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TINA THANKACHAN
 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.
 In
   COPD, less air flows in and out of the
 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.
 It is the 4th leading cause of mortality and
  12th leading cause of disability in the
  united states.
 In 2020 COPD is the 3rd leading cause of
  death.
 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)Genetics-Alpha 1-antitrypsin 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.
NUTRITION



               INFECTIONS

            SOCIO ECONOMIC STATUS




AGING POPULATION
 Abnormal inflammatory response of the
 lungs due to toxic gases.

 Responseoccurs in the airways
 ,parenchyma & pulmonary vasculature.

 Narrowing   of the airway takes place

 Destruction
           of parenchyma leads to
 emphysema.
 Destruction of lung parenchyma leads to an imbalance
  of proteinases/antiproteinases.
(this proteinases inhibitors prevents the destructive
  process)

              Pulmonary vascularchanges
    Thickening of vessels
    Collagen deposit
    Destruction of capillary       beds.

         Mucus hypersecretion(cilia dysfunction,airflow
    limitation,corpulmonale(RVF))


               Chronic cough and sputum production
   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.
 1) Bronchitis
 2) Emphysema
 Bronchitis :-
 Bronchitis (bron-KI-tis) is a condition in which
  the bronchial tubes become inflamed.
  acute (short term) and
 chronic (ongoing).
 Infections or lung irritants cause 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 atleast 3 months.
   Irritants irrritate the airway


   Excess mucus production

   Inflammation

   Cause the mucus secreting glands and goblet cells to
    increase in number.
   Ciliary function is reduced.

   More mucus production

Bronchial walls become thickened and lumen narrows and
  mucus plug the airway

Alveoli adjacent tto the bronchioles may
  become damaged and fibrosed.

 Alter function of alveolar macrophages.

                     infection
   sore throat,
   fatigue (tiredness),
   fever, body aches,
   stuffy or runny nose,
   vomiting, and
   Diarrhea
   persistent cough
   cough may produce clear mucus
   shortness of breath
   coughing,
    wheezing, and
   chest discomfort.
   The coughing may produce large amounts
    of mucus. This type of cough often is
    called a smoker's cough.
 History - medical history
 •Whether you've recently had a cold or
  the flu
 •Whether you smoke or spend time around
  others who smoke
 •Whether you've been exposed to dust,
  fumes, vapors, or air pollution -
 Mucus  -to see whether you have a
  bacterial infection
 chest x ray,
 lung function tests,
 CBC
 ABG analysis
 MEDICAL MANAGEMENT
 SURGICAL MANAGEMENT
 NURSING MANAGEMENT
 IMPROVE   VENTILLATION
1.   BRONCHO DILATORS LIKE BETA2
     AGONISTS(ALBUTEROL),ANTICHOLINERGIC
     S(IPRATROPIUM BROMIDE-ATROVENT).
2.   METHYLXANTHINES(THEOPHYLLINE,AMIN
     OPHYLLINE)
3.   CORTICOSTEROIDS
4.   OXYGEN ADMINISTRATION
   REMOVE BRONCHIAL SECRETION
   PROMOTE EXERCISES
   CONTROL COMPLICATIONS
   IMPROVE GENERAL HEALTH
 BULLECTOMY
    BULLAE ARE ENLARGED AIRSPACES THAT
  DO NOT CONTRIBUTE TO VENTILLATION BUT
  OCCUPY SPACE IN THE THORAX,THESE AREAS
  MAY BE SURGICALLY EXCISED
 LUNG VOLUME REDUCTION SURGERY
    IT INVOLVES THE REMOVAL OF A PORTION
  OF THE DISEASED LUNG PARENCHYMA.THIS
  ALLOWS THE FUNCTIONAL TISSUE TO EXPAND.
 LUNG TRANSPLANTATION
 ASSESSMENT
 PHYSICAL EXAMINATION
 DIAGNOSIS
 INTERVENTION
 IMPAIRED GAD EXCHANGE RELATED TO
  DECREASED VENTILLATION AND MUCOUS
  PLUGS
 INEFFECTIVE AIRWAY CLEARENCE RELATED
  TO EXCESSIVE SECRETION AND INEFFECTIVE
  COUGHING
 ANXIETY RELATED TO ACUTE BREATHING
  DIFFICULTIES AND FEAR OF SUFFOCATION
 ACTIVITY INTOLERENCE RELATED TO
  INADEQUATE OXYGENATION AND DYSPNOEA
 IMBALANCED NUTRITION LESS THAN BODY REQUIREMENT
            RELATED TO REDUCED APPETITE,DECREASED ENERGY LEVEL
            AND DYSPNOEA

 DISTURBED  SLEEP PATTERN RELATED TO
  DYSPNOEA AND EXTERNAL STIMULI
 RISK FOR INFECTION RELATED TO
  INEFFECTIVE PULMONARY CLEARENCE
 Definition:-Emphysema   is defined as
  enlargement of the air spaces distal to
 the terminal bronchioles, with
 destruction of their walls of the alveoli.
 Pathology :
 As the alveoli are destroyed the alveolar
  surface area in contact with the
  capillaries decreases.
 Causing dead spaces (no gas exchange
  takes place)
 Leads  to hypoxia.
 In later stages:
      CO2 elimination is disturbed and
  increase in CO2 tension in arterial blood
  causing

              Respiratory acidosis
 (Decrease pulmonary blood flowis
  increased forcing the RV to maintain high
  B.P. in PA.)
 Centrilobular-Therespiratory bronchiole
 (proximal and central part of the acinus)
 is expanded. The distal acinus or alveoli
 are unchanged. Occurs more commonly in
 the upper lobes.
 Panlobular-The entire respiratory acinus,
 from respiratory bronchiole to alveoli, is
 expanded. Occurs more commonly in the
 lower lobes, especially basal segments,
 and anterior margins of the lungs.
a)   History
b)   PFT
c)   Spirometry-to find out airflow
     obstruction.
d)   ABG analysis
e)   CT scan of the lung.
f)   Screening of alpha antitrypsin deficiency
g)   X-ray radiography may aid in the
     diagnosis.
 MEDICAL MANAGEMENT
 SURGICAL MANAGEMENT
 NURSING MANAGEMENT
 IMPROVE   VENTILLATION
1.   BRONCHO DILATORS LIKE BETA2
     AGONISTS(ALBUTEROL),ANTICHOLINERGIC
     S(IPRATROPIUM BROMIDE-ATROVENT).
2.   METHYLXANTHINES(THEOPHYLLINE,AMIN
     OPHYLLINE)
3.   CORTICOSTEROIDS
4.   OXYGEN ADMINISTRATION
   REMOVE BRONCHIAL SECRETION
   PROMOTE EXERCISES
   CONTROL COMPLICATIONS
   IMPROVE GENERAL HEALTH
 BULLECTOMY
    BULLAE ARE ENLARGED AIRSPACES THAT
  DO NOT CONTRIBUTE TO VENTILLATION BUT
  OCCUPY SPACE IN THE THORAX,THESE AREAS
  MAY BE SURGICALLY EXCISED
 LUNG VOLUME REDUCTION SURGERY
    IT INVOLVES THE REMOVAL OF A PORTION
  OF THE DISEASED LUNG PARENCHYMA.THIS
  ALLOWS THE FUNCTIONAL TISSUE TO EXPAND.
 LUNG TRANSPLANTATION
 ASSESSMENT
 PHYSICAL EXAMINATION
 DIAGNOSIS
 INTERVENTION
 IMPAIRED GAD EXCHANGE RELATED TO
  DECREASED VENTILLATION AND MUCOUS
  PLUGS
 INEFFECTIVE AIRWAY CLEARENCE RELATED
  TO EXCESSIVE SECRETION AND INEFFECTIVE
  COUGHING
 ANXIETY RELATED TO ACUTE BREATHING
  DIFFICULTIES AND FEAR OF SUFFOCATION
 ACTIVITY INTOLERENCE RELATED TO
  INADEQUATE OXYGENATION AND DYSPNOEA
 DISTURBED  SLEEP PATTERN RELATED TO
  DYSPNOEA AND EXTERNAL STIMULI
 RISK FOR INFECTION RELATED TO
  INEFFECTIVE PULMONARY CLEARENCE
 IMBALANCED NUTRITION LESS THAN BODY
  REQUIREMENT RELATED TO REDUCED
  APPETITE,DECREASED ENERGY LEVEL AND
  DYSPNOEA
   Respiratory insufficiency
   Respiratory failure
   Pneumonia
   Pneumothorax
   Pulmonary artery hypertension.
 TAKEYOUR MEDICATIONS REGULARLY AS
 PRESCRIBED,IF YOU HAVE ANY DOUBT RING
 YOUR HOSPITAL.

 EXERCISEREGULARLY EVERYDAY OR ELSE
 ATLEAST 4 OUT OF 7 DAYS.
THANK YOU!

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CHRONIC OBSTRUCTIVE PULMONARY DISEASE

  • 2.  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.
  • 3.  In COPD, less air flows in and out of the 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.
  • 4.
  • 5.  It is the 4th leading cause of mortality and 12th leading cause of disability in the united states.  In 2020 COPD is the 3rd leading cause of death.
  • 6.  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.
  • 7.  6)Genetics-Alpha 1-antitrypsin 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.
  • 8. NUTRITION INFECTIONS SOCIO ECONOMIC STATUS AGING POPULATION
  • 9.  Abnormal inflammatory response of the lungs due to toxic gases.  Responseoccurs in the airways ,parenchyma & pulmonary vasculature.  Narrowing of the airway takes place  Destruction of parenchyma leads to emphysema.
  • 10.  Destruction of lung parenchyma leads to an imbalance of proteinases/antiproteinases. (this proteinases inhibitors prevents the destructive process)  Pulmonary vascularchanges  Thickening of vessels  Collagen deposit  Destruction of capillary beds.   Mucus hypersecretion(cilia dysfunction,airflow limitation,corpulmonale(RVF))   Chronic cough and sputum production
  • 11. 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.
  • 12.  1) Bronchitis  2) Emphysema  Bronchitis :-  Bronchitis (bron-KI-tis) is a condition in which the bronchial tubes become inflamed.
  • 13.  acute (short term) and  chronic (ongoing).  Infections or lung irritants cause 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.
  • 14.  Chronic bronchitis:  It is defined as the presence of cough and sputum production for atleast 3 months.
  • 15. Irritants irrritate the airway  Excess mucus production  Inflammation  Cause the mucus secreting glands and goblet cells to increase in number.  Ciliary function is reduced.  More mucus production Bronchial walls become thickened and lumen narrows and mucus plug the airway 
  • 16. Alveoli adjacent tto the bronchioles may become damaged and fibrosed. Alter function of alveolar macrophages. infection
  • 17. sore throat,  fatigue (tiredness),  fever, body aches,  stuffy or runny nose,  vomiting, and  Diarrhea  persistent cough  cough may produce clear mucus  shortness of breath
  • 18. coughing,  wheezing, and  chest discomfort.  The coughing may produce large amounts of mucus. This type of cough often is called a smoker's cough.
  • 19.  History - medical history  •Whether you've recently had a cold or the flu  •Whether you smoke or spend time around others who smoke  •Whether you've been exposed to dust, fumes, vapors, or air pollution -
  • 20.  Mucus -to see whether you have a bacterial infection  chest x ray,  lung function tests,  CBC  ABG analysis
  • 21.  MEDICAL MANAGEMENT  SURGICAL MANAGEMENT  NURSING MANAGEMENT
  • 22.  IMPROVE VENTILLATION 1. BRONCHO DILATORS LIKE BETA2 AGONISTS(ALBUTEROL),ANTICHOLINERGIC S(IPRATROPIUM BROMIDE-ATROVENT). 2. METHYLXANTHINES(THEOPHYLLINE,AMIN OPHYLLINE) 3. CORTICOSTEROIDS 4. OXYGEN ADMINISTRATION
  • 23. REMOVE BRONCHIAL SECRETION  PROMOTE EXERCISES  CONTROL COMPLICATIONS  IMPROVE GENERAL HEALTH
  • 24.  BULLECTOMY BULLAE ARE ENLARGED AIRSPACES THAT DO NOT CONTRIBUTE TO VENTILLATION BUT OCCUPY SPACE IN THE THORAX,THESE AREAS MAY BE SURGICALLY EXCISED  LUNG VOLUME REDUCTION SURGERY  IT INVOLVES THE REMOVAL OF A PORTION OF THE DISEASED LUNG PARENCHYMA.THIS ALLOWS THE FUNCTIONAL TISSUE TO EXPAND.  LUNG TRANSPLANTATION
  • 25.  ASSESSMENT  PHYSICAL EXAMINATION  DIAGNOSIS  INTERVENTION
  • 26.  IMPAIRED GAD EXCHANGE RELATED TO DECREASED VENTILLATION AND MUCOUS PLUGS  INEFFECTIVE AIRWAY CLEARENCE RELATED TO EXCESSIVE SECRETION AND INEFFECTIVE COUGHING  ANXIETY RELATED TO ACUTE BREATHING DIFFICULTIES AND FEAR OF SUFFOCATION  ACTIVITY INTOLERENCE RELATED TO INADEQUATE OXYGENATION AND DYSPNOEA
  • 27.  IMBALANCED NUTRITION LESS THAN BODY REQUIREMENT RELATED TO REDUCED APPETITE,DECREASED ENERGY LEVEL AND DYSPNOEA  DISTURBED SLEEP PATTERN RELATED TO DYSPNOEA AND EXTERNAL STIMULI  RISK FOR INFECTION RELATED TO INEFFECTIVE PULMONARY CLEARENCE
  • 28.
  • 29.  Definition:-Emphysema is defined as enlargement of the air spaces distal to  the terminal bronchioles, with  destruction of their walls of the alveoli.  Pathology :  As the alveoli are destroyed the alveolar surface area in contact with the capillaries decreases.  Causing dead spaces (no gas exchange takes place)
  • 30.  Leads to hypoxia.  In later stages:  CO2 elimination is disturbed and increase in CO2 tension in arterial blood causing  Respiratory acidosis  (Decrease pulmonary blood flowis increased forcing the RV to maintain high B.P. in PA.)
  • 31.  Centrilobular-Therespiratory bronchiole (proximal and central part of the acinus) is expanded. The distal acinus or alveoli are unchanged. Occurs more commonly in the upper lobes.
  • 32.  Panlobular-The entire respiratory acinus, from respiratory bronchiole to alveoli, is expanded. Occurs more commonly in the lower lobes, especially basal segments, and anterior margins of the lungs.
  • 33. a) History b) PFT c) Spirometry-to find out airflow obstruction. d) ABG analysis e) CT scan of the lung. f) Screening of alpha antitrypsin deficiency g) X-ray radiography may aid in the diagnosis.
  • 34.  MEDICAL MANAGEMENT  SURGICAL MANAGEMENT  NURSING MANAGEMENT
  • 35.  IMPROVE VENTILLATION 1. BRONCHO DILATORS LIKE BETA2 AGONISTS(ALBUTEROL),ANTICHOLINERGIC S(IPRATROPIUM BROMIDE-ATROVENT). 2. METHYLXANTHINES(THEOPHYLLINE,AMIN OPHYLLINE) 3. CORTICOSTEROIDS 4. OXYGEN ADMINISTRATION
  • 36. REMOVE BRONCHIAL SECRETION  PROMOTE EXERCISES  CONTROL COMPLICATIONS  IMPROVE GENERAL HEALTH
  • 37.  BULLECTOMY BULLAE ARE ENLARGED AIRSPACES THAT DO NOT CONTRIBUTE TO VENTILLATION BUT OCCUPY SPACE IN THE THORAX,THESE AREAS MAY BE SURGICALLY EXCISED  LUNG VOLUME REDUCTION SURGERY  IT INVOLVES THE REMOVAL OF A PORTION OF THE DISEASED LUNG PARENCHYMA.THIS ALLOWS THE FUNCTIONAL TISSUE TO EXPAND.  LUNG TRANSPLANTATION
  • 38.  ASSESSMENT  PHYSICAL EXAMINATION  DIAGNOSIS  INTERVENTION
  • 39.  IMPAIRED GAD EXCHANGE RELATED TO DECREASED VENTILLATION AND MUCOUS PLUGS  INEFFECTIVE AIRWAY CLEARENCE RELATED TO EXCESSIVE SECRETION AND INEFFECTIVE COUGHING  ANXIETY RELATED TO ACUTE BREATHING DIFFICULTIES AND FEAR OF SUFFOCATION  ACTIVITY INTOLERENCE RELATED TO INADEQUATE OXYGENATION AND DYSPNOEA
  • 40.  DISTURBED SLEEP PATTERN RELATED TO DYSPNOEA AND EXTERNAL STIMULI  RISK FOR INFECTION RELATED TO INEFFECTIVE PULMONARY CLEARENCE  IMBALANCED NUTRITION LESS THAN BODY REQUIREMENT RELATED TO REDUCED APPETITE,DECREASED ENERGY LEVEL AND DYSPNOEA
  • 41. Respiratory insufficiency  Respiratory failure  Pneumonia  Pneumothorax  Pulmonary artery hypertension.
  • 42.  TAKEYOUR MEDICATIONS REGULARLY AS PRESCRIBED,IF YOU HAVE ANY DOUBT RING YOUR HOSPITAL.  EXERCISEREGULARLY EVERYDAY OR ELSE ATLEAST 4 OUT OF 7 DAYS.
  • 43.
  • 44.
  • 45.
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  • 47.
  • 48.
  • 49.