains thick mucus • The mucosa becomes infiltrated with lymphocytes, macs and plasma cells • The submucosa shows marked mucous gland hyperplasia, chronic inflammation and fibrosis

  31. Emphysema • Enlargement of the airspaces distal to the terminal bronchioles with destruction of alveolar walls • Is linked to chronic cigarette smoking but can be found in non-smokers with Alpha-1-antitrypsin deficiency • Irritants in smoke cause an influx of inflammatory cells into the alveoli. • proteolytic enzymes are released from leukocytes and destroy the alveolar walls • Oxygen radicals produced by cigarettes kill alveolar cells and leukocytes which releases even more enzymes • Elastase breaks down elastin fibers and its activity is increased • Oxygen radicals also inactivate antiproteolytic enzymes (Alpha 1 theory)

  32. Emphysema • Centrilobular • Widening of the airspaces in the center of a lobule • MC form and is found in smokers • Remaining bronchioles are infiltrated with antracotic macs and chronic inflammatory cells • Panacinar • Involves all the airspaces distal to the terminal bronchioles • Occurs with alpha 1 def.

  33. COPD—Emphysema (Pink Puffer) Figure 8-14A

  34. COPD—Chronic Bronchitis (Blue Bloater) Figure 8-14B

  35. Comparison of Chronic Bronchitis and Emphysema Table 8-2

  36. Asthma • Extrinsic • Intrinsic—attacks precipitated by: • Physical factors • Exercise • Psychological stress • Chemical irritants and air pollution • Bronchial infection • Aspirin

  37. Pathogenesis of Asthma Figure 8-15

  38. Histopathology of Asthma Figure 8-16

  39. Bronchodilators • Sympathomimetics • Albuterol (Ventolin) • MOA: beta-2 agonist which causes bronchodilation • Rapid onset of action • Indications: DOC for the treatment of acute asthma symptoms and prevent exercise induced asthma. • Side Effects: vasodilation, tachycardia, CNS stimulation. • Levalbuterol (Xopenex) • Less side effects than albuterol

  40. Bronchodilators • Salmeterol • MOA: long acting beta-2 agonist • Indications: chronic treatment of asthma or bronchospasm in adults. • Is not used for acute exacerbations • Epinephrine (Primatene Mist) • MOA: beta-2 bronchdilation, alpha-1 vasoconstriction and decreased secretions • Indications: emergent use for sever bronchoconstriction/vasodilation seen in anaphylaxis • Side Effects: tachycardia, CNS stimulation

  41. Bronchodilators • Ipratropium (Atrovent) • MOA: muscarinic antagonist which reverses AcH induced bronchconstriction • Indications: bronchospasm associated with COPD in adults • Side effects: very few systemic anticholinergic s/sx because it poorly crosses into the systemic circulation

  42. Corticosteroids • Drugs: Beclomethasone (Beclovent), Triamcinolone (Azmacort), Dexamethasone (Decadron) • Systemic • MOA: decrease inflammation and edema in respiratory tract. • Indications: asthma which can not be controlled by sympathomimetics alone • Side Effects: sodium/water retention, osteoporosis, PUD, avascular necrosis of the femoral head • Should be discontinued ASAP • Inhaled • MOA: same as systemic • Indications: same as systemic • Side Effects: don’t induce systemic toxicity. Their action is mostly in the lungs. They have an increased risk of oral thrush (Candida albicans infection)

  43. Lung Carcinoma • Most common malignant tumor of internal organs in the United States • Most often related to cigarette smoking • Rare before the age of 40 years, but its incidence rises with age • Poor prognosis

  44. Histogenesis of Lung Carcinoma Figure 8-25

  45. Histopathology of Lung Tumors • Squamous cell carcinoma • Adenocarcinoma • Large-cell undifferentiated carcinoma • Small-cell carcinoma • Mesothelioma --> Asbestos

  46. Clinical Features of Lung Cancer • Bronchial irritation • Local extension into the mediastinum or pleural cavity—pleural effusion • Distant metastases • Systemic effects of neoplasia • Paraneoplastic syndromes

  47. Metastases of Lung Carcinoma Figure 8-27