CHRONIC COUGH
DIFFERENTIAL DIAGNOSIS
*** Chronic Bronchitis
1. Definition Persistent cough with sputum
production for at least 3 months in
at least 2 consecutive years
Not fully reversible
2. Epidemiology 40-45 y/o
Higher in heavy smoker
men
3. Risk Factor Cigarette smoking
Airway hyper
responsiveness
Infection - exacerbation
4. Pathophysiology Hypersecretion of mucus in
the large airways
hypertrophy of submucosal
glands in the trachea and
bronchi
Hypersecretion in small
airways increase of goblet
cells in the bronchi and
bronchioles
Excessive mucus
production contributes to
airway obstruction
Hypertrophy of submucosal
gland and increase of
goblet cells thought to be
caused by cigarette
smoking and pollutants
5. Clinical Persistent productive cough is
Emphysema Asthma Lung Cancer
Abnormal permanent Increase responsiveness of Malignant mass arising from
enlargement of the airspaces tracheobronchial tree to the respiratory epithelium
distal to the terminal bronchiole, multiplicity of stimulus
accompanied by destruction of Most time fully
their wall, and without obvious reversible
fibrosis
Not fully reversible
50-75 y/o <10 y/o; <40 y/o Peaks at age 55-65
Higher in heavy smoker y/o
men Higher in men
Cigarette smoking Airway hyper Cigarette smoking
Airway hyper responsiveness Familial history of
responsiveness Familial history of lung cancer
Infection - exacerbation asthma
Protease-antiprotease activity.
Major lung protease comes from
neutrophil; major antiprotease is
1-Antitrypsin. Neutrophilic
proteases (elastase) have the
ability to digesting human lung.
This ability causing the
destruction of lung parenchyma.
Smokers has increase
neutrophil &macrophages
in the lungs
Smoking enhances the
activity of elastase;
macrophages elastase is
not inhibited by 1-AT
Smoking inhibit the action
of 1-AT
Do not occur until destruction of Episodic wheezing, cough and Main S & S
Manifestation the cardinal sign 1/3 of lung parenchyma dyspnea Cough is dry to
Cough early Dyspnea severe & early Onset: productive
Dyspnea mild & late Cough late Patient experience a Blood streaked
Sputum copious Sputum scanty sense of constriction sputum
Appearance blue bloaters Appearance pick puffer in the chest Long history of
Airway resistance Airway resistance Non productive cough smoking
increase slightly increase Harsh, audible Presentation of
Elastic recoil normal Elastic recoil low respiration (wheezing) unintentional weight
CXR prominent vessels; CXR hyperinflation; Prolonged expiration loss
large heart small heart Tachypnea, Horners Syndrome
Barrel chest Common weight loss tachycardia and Enopthalmos
Infection common Barrel chest systolic hypertension Ptosis,
Cor pulmonale common Obvious prolonged Barrel chest (increase Miosis
Hypercapnia expiration AP diameter) Ipsilateral loss of
Hypoxia Prolonged: sweating
Cyanosis blue bloaters Loss of adventitious Pancoasts syndrome
breath sound Local invasion in the
High-pitch wheezing superior part of
Accessory muscle lungs
becomes visibly active Involvement of C8,
Paradoxical pulse T1, & T2 nerves
develops involvement
End of episodes: Causing ulnar pain
Cough w/ thick, stingy Superior Vena Cava
mucus charcot- Vascular destruction
leyden crystal Pericardial
Wheezing is less tamponade
extreme Arrhythmias
Gasping type of Pleural effusion
respiration Hypoxemia
impending suffocation Dyspnea
Timing acute/sudden Lambert-Eaton myasthenic
episodes; may occur during syndrome
the night (nocturnal asthma) Muscle weakness
due to autoimmune
 antibodies
Dermatologic acanthosis
nigricans
Hypertrophic pulmonary
osteoarthropathy clubbing
of fingers
Paraneoplastic syndrome
ADH - hyponatremia
ACTH Cushings
syndrome
Hypercalcemia
Calcitonin -
hypocalcemia
Gonadotropins -
gynecomastia
Serotonin
carcinoid syndrome
6. Diagnosis Cannot be fully reversible Cannot be fully reversible Reversibility of 15% in Sputum cytology (4 slides)
N DLCO Decrease DLCO FEV1 after 2 puffs of - CXR hyperopacity on the
Increase RV CXR hyperlucency >1 cm with adrenergic agonist area of the mass
FEV1<FVC<VC bullae FEV1<FVC<VC CT Scan sensitivity
FEV1/FVC <0.7 Increase RV Sputum and blood Tissue biopsy
Increase TLC Helium test FEV1<FVC<VC eosinophilia bronchoscopy
FEV1/FVC < 0.7
Large increase TLC Helium test
7. Treatment Supportive: Supportive: Supportive: Definitive:
Smoking cessation Smoking cessation Removal of allergens Surgery
Supplemental oxygen Pharmacology: Quick relief:
Pharmacology: Bronchodilator Adrenergic stimulants
Bronchodilator Short acting (5-15mins)lasts 4-6h Catecholamines (30-90mins)
Short acting (5-15mins) lasts 4-6h Long acting (15-30mins)lasts 12h Fenoterol & Albuterol (4-6h)
Long acting (15-30mins) lasts 12h Anticholinergic (30- Salmeterol & Folmoterol (9-
Anticholinergic (30-60mins) lasts 60mins)lasts 4-6h 12h)
4-6h Theophyllines (12-24h oral Methylxanthines
Theophyllines (12-24h oral prep) prep) theophyllines, caffeine,
Inhaled glucocorticoid decrease Inhaled glucocorticoid theobromide controller
severity, need of hospitalization
and risk of exacerbation
N-Acetylcystein mucolytic &
antioxidant property
1-AT augmentation 1-AT def.
Non-pharmacology:
Vaccine influenza &
pneumococcal
Lung Transplant - pt65 y/o,
severe disability despite maximal
therapy, free of comorbid condition
decrease severity, need of
hospitalization and risk of
exacerbation
N-Acetylcystein mucolytic &
antioxidant property
1-AT augmentation 1-AT
deficiency
Non-pharmacology:
Vaccine influenza &
pneumococcal
Lung Transplant - pt65 y/o,
severe disability despite maximal
therapy, free of comorbid
condition
Lung Volume Reduction Surgery
(LVRS)
class, reduces nocturnal
symptoms.
Anticholinergics
ipratropium bromide (60-
90mins)
Long term Controller:
Glucocorticoids most
potent & most effective.
Parenteral & oral is most
beneficial for acute and
chronic attack. Inhaled is for
pt w/ persistent symptom.
Mast-cell stabilizing agents
cromolyn sodium and
nedocromil. Inhibit
degranulation of mast cell
preventing release of chemical
prophylaxis
Leukotrienes modifiers
Zileuton 5-LO synthesis
inhibitor
Zafirlukast & montelukast
LTD4 receptor antagonist