Pulmonary Diseases 2009 copy


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Pulmonary Diseases 2009 copy

  1. 1. Review of pulmonary diseases Dr. Hassan M. Abouelkheir BDS, MSC, PhD
  2. 2. 1- Chronic Obstructive Pulmonary Disease. • COPD is a group of conditions in which there is persistent difficulty in expelling (or exhaling) air from the lungs. It includes two diseases: • A- Chronic bronchitis • B- Emphysema.
  3. 3. A- Chronic bronchitis • bronchitis is defined as coughing and overproduction of mucus for at least 3 months of the year for more than 2 consecutive years. • Characterized by: • Irritation of the bronchial tubes (from smoking, air pollution, etc.) • Constant coughing causes damage to the bronchial tubes. • Reduced airflow to the lung (shortness of breath).
  4. 4. Chronic bronchitis (cont.) • The pathologic change consists of thickened bronchial walls with inflammatory cell infilterate, increase of the size of mucous glands & global cell hyperplasia. • Inflammation also causes the glands that line the bronchi to produce excessive amounts of mucus, further narrowing the airways and blocking airflow. • This leads to chronic productive cough with shortness of breath.
  5. 5. B- Emphysema • Is distention of the air spaces distal to the terminal bronchioles because of destruction of alveolar walls (septa). • It causes an overproduction of the enzyme elastase; one of the immune system's infection-fighting biochemicals. This results in irreversible destruction of a protein in the lung called elastin which is important for maintaining the structure of the walls of the alveoli. Obstruction occur by collapse of these unsupported and enlarged air spaces on expiration.
  6. 6. Emphysema (cont.) • Causes and symptoms: • Cigarette smoking is by far the most important risk factor. • Age: Chronic bronchitis is more common in people over 40 years old; emphysema occurs more often in people 65 years of age and older. • Socioeconomic class. COPD-related deaths are about twice as high among unskilled and semi-skilled laborers as among professionals.
  7. 7. Emphysema (cont.) • Family clustering. It is thought that heredity predisposes people in certain families to the development of COPD when other causes, such as smoking and air pollution, are present. • Lung infections. Lung infections make all forms of COPD worse. • In emphysema, shortness of breath on exertion is the predominant early symptom. Coughing is usually minor and there is little sputum.
  8. 8. COPD (cont.) • The first step in diagnosing COPD is a good medical evaluation, including a medical history and a physical examination of the chest using a stethoscope. • Additional tests can be ordered; Pulmonary function test by using spirometer
  9. 9. Additional diagnostic tests: • Using a spirometer, an instrument that measures the air taken into and exhaled from the lungs, the doctor will determine two important values: • (1) vital capacity (VC), the largest amount of air expelled after the deepest inhalation. • 2) forced expiratory volume (FEV1), the maximum amount of air expired in one second. The pulmonary function test can be performed in the doctor's office, but is expensive. • Chest x rays can detect only about half of the cases of emphysema. Chest x rays are rarely useful for diagnosing chronic bronchitis.
  10. 10. 2- Asthma • Is a chronic inflammatory respiratory disease consisting of recurrent episodes of dyspnea, coughing, and wheezing. • Characterized by: • Constriction of the airways in the lungs. • Swelling of the lining of the bronchial tubes in the lungs. • Secretion of excessive amounts of thick mucus.
  11. 11. Etiology: Types: 1- Extrinsic(allergic or atopic). 2- intrinsic (idiosyncratic). 3- drug induced. 4- exercise induced. 5- infectious. Allergic asthma is the most common 35% of adult cases is triggered by inhaled seasonal allergens such as polens, dust, house mites.
  12. 12. 1- Extrinsic(allergic or atopic): • Most common 35% of cases. • Triggered by inhaled allergen such as pollens, dust, house mites & animal danders. • It affects young adults and childern. • The complex of antigens with antibody causes degranulation of mast cells to secret bradykinins , histamine & prostaglandins. • These compounds causes bronchoconstriction increased vascular permeability.
  13. 13. 2- intrinsic (idiosyncratic). • It is associated with family history of allergy or with known causes. • Non response to skin tests with normal IgE . • Middle aged adults due to endogenous causes; emotional stress or vagal mediated response.
  14. 14. 3- drug induced: • Drugs such as aspirin, NSAIDs, Beta- blockers, angiotensin-converting enzyme inhibitors . • Food substances such as nuts, shellfish, strawberries, milk & food dye can trigger asthma.
  15. 15. 4- Exercise Induced: • It is stimulated by exertional activity. • The pathogenesis of this form is unknown. • Childern and young adults are more commenly affected. 5- infectious asthma: respiratory infection can develop bronchial constriction due to inflammatory response to infection.
  16. 16. Signs & symptomes: • Wheezing. • Shortness of breath, perhaps only with exercise . • Feeling a tightness in the chest. • Coughing, which may occur only at night . • Chronic asthma can be classified into; mild, moderate and sever according to the frequency of acute attacks and lung function.
  17. 17. Triggers of Attacks can be dentistry-related. Documented Cases include: • Tooth enamel dust (OOO 75:599,1993) • Methyl methacrylate (Thorax 39:712, 1984; Tubercle & Lung Dis 75:99,1994) • Menthol (J Investig Allergol Clin Immunol. 2001;11(1):56) • Aspirin-induced (Chest. 1994 Aug;106(2):654) • Toothpaste (J Aller Clin Immunol. 1992; N Engl J Med. 1990 323(26):1845) • Foreign bodies: Lego (N Engl J Med. 1996 334(6):406)11
  18. 18. Mediators of Asthma • Released from bronchial mast cells, alveolar macrophages, T lymphocytes and epithelial cells • Histamine, tryptase, leukotrienes and prostglandins • Early-phase response: injury from eosino- and neutrophils Bronchoconstriction • Late-phase: epithelial damage, airway edema, mucous hypersecretion, hyperresponsiveness of bronchial smooth muscle
  19. 19. Warning Signs of an Asthma Attack Irregular breathing: wheezing, labored breathing, cough Dyspnea, chest tightness Drop in FEV (<50% of optimum) Tachypnea, tachycardia Diaphoresis – sweating and paleness Pulsus paradoxus (decline of pulse magnitude, i.e. > 10 mm Hg in blood pressure, during inspiration compared to expiration)
  20. 20. Additional Features of Asthma Attack • Anxious or scared look • Flared nostrils during inhalation • Pursed lips breathing, Fast breathing • Hunched-over body posture; patient can't stand or sit straight and can't relax • Intercostal (between ribs or supraclavicular) depressions during inhalation Poor oxygenation (pulse oximeter, blue lips, nails, struggle to breathe) Emergency
  21. 21. Oral Manifestations -Asthma • Altered nasorespiratory function (mouth breathing) • Increased prevalence of caries with moderate to severe asthma. • B2 agonist decrease salivary flow by 20-35%, associated with increased # of lactobacilli • Misuse of inhaled corticosteroids increases the risk of oral candidiasis
  22. 22. Asthma -Complications • Most patients can expect reasonably good prognosis; however small % of patients progress to emphysema and respiratory failure or develop status asthmaticus • Status asthmaticus is the most serious complication associated with asthma • consists of a severe and prolonged asthmatic attack (lasts > 24 hours) and is refractory to usual therapy.
  23. 23. Asthma –Complications(cont.) • Signs include increased dyspnea, jugular venous pulsation, cyanosis and pulsus paradoxus (a fall in pulse magnitude as measured by ↓ systolic pressure with inspiration). It is often associated with infection. • Can lead to exhaustion, severe dehydration, peripheral vascular collapse and death.
  24. 24. •Chest x-rays (for hyperinflation) • Skin testing (for specific allergens) • Histamine or methacholine chloride challenge testing, • Sputum smears & blood counts (for eosinophilia) • Arterial blood gases, • Antibody-based enzyme- linked immunosorbent assay (ELISA) for measurement of environmental allergen exposure, and SPIROMETRY (a peak expiratory flow meter that measures pulmonary function Commonly ordered tests
  25. 25. Managing Asthma • Classification • Goal: limit exposure to triggering agents, allow normal activities, restore and maintain pulmonary function. • Choice of medication based on type & severity; and lifestyle change • Written action plan
  26. 26. Drugs used by Asthmatics • Anti-Inflammatory Agents (1st agents of choice) • Secondary Agents – Bronchodilators (can be faster acting – use in emergency) – Methylxanthines – Anticholinergic drugs
  27. 27. Additional Treatment approaches Systemic steroids +/- cyclosporine or methotrexate – for severe asthma NEW: Recombinant injectable humanized monoclonal antibody that binds IgE (Omalizumab [Xolair]; SubQ; Genetech/Novartis) prevents IgE from binding mast cell/basophil receptors It is effective in treating adults and children with asthma; allowed for withdrawal of inhaled steroids successfully in 55% of asthmatics (ADES HA, fever, urticaria and pruritis)
  28. 28. Dental Management of Asthmatic Patient Pretreatment Assessment: STABILITY – History (duration, severity, recent hospitalizations, respiration rate, eosinophil count, triggers) – Taking medicines (type, how much, today?), bring inhaler – Avoid triggers: cold air, dust, feathers or molds, animal dander, cigarette smoking, pollution, fragrances – Prophylax with inhaler – Being Stressed is a trigger • Use Anxiolytic: nitrous oxide, hydroxyzine (antihistamine + sedative.
  29. 29. Dental Management of Asthmatic Patient Treatment: avoid/reduce irritating odorants, sulfites, rotary-derived particulate matter, continue anxiolytic therapy, – Avoid barbiturates and narcotics, particularly meperidine. They are histamine-releasing drugs and can provoke an attack. Aspirin use can trigger an attack. . . – special needs for pt on systemic steroids
  30. 30. Dental Management of Asthmatic Patient Post treatment: avoid macrolide antibiotics with Theophylline (drug interaction). Asthma attack: act immediately; stop procedure, remove RD, administer SA-bronchodilator and O2, if no relief subQ epinephrine (1:1000) 0.3-0.5 mL, repeat inhaler and epinephrine q5 min as needed
  31. 31. 3-Tuberculosis Tuberculosis is a chronic, infectious disease that primarily attacks the lungs. • Mycobacterium tuberclosis is a bacterial causative organism. It is transmitted by salivary droplets. • An infectious disease of humans and animals caused by the tubercle bacillus and characterized by the formation of tubercles on the lungs and other tissues of the body, often developing long after the initial infection
  32. 32. Tuberculosis(cont.) • Tuberculosis (TB) is caused by a bacteria that primarily attacks the lungs. • An individual may be "TB infected," meaning the bacteria are in the body but are in an inactive state, walled off behind scab-like structures that are the body's defense mechanism. • Or have "TB disease," when the bacteria actively spread throughout the body and can cause damage to the lungs or other organs Scanning electron micrograph of Mycobacterium tuberculosis
  33. 33. Tuberculosis(cont.) Mode of transmission: 1- Air borne droplets of mucous or saliva by cough sneezing or talking. 2- ingestion (contaminated milk) rarely occur due to using pasteurized milk. Interval from infection to active TB ranges from few weeks to decades. • Active TB can be triggered when a person's immune system is weakened, such as from human immunodeficiency virus (HIV), malnutrition, or alcohol abuse. Mycobacterium tuberculosis (stained red) in sputum
  34. 34. Tuberculosis(cont.) • Pathogenesis: • TB infection begins when the mycobacteria reach the pulmonary alveoli, where they invade and replicate within alveolar macrophages.[19] The primary site of infection in the lungs is called the Ghon focus. • Bacteria are picked up by dendritic cells, which do not allow replication, although these cells can transport the bacilli to local (mediastinal) lymph nodes
  35. 35. Tuberculosis(cont.) • Further spread is through the bloodstream to the more distant tissues and organs where secondary TB lesions can develop in lung apices, peripheral lymph nodes, kidneys, brain, and bone. • Tuberculosis is one of granulomatous inflammatory conditions as a group of epithelioid macrophages surrounded by a lymphocyte cuff. • TB granuloma develops caseous necrosis at the center of tubercle. Tissue destruction and necrosis are balanced by healing and fibrosis. • Affected tissue is replaced by scarring and cavities filled with cheese-like white necrotic material
  36. 36. Tuberculosis(cont.) • Diagnosis: • 1- Tuberclin skin test: subcutaneous skin injection of purified protein derivatives of M. tuberculosis. • If the bacteria are present, whether active or inactive, the patch of skin will swell.
  37. 37. Tuberculosis(cont.) 2- Chest x-ray: Presence of cavitation in the lung of AP view of chest x-ray can help in TB diagnosis. 3- sputum culturing for detection of bacillus bacteria . X-ray of a patient with tuberculosis. A cavity- like lesion is visible on the upper-right lobe of the lung.
  38. 38. Interpretation of TST • > 5 mm: considered positive if close contact with infected person, abnormal chest x-ray, or HIV positive • >10 mm: considered positive if other medical risk factors present, foreigner, medically underserved, alcoholic, long-term care resident • > 15 mm: positive
  39. 39. Tuberculosis(cont.) • Signs & Symptoms: • A cough lasting three or more weeks that may produce discolored or bloody sputum • Unintended weight loss • Fatigue • Slight fever • Night sweats • Chills • Loss of appetite • Pain with breathing or coughing (pleurisy)
  40. 40. Tuberculosis(cont.) • Other sites of TB infections: • Scrofula:form of tuberculosis affecting the the neck lymph nodes, most common in children and is usually spread by unpasteurized milk from infected cows. Also called struma. • Milliary TB : spread of TB through the blood. • wasting disease; white plague: TB of the skin, because sufferers appear markedly pale.
  41. 41. Tuberculosis(cont.) Medical treatment: I) medical regimen: 1-- Patient education and compliance. 2- Appropriate selection of drugs. 3- Multiple drug use. 4- Drug administration continuance For a sufficient time. • It is treated with a regimen of strong antibiotics such as Rifampin and Isoniazid for six months to two years.
  42. 42. Tuberculosis(cont.) Dental management: • 1- active sputum- positive tuberculosis should not be treated on an outpatient basis. • 2- patient with a past history of TB: dentist should obtain medical history of treatment duration if less than 18 months or 9 months with physician consultation. • 3- patient with positive tuberculin test and give a history of active TB , prophylactic ionized may be started for 6 months to a year to prevent clinical disease. Normal treatment can be done without special precautions.
  43. 43. Tuberculosis(cont.) 4- patients with signs or symptoms suggestive of TB: If any symptoms of suggested TB such as non productive cough, pleuritic chest pain, fatigue, fever, dyspnea, hemoptysis, weight loss → dental care should not be provided and pt referred to physician.
  44. 44. Tuberculosis(cont.) • High-risk populations: • 1-THE ELDERLY:Many elderly patients developed the infection some years ago when the disease was more widespread. • 2-RACIAL AND ETHNIC GROUPS: • It is more common in blacks, who are more likely to live under conditions that promote infection. • two-thirds of all cases of TB in the United States affect African Americans, Hispanics, Asians, and persons from the Pacific Islands. • 3- LIFESTYLE FACTORS:HIV pts who have not yet developed clinical signs of AIDS. Alcoholics and intravenous drug abusers are also at increased risk of contracting tuberculosis.
  45. 45. THE END