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  1. RELIANCE COLLEGE OF NURSING SUBJECT- MEDICAL SURGICAL NURSING TOPIC CHRONIC OBSTRUCTIVE PULMONARY DISEASE Mr. om verma Msc lecturer medical surgical nursing
  2. INTRODUCTION  Chroinic obstructive pulmonary disease (COPD),refers to several disorders asthma , ,chronic bronchitis and emphysema, and cystic fibrosis 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.
  3. DEFINITION “Chronic obstructive pulmonary disease is a disease state define by airflow limitation that is not fully reversible.” Accd. To , Brunner & Suddarth
  4. classification  ASTHMA  CHRONIC BRONCHITIS  EMPHYSEMA  CYSTIC FIBROSIS
  5. •ASTHMA
  6. ASTHAMA  Asthma can be define as by broncho spasm broncho construction wheezing recurrent of dyspnea .  Bronchospasm means ( abnormal contraction of the smooth muscle of the bronchi )  Wheezing is a high pitched sound made while client breath )  according to Brunner and suddarth
  7.  Asthma is a disorder of bronchial airway define as periods of reversible broncho spasm . according to lippen cott Asthma is a chronic inflammatory disease of the airway that causes airway hyper-responsiveness ,mucosal edema and mucus edema. according to luck man
  8. TYPES OF ASTHMA  EXTRINSIC ( ALLERGIC)  INSTRINSIC ( NON ALLERGIC ) EXTRINSIC ( ALLERGIC) = patient with extrinsic asthma have some history of allergies resulting in a hyper sensitivity situation of an antigen -antibody type reaction . Family history hyper sensitivity and personal history of eczema , dermatitis and allergen such as pollen ( flower prag),molds ( fungal ) , animal dander , dust, insecticides , foods ( milk, sea food nuts )and certain drugs aspirin .
  9. INSTRINSIC ( NON ALLERGIC )  In non allergic asthmatic patent the increases hypersensitivity to stimuli such as infection ,exertion, drugs, climate changes and emotional stress ,anxiety , exercise , cold air , dry hyperventilation , smoke viruses .
  10. etiology  Family history -such as eczema , dermatitis  Allergy -such as dust ,insecticides , foods seafood  Emotional stress –strong emotional trigger the release of chemicals such as histamine and leukotrienes which an trigger the narrowing of airway .  Air pollution –cause irritate the airways and trigger asthma  Environmental changes -such as infection ,exercise ,living industrial area.  Certain drugs - such as aspirin
  11. Clinical manifestration  3 most common symptoms of asthma are  Coughing  Dyspnea  Wheezing  COUGHING – the asthmatic attack states suddenly with coughing an sensation of tightness in the chest.  DYSPNEA – Obstruction air flows creates the sensation of dyspnea patient sudden feel short of breath suffocation and drowning .  WHEEZING – patient condition feeling sweating ,tachycardia, fatigue ,and anxiety .
  12. DIAGNOSTIC TEST  Family history - occupational and environmental history  Sputum and blood test – may disclose eosinophilia (elevated levels of eosinophils) Chest radiograph- during acute episodes a chest radiograph may show hyperinflation and a flattened diaphragm. Positive skin test – to identification of specific allergens .
  13. PATHOPHYSIOLOGY  Due to etiological factors such as  Inhaled antigens • By producing antibodies immunoglobulin E(Ige) • It become attached to the receptor sites located on mast cells in the respiratory tract • When a reaction occurs between the antigen and antibody in the respiratory tract • Mast cells release hisatamin • swelling of membrane that line the airway (mucosal edema) • Reduced airway diameters • Contraction of the bronchial smooth muscle in the air way .
  14.  Causing further narrowing  Increases mucosa production ( hyper secretion )  Diminished airway size  Bronchospasm  Breathing difficulty  Then lead to asthma
  15. management Medical management 1. Achieve and maintain control of symptoms 2. Maintain pulmonary function as close to normal levels as possible . 3. Avoid adverse effects of asthma medication. 4.To give the oxygenation for breathing difficulty . 5. Suctioning for excessive mucus production. 6 to give antibiotics and anti inflammatory drugs . 7. Maintain normal activity level ,including exercise .
  16. pharmacological  Drugs  LEUKOTRIENE MODIFIERS INHIBITORS –  Antileukotriene block receptors or prevent bronchospasm  1. montelukast  2. zofirlukast  Action – helpful in improving airflow and asthma symptoms  BRONCHODILATORS  Albuterol  Metaproterenol  Pributerenol  ACTION –To prevent from bronchospasm and relief and control asthma symptoms.
  17.  LONG ACTING FORMS BETA 2 AGONISTS DRUGS  Salmeterol  Formeterol  Action- maintain the open airways for long term control.  Ant cholinergic drugs  1 –theophylline -prevent asthma episodes  SHORT ACTING BETA 2 AGONIST DRUG  Salbutamol is a short acting beta 2 agonist – used to prevent and treatment wheezing , shortness of breath ,coughing and chest tightness.  ATIBIOTICS –  Amoxicillin –treatment of upper and lower respiratory tract infection.
  18.  ANTI INFAMMATORY  Corticosteroid ( budesonide)  Cromolyn sodium oral inhalation ( anti inflammatory agents)  Dexamethasone oral to prevent the release of substances in the body that cause inflammation.
  19. COMPLICATION  RESPIRATORY FAILURE –fails in one and both of its gas exchange function.  PNEUMONIA – inflammation lungs parenchyma cells.  ATELECTASIS- a compete or partial collapse of a lung or lobe of a lungs .  DEHYDRATION – Deficit of total body fluid.  HYPOXEMIA- an abnormal low concentration of oxygen in the blood .
  20. CHRONIC BRONCHITIS
  21. CHRONIC BRONCHITIS Lung damage and inflammation in the large airways results in chronic bronchitis. Chronic bronchitis is defined in clinical terms as a cough with sputum production on most days for 3 months of a year, for 2 consecutive years. Chronic bronchitis is excessive production of mucus in the bronchi accompanied by a recurrent cough that persists for at least 3 months of the year.
  22.  ETIOLOGY:-  Recurring respiratory tact infections  Heredity  Aging –change in the respiratory and pulmonary immune system  Cigarette smoking –damaging airways and the small air sac found in lungs  Exposure to airborne chemical –occupational industrial area.  Secondhand smoke- exhaled bye a smoker is given off by burning tobacco and is inhaled by person near by called secondhand smoker.  Dust –over the long period of time in suffering from dust  Air pollution  Bacterial infection mycoplasm ,pneumococcus  Virus such as influenza
  23.  Alpha -1 antitrypsin deficiency- means lack a proteine in blood called alpha -1 antitrypsin .  This protein helps protect lungs from damage.
  24. CLINICAL MANIFESTRAST  Frequent productive cough during most winter months  Brancospasm  Hypoxemia- deficiency in the amount of o2 reaching the tissues .  Hypercapnea –increase co2 collect in the blood stream.  Frequent respiratory infection  The bluish-red color of the skin results from polycythemia – is a condition that results in an increase level of circulating blood cells in the blood stream.  Cyanosis  Emphysema-is damage the air sac in lungs
  25. PATHOPHYSIOLOGY Smoke and irritants Hyperplasia and hypertrophy of goblet cells & mucous glands of airway Increased mucous production narrowing of airway and mucous secretion Infiltration (enter)of airway walls with inflammatory cells Scarring and remodeling resulting in thickening and narrowing of the airway Limitation of airflow
  26. DIAGNOSTIC TEST 1. History taking 2. Physical examination (Crackles sound,Presence of S3 sound) 3. Blood test= the concentrate of red blood cells which may be increased due to the chronic lack of o2 . 4. X- ray of the lungs (increased fluid in the alveolar walls, pleural effusion (an abnormal collection of fluid in the pleural space).) x-ray picture of lungs and show signs of infection such as pneumonia or a collapsed lung . 5. PFT- are non invasive tests that show how well the lungs are working . The teat measured lung volume ,capacity ,rate of flows ,and gas exchange. 1. Arterial blood gas analysis(ABG)
  27.  SPUTUM TEST- is a find germs such as bacteria or a fungal that cause infection  ABG-test is a blood gas test of blood from an artery ,that measure the amount of certain gases such as oxygen, and carbon dioxide dissolved in artrial blood  SPIROMETRY= is the best test to detect airflow limitation and obstruction
  28. MANAGEMENT  MEDICAL MANAGEMENT  Stop smoking.  The dangers of secondhand smoke are well documented. Children should never be exposed to secondhand smoke inside the home.  Avoid exposure to irritants. Proper protection in the workplace is vital to preventing exposure.  Avoiding long exposure to air pollution from heavy traffic may help prevent bronchitis.  Proper nutrition  Control of environmental temperature and humidity
  29. PHARMACHOLOGICAL  Antibiotics –tetracycline's inhibits bacterial growth  Bronchodilators- a bronchodilator is a substance that dilates the bronchi and bronchioles  Steroids- corticosteroids helps decrease inflammation in airways.  Antimicrobial therapy with tetracycline ,ampicilline,amoxicilline.
  30.  Segmentectomy - removal of single segment of a lung lobe  Lobectomy- surgery to removal one of the lobe of the lungs
  31. •EMPHYSEMA
  32. EMPHYSEMA  Lung damage and inflammation of the air sacs (alveoli) results in emphysema. Emphysema is defined as enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls.  The destruction of air space walls reduces the surface area available for the exchange of oxygen and carbon dioxide during breathing.  destruction of the wall of the alveoli with resulting enlargement of abnormal air spaces .
  33. TYPES 1. PANLOBULAR = Is destruction of the bronchioles alveolar duct and alveoli 2.CENTRILOBULAR= in these emphysema the primary area invovelment is the center part of lobule and respiratory bronchioles enlarged the wall are destroyed
  34. ETIOLOGY Genetic = the inherited condition known as alpha 1 antitrypsin deficiency result in the most severe from of hereditary emphysema Idiopathic Smoking Air pollution Deficiency of Alfa anti trypsin-congenital condition known as alfa anti trypsin deficiency Environmental factors such as occupational exposurs Lungs disease = tb, pneumonia , Alpha -1 antitrypsin deficiency- means lack a protein in blood called alpha -1 antitrypsin . This protein helps protect lungs from dam
  35. PATHOPHYSIOLOGY Recurrent infection and irritants Excessive mucus production Loss of elastic recoil of the airway Enlargement of air spaces distal to the terminal bronchioles Destruction of the wall of alveoli Hyperinflation ( over distention)of the alveoli Narrowing of small alveoli Reduced surface area for gas exchange Breathlessness
  36. SIGNS AND SYMPTOMS  Essentials of diagnosis include:  History of cigarette smoking.  Chronic cough and sputum production (in chronic bronchitis)  Dyspnea (in emphysema) shortness of breath  Wheezing= high pitched sound made while breathing . Cyanosis . Chest pain Hypoxemia Anorexia lack of appetite
  37. DIAGNOSIS HISTORY COLLECTION  The diagnosis of COPD should be considered in anyone who has  Dyspnea,  Chronic cough or sputum production,  and history of exposure to risk factors for the disease such as regular tobacco smoking.
  38. SPIROMETRY The diagnosis of emphysema is confirmed by spirometry, a test that measures breathing. Spirometry also measures the forced vital capacity (FVC) which is the greatest volume of air that can be breathed out in a whole large breath. .
  39. OTHER TESTS On chest x-ray the classic signs of COPD are over- expanded lung (hyperinflation), a flattened diaphragm, increased retrosternal airspace, and bullae. BLOOD TESTS ABG=A blood sample taken from an artery can be tested for blood gas levels which may show low oxygen levels (hypoxemia) and/or high carbon dioxide levels (respiratory acidosis). A blood sample taken from a vein may show a high blood count (reactive polycythemia), a reaction to long-term hypoxemia.
  40. MANAGEMENT  There is currently no cure for COPD; however, COPD is both a preventable and treatable disease. The major current directions of COPD management are  to assess and monitor the disease,  reduce the risk factors,  manage stable COPD,  prevent and treat acute exacerbation.
  41. MEDICAL MANAGEMENT BRONCHODILATORS Bronchodilators are medicines that relax smooth muscle around the airways, increasing the calibre of the airways and improving air flow.
  42. β2 agonists β2 agonists stimulate β2 receptors on airway smooth muscles, causing them to relax. There are several β2 agonists available. Albuterol (common brand name: Ventolin) and terbutaline are widely used short acting β2 agonists and provide rapid relief of emphysema symptoms. Long acting β2 agonists (LABAs) such as salmeterol and formoterol are used as maintenance therapy and lead to improved airflow, exercise capacity, and quality of life.
  43. Anticholinergics  .  Anticholinergic drugs. Regular use is associated with improvements in airflow
  44. Corticosteroids  Corticosteroids act to reduce the inflammation in the airways, reducing lung damage and airway narrowing caused by inflammation.  Some of the more common corticosteroids in use are prednisone, fluticasone, budesonide, mometasone, and beclomethasone. Corticosteroids are used in tablet or inhaled form to treat and prevent acute exacerbations of COPD.
  45. Other medication  Expectorant- bromhexine, potassium iodide, sodium citrate,  Mucolytic- ambroxol,acetyl cystine clearance of mucus( also used in pcm poisoning.)  Mast cell stabilizer- sodium chromo glycate, ketotifen.
  46. Supplemental oxygen  Supplemental oxygen can be given to people with emphysema who have low oxygen levels in the body.  Oxygen is provided through tubing via a nasal cannula or oxygen mask.  Long-term oxygen therapy for at least 16 hours a day can improve the quality of life and survival for people with COPD
  47. NUTRITIONAL MANAGEMENT  who are underweight can improve their breathing muscle strength by increasing their calorie intake. When combined with regular exercise or a pulmonary rehabilitation programme, this can lead to improvements in COPD symptoms.  High protein diet for the regeneration of tissue due to recurrent infection.  Vitamins supplement to prevent infection.  Frequent diet with adequate fluid
  48. SURGICAL MANAGEMENT  A bullectomy is the surgical removal of a bulla, a large air-filled space that can squash the surrounding, more normal lung.  Lung volume reduction surgery is similar; parts of the lung that are particularly damaged by emphysema are removed allowing the remaining, relatively good lung to expand and work better.  Lung transplantation is sometimes performed for severe COPD, particularly in younger individuals.
  49. COMPLICATION  PNEUMONIA  COLLAPSED LUNGS  RECURRENT RESPIRATORY INFECTION
  50. NURSING MANAGEMENT  IMPAIRED GAS EXCHANGE DUE TO CHRONIC INHALATION OF TOXINS.  SELF CARE DEFICIET RELATED TO FATIGUE  NUTRITION IMBALANCE LESS THEN BODY REQUIREMENT  FLUID VOLUME DEFICEY RELATED TO EXCESSIVE SPUTUM PRODUCTION  FEAR RELATED TO COMPLICATIONS OF DISEASE.
  51. •CYSTIC FIBROSIS
  52. introduction  Cystic fibrosis is a serious genetic condition that causes severe damage to the respiratory and digestive systems. This damage often results from a buildup of thick, sticky mucus in the organs. The most commonly affected organs include the:  lungs  pancreas  liver  intestines
  53. CYSTIC FIBROSIS  Cystic fibrosis (CF) is caused by a defective gene which tells the body to produce abnormally thick and sticky fluid, called mucus  ( Cystic fibrosis transmembrane conductance regulator. )  a hereditary disorder affecting the exocrine glands. It causes the production of abnormally thick mucus, leading to the blockage of the pancreatic ducts, intestines, and bronchi and often resulting in respiratory infection.
  54. ETIOLOGY  A defect in the CFTR gene causes cystic fibrosis (CF). This gene makes a protein that controls the movement of salt and water in and out of your body's cells. This causes thick, sticky mucus and very salty sweat.  Family history. Because cystic fibrosis is an inherited disorder, it tends to run in families.  Race. Although cystic fibrosis occurs in all races, it is most common in white people of northern European ancestry.
  55.  ABNORMAL SODIUM AND CHLORIDE TRANSPORT  across cell membrane, causing thick secretion in lung  BACTERIAL INFECTION  Staphylococcus aureus: This is commonly carried on the skin and nose. Pseudomonas aeruginosa: This is the main most common bacteria responsible for lung injury in CF
  56. Clinical manifestation  Respiratory signs and symptoms  The thick and sticky mucus associated with cystic fibrosis clogs the tubes that carry air in and out of your lungs. This can cause signs and symptoms such as:  A persistent cough that produces thick mucus (sputum)  Wheezing  Breathlessness  Exercise intolerance + is a condition of inability or decreased ability to perform physical exercise  Repeated lung infections  Inflamed nasal passages or a stuffy nose
  57. • Salty tasting skin (salt loss when sweating) leading to dehydration • Greasy, light coloured, foul smelling stools or diarrhoea
  58. pathophysiology • Due to etiological factors such as • CFTR loss of its function as a chloride ion transporter caused by misfolding protein • Abnormal sodium and chloride transport across cell membrane, causing thick tenacious ( strictly ) secretion in lung Mucus builds up and obstructs airways • Build up also makes a suitable environment for bacterial growth  Bacterial growth increases risk of infections  Repeated infections cause lung damage  Than lead to cystic fibrosis
  59. Diagnostic test  THE IMMUNOREACTIVE TRYPSINOGEN TEST  is a standard newborn screening test that checks for abnormal levels of the protein called IRT in the blood. A high level of IRT may be a sign of cystic fibrosis. However, further testing is required to confirm the diagnosis.  Sweat Chloride Test  THE SWEAT CHLORIDE TEST  is the most commonly used test for diagnosing cystic fibrosis. It checks for increased levels of salt in the sweat. The test is performed by using a chemical that makes the skin sweat when triggered by a weak electric current. Sweat is collected on a pad or paper and then analyzed. A diagnosis of cystic fibrosis
  60.  SPUTUM TEST  During a sputum test, the doctor takes a sample of mucus. The sample can confirm the presence of a lung infection. It can also show the types of germs that are present and determine which antibiotics work best to treat them.  CHEST X-RAY  A chest X-ray is useful in revealing swelling in the lungs due to blockages in the respiratory passageways.
  61.  CT SCAN These images allows your doctor to view internal structures, such as the liver and pancreas, making it easier to assess the extent of organ damage caused by cystic fibrosis.  PULMONARY FUNCTION TESTS (PFTS)  Pulmonary function tests (PFTs) determine whether your lungs are working properly. The tests can help measure how much air can be inhaled or exhaled .
  62. Pharmacological management  Eg 1.Antibiotics to prevent and treat lung and sinus infections Eg:Azithromycin  Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen and indomethacin, may help reduce any pain and fever associated with cystic fibrosis.  Bronchodilators relax the muscles around the tubes that carry air to the lungs, which helps increase airflow. You can take this medication through an inhaler or a nebulizer.
  63. Surgical  A lung transplant involves removing a damaged lung and replacing it with a healthy one, usually from a deceased donor.
  64. THANK YOU
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