a.

Acute cough
DISEASES OF THE PULMONARY SYSTEM ➔ Resolves within 2 to 3 weeks of the onset of
I. Clinical Manifestations of a pulmonary disease illness or resolves with treatment of the
a. Cough underlying condition.
b. Dyspnea ➔ Result of
c. Hypoxia/Hypoxemia ◆ upper respiratory tract infections
d. Cyanosis ◆ allergic rhinitis
e. Hemoptysis ◆ acute bronchitis
f. Clubbing ◆ Pneumonia
II. Infections of the Lungs ◆ congestive heart failure
a. Pneumonia ◆ pulmonary embolus, or aspiration.
i. Viral / Influenza
ii. Bacterial b. Chronic cough
A. Streptococcus pneumoniae ➔ Persisted for more than 3 weeks, although 7 or 8
B. Staphylococcus aureus weeks may be a more appropriate timeframe
C. Mycoplasma pneumoniae because acute cough and bronchial
D. Klebsiella pneumoniae hyperreactivity can be prolonged in some cases
E. Mycobacteria of viral infection.
F. Pneumocystis carinii ➔ In individuals who do not smoke, chronic cough
iii.Fungal is commonly caused by:
A. Primary Pathogenic Fungi ◆ postnasal drainage syndrome
B. Opportunistic Fungi ◆ non-asthmatic eosinophilic bronchitis
a. Aspergillus fumigatus ◆ asthma
b. Cryptococcus neoformans ◆ gastroesophageal reflux disease.
c. Candida albicans ➔ In persons who smoke,
III. Chronic Obstructive Pulmonary Diseases ◆ `chronic bronchitis
a. Emphysema ◆ most common cause of chronic cough,
b. Chronic Bronchitis ➔ Lung cancer to be considered
IV. Airway Hypersensitivity ➔ ACE inhibitors
a. Asthma
A. DYSPNEA

CLINICAL MANIFESTATION OF PULMONARY

What is it?
DISEASES
A. COUGH ➔ Dyspnea is defined as “a subjective experience
What is it? of breathing discomfort that is comprised of
qualitatively distinct sensations that vary in
➔ Cough is a protective reflex that helps clear the intensity.
airways by anexplosive expiration. Inhaled ➔ Multiple factors:
particles, accumulated mucus, inflammation, or ◆ Physiological
the presence of a foreign body initiates the cough ◆ Psychological
reflex by stimulating the irritant receptors in the ◆ Social
airway. ◆ Environmental
➔ There are few such receptors in the most distal ◆ It is often described as breathlessness,
bronchi and the alveoli; thus it is possible for air hunger, shortness of breath, labored
significant amounts of secretions to accumulate in breathing, and preoccupation with
the distal respiratory tree without cough being breathing.
initiated. ➔ Pulmonary disease, or many other conditions
➔ The cough reflex consists: such as pain, heart disease, trauma, and
◆ Inspiration anxiety.
◆ closure of the glottis and vocal cordS ➔ The signs of dyspnea:
◆ contraction of the expiratory muscles ◆ flaring of the nostrils
◆ reopening of the glottis, > forceful ◆ use of accessory muscles of respiration
expiration that removes the offending ◆ retraction (pulling back) of the
matter. intercostal spaces.
➔ Cough occurs frequently in healthy individuals; ◆ retractions of tissue between the ribs
however, those with an inability to cough (subcostal and intercostal retractions)
effectively are at greater risk for pneumonia. – lung parenchyma in origin
● more commonly in children.
1
 A. HYPOXIA, HYPOXEMIA C. HEMOPTYSIS

Hypoxemia ➔ Hemoptysis is the expectoration of blood or

➔ Reduced oxygenation of arterial blood bloody secretions.
(reduced Pao2)
➔ Confused with hematemesis, which is the
➔ Respiratory alterations
vomiting of blood.
Hypoxia ➔ Blood produced with coughing is usually bright
➔ reduced oxygenation of cells in tissues red, has an alkaline pH, and is mixed with
➔ may be caused by alterations of other systems frothy sputum.
as well. ➔ Blood that is vomited is dark, has an acidic pH,
and is mixed with food particles.
*Although hypoxemia can lead to tissue hypoxia, tissue ➔ Indicates infection or inflammation that
hypoxia can result from other abnormalities unrelated
damages the bronchi (bronchitis,
to alterations of pulmonary function, such as low
bronchiectasis) or the lung parenchyma
cardiac output or cyanide poisoning.
(pneumonia, tuberculosis, lung abscess)
➔ Other causes include cancer and pulmonary
Hypoxemia results from problems with one or more of
infarction.
the major mechanisms of oxygenation:
➔ The amount and duration of bleeding provide
important clues about its source.
1. Oxygen delivery to the alveoli
➔ Bronchoscopy, combined with chest computed
a. Oxygen content of the inspired air (Fio2)
tomography (CT), is used to confirm the site of
b. Ventilation of the alveoli
bleeding.
2. Diffusion of oxygen from the alveoli into the blood
a. Balance between alveolar ventilation and
D. CLUBBING
perfusion match)
b. Diffusion of oxygen across the alveolar
➔ Clubbing is the selective bulbous enlargement
capillary barrier
of the end (distal segment) of a digit (finger or
3. Perfusion of pulmonary capillaries
toe)
➔ Its severity can be graded from 1 to 5 based on
B. CYANOSIS
the extent of nail bed hypertrophy and the
amount of changes in the nails themselves or
➔ Cyanosis is a bluish discoloration of the skin
as early, moderate or severe.
and mucous membranes caused by increasing
➔ It is usually painless.
amounts of desaturated or reduced
➔ Commonly associated with diseases that cause
hemoglobin (which is bluish) in the blood.
chronic hypoxemia
➔ It generally develops when 5 g of hemoglobin
◆ Bronchiectasic
is desaturated, regardless of hemoglobin
◆ Cystic fibrosis
concentration.
◆ Pulmonary fibrosis
◆ Lung abscess
a. Peripheral cyanosis
➔ Slow blood circulation in fingers and toes ◆ Congenital heart disease.
➔ Most often caused by poor circulation resulting ◆ Lung cancer - even without hypoxemia
from intense peripheral vasoconstriction, such because of the effects of inflammatory
as that observed in persons who have Raynaud cytokines and growth factors
(hypertrophic osteoarthropathy)
disease, are in cold environments, or are
severely stressed.
➔ Best observed in the nail beds.

b. Central cyanosis
➔ caused by decreased arterial oxygenation (low
Pao2) from pulmonary diseases or pulmonary
or cardiac right-to-left shunts.
➔ Best detected in buccal mucous membranes
and lips.

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 II. INFECTIONS OF THE LUNGS ● Incubation Period: 1-4 days
● Contagious for: 1day Before Syx Onset, and the
Pneumonia next 7days.
Definition: infection of the pulmonary parenchyma ● Viral-Induced Epithelial Dysfunction &
Destruction
Normal lung defenses
● cough reflex, reflex closure of the glottis Clinical Features
● tracheobronchial mucociliary transport ● Symptoms: Chills, Fatigue, Cough,
● alveolar macrophages ● Myalgias, Arthralgias, Headache Signs: High
● inflammatory immune system response Fever (<42C); But Chest Clear (Unless 2o
Bacterial Pneumonia)
Risk factors impairing lung defenses ● Complications: Secondary Bacterial
● smoking, toxic inhalation, aspiration, ● Pneumonia, Otitis Media, Sinusitis
mechanical obstruction, ETT/NTT intubation,
respiratory therapy, pulmonary edema, Diagnosis
hypoxemia, acidosis immunosuppression,
splenectomy, uremia, DM, malnutrition, elderly ● Clinical Diagnosis (Signs & Symptoms)
age, decreased LOC ● +/- Nasopharyngeal Swabs
● +/- Serology
Pathogenesis ● NB: CXR is usually Normal

aspiration of upper airway organisms. Treatment and Prevention

●
pneumoniae, S. pyogenes, Mycoplasma, H.
● Primarily Supportive Treatment:
influenzae, M. catarrhalis
● Bed Rest, Fluid, Paracetamol/Analgesics,
● inhalation of infectious aerosols:
Antitussives, Decongestants
● Mycoplasma, TB, influenza, Legionella,
● +/- Antivirals (Effective within 48 hours of
Histoplasma, C. psittaci, Q fever
onset):
● other: hematogenous (S. aureus,
● Oseltamivir (Tamiflu TM) / Zanamivir (Relenza
Fusobacterium), direct (trauma)
TM) > Reduce <24hrs of Symptoms
Clinical presentation ● Vaccine: FluVax is recommended Annually for
Everyone
● Typical and atypical pneumonia syndromes
but in real life it's often difficult to differentiate ** Vaccine is reformulated each year to include current
typical from atypical infections (See table at serotypes
PowerPoint)
B. BACTERIAL
● Elderly often present atypically; altered LOC is
sometimes the only sign
i. Streptococcus pneumoniae
● Epidemiology affects clinical presentation and
➔ most common bacterial pneumonia
treatment
➔ at risk: secondary complication to a viral RTI

General Pneumonia Triad (WHO):

Clinical presentation
➔ abrupt onset with fever, rigor, pleurisy, and
● Fever
"rusty" sputum; watch for meningeal
● Tachycardia
involvement
● Tachypnea (+/- Breathlessness)
CXR (Chest radiography)
A. VIRAL PNEUMONIA ➔ classically causes a lobar consolidation
Sputum
SEASONAL FLU (INFLUENZA A & B) ➔ PMNs and gram-positive oval-shaped
Etiology diplococci
➔ Influenza Virus A & B for adults (<10% of Labs
pneumonia among adults) ➔ leukocytosis (10,000-30,000 is common, but
➔ Most common cause of pneumonia in children may be leukopenic on admission)
(usually RSV) Treatment
➔ penicillin G (erythromycin if penicillin allergic;
Pathogenesis vancomycin, ceftriaxone or cefotaxime if
resistant) x 7-10 days
● Transmission: airborne spread. Droplet Prevention: Pneumovax (give once only)
3
 ii. Staphylococcus aureus iv. Klebsiella pneumoniae

➔ sudden onset bronchopneumonia ➔ at risk: alcoholics

➔ at risk: secondary complication of influenza
infection or in hospitalized patients with Clinical presentation:
underlying disease, severe diabetes, drug
abusers, immunocompromised. ➔ explosive onset of fever, prostration; similar to
pneumococcus; bloody sputum ("red currant
Clinical presentation jelly")
➔ high fever, chills, progressive dyspnea,
cyanosis, cough, pleuritic pain, quite Complications:
toxic-appearing
➔ rapid cavitation, abscess, high mortality
Complications:
➔ Cavitation (necrotizing pneumonia), CXR:
pneumothorax, empyema, pneumatoceles in
➔ classically lobar consolidation with bulging
children
fissure
Sputum
Sputum:
➔ PMNs and gram-positive cocci in clusters,
chains, and pairs
➔ large gram-negative encapsulated rods

Treatment
Treatment:
➔ Cloxacillin or vancomycin (if penicillin allergic)
x 7-10 days and drain any empyema ➔ cephalosporin and aminoglycoside; adequate
drainage of empyema (can cause extensive
scarring)
iii. Mycoplasma pneumoniae

➔ most common atypical pneumonia; "walking

pneumonia" v. Pneumocystis carinii
➔ at risk: young adults (especially 5-15 years old)
➔ incubation: 12-14 days (insidious onset) ➔ at risk: patients on immunosuppressants (e.g.
transplant recipients) or chemotherapy, AIDS
Clinical presentation: when CD4 count < 200
➔ constitutional illness with fever, persistent
hacking cough +/– scant sputum, chills Clinical presentation:
uncommon ➔ atypical, concurrent opportunistic infections
➔ Extrapulmonary features: headache, diarrhea,
non-exudative pharyngitis, skin (e.g. erythema CXR
multiforme), arthralgia, myalgia, hemolytic ➔ diffuse interstitial infiltration, often isolated to
crises, bullous myringitis, CNS (e.g. myelitis, upper lobes
Guillain-Barré syndrome, meningoencephalitis)
CXR Sputum:
➔ Classically worse than clinical presentation; ➔ Giemsa stain; lower yield in patients on
usually bilateral, patchy air-space diseases prophylaxis; diagnosis may require BAL or
Sputum transbronchial biopsy
➔ more mononuclear cells and fewer PMNs than
bacterial pneumonia, but mycoplasma not Treatment:
visualized ➔ TMP-SMX, pentamidine, TMP-dapsone,
Labs clindamycin-primaquin, atovaquone; add
➔ complement fixation shows significant titre rise corticosteroids if PaO2 < 70 mm Hg or AaDO2 >
in up to 80%, anti-I (IgM) increased in 50%, 35 mm Hg
cold agglutinins, WBC not significantly
increased (PMNs slightly elevated) Prevention:
Treatment: ➔ in AIDS, after an episode of PCP or when CD4
➔ macrolide, newer generation quinolones, count < 200 use TMP-SMX, TMP-dapsone, or
doxycycline x 10-14 days pentamidine

4
 vi. Mycobacterium tuberculosis
Pathogenesis
➔ inhalation of aerosolized droplets from close
contacts
➔ primary TB: development of granulomatous
reactions in the lungs, +/– local spread to
lymph nodes and hematogenous to
distantorgans (extrapulmonary TB, e.g.
kidneys, bone)
➔ lesions usually heal and fibrose in the
immunocompetent
➔ secondary/post-primary TB: reactivation of
dormant organisms and proliferation in
aging/immunocompromised patients
Clinical presentation
➔ usually asymptomatic but may have fever,
lassitude, erythema nodosum, cough, sputum
➔ post-primary TB: reactivation of dormant
organisms in immunocompromised patients;
➔ early systemic symptoms:
◆ Malaise, fever, sweats, anorexia, weight
loss
➔ late localizing symptoms: dyspnea, pleuritic
chest pain, cough, purulent sputum,
hemoptysis
➔ Miliary TB (post-primary dissemination of
multiple tiny granulomas
immunocompromised patients):
◆ fever, anemia, splenomegaly, meningitis
➔ primary TB: nonspecific lower lobe calcified
infiltrates, hilar and paratracheal node
enlargement, pleural effusion
➔ post-primary TB: cavitation in apical regions
and posterior segment of upper lobe and/or
superior segment of the lower lobes +/–
calcification
➔ Miliary TB: uniformly distributed, very fine
nodules (like seeds) throughout
Investigations
➔ culture of involved sites and identification of
acid-fast bacilli (Ziehl-Nielsen stain)
➔ Mantoux Skin Test (see below)
➔ CXR
C. FUNGAL
i. PRIMARY PATHOGENIC FUNGI
Etiology
➔ Histoplasma capsulatum, Coccidioides immitis,
Blastomyces dermatitidis
Pathogenesis
➔ Primary granulomatous lung infection
➔ systemic hematogenous dissemination
➔ fungus is usually destroyed if patient
immunocompetent
➔ persists as chronic systemic granulomatous
infection in immunocompromised
Clinical presentation
➔ Usually asymptomatic or mild respiratory
illness
➔ Acute pneumonia that resolves with granuloma
formation and calcification
➔ Chronic cavitary pneumonia clinically and
radiologically like TB or CA
➔ Disseminated disease: meninges, brain, bone,
liver, spleen, kidney, joints
Diagnosis
➔ Tissue biopsy for staining and culture
Treatment
➔ Amphotericin B, itraconazole
ii. OPPORTUNISTIC FUNGI
a. Aspergillosis
Etiology
in ➔ mostly Aspergillus fumigatus
Clinical Presentation
➔ allergic bronchopulmonary aspergillosis (see
Pulmonary Infiltrates with Eosinophilia)
➔ Aspergilloma (fungus ball)
Noninvasive ball of hyphae colonizes a preexisting
lung cavity
➔ Ranges from asymptomatic to massive
hemoptysis
◆ CXR
§ round opacity surrounded by a thin lucent rim of air,
often in upper lobes (“air crescent” sign)
Invasive aspergillosis
➔ at risk: immunosuppressed, especially
neutropenics
➔ severe symptoms with fever, cough, dyspnea,
pleuritic pain, tends to cavitate CXR: local or
diffuse infiltrates +/– pulmonary infarction
Endobronchial pulmonary aspergillosis
➔ at risk: chronic lung disease
➔ chronic cough and hemoptysis
Treatment
➔ amphotericin B, itraconazole; resection of
aspergilloma
5
 b. Cryptococcosis
Etiology
➔ Cryptococcus neoformans
Clinical presentation
➔ acute: usually resolves spontaneously in the
immunocompetent
➔ chronic: intense pulmonary granulomatous
reaction with hematogenous spread to brain
causing fatal meningoencephalitis if not
treated; immunocompromised patients at risk
Treatment
➔ amphotericin B +/– flucytosine
c. Candidiasis
Etiology
➔ Candida albicans
Clinical presentation
➔ fever, septicemia
➔ usually hematogenous spread to lungs
➔ CXR: diffuse, vaguely nodular infiltrate visible
only when numerous abscesses are present
Treatment:
➔ amphotericin B, fluconazole
III. CHRONIC OBSTRUCTIVE PULMONARY
DISEASES OF THE LUNGS
I. COPD
➔ HEAVILY ASSOCIATED WITH SMOKING
➔ characterized by progressive development of
airflow limitation that is irreversible/minimally
reversible
➔ includes chronic bronchitis and emphysema;
usually coexist to variable degrees in most
patients - five pathophysiological processes
associated with COPD
1. Inflammatory narrowing of respiratory and
membranous bronchioles
2. Proteolytic digestion of connective tissue
framework of the lung resulting in decreased
parenchymal tethering of airways
3. Loss of alveolar surface area and capillary bed
4. Lung hyperinflation caused by loss of lung elastic
recoil
5. Increased pulmonary vascular resistance caused
by vasoconstriction and loss of capillary bed
Risk Factors
➔ Smoking is the most important risk factor.
➔ minor risk factors include:
◆ environmental factors: air pollution,
occupational exposure, IV drug abuse
or talcosis
◆ treatable factors: low BMI,
α-1-antitrypsin deficiency, bronchial
hyperactivity
➔ demographic factors: age, family history, male
sex, history of childhood respiratory infections
and socioeconomic status
a. Emphysema
Pathologic definition:
➔ dilatation and destruction of air spaces distal
to the terminal bronchiole without obvious
fibrosis
➔ decreased elastic recoil of lung parenchyma
causes decreased expiratory driving pressure,
airway collapse, and air trapping
➔ 2 types:
◆ centriacinar (respiratory bronchioles
predominantly affected)
● typical form seen in smokers
● primarily affects upper lung
zones
◆ panacinar (respiratory bronchioles,
alveolar ducts, and alveolar sacs
affected)
● responsible for less than 1% of
emphysema cases
● primarily affects lower lobes
b. Chronic Bronchitis
➔ A clinical diagnosis
Definition:
➔ Chronic cough and sputum production on most
days for at least 3 consecutive months in 2
successive years
➔ Obstruction due to narrowing of the airway
lumen by mucosal thickening and excess
mucus
➔ Usually due to smoking but air pollution
increasingly important
➔ Exacerbations due to respiratory tract
infections (typically viral), air pollution,
bronchospasm, mucus plugging, and CHF
➔ some have features of asthma and chronic
bronchitis (asthmatic bronchitis)
6
 IV. AIRWAY HYPERSENSITIVITY ◆ Mild Asthma: Inhaled Corticosteroids
(Budesonide or Fluticasone) Or Inhaled
ASTHMA Antimuscarinic (Ipratropium Bromide) – If
What is Asthma? ICS-Intolerant.
➔ A chronic Inflammatory Disorder of the ◆ Moderate Asthma: LABA + Inhaled
Airways > Episodic, Reversible Constriction. Corticosteroid Combinations Symbicort
[Budesonide + formoterol] or Seretide
Etiology [Fluticasone + Salmeterol
Types: ◆ Severe Asthma: Oral Leukotriene Inhibitors
1. Atopic (Allergic) Asthma (Type 1 (Singulair [Montelukast])
Hypersensitivity Reaction - IgE.)
2. Non-Atopic Asthma (Viral - Induced / Drug -
Induced (Eg. Aspirin)/Occupational)
Environmental Triggers
- (Dust / Pollen / Dander / Mould/ Smoke/
Pollution/Perfume/Cold Air)
- Genetic – (FamHx is Common)

Pathophysiology:
A. Type 1 Hypersensitivity Reaction:
➔ Rapid Immune Reaction to a
Previously-Sensitized Antigen >
Mast-Cell/Basophil Degranulation > Release
Inflammatory Mediators >

I. Initial (Early) Phase:

➔ Vasodilation & inc Permeability (Bronchial
edema)
➔ Smooth Muscle Spasm (Bronchoconstriction)
➔ Epithelial Damage > dec Mucociliary Function >
Mucus Accumulation.

II. Late Phase:

➔ Immune-Mediated Epithelial Damage
➔ Dec. Mucociliary Function > Accumulation of
Mucus

Clinical Features:
➔ Asymptomatic between ‘Attacks’ – (But
➔ may have Allergic Rhinitis, Hives or Eczema)
➔ ‘Attacks’ of Severe Dyspnea & Wheezing -
(Often Triggered by Allergen
(Pollens/Dust/Animal Dander)

Complications:
➔ “Status Asthmaticus: Acute Asthma –
➔ Unresponsive to Bronchodilators
/Corticosteroids. (Can be Fatal)

Diagnosis:
Clinical Features:
➔ Dyspnea, Wheeze, Cough
➔ Chest Tightness
➔ Tachypnea, Hyperinflation, Inc Resp. Effort

Management:
➔ Prevention: