COPD

1. Definition: The American thoracic society defines COPD as a disease state

characterised by the presence of airflow obstruction due to Emphysema or Chronic
Bronchitis.

Chronic
Emphysema
Bronchitis

COPD

Emphysema: (Pink Puffers) Abnormal permanent enlargement of the air spaces

distal to terminal bronchioles, accompanied by destruction of their walls without
significant fibrosis.
 Types of emphysema on the basis of anatomical distribution:
Types Centriacinar Panacinar Distal acinar Irregular
Definition Central and Whole acinus Distal part of Acinus
proximal part of is affected. acinus is irregularly
acini is affected. affected.
affected.
Cause Smoking is the Alpha 1 Cause is Secondary to
main cause. antitrypsin unknown. inflammatory
deficiency is diseases.
the main
cause.
Lung part Lung upper Lower lobe is
Upper half Clinically
lobe is affected. affected.
lung is asymptomatic.
affected.
Centiacinar and Panacinar are clinically important types.
 Pathogenesis of Emphysema:

Emphysema
Enviornmental Exposure Genetic Factors
Tobacco smoke, biomassfuels and others TGF-B1 Polymorphism, alpha 1 antitrypsin deficiency

Cells Affected
Inflammatory cells Epithelial cells Mesenchymal cells

Cellular Injury
Cytokines, Proteases, Elastases causes Impaired proliferation, Apoptosis,
Apoptosis, Necrosis
ECM degradation decreased matrix synthesis
  Morphological Features of Emphysema:
Centiacinar Panacinar
Deeper pink lungs Pale lungs
Less voluminous Voluminous
Upper 2/3rd of lungs severely affected Lower Lung affected

 Microscopic Features of Emphysema:

o Destruction of alveolar walls without fibrosis
o Enlarged air spaces
o Loss of alveolar capillaries
o Loss of elastic tissues
o Bronchiolar inflammation
Chronic Bronchitis: (Blue Bloaters) Presence of persistent productive cough for atleast 3
consecutive months in atleast 2 consecutive years. 20-25% Men of age 40-65 years are at
risk. In early stage there is the production of mucoid sputum with no airflow obstruction but
in later stage chronic airway obstruction occurs.
 Pathogenesis of Chronic Bronchitis:

Hypertrophy Increase mucin

of mucus secreting Goblet
cells in epithelium
Risk Factor glands in of small small
trachea and bronchi and
bronchi brochioles
Mucus
Hypersecretion
Recruitment of CD8+
lymphocytes,
Risk Factor macrophages & Inflammation
neutrophils

 Morphological/Histological Features of Chronic Bronchitis:

o Hyperaemic & swollen blood vessels
o Enlarged mucus secreting glands on histologic examination
o Inflammatory cells are present

2. Epidemiology: 4th leading cause of death, COPD affects more than 10% of US adult
population. The NHLBI estimates that 14 million Americans have been diagnosed
with COPD. With COPD and Asthma over 120,000 death reported annually. The
death rate from COPD is increasing rapidly, especially among elderly men.
3. Risk factors: Tobacco smoke, air pollutants, biomass fuel, older age and genetic
factors.
4. Stages: There are 4 stages of COPD according to GOLD STAGING SYSTEM. In
this system measure the FEV in 1 second.
 a) Mild COPD: FEV1 about 80% or more of normal.
b) Moderate COPD: FEV1 b/w 50 & 80% of normal.
c) Severe COPD: FEV1 b/w 30 & 50% of normal.
d) Very severe: FEV1 less than 30% of normal.
5. Lab findings: Spirometry provides objective information about pulmonary function
and assess the results of therapy. In Pulmonary Function Test check the ratio of
FEV1/FVC. In COPD patient the value of FEV1/FVC ratio is low (FEV= 80% -
120%). Lung volume measurements reveal increases RV & Total lung capacity.
6. Imaging: Radiographs of patients with chronic bronchitis shows only non-specific
peribronchial & perivascular markings. Radiographs are insensitive for emphysema.
CT scan of chest more sensitive and specific for the diagnosis of emphysema rather
than chronic bronchitis. Doppler Echocardiography to check the pulmonary
hypertension.
7. Sign & Symptoms: Excessive cough, wheezing, sputum production, dyspnea.
Hypoxia, hypercapnia. Cyanosis & acidosis also shown in pts with chronic bronchitis.
8. Differential diagnosis: Bronchial asthma, bronchiectasis, cystic fibrosis,
bronchopulmonary mycosis and central airflow obstruction.
9. Complications: Pulmonary HTN, recurrent infection, core pulmonale, atrial
dysrhythmias, RHF, pulmonary thrombo embolism, pneumonia, chronic respiratory
failure, coma & death.
10. MNT:
11. Prognosis: Check the degree of Pulmonary dysfunction is an important predictor of
survival: median survival of patients with FEV1 less than or equal to 1L is about 4
years. BODE index is a tool that predicts death & hospitalization better than FEV1
alone. BODE index includes BMI, Airway obstruction, dyspnea and exercise
capacity.
12. Prevention: Elimination of long term exposure to tobacco smoke. Vaccination
against seasonal influenza & pneumococcal infections may be beneficial. Lifestyle
and dietary modifications.
13. Treatment:
a) Smoking cessation
b) Oxygen therapy
c) Inhale bronchodilators (Anticholinergic ipratropium bromide and B-2 agonist
e.g. albuterol, metaproterenol)
d) Corticosteroids through nebulizer
e) Theophylline (bronchodilator)
f) Antibiotics (doxycycline, trimethoprim-sulfamethoxazole, cephalosporin)
g) Pulmonary rehabilitation (graded aerobic physical exercise programs e.g.
walking 20 minutes 3 times per week)
h) Other measures: use of adequate systemic hydration, effective cough training
methods & alpha 1 antitrypsin replacement therapy in emphysema.
i) Surgery: Lung Transplant, Lung volume reduction surgery & Bullectomy.
14. When to Refer:
 COPD onset occurs before the age of 40
 Frequent exacerbations
 Severe or rapidly progressive COPD
 Need for long term oxygen therapy
 Onset of comorbid illness (heart failure or lung cancer)
15. When to admit:
  Severe symptoms or acute worsening that fails to respond to out-patient
management
 Acute or worsening hypoxemia, hypercapnia, peripheral edema & change in
mental status and to maintain sleep, nutrition and hydration status.
Asthma
1. Definition: Chronic inflammatory disorder of airways, caused by recurrent episodes
of wheezing, breathlessness, chest tightness, cough particularly at night or early
morning.
2. Hallmarks:
 Increase mucus secretion
 Hypertrophy & hypersensitivity of smooth muscle cells
 Inflammation with eosinophils unlike chronic bronchitis
3. Epidemiology: Worldwide, it is estimated that approximately 334 million people
currently suffer from asthma, and 250,000 deaths are attributed to the disease each
year. The prevalence of the disease is continuing to grow, and the overall prevalence
is estimated to increase by 100 million by 2025.
4. 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 substances, such as pollen, dust mites, mold spores, pet dander or
particles of cockroach waste
 Respiratory infections, such as the common cold
 Physical activity (exercise-induced asthma)
 Cold air
 Air pollutants and irritants, such as smoke
 Certain medications, including beta blockers, aspirin, ibuprofen
(Advil, Motrin IB, others) and naproxen (Aleve)
 Strong emotions and stress
 Sulphites and preservatives added to some types of foods and beverages,
including shrimp, dried fruit, processed potatoes, beer and wine
 Gastroesophageal reflux disease (GERD), a condition in which stomach
acids back up into your throat
5. Risk factors: A number of factors are thought to increase your chances of developing
asthma. These include:
 Having a blood relative (such as a parent or sibling) with asthma
 Having another allergic condition, such as atopic dermatitis or allergic
rhinitis (hay fever)
 Being overweight
 Being a smoker
 Exposure to exhaust fumes or other types of pollution
 Exposure to occupational triggers, such as chemicals used in farming,
hairdressing and manufacturing
6. Pathogenesis: TH2 cells reaction against environmental agents. In inflammation TH2
cells secrete and activates cytokines such as IL-4, IL-5 & IL-13. IL-4 produce IGE
antibody, coats mast cells which when exposure to allergen releases histamine
granules. These granules undergo two phases i.e. Early phase: Bronchoconstriction,
increase mucus production & vasodilation. Late phase: Inflammation and activation
of eosinophils, neutrophils & T-cells.
IL-4 activates eosinophils and IL-13 stimulates mucus production.
 Airway remodelling: Structural changes in bronchial wall by repeated exposure of
inflammation. Structural changes such as hypertrophy of bronchial smooth muscles &
mucus glands, increase vascularity & deposition of sub epithelial collagen.

7. Types:

Atopic Asthma Non-Atopic Drug Induced Occupational

Asthma Asthma
Most common type No allergic Pharmacological Due to repeated
with allergic sensitization agents provokes exposure with
sensitization Asthma e.g. Aspirin fumes, organic or
chemical dust &
gasses
Example of type I Virus induced Mechanism
IGE mediated respiratory unknown
Hypersensitivity infection
Allergic reactions Positive family Aspirin inhibits
precedes by history is less cyclooxygenase
positive family common, Inhaled pathway of
history, allergic air pollutant arachidonic acid
rhinitis, urticarial, metabolism without
eczema & affecting
environmental lipoxygenase route,
antigens such as shifting balance of
dust, pollen & production towards
certain foods leukotrienes that
cause
bronchospasm
Diagnosis: Diagnosis: Aspirin sensitive
Skin test: with Negative skin test pts suffers recurrent
offending antigens rhinitis, nasal
result in immediate polyps, urticarial &
wheal & flare bronchospasm
reactions
Serum RASTs test:
identify the
presence of IGE
specific for allergy

8. Asthma classification
 Mild intermittent: Mild symptoms up to two days a week and up to two nights
a month
 Mild persistent: Symptoms more than twice a week, but no more than once in a
single day
 Moderate persistent: Symptoms once a day and more than one night a week
 Severe persistent: Symptoms throughout the day on most days and frequently at
night
9. Diagnosis: Through physical examination and lab tests
Lab tests: Lung function tests to determine how much air moves in and out as you
breathe. Lung function tests often are done before and after taking a medication called
a bronchodilator (brong-koh-DIE-lay-tur), such as albuterol, to open your airways. If
your lung function improves with use of a bronchodilator, it's likely you have asthma.
These tests may include:
 Spirometry. This test estimates the narrowing of your bronchial tubes by
checking how much air you can exhale after a deep breath and how fast
you can breathe out.
 Peak flow. A peak flow meter is a simple device that measures how hard
you can breathe out.
 Methacholine challenge. Methacholine is a known asthma trigger that,
when inhaled, will cause mild constriction of your airways. If you react to
the methacholine, you likely have asthma. This test may be used even if
your initial lung function test is normal.
 Nitric oxide test. This test, though not widely available, measures the
amount of the gas, nitric oxide that you have in your breath. When your
airways are inflamed — a sign of asthma — you may have higher than
normal nitric oxide levels.
 Imaging tests. A chest X-ray and high-resolution computerized tomography
(CT) scan of your lungs and nose cavities (sinuses) can identify any
structural abnormalities or diseases (such as infection) that can cause or
aggravate breathing problems.
 Allergy testing. This can be performed by a skin test or blood test. Allergy
tests can identify allergy to pets, dust, mold and pollen. If important allergy
triggers are identified, this can lead to a recommendation for allergen
immunotherapy.
 Sputum eosinophils. This test looks for certain white blood cells
(eosinophils) in the mixture of saliva and mucus (sputum) you discharge
during coughing. Eosinophils are present when symptoms develop and
become visible when stained with a rose-colored dye (eosin).
 Provocative testing for exercise and cold-induced asthma. In these tests,
your doctor measures your airway obstruction before and after you perform
vigorous physical activity or take several breaths of cold air.
10. Sign & symptoms: Asthma signs and symptoms include:
 Asthma attack lasts 1 to several hours
 Shortness of breath
 Chest tightness or pain
 Hyperinflation of lungs with air trapped distal to bronchi
 Bronchi filled with mucus & debris
 Hypercapnia, acidosis & hypoxia
 Trouble sleeping caused by shortness of breath, coughing or wheezing
 Wheezing sound when exhaling (wheezing is a common sign of asthma in
children)
  Coughing or wheezing attacks that are worsened by a respiratory virus, such as
a cold or the flu
11. Complications: Permanent narrowing of the bronchial tubes (airway remodelling)
that affects how well you can breathe.
12. MNT:
13. Prognosis: The prognosis of adult asthma is not as well-described as that of chronic
obstructive pulmonary disease. Although complete remission is possible, remission
rates are low and limited to milder cases. Permanent lung function impairment
develops in some asthmatic patients, and this risk is increased in smokers
14. Prevention:
 Follow your asthma action plan
 Get vaccinated for influenza and pneumonia
 Identify and avoid asthma triggers
 Monitor your breathing
 Identify and treat attacks early
 Take your medication as prescribed
 Pay attention to increasing quick-relief inhaler use 
15. Treatment:
 Long-term control medications reduce the inflammation in your airways such
as Inhaled corticosteroids (fluticasone, budesonide, ciclesonide)
Leukotriene modifiers (montelukast, zafirlukast) Long-acting beta agonists
(formoterol, salmeterol) Theophylline.
 Quick-relief inhalers (bronchodilators) quickly open swollen airways such as
Short-acting beta agonists (albuterol, levalbuterol) Ipratropium (Atrovent)
Oral and intravenous corticosteroids
 Lifestyle modification by avoiding triggers and stay healthy

Medical Nutrition therapy

 The nutritionist or dietetian address the dietary triggers, corrects energy and
nutrient deficiencies and excesses in the diet, educates the patient on a
personalized diet that provides optimal levels of nutrients, monitors growth
in children, and watches for food-drug interactions.
 Modulation of antioxidant intake with nutritional supplementation has a
beneficial effect on the severity and progression of asthma. Although a slight
inverse association was seen between low vitamin E intakes and wheezing
symptoms, no association was found between vitamin E and asthma.
 A diet rich in antioxidants and monounsaturated fats are good for asthma
patients.
 Supplementation of vitamin C and zinc also have been reported to improve
asthma symptoms and lung function.
 Insufficient serum level of vitamin D was associated with an increase in
asthma exacerbation in the form of ER visits and hospitalizations.

Foods allowed Reason to give

Apple Increased lung function
Banana Antioxidant, potassium presences
improve lung functions.
Cantaloupe Prevent from lung damage (presence
antioxidant vit.C
Carrots Beta carotene presence that reduce the
exercise induced asthma
Coffee Bronchodilators improve airflow
Garlic Allicin destroy free radicals
Ginger Relax the airways

Foods avoided Reason not to give

Dried fruits Sulfites(type of preservative worsen
for asthma
Cabbagge Gas producing vegetables(chest
tightness and trigger asthma flares