Self-Study Questions for the Respiratory Pathophysiology Unit

1. What determines FRC (functional residual capacity)?

page 14 of syllabus, section V. at the bottom of the page
2. Name at least three factors that can reduce airway resistance.
page 22, top of page under D.
3. List at least two factors that can shift the oxygen hemoglobin desaturation curve to the
LEFT.
page 40, figure 2
4. Calculate the alveolar-arterial oxygen gradient for a patient with the following set of arterial
blood gases: pH 7.08; PaCO2 80; PaO2 40; HCO3- 24.
page 37
5. What is your interpretation of the following arterial blood gas: pH 7.08; PaCO2 80; PaO2 40;
HCO3- 24?
page 45, top sections
6. Which of the following types of pulmonary vessels (arterial, venous &/or lymphatic) is/are
found in the connective tissue adjacent to airways?
arterial (bronchial and pulmonary) and lymphatics
7. Name at least two major differences between the histology of bronchi and bronchioles.
bronchi have plates of hyaline cartilage and submucosal glands; bronchioles don't
8. List at least three differences between the pathology of centrilobular and panlobular
emphysema.
centrilobular emphysema involves the center of the lobules to a greater extent, as
opposed to being distributed uniformly throughout the lobules
centrilobular emphysema is more severe in the upper lobes; panlobular emphysema is
more severe in the lower lobes
centrilobular emphysema usually has significant accompanying anthracosis; panlobular
emphysema, if caused by alpha1-antitrypsin deficiency alone, does not

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9. Name at least two similarities and two differences between the microscopic pathology of
chronic bronchitis and asthma.
similarities: airways with smooth muscle hyperplasia, inflammation and edema,
increased mucus production
differences: inflammation in asthma typically has a prominent infiltrate of eosinophils,
whereas chronic bronchitis usually has just "generic" acute and chronic inflammatory
cells; asthma has sub-basement membrane fibrosis, which is not present in chronic
bronchitis
10. What features would make you consider a diagnosis of cystic fibrosis rather than immotile
cilia syndrome in a 9 year-old child?
thick mucus; high sweat chloride; multiorgan involvement, especially pancreas; sputum
cultures growing resistant Pseudomonas
11. Why does infant respiratory distress syndrome potentially lead to pulmonary hypertension?
hypoxia pulmonary vasoconstriction vessel remodeling pulmonary hypertension
right heart strain and failure
12. List one diagnosis associated with each of the five classes of pulmonary hypertension.
pages 116-118
13. Name at least two risk factors for pulmonary thromboembolism.
page 126
14. Define paradoxical thromboembolism.
a deep venous thrombus gains access to the systemic circulation via an opening
between the right and left sides of the heart (e.g., ASD, VSD, patent foramen ovale)
15. Name an anticoagulant drug which does NOT depend on renal function for elimination.
argatroban
16. How do you monitor warfarin (Coumadin) for effectiveness?
INR
17. What laboratory tests on pleural fluid would indicate the fluid is a transudate? Why is it
important to distinguish a transudate from an exudate?
low protein and LDH; transudates are managed by treating the underlying condition

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18. If the majority of cells found in pleural fluid are lymphocytes, what disease(s) would you be
considering?
tuberculosis and malignancy
19. Describe the main differences between simple and complicated coal workers'
pneumoconiosis.
simple CWP is characterized by scattered small coal macules or nodules without
significant fibrosis; complicated CWP is characterized by large accumulations of carbon
pigment with significant fibrosis, leading to complications such as pulmonary
hypertension
20. The function of which pulmonary cell type is severely impaired in individuals with silicosis?
macrophage
21. List two important functions of
the cell type indicated by the arrows
in this photomicrograph of injured
lung.
type II pneumocytes produce surfactant
and are the regenerative cell type capable
of differentiating into both type I and II
pneumocytes after lung injury

22. What are some clinical clues that a patient is likely to have bacterial pneumonia rather than
just a bad cold?
top of page 215
23. Why does the absence of a spleen increase the risk for the development of Streptococcus
pneumoniae pneumonia?
The spleen puts opsonins on encapsulated bacteria making it easier for macrophages to
recognize and engulf them; with no spleen, no opsonins

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24. For the three major fungal pulmonary infectious diseases that can affect immunocompetent
individuals (blastomycosis, coccidioidomycosis and histoplasmosis), describe the areas in the
U.S. where these diseases are endemic, as well as the characteristic microscopic morphology
of the pathogenic organisms.
blastomycosis southeastern and central U.S.; large, broad-based budding yeasts at
body temperature
coccidioidomycosis western and southwestern U.S.; spherules with endospores at
body temperature
histoplasmosis Ohio and Mississippi river valleys; tiny, intracellular yeast at body
temperature
all 3 are dimorphic fungi, so are present as much more hardy forms (conidia) in the soil
25. Name at least three conditions which increase the risk for progression from latent
tuberculosis infection (LTBI) to active tuberculosis (TB disease).
top of page 230
26. If a patient is not doing well on a 4-drug treatment regimen for tuberculosis, what would be
the problem in adding a 5th drug to help?
page 232
27. Why do we start therapy for tuberculosis with 3-4 drugs?
page 232
28. What pathology MOST supports a diagnosis of idiopathic pulmonary fibrosis?
fibroblastic foci; heterogeneous pathology worse at the lung bases and under the pleura
29. Which of the idiopathic interstitial lung diseases have a strong association with smoking?
desquamative interstital pneumonitis (DIP), pulmonary Langerhans cell histiocytosis
idiopathic pulmonary fibrosis also has an association with smoking, but not as strong as
the two above
30. If a 30 year-old African American woman presents to your office with exertional dyspnea and
a dry cough, has a moderate restrictive defect on pulmonary function testing and has a chest Xray showing bilateral hilar lymphadenopathy, you would be able to guess the diagnosis. So why
would you need a biopsy?
rule out infection or malignancy before starting therapy for sarcoidosis

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31. List at least three non-infectious causes of granulomatous inflammation in the lung.
sarcoidosis, berylliosis, hypersensitivity pneumonitis
32. What factors would lead you to believe that a patient with suspected idiopathic pulmonary
fibrosis would NOT need an open lung biopsy?
classic high resolution CT findings in the appropriate clinical setting
33. What is the most common mechanism causing hypoxemia?
V/Q mismatch
34. When evaluating a patient, what factors might lead you to start mechanical (or assisted)
ventilation?
page 321, middle of page
35. For which cell type of lung cancer would you most likely expect hemoptysis (coughing up
blood)?
squamous cell carcinoma more locally destructive malignancy that usually erodes into
the central airways; remember that it can also cavitate
another important concept (which may not have been emphasized) is that there is one
paraneoplastic syndrome more commonly seen with squamous cell carcinoma than with
small cell carcinoma; this is ectopic secretion of PTHrP, which can produce
hypercalcemia
36. Compare and contrast the development of squamous cell carcinoma and adenocarcinoma
of the lung from normal epithelium to premalignant lesions to an invasive malignancy.
squamous cell carcinoma: pseudostratified ciliated columnar epithelium undergoes
squamous metaplasia as a result of chronic injury due to irritants (e.g., in cigarette
smoke)
then with exposure to numerous chemical carcinogens (initiators and promoters) in
cigarette smoke, squamous metaplasia may develop into progressively more severe
squamous dysplasia
with subsequent genetic abnormalities, the severely dysplastic squamous epithelial cells
can develop the ability to invade and progress to invasive squamous cell carcinoma
adenocarcinoma: with carcinogenic exposures, normal distal airway and alveolar
epithelium (which is glandular) can develop into atypical adenomatous hyperplasia (an
incidental finding)
with further genetic abnormalities, this can progress into adenocarcinoma in situ and
then ultimately into invasive adenocarcinoma

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37. How does a pathologist distinguish between a typical carcinoid tumor and small cell lung
carcinoma?
macroscopically, a typical carcinoid is usually well-defined, as opposed to the infiltrating
growth pattern of small cell carcinoma (often adjacent to airways as was discussed
yesterday)
microscopically, similarities between the two include the fact that they both have the
characteristic "salt and pepper" chromatin pattern of neuroendocrine cells, and both are
highly vascular
however, after that, their histologic appearance diverges; a typical carcinoid is
composed of a monotonous population of neuroendocrine cells with regular round
nuclei and more cytoplasm than is typical of small cell carcinoma; in addition, cytologic
atypia and mitotic figures are absent
small cell carcinoma is comprised of neuroendocrine cells with very scanty cytoplasm,
that frequently mold to one another; there is evidence of a high proliferative rate (e.g.,
mitotic figures, tumor cell necrosis), as well as cellular fragility (smeared DNA producing
the fairly reproducible crush artifact)
38. Who should be screened for lung cancer based on the National Lung Screening Trial?
smokers age 55-77, still within 15 years of quitting, 30 pack year smoking history
39. What is the clinical relevance of the long latency period for lung cancer (from the first
malignant cell to clinical manifestations)?
diagnosis is late
40. Define what is meant by a paraneoplastic syndrome and provide at least three examples.
signs/symptoms occurring in a minority of patients with malignancies that cannot be
attributed to tumor growth and spread or endogenous hormone synthesis
examples include tumor cell production of procoagulants or ectopic hormones (e.g.,
small cell carcinoma producing ACTH or ADH; squamous cell carcinoma producing
PTHrP)
other examples include cross-reacting immune responses between tumor cell antigens
and normal tissue components (e.g., Lambert-Eaton myasthenic syndrome, cerebellar
degeneration)
41. How can you differentiate non-REM from REM sleep?
pages 334-335

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42. Name at least one Dont of good sleep hygiene which you yourself are guilty of.
this is personal but check page 336 at the bottom
43. List at least three of the parameters monitored during a polysomnogram (sleep study).
page 338
44. List at least three causes of excessive daytime sleepiness.
obstructive sleep apnea, narcolepsy, inadequate sleep, poor sleep hygiene
45. What are the three changes in pulmonary mechanics that occur as people age?
page 352 I. A.