2. Bronchiectasis
It is characterized by chronic permanent dilation and
destruction of bronchi due to destructive changes in
elastic and muscular layers of bronchial walls that
may be diffuse or localized resulting in impairment of
drainage of bronchial secretions. Accumulation of
secretions leads to infection
In Pakistan pulmonary TB is the major cause!!
4. Bronchiectasis: Clinical
Clinical:
Cough (90 %): Chronic productive cough,There is also
halitosis
Daily sputum production (76%): Sputum is purulent,
more in the mornings
Dyspnea (72%)
Hemoptysis (56%): Slight, massive or recurrent
On Examination:
Weight loss, anorexia, clubbing of fingers/
Auscultation: Coarse crepitation's will be heard over
the affected areas, commonly at lung bases
5. Investigations:
Sputum: C/S:
May reveal S.Aureus, Pseudomonas Aeruginosa, Aspergillus
AFB:
Mycobacterium tuberculosis
Assessment of ciliary function:
It’s the time taken for a small pellet of saccharin placed in the
anterior chamber of the nose to reach the pharynx when the
patient can taste it, it should not exceed 20 minutes.
Electron microscopy:
To check cilia
X-ray Chest:
May be normal or may show dilated bronchi with thickened
bronchial walls and sometimes multiple cysts containing fluid.
7. High resolution CT scan
High sensitivity and specificity
Train track sign:
the bronchial wall is thickened and visible; the bronchi
lose the trend of narrowing from proximal to distal
end
Diamond ring sign:
Dilated bronchi appear as ring structures.
8.
9. Bronchoscopy
Evaluating the airways for lesions
Assessing the cause of hemoptysis
Localizing the source of hemoptysis
10. Treatment
Medical management:
1. Bronchodilators
2. Postural drainage
3. Antibiotic therapy: Depending on C/S
Surgical Management
1. When its unilateral, confined to a lobe or segment
and patient is not responding to treatment, surgical
resection is required
11. COPD
It’s a disease characterized by presence of air flow
obstruction due to chronic bronchitis or emphysema.
Chronic bronchitis: Clinical disorder characterized by
productive cough on most of the days for atleast 3
consecutive months for more that 2 successive years.
Emphysema: Abnormal and permanent dilation of air
spaces lying beyond the terminal bronchioles
accompanied by destruction of their walls
12. Risk Factors
Cigarettes (80 to 90% of cases in the US).
Possible exposure to secondhand smoke
Environmental factors such as respiratory
infections
Industrial exposures
Air pollution
Genetic predisposition (e.g. alpha-1
antitrypsin deficiency)
13. releaserelease
Inflammatory Process in COPD
NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease. April 2001 (Updated 2003).
Barnes PJ. Chronic obstructive pulmonary disease. N Engl J Med. 2000;343:269-280.
activatesactivatesactivatesactivates
NeutrophilsNeutrophilsNeutrophilsNeutrophils
Macrophages inMacrophages in
respiratoryrespiratory
tracttract
Macrophages inMacrophages in
respiratoryrespiratory
tracttract
ProteasesProteasesProteasesProteases stimulatestimulatestimulatestimulate
releaserelease
ParenchymalParenchymal
DestructionDestruction
15. COPD
Diagnostic tests
Clinical Features
Physical examination
Sample of sputum
Chest x-ray
High-resolution CT (HRCT scan)
Pulmonary function test (spirometery)
Pulse oximeter
16. Clinical Features
Cough: Repeated attacks of productive cough, especially
during winter and later it becomes constant. There is
tightness in the chest especially in the morning
Expectoration: Sputum is little, mucoid and tenacious.
Purulent sputum is indicative of infection.
Dyspnea: Noted in heavy exertion, condition progresses it
occurs with mild activity and at rest.
17. Examination:
Inspection: Patient has dyspnea/ Accessory muscles
are used/ Pursing of lips/ Indrawing of supraclavicular
fossae and intercostal spaces during inspiration/
Chest becomes barrel shaped
Palpation: Apex beat not palpable/ Chest expansion
becomes decreased
Percussion: Hyper-resonant
Auscultation: Breath sounds decreased/ Coarse
crepitation's at lung bases during inspiration and
expiration
18. COPD Patients—Not Necessarily
the Stereotype
Stereotypical pictures of COPD patients
31
Blue BloaterBlue BloaterPink PufferPink Puffer
19.
20. Reduced expiratory flow rate, destruction of alveoli, and short
exhalation time lead to…
Low, Flattened DiaphragmLow, Flattened Diaphragm Increased A-P DiameterIncreased A-P Diameter
Air TrappingAir Trapping
Hyperinflation
22. Sputum C/S: It may reveal streptococcal pneumonia,
HI, Moraxella catarrhalis
Alpha 1-Antitrypsin: 2-4g/L
CBC: Hemoglobin level and PCV can be elevated as
a result of persistent hypoxaemia
23. Diagnosis of COPD
Role of Spirometry
• Expiratory airflow limitation is the hallmark physiologicExpiratory airflow limitation is the hallmark physiologic
change of COPDchange of COPD
• FEVFEV11, FVC, FEV, FVC, FEV11/FVC all decrease/FVC all decrease
• Spirometry is “the gold standard”—most reproducible,Spirometry is “the gold standard”—most reproducible,
standardized, objective way of measuring airflow limitationstandardized, objective way of measuring airflow limitation
24.
25. GOLD Stages of COPD
NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease. April 2001 (Updated 2003).
26.
27. Asthma
Asthma is a chronic lung-disease that inflames and
narrows the airways (tubes that bring air into and out
of an individual’s lungs).
Asthma is the most common chronic disease among
children.
Extrinsic (70%) is due to IgE and Th2 mediated
responses to environmental antigens
Intrinsic (30%) is Triggered by non immune stimuli:
Aspirin, stress, exercise, viral infections
28. What substances trigger asthma?
Type of Substance Examples
Air pollutants, including dusts,
smoke, mists & fumes
Diesel exhaust; tobacco smoke;
mineral, rock, coal, & wood dusts;
gases; fumes & vapors from aerosol
agents, chemicals, cleaning materials,
solvents, paints, welding & from heating
& cooling metals quickly
Pollens, mites & molds Trees, flowers, weeds, hay, plants
Animal dander Birds, cats, dogs
Medications Aspirin, anti-inflammatory drugs
Foods Egg, wheat, nuts
29.
30. Mediators
Leukotrienes C4, D4, E4:
Prolonged bronchoconstriction, increased mucin secretion
Acetylcholine:
Stimulation of muscaranic receptors, Inc. Muscle contraction
Histamine:
Causes bronchospasm
Prostaglandin D2:
Elicits Bronchoconstriction
Eosinophils:
Late phase reaction starts 4-8hrs later and persists for 12-
24hrs, it produces leukotrienes, and its toxic to airways
31.
32.
33. Symptoms
Common symptoms of asthma include:
Coughing
Wheezing
Tightness in the chest
Shortness of breath
34. Diagnosis
History :
Periodic attacks / Family history / Seasonal / Early morning
On Examination:
Mild attack:
1. Slight tachycardia/ tachypnea
2. Mild diffuse wheezing
Moderate attack:
1. Use of accessory muscles, retraction of Intercostal muscles
2. Decreased breath sounds, loud wheezing
Severe attack:
1. Fatigue, cyanosis
2. Inaudible breath sounds ( Silent chest)
3. Inability to maintain lying position
35. Investigations
Chest X-ray:
Hyper inflated lungs
Blood tests:
Eosinophils and IgE are usually increased
Skin prick test:
Should be performed in all cases of asthma to help
identify allergic causes
37. Step 1: Mild intermittent asthma
Step 5: Continuous or frequent
use of oral steroids
Step 4: Persistent poor control
Step 3: Add-on therapy
Step 2: Regular preventer therapy
Management
• Learning to recognize one’s own triggers and taking steps
to avoid them./Avoid aggravating factors:
• Stepwise management of asthma in adults
38. Step 1: Mild intermittent asthma
Inhaled short acting ß2 agonist as required
Stepwise management of asthma in adults
39. Step 2: Regular preventer therapy
Inhaled steroids should be prescribed for patients:
With exacerbation of asthma in the last 2 years
Using inhaled beta2 agonists three times a week or more
Symptomatic three times a week or more
Waking one night a week or more
Start patients at inhaled steroid dose appropriate to disease severity (e.g.
adults: 400 micrograms per day; beclomethasone), higher doses in smokers
are required
Use lowest dose at which effective control of asthma is maintained
AE: Oropharyngeal candidiasis/ Dec bone growth
Inhaled steroids are the most effective preventer drug for adults and
children for achieving overall treatment goals
40. Stepwise management of asthma in adults
Step 3: Add-on therapies
1. Check inhaler technique
2. Add inhaled long-acting ß2 agonist (LABA) ex: Salmetrol (12hrs)
3. Assess control of asthma:
• Good response to LABA – continue LABA
• Benefit from LABA but control still inadequate – continue LABA and
increase inhaled steroid dose to 800 micrograms/day * (if not already on
this dose)
• NO response to LABA – stop LABA and increase inhaled steroid to
800 micrograms/day *. If control still inadequate, institute trial of other
therapies
(e.g. leukotriene receptor antagonist or SR theophylline)
Step 1: Mild intermittent asthma
Step 2: Regular preventer therapy
Start at dose of inhaled
steroid appropriate to
severity of disease.
41. Stepwise management of asthma in adults
Step 3: Add-on therapies
1. Check inhaler technique
2. Add inhaled long-acting ß2 agonist (LABA) ex: Salmetrol (12hrs)
3. Assess control of asthma:
• Good response to LABA – continue LABA
• Benefit from LABA but control still inadequate – continue LABA and
increase inhaled steroid dose to 800 micrograms/day * (if not already on
this dose)
• NO response to LABA – stop LABA and increase inhaled steroid to
800 micrograms/day *. If control still inadequate, institute trial of other
therapies
(e.g. leukotriene receptor antagonist or SR theophylline)
Step 1: Mild intermittent asthma
Step 2: Regular preventer therapy
Start at dose of inhaled
steroid appropriate to
severity of disease.
42.
43. Step 4: Persistent poor control
Consider trials of:
• increasing inhaled steroid up to 2000mcg/day *
• Addition of oral therapy(e.g. leukotriene
receptor antagonist, SR theophylline, ß2 agonist
tablet)
Step 1: Mild intermittent asthma
Step 3: Add-on therapy
Step 2: Regular preventer therapy Start at dose of inhaled
steroid appropriate to
severity of disease.
Stepwise management of asthma in adults
44. Step 5: Continuous or frequent use of oral steroids
Use daily steroid tablet in lowest dose providing adequate control
Maintain high dose inhaled steroid at 2000mcg/day *
Consider other treatments to minimise the use of steroid tablets
AE: When use is >3months or receiving more than 3-4 courses
Step 1: Mild intermittent asthma
Step 3: Add-on therapy
Step 2: Regular preventer therapy
Start at dose of inhaled
steroid appropriate to
severity of disease.
Step 4: Persistent poor control
Stepwise management of asthma in adults
45. Step-down therapy
Once asthma control is established, the dose of
C/S should be titrated to the lowest dose at which
control is maintained.
Decreasing the dose by 25-50% every 3 months
is a reasonable strategy
The diagram below shows the mucus development in a lung with Bronchiectasis (on the right), and a normal lung on the left…. The term ‘bronchiectasis’ is used to describe abnormal and permanently dilated airways.
Middle lobe syndrome/
Kartagener syndrome: A genetic syndrome that is characterized by sinusitis, bronchiectasis (widening and inflammation of the bronchi), dextrocardia (heart on the right side of the chest), and infertility.
Emperical Antipseudomonal antibiotics//// LOBE drained has to be uppermost/// 5-10 min daily twice a day
>10 pack years=20 cigarettes per day per year=1 pack year
Infections decrease in FEV1---) Adenovirus in lung tissue may increase lung damage, HIV Inc chances of emphysema
Key Points:
Inflammation in COPD is associated with edema of the mucosa, hypersecretion of mucus, and fibrosis. The latter develops after chronic inhalation of toxic particles, the most important of these being from tobacco smoke.
The parenchymal destruction is characterized by loss of alveolar attachments, destruction of alveolar walls, and a decrease in the elastic recoil that keeps the airways open during expiration. Airways collapse.
NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease. Bethesda, Md: National Institutes of Health; April 2001 (Updated 2003). NHLBI/WHO Workshop Report, NIH publication 2701.
American Thoracic Society Statement. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1995;152(suppl 5):S77-S120.
The National Lung Health Education Program Executive Committee. Strategies in preserving lung health and preventing COPD and associated diseases: the National Lung Health Education Program (NLHEP). Chest. 1998;113(suppl 2):123S-163S.
Key Points:
In severe COPD, two stereotypes—the pink puffer and the blue bloater—help define the extremes of the disease.
Most patients have features of both stereotypes.
The pink puffer is typically an asthenic, barrel-chested, emphysematous patient who exhibits pursed-lip breathing, who has no cyanosis or edema, and who sits forward with hands on thighs or knees to assist in inspiration (Tripod position). Usually, such a patient uses extrathoracic muscles to breathe, produces minimal sputum, and experiences little fluctuation in the day-to-day level of dyspnea. Diaphragmatic excursions are reduced, and breath and heart sounds are distant. The barrel-shaped chest is nonspecific because elderly persons commonly have increased lung compliance and larger resting lung volumes.
The blue bloater is typically overweight, cyanotic, edematous, and has a chronic productive cough. Generally, they have dyspnea at rest. Elderly blue bloaters are uncommon because blue bloaters often have cor pulmonale, which rapidly leads to death if not treated appropriately. It is not uncommon for early use of supplemental oxygen.
It is not correct to assume that the pink puffer has predominantly emphysema and the blue bloater predominantly bronchial disease.
Terry PB. Chronic Obstructive Pulmonary Disease. In: Merck Manual of Geriatrics.
Whitehouse Station, NJ: Merck & Co, Inc.; 2003.
Thin, breathless, maintain a normal PaCO2 until the late stage…. BLUE: Develop hypercapnia earlier and develop edema and secondary edema//
Alveolar ventilation
Hyperinflation of the lungs in COPD occurs because of progressive destruction of the alveoli, reduced expiratory flow rate, and the relatively short time of exhalation that COPD patients experience because of obstruction to airflow.
Cholinergic tone contributes to reduced expiratory flow rate and inadequate exhalation time.
Other complications are the fact that chest wall recoil remains inward, which results in a threshold load at the start of inspiration; and the flattened, shortened diaphragm muscle, which leads to inefficiency in force generation.
Patients work harder to breathe.
The posteroanterior (PA) and lateral chest radiographs shown here illustrate advanced findings of COPD and hyperinflation. Chest radiograph changes occur late. The expanded chest, retrosternal air space, low and flat diaphragm, and decrease in peripheral vascularity highlight the major radiographic findings. Hyperinflation is readily apparent.
Axial CT image of the lung of a person with end-stage bullus emphysema
FEV1 = forced expiratory volume in 1 second (the volume of air that is forcefully expelled in the first second of a forced expiration starting from full inspiration). A patient with unobstructed airflow should be able to exhale the majority of air (80%) from their lungs within the first second of forced expiration.
FVC = forced vital capacity. FVC is the maximum volume of air in liters that can be forcibly and rapidly exhaled following a maximum inspiration. A “normal” FVC in a healthy adult is approximately 80% of predicted or greater.
Predicted values are determined by a combination of factors including age, gender, height, and race.
Airway obstruction is characterized by a decrease in the FEV1/FVC ratio. A ratio of less than 70% in adults indicates airway obstruction.
If FEV1 returns to the predicted normal range after administration of a bronchodilator, the patient’s airflow limitation is likely caused by asthma.
Spirometry should be performed again after administering a bronchodilator such as albuterol to ascertain postbronchodilator readings and determine the amount of reversibility.
Patients with COPD commonly have significant improvements in spirometry following inhaling bronchodilators, but will not return to a normal range.
Global initiative for chronic obstructive lung disease///The worse a person's airflow limitation is, the lower their FEV1. As COPD progresses, FEV1 tends to decline//
FEV1% predicted, which is defined as FEV1% of the patient divided by the average FEV1% in the population for any person of similar age, sex and body composition.
Smoking cessation/ Mild: Short acting: Salbutamol, Terbutaline, Ipratropium/ Moderate: Longer acting B2 agonists Salmetrol, formoterol, tiotropium bromide, Pulmonary rehab: Exercise should be encouraged, breathlessness whilst distressing is not dangerous, 2-3 sessions per week, last b/w 6-12 weeks.
Severe: Inhaled steroids
Very severe: O2 therapy: Long term O2 therapy, Minimum 15hrs/day Inc SaO2 to 90%
Surgery: Bullectomy/ Lung transplant/ LVRS (Lung volume reduction surgery)
Oral C/s: Prednisolone, improves lung function 30mg for 10 days
Asthma is a chronic disease affecting the lungs. It inflames and narrows the airways making breathing hard for those with asthma.
It is the most common chronic disease among children.
http://www.who.int/respiratory/asthma/en/
IL4 Ige/ IL5 activates eosinophils/
Image: http://www.nhlbi.nih.gov/health/dci/Diseases/Asthma/Asthma_WhatIs.html
Figure A: location of lungs in the body and airways in the lungs.
Figure B: a normal, non-asthmatic airway.
Figure C: an airway during asthmatic symptoms. The airway is narrowed, limiting air flow. Tightened muscles constrict air flow, as do inflamed and thickened airways. Excess mucus clogs the airway.
Thickening of BM, Edema and inflammation of bronchial walls, presence of eosinophils, increased submucosal glands, Hypertrophy of bronchial muscle walls
Atopy is the inherited predisposition to develop an antibody called immunoglobulin E (IgE) in response to exposure to environmental allergens. This can be measured in the blood.
Asthma symptoms include, but are not limited to, coughing, wheezing, chest tightness, and shortness of breath.
Coughing related to asthma often interferes with sleep and is worse at night or early in the morning.
Shortness of breath may present itself as the inability to catch one’s breath or out of breath (quick inhaling and exhaling).
http://www.nhlbi.nih.gov/health/dci/Diseases/Asthma/Asthma_SignsAndSymptoms.html
12% AND 200 ML REVERSIBILTY
Note the downward pathway – regular review and assessment – dose titration.
Long term medications, typically taken daily, are one way to control and manage asthma symptoms.
There are a variety of long term medications one can take.
Inhaled corticosteroid – most commonly prescribed long term asthma medication. These have a relatively low risk of side effects and are generally safe for long-term use.
Leukotriene modifiers – help prevent asthma symptoms for up to 24 hours. Have been linked to psychological reactions such as agitation, aggression, hallucinations, depression and suicidal thinking.
Long-acting beta agonists – open the airways and reduce inflammation, but have been linked to severe asthma attacks. Should be taken in combination with an inhaled corticosteroid.
Combination inhalers – contain a long-acting beta agonist along with a corticosteroid. Since it contains a long-acting beta agonist, these medications may increase your risk of having a severe asthma attack.
Bit about height – still concerns about systemic activity – case reports about idiosyncratic effects on growth.
Case reports of hypoadrenal crises with hypoglycaemia in kids – mostly related to fluticasone.
Added in bottom statement from another slide
Note bit about stopping LABA if doesn’t work.
Is this realistic? Does it happen?
Note bit about stopping LABA if doesn’t work. (Sustained release)
Is this realistic? Does it happen?
Asthma medications and personal responsibility are the key for controlling symptoms.
Medications include long-term (taken daily) and quick relief (taken at the onset of an asthma attack to alleviate symptoms).