Asthma and COPD PATHOPHYSIOLOGY .pptx

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1. ASTHMA

2. D E F I N I T I O N : Asthma is a chronic heterogeneous disease of the lower airways characterized by chronic inflammation and airway hyper-reactivity leading to cough, wheeze, difficulty in breathing, and chest tight ness. It is usually characterized by chronic airway inflammation , bronchial reversible obstruction and hyperresponsiveness to direct or indirect stimuli.

3. CAUSES : Asthma triggers Exposure to various irritants and substances that trigger allergies (allergens) can trigger signs and symptoms of asthma . Asthma triggers are different from person to person and can include: Airborne allergens , such as pollen, dust mites, mold spores, pet dander or particles of cockroach waste Respiratory infections, such as the common cold Physical activity Cold air Air pollutants and irritants , such as smoke

4. Certain medications , including beta blockers , aspirin , and nonsteroidal anti-inflammatory drugs, such as ibuprofen and naproxen sodium Strong emotions and stress P reservatives added to some types of foods and beverages , including , dried fruit, processed potatoes, beer and wine Gastroesophageal reflux disease (GERD), a condition in which stomach acids back up into your throat

5. RI S K F A C T O R : Family history Viral respiratory infections Allergies Occupational exposures Smoking Air Pollution Obesity

6. Types of Asthma: Allergic Asthma (extrinic asthma) Non-Allergic Asthma ( intrinsic asthma) Mixed Asthma Cough-Variant Asthma (very common in children) Exercise Induced Asthma Noctornal Asthma Occupational Asthma

7. A . A ller g i c A st h m a : When the symptoms are induced by a hyperimmune response to the inhalation of specific allergens. Type –I (IMMEDIATE ) hypersensitivity reaction is the basis of the IgE . When person come across an allergy trigger , our body makes molecules called IgE antibodies . These trigger a series of reaction that cause swelling , runny nose and sneezing. Extrinsic asthma symptoms occur in response to allergens, such as dust mites, pollen, and mold . It is also called allergic asthma and is the most common form of asthma.

8. B. Non –Allergic Asthma: This type of asthma is triggered by the presence of irritants in the air that are not related to allergies . This irritants stimulate parasympathetic nerve fibers in the airways causing broncho-constriction and inflammation. Non-allergic asthma is triggered by factors other than allergens. These can include : Viral respiratory infections Exercise Irritants in the air Stress Drugs and certain food additives Weather conditions

9. C. Mixed Asthma: Mixed asthma is the combination of both allergic and non-allergic asthma . This is the most common form of asthma.

10. D . C O U G H – V A R I A N T A S T H M A : Cough variant asthma is a type of asthma that features a dry, non productive cough . There may be no traditional asthma symptoms, such as wheezing or shortness of breath . An ongoing cough is often the only symptom. Cough variant asthma (CVA) is a common asthma variation in children.

11. E. EXERCISE INDUCE ASTHMA: Exercise-induced asthma is asthma that is triggered by vigorous or prolonged exercise or physical exertion . Most people with chronic asthma experience symptoms of asthma during exercise.

12. F. O C C U P A T I O N A L A S T H M A : People with this condition usually work around chemical fumes , dust or other irritants in the air . If you’ve been diagnosed with asthma that has another cause, it can be worsened by airborne irritants at work. Triggers may include chemicals used in manufacturing; paints; cleaning products; dusts from wood, grain and flour; latex gloves; certain molds; animals; and insects.

13. Normal and Bronchial Asthma Tissues 

14. PATHOPHYSIOLOGY:

15. PATHOPHYSIOLOGY:

16. Asthma is associated with T-helper cell type-2 (Th-2) immune responses. Its may include allergic and non-allergic stimuli. which produces a cascade of events leading to chronic-airway inflammation. Elevated levels of Th-2 cells in airways releases specific cytokines including IL-4,IL-5,IL-9 and IL-13 and promote eosinophilic inflammation and immunoglobulin E (IgE) production. IgE production in turns triggers releate of inflammatory mediators,

17. such as histamine and cysteinyl leukotrienes, that cause bronchospasm (contraction of the smooth muscle in the airways), edema, and increased mucous secretion, which lead to the characteristic symptoms of asthma.

18. IL-4 drives Th2 cell differentiation and mediates the production of downstream Type 2 cytokines IL-13 mediates goblet cell hyperplasia and increased mucus secretion , and promotes airway obstruction , bronchial hyperactivity, smooth muscle hypertrophy , and airway remodelling. IL-4 and IL-13 play an important role in class switching of B cells to produce IgE. IL-5 mediates the differentiation of eosinophils in bone marrow; IL-4 and IL-13 drive the tracking of eosinophils to sites of inflammation.

19. IL-4 drives Th2 cell differentiation IL-4 and IL-13 promote class switching of B cells to produce IgE. AL L E RGI C - ASTHMA

20. DIAGNOSIS: Patient history Physical Examination Chest X-ray Pulmonary Function Test Blood and Sputum Test Allergy Prick skin Test Spirometry Test FEV ( Force Expiratory Volume) FVC ( Force Vital Capacity)

21. D R UG S F O R A S T HM A :

22. BRONCHODILATORS: Beta-2 agonists : Beta-2 agonists are bronchodilators that play an important role in asthma control and treatment of acute exacerbations. They bind to the beta-2 adrenergic receptors on the bronchial smooth muscle cells, causing smooth muscle relaxation and bronchodilation. Increased levels of energy –producing cAMP. This is done by competitively inhibiting phosphodiesterase(PDE ) ,the enzyme, that breaks the cAMP. Its result into decreased cAMP levels, cause SM relaxation,bronchodialation and increased air flow.

23. L E UK OT R IEN E A NT A G O N I S T S : Leukotrienes are lipid mediators involved in bronchoconstriction and airway inflammation . Leukotriene-modifying drugs, including zafirlukast, montelukast, and zileuton, work by inhibiting leukotriene synthesis or as competitive antagonists of the leukotriene receptors . Cysteinyl leukotrienes are released from mast cells and eosinophils and are involved in bronchial smooth muscle contraction and increased mucus secretion. By working as receptor antagonists and inhibiting leukotriene synthesis, these drugs downregulate airway inflammation; they have also been shown to improve asthma symptoms and lung functi on and serve as an add-on therapy to ICS. Current guidelines recommend the use of leukotriene receptor antagonists only as an alternative treatment to ICS in those with moderate persistent asthma who cannot tolerate ICS and as an add-on therapy to those receiving combined LABA/IC S.

24. MAS T C E L L ST A BILI Z E RS : Its inhibits degranulation of mast cells . Release of mediators like histamines,LT,IL is inhibited. Chemotaxis of inflammatory cells is inhibited . Bronchial hyperactivity of histamine is reduced. Bronchospam due to various stimuli is prevented. It can’t be used to prevent attack of asthm a because it does not affect the constrictor action .

25. COTICOSTEROIDS: Corticosteroids are not bronchodialators . It is given as prophylactic medications,use alone or combined with beta- agonists. Inhibition of phospholipase A2 , decreased prostaglandin and leukotrienes . Mast cell stabilization ,decreased histamine release. Upregulation of beta2 receptors .

26. A N T I- Ig E A N T IB O D Y : The drug omalizumab is actually a humanized monoclonal antibody. It is administered I.M or S.C . It neutralizes free IgE in circulation without activating mast cellls and other inflammatory cells. So IgE level in plasma is down and so,mast cell-IgE mediated histamine release is inhibited . cause bronchoconstriction

27. Asthma comorbidities and stroke: Asthma is not an exception and there list of commonly encountered comorbidities includes chronic rhinitis, chronic sinusitis/rhino-sinusitis, gastro-esophageal reflux disease, obstructive sleep apnea/sleep-disordered breathing, psychological disturbances (particularly depression and anxiety disorders), chronic/recurrent respiratory infections , hyperventilation syndrome, hormonal disturbances and other . There are also possible emerging comorbid conditions such as cardiovascular, obesity, metabolic syndrome, diabetes mellitus, degenerative joint disease/arthritis and psychiatric diseases. Some of these comorbidities lead to an increased risk of stroke and are highly prevalent in asthma patient . This raises the question that the increased risk of stroke in asthma patients may be due to confounding effect. Nevertheless, the important point is that proper screening and diagnosis of comorbidities in asthmatics is essential for preventing serious complications including stroke .

28. Bronchial Thermoplasty: Bronchial thermoplasty (BT) offers a nonpharmacologic therapy for those with asthma unresponsive to standard treatment with ICS and bronchodilators. Bronchial thermoplasty is a treatment for severe asthma approved by the FDA in 2010 involving the delivery of controlled, therapeutic radiofrequency energy to the airway wall, thus heating the tissue and reducing the amount of smooth muscle present in the airway wall. BT uses thermal energy to bronchoscopically ablate airway smooth muscles to decrease bronchoconstriction and airway hyperplasia . The effectiveness of this treatment was initially seen in the AIR (ASTHMA INTERVENTION RESEARCH) trial in 2007, which randomised patients with moderate or severe asthma to BT or a control group.

29. COPD is also known as chronic obstructive lung disease (COLD), chronic obstructive airway disease (COAD), chronic airflow limitation (CAL) and chronic obstructive respiratory disease (CORD) Chronic obstructive pulmonary disease (COPD) refers to chronic bronchitis and emphysema , a pair of two commonly co-existing diseases of the lungs in which the airways become narrowed. This leads to a limitation of the flow of air to and from the lungs causing shortness of breath.

30. I n COPD, less air flow s in and out of t he airways because of one or more of the following: The airways and air sacs lose their elastic quality . The walls between many of the air sacs are destroyed. The walls of the airways become thick and inflamed . The airways make more mucus than usual , which tends to clog them.

31. A cute (short term) and chronic (ongoing). Infection s or lung irritants cau s e acute bronchitis. Chronic bronchitis is an ongoing serious condition . It occurs if the lining of the bronchial tubes is constantly irritated and inflamed causing a long-term cough with mucus. Chronic bronchitis: It is defined as the presence of cough and sputum production for at least 3 months.

32. 1) Smoking 2) Occupational exposures- exposure to workplace dusts found in coal mining, gold mining, and the cotton textile industry and chemicals such as cadmium, isocyanates, and fumes from welding have been implicated in the development of airflow obstruction . 3) Air pollution 4) sudden airway constriction in response to inhaled irritants 5) Bronchial hyperresponsiveness is a characteristic of asthma . 6) Genetic s -A l pha 1 -antitr y psin deficiency is a genetic condition that is responsible for about 2% of cases of COPD. In this condition , the body does not make enough of a protein , alpha 1-antitrypsin . Alpha 1- antitrypsin protects the lungs from damage caused by protease enzymes , such as elastase and trypsin that can be released as a result of an inflammatory response to tobacco smoke.

33. NUTRITION INFECTIONS SOCIO ECONOMIC STATUS AGING POPULATION

34. Chronic cough Sputum production Wheezing Chest tightness Dyspnoea on exertion Wt.loss Respiratory insufficiency Respiratory infections Barrel chest- chronic hyperinflation leads to loss of lung elasticity.

35. History PFT Spirometry-to find out airflow obstruction. ABG analysis CT scan of the lung. Screening of alpha antitrypsin deficiency X-ray radiography may aid in the diagnosis.

36. IMPROV E VENTILL A TION BRONCHO DILATORS LIKE BETA2 AGONISTS(ALBUTEROL), ANTICHOLINERGIC S(IPRATROPIUM BROMIDE-ATROVENT). METHYLXANTHINES(THEOPHYLLINE,AMIN OPHYLLINE) CORTICOSTEROIDS OXYGE N A D MINIST R A TION

37. ⦿ BUL L EC T OMY BULLAE ARE ENLARGED AIRSPACES THAT DO NOT CONTRIBUTE TO VENTILLATION BUT OCCUPY SPACE IN THE THORAX,THESE AREAS MAY BE SURGICALLY EXCISED ⦿ LUNG VOLU M E RED U CTION SUR G E R Y IT INVOLVES THE REMOVAL OF A PORTION OF THE DISEASED LUNG PARENCHYMA.THIS ALLOWS THE FUNCTIONAL TISSUE TO EXPAND. ⦿ LUNG TRANSPLAN T A TION

38. TAKE YOUR MEDICATIONS REGULARLY AS PRESCRIBED,IF YOU HAVE ANY DOUBT RING YOUR HOSPITAL. EXERCISE REGULARLY EVERYDAY OR ELSE ATLEAST 4 OUT OF 7 DAYS.