This document provides information on Chronic Obstructive Pulmonary Disease (COPD) and some of its components. It begins with an introduction defining COPD and its causes as disorders that narrow the airways and limit airflow. It then discusses specific conditions like asthma, chronic bronchitis, and emphysema. For each condition, it covers definitions, classifications, etiology, clinical manifestations, diagnostic tests, pathophysiology, management, pharmacological treatments, and potential complications. The document aims to educate on COPD and its subtypes through detailed descriptions and explanations.

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