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Dr. RAJENDRAN’S INSTITUTE OF MEDICAL EDUCATION
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PNEUMONIA AND LUNG ABSCESS (57 MCQs)
1) What type of cells line the large airways?
a. IgA secreting cells
b. Ciliated columnar epithelial cells
c. Type 1 and 2 cells
d. Macrophages
Ans - B
80% of the cells lining the central airways are ciliated, pseudostratified, columnar epithelial cells.
Each ciliated cell contains about 200 cilia (See figure below). The cilia beat at 1000 times per
minute. There is a fast forward stroke and a slower backward recovery. Ciliary motion is
coordinated so that each wave is propagated toward the oropharynx. The cilia are covered by a
liquid film that is 5 to 10 um thick. It is composed of two layers. The outer layer (or gel layer) is
viscous. It traps deposited particles. The cilia beat in the less viscous inner layer (sol layer).
During the forward stroke, the tips of the cilia just touch the viscous gel and propel it toward the
oropharynx. During recovery, the cilia move entirely within the low-resistance sol layer. Ciliated
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cells are interspersed with mucus-secreting cells in the trachea and bronchi but not in the
bronchioles.
2) Which is present in the fluid lining the alveolar walls?
a. Surfactant
b. Fibronectin
c. Immunoglobulin
d. Macrophages
e. All of the above
Ans - E
The epithelial lining fluid contains surfactant, fibronectin, and immunoglobulin.
Fibronectin is a large surface protein secreted by macrophages and platelets. Fibronectin is the
receptor for the normal gram-positive flora of the oropharynx. Fibronectin is a commonly used
receptor for binding by pathogens.
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The immunoglobulins opsonize or lyse pathogens deposited on the alveolar surface.
The alveolar macrophages, lymphocytes, and a few polymorphonuclear leukocytes are loosely
attached to the lining cells or lying free within the lumen.
From blood to air, the alveolar walls consist of the endothelium that lines the capillaries, the
capillary basement membrane, the interstitial tissue, the alveolar basement membrane, the
alveolar lining epithelial cells (flattened type 1 pneumocytes that cover 95% of the alveolar
surface or rounded, granular, surfactant-producing type 2 pneumocytes), and epithelial lining
fluid.
3) What keeps the lower respiratory tract normally sterile?
a. Sneezing
b. Cough reflex
c. Ciliary action
d. Alveolar macrophages
e. All of the above
Ans - E
Infectious particles deposited on the nasal surfaces are removed by sneezing.
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Reflex closure of the glottis and cough protect the lower respiratory tract. Impairment of the
cough reflex increases the risk of pneumonia. Causes of loss or suppression of the cough reflex
include coma, anesthesia, neuromuscular disorders, drugs, and chest pain.
Those particles deposited on the tracheobronchial surface are swept by ciliary motion toward the
oropharynx. Mucociliary dysfunction increases the risk of pneumonia. Causes of mucociliary
dysfunction include cigarette smoke, inhalation of hot or corrosive gases, viral infections, or
genetic disturbances (e.g., the immotile cilia syndrome or Kartagener syndrome and cystic
fibrosis).
Particles that bypass the above defenses in the airways and get deposited on the alveolar surface
are cleared by phagocytic cells and humoral factors. Alveolar macrophages are the major
phagocytes in the lower respiratory tract. Some phagocytosed microorganisms are killed. Other
microorganisms can persist within the macrophage (e.g., Mycobacterium tuberculosis,
Legionella). Dysfunction of alveolar macrophages increases the risk of pneumonia.
See figure below. The common pathogenetic mechanism is attachment of the organisms to the
upper respiratory tract epithelium. This is followed by necrosis of the cells lining the respiratory
tract, an inflammatory response and outpouring of fluid into alveolar spaces.
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4) Which statement(s) is/are true?
a. 80% of the cells lining the central airways are ciliated
b. Epithelial lining fluid contains immunoglobulin
c. Lower respiratory tract is normally sterile
d. All
Ans - D
When small numbers of low-virulence microbes are deposited in the lungs, immune defenses
(e.g., mucociliary escalator, antimicrobial proteins in airway surface liquid and alveolar
macrophages) eradicate the infection. In contrast, numerous or more virulent microbes elicit an
inflammatory response that helps to rid the lungs of infecting microbes.
During pulmonary infection, neutrophils migrate out of the pulmonary capillaries and into the air
spaces. Neutrophils kill ingested microbes with reactive oxygen species (e.g., hypochlorite),
antimicrobial proteins (e.g., bactericidal permeability-inducing protein and lactoferrin), and
degradative enzymes (e.g., elastase).
Acute inflammation is an essential immune response in the lungs. At the same time, it also
contributes directly to lung injury and abnormal pulmonary function. The neutrophil products
such as reactive oxygen species and proteases released to kill microbes also kill host cells and
damage host tissues.
5) Defects in cell-mediated immunity leads to increased infections with all except
a. Mycobacteria
b. Herpesviruses
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c. Pneumocystis carinii
d. Pyogenic bacteria
Ans - D
Cell-mediated immune defects lead to increased infections with intracellular microbes such as
mycobacteria and herpesviruses as well as with microorganisms of very low virulence, such as
Pneumocystis carinii. Neutrophil and complement defects and humoral immunodeficiency
typically lead to an increased incidence of infections with pyogenic bacteria.
6) What is pneumonia?
a.
Any infection of the lung parenchyma
b. Infection of alveoli
c. Infection below trachea
d. Infection below bronchi with or without alveolar involvement
Ans - A
Pneumonia is broadly defined as any infection of the lung parenchyma (although the same term is
used for many interstitial lung diseases that are not infectious in origin, such as usual interstitial
pneumonia). Pneumonias can be classified by the specific etiologic agent (e.g., pneumococcal,
staphylococcal) or by the clinical setting in which the infection occurs (e.g., community acquired
or acquired in a hospital). Classifying into community acquired pneumonia or nosocomial
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pneumonia narrows the list of suspected pathogens for giving empirical antimicrobial therapy.
See table below.
THE PNEUMONIA SYNDROMES
Community-acquired acute pneumonia

Streptococcus pneumoniae

Mycoplasma pneumoniae

Haemophilus influenzae

Chlamydia spp. (C. pneumoniae, C. psittaci, C. trachomatis)

Staphylococcus aureus

Legionella pneumophila

Viruses: RSV, parainfluenza virus (children); influenza (adults); adenovirus; SARS
Nosocomial pneumonia

Streptococcus pneumoniae

Gram-negative bacilli

Staphylococcus aureus
Aspiration pneumonia

Anaerobic oral flora (Bacteroides, Prevotella, Fusobacterium, Peptostreptococcus),
admixed with aerobic bacteria (Streptococcus pneumoniae, Staphylococcus aureus,
Haemophilus influenzae, and Pseudomonas aeruginosa)
Chronic pneumonia

Mycobacterium tuberculosis and atypical mycobacteria

Nocardia

Actinomyces
Necrotizing pneumonia and lung abscess

Anaerobic bacteria (extremely common), with or without mixed aerobic infection

Staphylococcus aureus, Klebsiella pneumoniae, Streptococcus pyogenes, and type 3
pneumococcus (uncommon)
Pneumonia in the immunocompromised host

Cytomegalovirus
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
Pneumocystis jerovicii

Mycobacterium avium-intracellulare

Invasive aspergillosis

Invasive candidiasis

"Usual" bacterial, viral, and fungal organisms (listed above)
7) What is the most common mechanism for the production of pneumonia?
a. Aspiration
b. Inhalation
c. Hematogenous dissemination
d. Direct inoculation
Ans - A
The major route of infection is microaspiration from a previously colonized oropharynx. Most
pulmonary pathogens originate in the oropharyngeal flora. Aspiration of these pathogens is the
most common mechanism for the production of pneumonia. The gingival crevices and dental
plaques are sources of anaerobic pulmonary pathogens (e.g., Porphyromonas gingivalis,
Prevotella melaninogenica, Fusobacterium nucleatum, Actinomyces spp., spirochetes, and
anaerobic streptococci).
Inhalation of suspended aerosolized microorganisms is the mechanism of infection for viruses,
Legionella, and tuberculosis.
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8) Aspiration of oropharyngeal secretions into the lower respiratory tract
a. Common during sleep in healthy adults
b. Common in those with an impaired level of consciousness
c. Risk is increased in those with nasogastric tube
d. All are true
e. All are false
Ans - D
About 50% of healthy adults aspirate oropharyngeal secretions into the lower respiratory tract
during sleep.
Aspiration is more frequent in those with an impaired level of consciousness (e.g., alcoholics;
drug abusers; and patients who have had seizures, strokes, or general anesthesia), neurologic
dysfunction of the oropharynx, and swallowing disorders.
Nasogastric or endotracheal tubes increase the risk. Nasogastric tubes can facilitate the transfer
of gastric bacteria to the pharynx.
9) Gram-negative bacillary colonization of the oropharyngeal mucosa
a. Is common in health
b. Is due to decreased salivary proteolytic activity
c. Is due to increase in fibronectin
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d. All are true
e. All are false
Ans - E
All are false statements. Aerobic gram-negative bacillary colonization of the oropharyngeal
mucosa is unusual in healthy persons (<2%).
Frequency increases with hospitalization, worsening debility, severe underlying illness,
alcoholism, diabetes, and advanced age. This may be due to increased salivary proteolytic
activity, which destroys fibronectin.
Fibronectin is a glycoprotein coating the surface of the mucosa. Fibronectin is the receptor for
the normal gram-positive flora of the oropharynx. Loss of fibronectin exposes the receptors for
aerobic GNB on the epithelial cell surface.
10) Which pneumonia is typically not acquired by inhalation?
a. Legionellosis
b. Psittacosis
c. Histoplasmosis
d. Q fever
e. Staphylococcus
Ans - E
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Pneumonia typically acquired by inhalation includes tuberculosis, influenza, legionellosis,
psittacosis, histoplasmosis, Q fever, and Hantavirus pulmonary syndrome.
Hematogenous dissemination from an extrapulmonary site is usually due to staphylococcus
aureus. Hematogenous dissemination to the lungs occurs in IV drug users with bacterial
endocarditis and in patients with IV catheter infections. Fusobacterium infections of the
retropharyngeal tissues (Lemierre's syndrome - i.e., retropharyngeal abscess and jugular venous
thrombophlebitis) also disseminate hematogenously to the lungs.
11) Lobar pneumonia is
a.
Involvement of an entire lobe
b. Involvement of alveoli contiguous to bronchi
c. Presence of cavities < 2 cm in diameter
d. Presence of one or more cavities > 2 cm in diameter
Ans - A
The pneumonic process may involve primarily the interstitium or the alveoli. Involvement of an
entire lobe is called lobar pneumonia. See figures below.
When the process is restricted to alveoli contiguous to bronchi, it is called bronchopneumonia.
Patchy consolidation of the lung is the dominant characteristic of bronchopneumonia. Confluent
bronchopneumonia may be indistinguishable from lobar pneumonia.
Cavities develop when necrotic lung tissue is discharged into communicating airways. This
results in either necrotizing pneumonia or lung abscess. Necrotizing pneumonia is multiple small
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cavities < 2 cm in diameter. Lung abscess is presence of one or more cavities > 2 cm in diameter.
Lobar pneumonia
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Bronchopneumonia
12) All are pathological stages of lobar pneumonia except
a. Congestion
b. Red hepatization
c. Gray hepatization
d. Resolution
e. Pleurisy
Ans - E
The four stages of the inflammatory response in lobar pneumonia are congestion, red
hepatization, gray hepatization, and resolution. In the first stage of congestion, there is vascular
engorgement, intra-alveolar fluid with few neutrophils, and often numerous bacteria.
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In red hepatization, the lobe is red, firm, and airless, with a liver-like consistency, hence the term
hepatization. Red color is due to massive exudation of red cells. Neutrophils and fibrin also fill the
alveolar spaces.
In the stage of gray hepatization, there is progressive disintegration of red cells. The
fibrinosuppurative exudate persists, giving the gross appearance of a grayish brown, dry surface.
In the final stage of resolution, the exudate in the alveolar spaces undergoes enzymatic digestion.
The product is semifluid, debris that is resorbed, ingested by macrophages, coughed up, or
organized by fibroblasts growing into it. Lung tissue destruction and necrosis result in the
formation of lung abscess.
Pleuritis is often present in the early stages if the consolidation extends to the surface. Spread of
infection to the pleural cavity causes empyema.
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