CARDIO- PULMONARY PATHOLOGY

CPP PRE QUIZ 8 E. Furrier’s lung

7. What is the pathophysiology of acute
1. All of the following pneumoconiosis from
hypersensitivity pneumonitis?
exposure to inorganic dusts causes lung
A. Proliferation of bone- marrow derived
fibrosis, except:
fibrocytes inducing lung inflammation
A. Byssinosis
and fibrosis
B. Asbestosis
B. Immune mediated response of small
C. Coal worker’s pneumoconiosis
inhaled antigens in distal airways and
D. Silicosis
alveoli
E. None of the above
C. Exposure to cigarette smoke inducing
2. This test is more sensitive for the detection
proliferation of inflammatory
of pleural thickening for patients with history
mediators in the alveoli
of asbestos exposure
D. Genetic mutation leading to
A. Chest Xray
hypersensitivity reaction in smaller
B. High resolution CT scan scan
airways and alveoli
C. Chest ultrasound
E. Respiratory infection causing
D. MRI of the chest
inflammatory response in alveoli
E. Lung biopsy
8. What are the 2 major risk factors for
3. All of the following are specific work
obstructive sleep apnea?
practices that should be asked during
A. Menopausal women and obesity
patient’s history and occupational or
B. Obesity and positive family history of
environmental exposure in patients
OSA
considering with pneumoconiosis, except:
C. Mandibular retrognathia and
A. Smoking history
adenotonsillar hypertrophy
B. Chemical odors
D. Male sex and obesity
C. Presence of visible dusts
E. Genetic syndromes (down’s
D. Size and ventilation of workspaces
syndrome) and endocrine syndrome
E. Whether co-workers have similar
(hypothyroidism)
complaints
9. All of the following factors must be
4. Which of the following organic dust is the
evaluated to check on the asthma control of
culprit of patients with occupational lung
a patient, except:
disease called byssinosis?
A. Hospital admissions
A. Coal dust
B. Need for reliever/ rescue treatment
B. Grain dust
C. Limitations of activities
C. Cobalt
D. Daytime and nocturnal symptoms
D. Beryllium
E. None of the above
E. Cotton dust
10. What is in the indication of a need for regular
5. Which type of pneumoconiosis is a risk factor
controller therapy in asthma?
for developing mesothelioma?
A. Use of a reliver medication once a
A. xAsbestos
week
B. Byssinosis
B. Use of a reliver medication >2x a
C. Coal worker’s pneumoconiosis
week
D. Silicosis
C. Use of a reliver medication >3x a
E. Berylliosis
week
6. Which of the following hypersensitivity
D. Use of a reliver medication once a
pneumonitis is associated with exposure to
month
bacterial or fungal antigens such as grain,
E. Use of a reliver medication >2x a
moldy hay or silage?
month
A. Bagassosis
B. Miller’s lung
C. Farmer’s lung
D. Poultry worker’s lung
HYPERSENSITIVITY PNEUMONITIS
OCCUPATIONAL AND ENVIRONMENTAL LUNG DISEASE
CARDIO- PULMONARY PATHOLOGY
HYPERSENSITIVITY PNEUMONITIS
INTRODUCTION AND DEFINITION
➢ Extrinsic allergic alveolitis
➢ Pulmonary disease due to inhalation exposure
to a variety of antigens leading to an
inflammatory response of the alveoli and
small airways
➢ Sensitization to an inhaled antigen as
manifested by specific circulating IgG
antibodies (necessary for the development of
HP)
➢ Systemic manifestations such as fever and
fatigue can accompany respiratory symptoms
➢ Decreased risk of developing HP in smokers
(unexplained)
PATHOPHYSIOLOGY
➢ Immune- mediated condition that occurs in
response to inhaled antigens that are small
enough to deposit in distal airways and alveoli
➢ Condition with a TH1 inflammatory pattern
and TH17 lymphocyte subsets may be
involved
• CHRONIC HP
- bone marrow – derived fibrocytes
may contribute to lung
inflammation and fibrosis.
CLINICAL PRESENTATION
➢ traditionally categorized as acute, subacute
and chronic hypersensitivity pneumonitis
OCCUPATIONAL AND ENVIRONMENTAL LUNG DISEASE
➢ HP study group
• Best to describe HP in bipartite
fashion, with one group featuring
recurrent systemic signs and
symptoms and the other featuring
more severe respiratory findings
1. ACUTE HP
✓ Manifest 4-8 hrs. after exposure to
inciting Ag
✓ Systemic symptoms: fever, chills, and
malaise + dyspnea
✓ Resolve within hours to days if no
further exposure to the offending Ag
2. SUBACUTE HP
✓ Resulting from ongoing Ag exposure
✓ More gradual onset of respiratory
(quit severe) and systemic symptoms
over the course of weeks
✓ Resolution of the symptoms within
weeks to months with Ag avoidance
3. CHRONIC HP
✓ Insidious onset of symptoms, with
poorer prognosis
✓ Symptoms: progressive dyspnea,
cough, fatigue, weight loss and
clubbing of the digits
✓ Irreversible component to the
respiratory impairment, not
responsive to removal of the
responsible Ag
✓ Disease progression of chronic to lung
fibrosis and hypoxemic respiratory
failure similar in idiopathic pulmonary
fibrosis (IPF)
✓ Fibrotic lung disease- feature of
exposure to bird Ag
✓ Emphysematous phenotype – in
farmer’s lung
DIAGNOSIS
➢ History of exposure to an offending antigen
➢ Respiratory and systemic symptoms
➢ Additional workup in establishing an
immunologic and physiologic response to
inhalation antigen exposure:
• Chest imaging
• Pulmonary function testing (PFT)
• Serologic studies
• Bronchoscopy
• Lung biopsy
➢ Re- exposure to the offending environment
may be performed to aid in confirming the
diagnosis of HP
HYPERSENSITIVITY PNEUMONITIS
CARDIO- PULMONARY PATHOLOGY

1. CHEST IMAGING honeycombing in advanced cases (similar to

IPF)

CLINICAL PREDICTION RULE

(HP STUDY GROUP)

➢ 6 statistically significant predictors for HP

• Exposure to an antigen known to
cause HP (strongest predictor)
presence of serum precipitins
• Recurrent symptoms
• Symptoms occurring 4-8 hrs. after
antigen exposure
2. PULMONARY FUNCTION TESTING • Crackles on inspiration
✓ Either restrictive or obstructive PFTs, • Weight loss
hence not useful in establishing the ➢ Differential diagnosis
diagnosis • Respiratory infection
✓ Use in characterizing the physiologic • Interstitial lung disease – IPF or Non-
impairment of an individual patient Specific Interstitial Pneumonitis (NSIP)
3. SERUM PRECIPITINS • Sarcoidosis
✓ Panels that test for several specific • Organic toxic dust syndrome (OTDS)
serum precipitins often provide false-
negative results TREATMENT
✓ Presence of an immunologic response
alone is not sufficient for establishing ➢ Mainstay of treatment: Antigen Avoidance
the diagnosis
• Careful exposure history
4. BRONCHOSCOPY
- To identify the potential offending
✓ With bronchoalveolar lavage (BAL)
antigen and to identify the
✓ BAL lymphocytosis is characteristics
location where a patient is
finding
exposed
✓ In active smokers, a lower threshold
• Modify the environment to minimize
should be used to establish BAL
patient exposure
lymphocytosis, (smoking will result in
- removal of birds, removal of
lower lymphocyte percentages)
molds, and improved ventilation
✓ Most have a CD4+/ CD8+ lymphocyte
• Personal protective equipment
ratio of <1 (not specific finding)
- respirators and ventilated
5. LUNG BIOPSY
helmets
✓ Tissue samples obtained by a
➢ HP- self – limited disease, thus pharmacologic
bronchoscopic approach
is generally not necessary
(transbronchial biopsy) or surgical
➢ Role for glucocorticoid therapy – called
approach (video assisted
subacute and chronic HP (severe symptoms)
thoracoscopy or open approach)
➢ Accelerate the resolution of symptoms
✓ Not absolutely necessary to establish
➢ Prednisone therapy initiated at 0.5- 1 mg/kg
the diagnosis of HP
of ideal body weight per day (not to exceed 60
mg/ d or alternative glucocorticoid
COMMON HISTOLOGIC FEATURE IN HP
equivalent) over a duration of 1-2 weeks,
followed by a tapper over the next 2-6 weeks
➢ Presence of noncaseating granulomas of small
➢ Chronic HP with extensive lung fibrosis – lung
airways (loose and poorly defined)
transplantation
➢ Patchy distribution of mixed cellular infiltrate
with a lymphocytic predominance (alveolar
spaces and interstitium )
➢ Bronchiolitis with the presence of organizing
exudate
➢ Fibrosis (Chronic HP)- fibrotic changes may be
focal or diffuse and severe with
HYPERSENSITIVITY PNEUMONITIS
OCCUPATIONAL AND ENVIRONMENTAL LUNG DISEASE
CARDIO- PULMONARY PATHOLOGY
OCCUPATIONAL AND ENVIRONMENTAL
LUNG DISEASE
HISTORY AND EXPOSURE ASSESSMENT
➢ Patient’s history is very important in assessing
any potential occupational or environmental
exposure
➢ Inquiry into specific work practices include:
• Specific contaminants involved
• Presence of visible dusts
• Chemical odors
• Size and ventilation of workspaces
• Use of respiratory protective
equipment
• whether co- workers have similar
complaints
➢ short- term and long-term exposures to
potential toxic agents in the distant past
LABORATORY TESTS
➢ exposures to inorganic and organic dusts can
cause interstitial lung disease
• restrictive pattern
• decreased diffusing capacity
➢ exposures to a number of dusts or chemical
agents- result in occupational asthma or COPD
characterized by airway obstruction
➢ measurement of change in FEV1 before and
after a working shift
• used to detect an acute
bronchoconstrictive response
➢ chest radiograph
• detect and monitor the pulmonary
response to mineral dusts, certain
metals and organic dusts capable of
inducing hypersensitivity pneumonitis
➢ International Labour
• Organization (ILO) international
Classification Of Radiographs of
Pneumoconioses classifies chest
radiograph by :
Nature and Size of opacities
Extent of involvement of the
parenchyma
➢ Useful for epidemiologic studies and
screening large numbers of workers, but not
on an individual worker’s chest radiograph
OCCUPATIONAL AND ENVIRONMENTAL LUNG DISEASE
➢ High- resolution CT scan (HRCT)
• More sensitive for the detection of
pleural thickening, for patients with a
history of asbestos exposure
➢ Skin prick testing or specific IgE antibody titers
• For evidence of immediate
hypersensitivity to agents capable of
inducing occupational asthma (flour
antigens in bakers)
➢ Specific IgG precipitating antibody titers
• For agents capable of causing
hypersensitivity pneumonitis (pigeon
antigen in bird handlers)
➢ Assays for specific cell- mediated immune
responses
• Beryllium lymphocyte proliferation
testing in nuclear workers
• Tuberculin skin in health care workers
➢ Bronchoscopy to obtain transbronchial
biopsies of lung tissue
➢ Video- assisted thoracoscopic surgery (larger
sample of lung tissue )
• Determine the specific diagnosis of
environmentally induced lung disease
(hypersensitivity pneumonitis or giant
cell interstitial pneumonitis due to
cobalt exposure)
DETERMINANTS OF INHALATIONAL
EXPOSURE
➢ Chemical and physical characteristics of
inhaled agents affect both the dose and the
site of deposition in the respiratory tract
HYPERSENSITIVITY PNEUMONITIS
CARDIO- PULMONARY PATHOLOGY

HYPERSENSITIVITY PNEUMONITIS
OCCUPATIONAL AND ENVIRONMENTAL LUNG DISEASE
CARDIO- PULMONARY PATHOLOGY

PNEUMOCONIOSES

➢ Interstitial fibrosis due to occupational

exposure
➢ Requires chronic exposure to small particles
that are fibrogenic

HYPERSENSITIVITY PNEUMONITIS
OCCUPATIONAL AND ENVIRONMENTAL LUNG DISEASE
CARDIO- PULMONARY PATHOLOGY

HYPERSENSITIVITY PNEUMONITIS
OCCUPATIONAL AND ENVIRONMENTAL LUNG DISEASE
CARDIO- PULMONARY PATHOLOGY
CPP POST QUIZ 8
1. Measurement of change in what pulmonary
function test before and after a working shift
is used to detect an acute broncho
constrictive response in pneumoconiosis?
A. FVC
B. TLC
C. FEV1
D. FEV1/ FVC ratio
E. VC
2. Which of the following pneumoconiosis is
associated with greater risk of acquiring
pulmonary tuberculosis because it causes
alveolar macrophage dysfunction?
A. Asbestosis
B. Byssinosis
C. Coal worker’s pneumoconiosis
D. Silicosis
E. Berylliosis
3. Which of the following inhaled agents
absorbed in the lining fluid of the upper and
proximal airways and produce irritative and
bronchoconstriction?
A. Nitrogen dioxide
B. Sulfur dioxide
C. Ammonia
D. A and B
E. B and C
4. Which of the following condition is an
important cause of acute cardiorespiratory
failure among firefighters and fire victims
due to inhalation of toxic agents such as
carbon monoxide, cyanide and hydrochloric
acid?
A. Hypersensitivity pneumonitis
B. Metal fume fever
C. Smoke inhalation
D. Polymer fume fever
E. Byssinosis
5. All of the following association of the
following pneumoconiosis with its
occupational exposures and associated
respiratory conditions are true, except:
A. Byssinosis- asthma like syndromes
B. Cobalt exposure- giant cell interstitial
pneumonitis
C. Asbestosis- lung cancer
D. Berylliosis – processing alloys for high-
tech industries
E. Silicosis – mesothelioma
6. Which of the following pneumoconiosis may
show profuse miliary infiltration or
consolidation on chest radiograph and a
characteristics HRCT pattern known as “crazy
paving” as seen in the picture?
OCCUPATIONAL AND ENVIRONMENTAL LUNG DISEASE
A. Silicosis
B. Berylliosis
C. Asbestosis
D. Coal worker’s pneumoconiosis
E. Byssinosis
7. All of the following statements are true
regarding hypersensitivity pneumonitis (HP)
except:
A. There is an unexplained increased risk
of developing HP among smokers
B. HP is due to inhalational exposure to
a variety of antigens leading to
inflammatory response to alveoli and
small airways
C. Fever and fatigue can accompany
respiratory symptoms
D. HP is also called extrinsic allergic
alveolitis
E. Sensitization to an inhaled antigen is
manifested as specific circulating igG
antibodies
8. Which of the following occupational lung
disease is commonly associated with chronic
granulomatous inflammatory disease that is
similar to sarcoidosis?
A. Coal worker’s pneumoconiosis
B. Chronic beryllium disease
C. Byssinosis
D. Complicated silicosis
E. Asbestosis
9. What is the mainstay of treatment in
patients with hypersensitivity pneumonitis?
A. Lung transplantation
B. Smoking cessation
C. Antigen avoidance
D. Glucocorticoid therapy
E. All of the above
10. What are the 2 most common antigenic
bacterial and fungal causes of
hypersensitivity pneumonitis?
A. Staphylococcus and candida
B. Mycobacteria and botrytis
C. Actinomycetes and aspergillus
D. Bacillus and penicillium
E. Clostridium and sitophilus
HYPERSENSITIVITY PNEUMONITIS