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
Emphysema Asthma Lung Ca
Abnormal permanent Increase responsiveness of Malignant mass
enlargement of the airspaces tracheobronchial tree to the respiratory e
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
Higher in heavy smoker y/o
men Higher in
Cigarette smoking Airway hyper Cigarette
Airway hyper responsiveness Familial
responsiveness Familial history of lung can
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
 Excessive mucus neutrophil &macrophages
production contributes to in the lungs
airway obstruction Smoking enhances the
Hypertrophy of submucosal activity of elastase;
gland and increase of macrophages elastase is
goblet cells thought to be not inhibited by 1-AT
caused by cigarette Smoking inhibit the action
smoking and pollutants of 1-AT
5. Clinical Persistent productive cough is 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
Cough early Dyspnea severe & early Onset: producti
Dyspnea mild & late Cough late Patient experience a Blood st
Sputum copious Sputum scanty sense of constriction sputum
Appearance blue bloaters Appearance pick puffer in the chest Long his
Airway resistance Airway resistance Non productive cough smoking
increase slightly increase Harsh, audible Presenta
Elastic recoil normal Elastic recoil low respiration (wheezing) unintent
CXR prominent vessels; CXR hyperinflation; Prolonged expiration loss
large heart small heart Tachypnea, Horners Syndro
Barrel chest Common weight loss tachycardia and Enoptha
Infection common Barrel chest systolic hypertension Ptosis,
Cor pulmonale common Obvious prolonged Barrel chest (increase Miosis
Hypercapnia expiration AP diameter) Ipsilater
Hypoxia Prolonged: sweating
Cyanosis blue bloaters Loss of adventitious Pancoasts synd
breath sound Local inv
High-pitch wheezing superior
Accessory muscle lungs
becomes visibly active Involvem
Paradoxical pulse T1, & T2
develops involvem
End of episodes: Causing
Cough w/ thick, stingy Superior Vena C
mucus charcot- Vascular
leyden crystal Pericard
 Wheezing is less tampona
extreme Arrhythm
Gasping type of Pleural e
respiration Hypoxem
impending suffocation Dyspnea
Timing acute/sudden Lambert-Eaton m
episodes; may occur during syndrome
the night (nocturnal asthma) Muscle w
due to au
antibodi
Dermatologic a
nigricans
Hypertrophic pu
osteoarthropath
of fingers
Paraneoplastic s
ADH - hy
ACTH C
syndrom
Hyperca
Calciton
hypocalc
Gonadot
gynecom
Serotoni
syndrom
6. Diagnosis Cannot be fully reversible Cannot be fully reversible Reversibility of 15% in Sputum cytology
N DLCO Decrease DLCO FEV1 after 2 puffs of - CXR hyperopa
Increase RV CXR hyperlucency >1 cm with adrenergic agonist area of the mass
FEV1<FVC<VC bullae FEV1<FVC<VC CT Scan sensit
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
Supplemental oxygen
Pharmacology:
Bronchodilator
Short acting (5-15mins) lasts 4-6h
Long acting (15-30mins) lasts 12h
Anticholinergic (30-60mins) lasts
4-6h
Theophyllines (12-24h oral prep)
Inhaled glucocorticoid decrease
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
Smoking cessation
Pharmacology:
Bronchodilator
Short acting (5-15mins)lasts 4-6h
Long acting (15-30mins)lasts 12h
Anticholinergic (30-
60mins)lasts 4-6h
Theophyllines (12-24h oral
prep)
Inhaled glucocorticoid
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)
Removal of allergens Surgery
Quick relief:
Adrenergic stimulants
Catecholamines (30-90mins)
Fenoterol & Albuterol (4-6h)
Salmeterol & Folmoterol (9-
12h)
Methylxanthines
theophyllines, caffeine,
theobromide controller
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