Asthma is a chronic inflammatory disease of the airways characterized by variable airflow obstruction that is usually reversible. It affects people of all ages but predominantly early in life. The prevalence of asthma is approximately 10-12% of the population and it is both common and exacerbated by smoking. Diagnosis involves demonstrating variable airflow obstruction and its reversibility via spirometry and peak flow measurement. Management focuses on avoidance of triggers, bronchodilators for acute exacerbations, and inhaled corticosteroids for chronic control. Chronic obstructive pulmonary disease (COPD) is a progressive lung disease characterized by airflow limitation that is not fully reversible. Risk factors include cigarette smoking and occupational exposures. Symptoms include cough, sputum production and

1. Asthma
Salahadin A. (B.Pharm)
Lecturer and clinical pharmacist
Jan, 2013

2. Definition
 a syndrome characterized by airflow
obstruction that varies markedly
 relieved spontaneously or with Bronchodilator
± Corticosteroids
 Chronic inflammatory disease of airways
 ↑ responsiveness of tracheobronchial tree
 Physiologic manifestation: Air Way narrowing
which is usually reversible
 Clinical manifestations: a triad of paroxysms
of cough, dyspnea and wheezing

3. Disease Pattern
 Episodic --- acute exacerbations
interspersed with symptom free periods
 Chronic --- daily Airway obstruction which
may be mild, moderate or severe ±
superimposed acute exacerbations
 Life-threatening--- slow-onset or fast-
onset (fatal within 2 hours)

4. Prevalence
 All ages, predominantly early life with peak
age of 3 years
 Adults: ~10–12% population
 Children: 15% population
 50% dx <10y,85% dx <40y, 15% dx > 40y
 2:1 male/female preponderance in
childhood ; equalize in adults
 Asthma is both common and frequently
complicated by the effects of smoking on
the lungs

5. Etiology
 Allergic/atopic/early onset asthma---
rhinitis,
urticaria, eczema, (+)skin tests, ↑IgE,(+)
response to provocation tests with
aeroallergens.
 Idiosyncratic/non-atopic/intrinsic
asthma/late onset asthma--- no allergic
diseases,(-)skin tests, normal IgE,
symptoms when upper resp infection, sx
lasting days or months and usually have

6. Risk Factors

15. Triggers of acute asthmatic
episodes
 Allergens - pollen
 Pharmacologic
stimuli such as
aspirin, NSAIDS, β-
blockers,
preservatives,col
agent
 Environment
pollutionozone,SO2,
NO2
 Occupational- metal
•Infection- resp viruses
•Exercise –cold dry air
→thermally-induced
hyperemia and
microvascular
engorgement
•Emotional stress

16. DIAGNOSIS : CLINICAL
 Episodic asthma: Paroxysms of wheeze, dyspnoea
and cough, asymptomatic between attacks.
 Acute severe asthma: Upright position, use
accessory resp muscles, can’t complete
sentences in one breath, tachypnea > 30/min,
tachycardia > 110/min, PEF < 50% of pred or
best, pulsus paradoxus, chest hyperresonant,
prolonged expiration, breath sounds
decreased, inspiratory and expiratory rhonchi.

17. Cont..
 Life-threatening features: PEF < 33% of pred
or best, silent chest, cyanosis, bradycardia,
hypotension, feeble respiratory effort,
exhaustion, confusion, coma, PaO2 < 60,
PCO2 normal or increased, acidosis (low pH
or high [H+]).
 Chronic asthma: Dyspnea on exertion,
wheeze, chest tightness and cough on daily
basis, usually at night and early morning;
intercurrent acute severe asthma
(exacerbations) and productive cough
(mucoid sputum), recurrent respiratory

18. DIAGNOSIS : PHYSIOLOGIC
 Demonstration of variable airflow obstruction with
reversibility by means of FEV1 and PEF
measurement (spirometer and peak flow meter).
1. FEV1 < 80% of pred – PEF < 80% of pred.
2. Reversibility: A good bronchodilator response is a
12% or 200ml improvement in FEV1 15 min after
inhalation of 200ug salbutamol (2 puffs).
3. Diurnal peak flow variation: Normal variation:
Morning PEF 15% lower than evening PEF. With
asthma this variation is > 15% (morning dipping).

19. Cont..
4. Provocation studies:AHR
(a) Exercise: A 15% drop in FEV1 post
exercise indicates exercise induced asthma.
(b) Metacholine challenge: A 20% reduction in
FEV1 at Metacholine concentrations <
8mg/ml indicates bronchial hyperreactivity.
 This is expressed as a PC20 value of eg 0.5mg/ml
(= a 20% reduction in FEV1 at 0.5mg/ml
Metacholine).

20. DIAGNOSIS :IMMUNOLOGIC
 Skin prick wheal and flare response.
 IgE.
 Eosinophil cationic protein (ECP).
 Peripheral blood and sputum eosinophilia.

21. DIAGNOSIS : RADIOLOGY
Chest XR may be normal between
attacks.
With attacks hyperinflation may be
found.
In complicated asthma segmental
lobar collapse (mucous plugs) and
pneumothorax can occur.

22. DIFFERENTIAL DIAGNOSIS
1. Upper airway obstruction – glottic
dysfunction.
2. Acute LV failure – pulmonary oedema.
3. Pulmonary embolism.
4. Endobronchial disease.
5. Chronic bronchitis.
6. Eosinophilic pneumonia.
7. Carcinoid syndrome.
8. Vasculitis.

23. Risk factors for a fatal asthma
attack
Previous severe exacerbation (eg,
intubation or ICU admission)
Two or more hospitalizations for asthma in
the past year
Three or more emergency department
visits for asthma in the past year
Hospitalization or emergency department
visit for asthma in the past month

24. Risk factors for a fatal asthma
attack…
Use of more than two canisters of
short-acting beta agonist per month
Difficulty perceiving asthma symptoms
or severity of exacerbations
Low socioeconomic status, inner city
residence, illicit drug use, major
psychosocial problems
Comorbidities, such as cardiovascular,
chronic lung, or psychiatric disease

25. Criteria for Admission or
Discharge
The severity of the attack and response
to initial emergency room therapy
Risk factors for asthma mortality

26. Classification of Severity
CLASSIFY SEVERITY
Clinical Features Before Treatment
Symptoms Nocturnal
Symptoms
FEV1 or PEF
STEP 4
Severe
Persistent
STEP 3
Moderate
Persistent
STEP 2
Mild
Persistent
STEP 1
Mild
Intermittent
Continuous
Limited physical
activity
Daily
Attacks affect activity
> 1 time a week
but < 1 time a day
< 1 time a week
Asymptomatic and
normal PEF
between attacks
Frequent
> 1 time week
> 2 times a month
< 2 times a month
<60% predicted
Variability > 30%
60 - 80% predicted
Variability > 30%
>80% predicted
Variability 20 - 30%
>80% predicted
Variability < 20%
The presence of one feature of severity is
sufficient to place patient in that category.

27. MANAGEMENT
 Avoidance of allergen and triggers – may be
impractical→adjust Rx.

28. Cont..
 Acute severe asthma:
1. Immediate Rx: O2 40-60% via mask or
cannula + β2 agonist (salbutamol 5mg) via
nebulizer + Prednisone tab 30-60mg and/or
hydrocortisone 200mg IV.
 With lifethreatening features add 0.5mg
ipratropium to nebulized β2 agonist +
Aminophyllin 250mg IV over 20 min or
salbutamol 250ug over 10 min.
2. Subsequent Rx: Nebulized β2 agonist 6
hourly + Prednisone 30-60mg daily or
hydrocortisone 200mg 6 hourly IV + 40-60%

29. Cont..
No improvement after 15-30 min:
Nebulized β2 agonist every 15-30 min +
Ipratropium.
Still no improvement: Aminophyllin
infusion or alternatively salbutamol
infusion.
Monitor Rx: Aminophyllin blood levels +
PEF after 15-30 min + oxymetry (maintain
SaO2 > 90) + repeat blood gases after 2
hrs if initial PaO2 < 60, PaCO2 normal or
raised and patient deteriorates.

30. Complications of acute asthma
Pneumo-thorax, Pneumo-mediastinum,
Pneumo-percardium, subcutaneous
emphysema
Mucus plugging, atelectasis
Anoxic brain damage
Theophylline toxicity

31. Discharge medications and
planning
 Short-acting β2-agonist
 Prednisone 30-60 mg daily x 5-14 days (no
taper needed for patients not previously on
steroids)
 Inhaled corticosteroids at 500-1000 ug/day of
fluticasone or equivalent (Combination
inhaler)
 Education
 Proper technique in the use of inhalers
 Roles of bronchodilators versus anti-
inflammatory agents
 Written action plan

32. Mortality
Deaths from asthma are uncommon
Risks for death:-
poorly controlled disease with frequent
use of bronchodilator inhalers
lack of corticosteroid therapy
previous admissions to the hospital with
near-fatal asthma

33. Chronic Obstructive Pulmonary
Disease (COPD)

34. COPD
 Definition - a disease state characterized by
airflow limitation that is not fully reversible
COPD includes
 Emphysema - an anatomically defined
condition characterized by destruction and
enlargement of the lung alveoli
 Chronic bronchitis - a clinically defined
condition with chronic cough and phlegm
 Small airways disease - a condition in which
small bronchioles are narrowed

35.  COPD is present only if chronic airflow
obstruction occurs
 chronic bronchitis without chronic airflow
obstruction is not included within COPD .
EPIDEIMOLOGY
 fourth leading cause of death in US
 affects >16 million persons in US
 GOLD estimates suggest that COPD will
rise from the sixth to the third most
common cause of death worldwide by
2020.

36. Risk Factors
 Cigarette Smoking
 Airway Responsiveness
 Respiratory Infections
 Occupational Exposures
 Ambient Air Pollution
 Passive, or Second-Hand, Smoking
Exposure
 Genetic α1 Antitrypsin Deficiency????

37. Natural History
.The effects of cigarette smoking on
pulmonary function appear to depend on
The intensity of smoking exposure
Timing of smoking exposure during
growth
The baseline lung function of the
individual
.Genetic factors likely contribute to the
level of pulmonary function achieved
during growth and to the rate of decline
in response to smoking and potentially

39. Pathogenesis

40. Pathophysiology
 Airflow Obstruction
o Persistent reduction in forced expiratory flow
rates .
o reduced FEV1
o reduced ratio of FEV1/FVC
 Hyperinflation
o Increases in the residual volume and the
residual volume/total lung capacity ratio
 Gas Exchange
o Non uniform distribution of ventilation
o Ventilation-perfusion mismatching

41. Clinical Presentation
History
 Risk factors
 cough, sputum production, and exertional
dyspnea
 symptoms for months or years before seeking
medical attention
 Activities involving significant arm work,
particularly at or above shoulder level, are
particularly difficult for patients with COPD
 activities that allow the patient to brace the arms
and use accessory muscles of respiration are
better tolerated

42. Classification of COPD

44. Physical Findings
Early stages of COPD
 Normal physical examination
Current smokers - signs of active
smoking ( an odor of smoke or nicotine
staining of fingernails )

45. severe disease
 prolonged expiratory phase and expiratory
wheezing
 signs of hyperinflation ( a barrel chest and
enlarged lung volumes with poor
diaphragmatic excursion)
 use of accessory muscles of respiration,
sitting in the characteristic "tripod"

46. Advanced disease
 systemic wasting - significant weight loss,
bitemporal wasting, and diffuse loss of
subcutaneous adipose tissue
 paradoxical inward movement of the rib
cage with inspiration (Hoover's sign)
 Signs of overt right heart failure
 Clubbing of the digits is not a sign of COPD

47. Laboratory Findings
 Arterial blood gases and oximetry
 Hematocrit – Secondary polycythemia
 Pulmonary function testing
-reduction in FEV1 and FEV1/FVC
-lung volumes may increase, resulting in
an increase in total lung capacity, functional
residual capacity, and residual volume

48. Spirometry(V-T curves)

50. CXR

51. Cont…
 Echocardiography - rt ventricular
hypertrophy
 Testing for α1AT deficiency

52. Management
 Stable Phase COPD
Pharmacologic
 Bronchodilators
 Glucocorticoids
 Oxygen
 Others - α1AT augmentation therapy

53. Non-pharmacologic
 Smoking Cessation
 General Medical Care
 Pulmonary Rehabilitation
 Lung Volume Reduction Surgery (LVRS)
 Lung Transplantation

54. Exacerbations of COPD
 Bronchodilators
 Antibiotics
 Glucocorticoids
 Oxygen
 Mechanical Ventilatory Support

55. Mild to moderate exacerbations
Streptococcus pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
Chlamydia pneumoniae
Mycoplasma pneumoniae
Viruses
Severe exacerbations
Pseudomonas species
Other gram-negative enteric bacilli
Common Infectious Causes of COPD
Exacerbations

56. Mild to moderate exacerbations
First-line antibiotics
 Doxycycline (Vibramycin), 100 mg twice daily
 Trimethoprim-sulfamethoxazole (Bactrim DS, Septra DS), one
tablet twice daily
 Amoxicillin-clavulanate potassium (Augmentin), one 500 mg/125
mg tablet three times daily or one 875 mg/125 mg tablet twice daily
Alternative antibiotics
 Macrolides
 Clarithromycin (Biaxin), 500 mg twice daily
 Azithromycin (Zithromax), 500 mg initially, then 250 mg daily
 Fluoroquinolones
 Levofloxacin (Levaquin), 500 mg daily
 Gatifloxacin (Tequin), 400 mg daily
 Moxifloxacin (Avelox), 400 mg daily
Antibiotic Choices for COPD
Exacerbations

57. Moderate to severe exacerbations: Recommend IV
antibiotics
Cephalosporins
 Ceftriaxone (Rocephin), 1 to 2 g IV daily
 Cefotaxime (Claforan), 1 g IV every 8 to 12 hours
 Ceftazidime (Fortaz), 1 to 2 g IV every 8 to 12 hours
Antipseudomonal penicillins
 Piperacillin-tazobactam (Zosyn), 3.375 g IV every 6 hours
 Ticarcillin-clavulanate potassium (Timentin), 3.1 g IV every 4 to 6
hours
Fluoroquinolones
 Levofloxacin, 500 mg IV daily
 Gatifloxacin, 400 mg IV daily
Aminoglycoside
 Tobramycin (Tobrex), 1 mg per kg IV every 8 to 12 hours, or 5 mg
per kg IV daily
Antibiotic Choices for COPD
Exacerbations

58.  For severe exacerbations of COPD
requiring inpatient therapy,
methylprednisolone sodium succinate
(Solu-Medrol) is commonly used initially.
 Dosage: Commonly 60mg or 125mg every
six to twelve hours depending on severity of
exacerbations
After two to three days of intravenous
therapy, the patient can be switched to orally
administered prednisone in a starting
dosage of 60 mg daily for a total of two
Corticosteroids in COPD
Exacerbations

59. References
1. Marie A. Chisholm-Burns. Pharmacotherapy
principles & practice. Chisholm-burns Ma,
editor: The Mc-Graw Hill Companies, Inc. ;
2008.
2. Joseph T. Dipiro P, Exexutive and Dean
Professor, South Carolina College of Pharmacy,
University of South Carolina. Pharmacotherapy
A Pathophysiologic Approach. Seventh Edition
ed. : Mc-Graw-Hill; 2008.
3. Koda-Kimble MAY, LloydYee. Applied
Therapeutics: The Clinical Use of Drugs, 9th
Edition. Koda-Kimble MAY, LloydYee, editor:
Copyright ©2009 Lippincott Williams & Wilkins;