Study Guide

PART 1:   Concepts of Pulmonary Pathophysiology

1. (a) Discuss how chronic elevation of paCO2 levels in a patient with chronic lung disease may cause a “resetting” of the homeostatic set point of the central chemoreceptors for CO2.  

  • This can lead to a gradual increase in the baseline levels of carbon dioxide tolerance, resulting in a blunted response to respiratory stimuli. Consequently, patients may exhibit hypoventilation and a reduced ability to sense hypercapnia, which complicates the clinical management of their respiratory status.

(b) Considering this pathophysiologic mechanism, why is it important to use caution when administering oxygen to patients with chronic lung disease?

  • Administering high levels of oxygen may further suppress the central respiratory drive, as these patients often rely on hypoxic drive for stimulation of ventilation. If oxygen concentrations are increased significantly, they may experience a reduction in their respiratory rate, leading to exacerbation of hypercapnia and subsequent respiratory acidosis, which can be particularly detrimental in managing their overall clinical state.

2. (a) Differentiate between the terms “airway resistance” and “tissue resistance.”

  • Airway Resistance: Resistance to flow through the airwaysthat occurs due to factors such as airway diameter, mucus production, and bronchoconstriction.

  • Tissue Resistance: Resistance encountered in the lung parenchyma that affects the expansion and contraction of lung tissue, influenced by the elastic properties of the lung and chest wall.

(b) Regarding airway resistance:

  • Discuss how a decrease in airway radius causes increased resistance to flow of air through the airways.

  • How do airway wall edema, mucus obstruction, and bronchoconstriction increase airway resistance?

(c) Regarding tissue resistance:

  • Differentiate between compliance and elastance.

  • How does a decrease in compliance causes decreased gas exchange?

  • How does a decrease in elastance cause decreased gas exchange?

3.  Discuss how gas diffusion across the alveolar-capillary surface can be decreased by.

  • decreased inflation of alveoli

  • decreased blood flow through pulmonary capillaries (decreased pulmonary perfusion)

  • pathology of the interstitial space between the alveoli and pulmonary capillaries (such as excess interstitial fluid or interstitial scarring/fibrosis). 

4. (a) Describe the meaning of the physiologic concept “work of breathing.”  

(b) Would pulmonary pathophysiology be more likely to cause an increase or decrease in the work of breathing? Why?

(c) Describe clinical manifestations that reflect an increase in the work of breathing.

(d) Discuss how an increased work of breathing would increase the need for energy.

5.  Interpret the meanings of increases/decreases in the following diagnostic assessments of respiratory function:

a.) Oxygen saturation level – obtained from 2 different sources:

  • SpO2 – peripheral oxygen saturation (reading obtained from a pulse oximeter device)

  • SaO2 –  oxygen saturation in arterial blood (reported as part of ABG results)

b.) Arterial Blood Gases (pH, paO2, paCO2, bicarbonate)

c.) Pulmonary Function Tests (particularly the DLCO, FEV1, and pre/post bronchodilator tests). 

d.) Peak Expiratory Flow Rate (PEFR)

PART 2:   Common Respiratory Disorders

6. Discuss the pathophysiology and clinical diagnostic indications of acute respiratory failure.

7. a.) Differentiate between the pathophysiology of upper and lower respiratory tract infections.  

b.) Differentiate common infections of the upper and lower respiratory tract (common cold, rhinitis, sinusitis, laryngitis, influenza, acute bronchitis, and bronchiolitis)

8. Discuss the pathophysiology of pneumonia.

a.) Which part of the lungs are affected in pneumonia? Discuss how the pathophysiologic changes in pneumonia cause gas exchange to be decreased.

  b.) Describe types of microbial pathogens that cause pneumonia.

c.) Differentiate between “hospital acquired pneumonia” and “community acquired pneumonia.”

d.) Differentiate between lobar pneumonia and bronchopneumonia.

e.) Differentiate the 4 phases of acute bacterial pneumonia and the pathophysiologic events that occur in each phase (edema, red hepatization, grey hepatization, resolution). 

e.) What is the pathophysiologic origin of the “rust-colored sputum” that often occurs in pneumonia?

f.) Discuss the pathophysiology of pleuritis (pleurisy) and pleuritic pain. Why does pleuritic pain often occur with pneumonia?

9. Discuss the pathophysiology of tuberculosis.

  1. Identify which part of the lungs are affected.

  2. Identify the causative organism.  Describe unique characteristics of this organism that make it so pathogenic.

  3. Identify the type of hypersensitivity response is demonstrated in TB skin testing. (Type I, II, III, or IV).  Does that immune response reflect the activity of the humoral or cellular branch of the adaptive immune response?

  4. Describe how the formation of pulmonary granulomas (Ghon foci / Ghon complexes) in tuberculosis reflect the immune response to the TB organism.

10. Identify risk factors for fungal respiratory infections and discuss why fungal infections are more common in persons with reduced immune function. 

11. a.) Discuss the general pathophysiology of common types of respiratory tract malignancies.

b.) Differentiate clinical manifestations associated with laryngeal cancer versus lung cancers.

12. Discuss anatomic and immunological characteristics that place children at higher risk from acute respiratory infections. 

13. Discuss the pathophysiology of epiglottitis (inflammation of the epiglottis).  

a.) Describe the location and function of the epiglottis.  

b.) Describe common clinical manifestations of epiglottitis.

c.) Discuss the most life-threatening risk to a patient with epiglottitis. 

14. Discuss the pathophysiology and common clinical manifestations of the childhood respiratory infections epiglottitis, acute laryngotracheal bronchitis (croup), and bronchiolitis.   

15.  Describe the pathophysiology of Respiratory Distress Syndrome of the Newborn (or Neonatal Respiratory Distress Syndrome). 

PART 3:   Disorders of Oxygenation & Ventilation

16. Describe situations that increase risk for aspiration and how aspiration can cause pneumonia.  

Why is it more common to aspirate into the right mainstem bronchus than the left? 

17. Discuss the pathophysiology of atelectasis and differentiate between compression atelectasis and absorption atelectasis. 

18. a.) Discuss the pathophysiology of pulmonary edema.  Describe the role of surfactant in preventing pulmonary edema.

b.) Discuss 4 alterations that can lead to pulmonary edema.  (RECALL the 4 pathophysiologic causes of interstitial edema from the unit on fluid & electrolyte pathophysiology. These are the SAME mechanisms that reflect disruption in the balance of the Starling Forces at the level of the capillaries. The alveolar-capillary interface is a specialized form of capillary bed.)

19. a.) Discuss the pathophysiology of pneumothorax. 

b.) Describe the meaning of the term “spontaneous pneumothorax.”

c.) Differentiate the pathophysiology and clinical manifestations of open (communicating) pneumothorax and tension pneumothorax.  Which is more immediately life threatening? Why?

20. Discuss the pathophysiology of pleural effusion (including the type of fluid involved in each type. 

  • Transudative pleural effusion

  • Exudative pleural effusion (empyema)

  • Hemothorax

  • Chylothorax

21. a.) Discuss the pathophysiology of Acute Respiratory Distress Syndrome (ARDS). 

b.) Discuss some mechanisms of lung injury that can lead to the development of ARDS.  

c.) Differentiate the pathophysiology of Acute Respiratory Distress Syndrome (ARDS) from the pathophysiology of Respiratory Distress Syndrome of the Newborn (Neonatal RDS).

  • Which disorder is caused by a primary deficiency of surfactant?  (Primary deficiency refers to inadequate production of surfactant because cells that produce surfactant are not yet fully developed – i.e,. a developmental deficiency.)

  • Which disorder is associated with a secondary deficiency of surfactant because of damage to the alveoli?   (Secondary deficiency refers to a surfactant deficiency that occurs because cells that produce surfactant have been damaged by some type of cell injury.)

22. Discuss the pathophysiology of asthma, and the common clinical manifestations of asthma.

a.) Describe how inflammation causes the clinical manifestations of asthma (including how decreasing airway inflammation can reverse the airway changes).

b.) Describe how each of the following asthma components contributes to obstruction to the outflow of air:  airway edema, mucus secretion into airways, bronchoconstriction.

  1. Differentiate how the following diagnostic tests measure the degree of airway obstruction: 

  • Forced Expiratory Volume in 1 second (FEV1) – measured in pulmonary function test

  • Peak Expiratory Flow Rate – measured by portable hand-held meter

d.) Describe the mechanism that produces hyperexpanded alveoli and “air trapping” in asthma.

e.) Differentiate the pathology of allergic asthma VERSUS nonallergic asthma.  Describe the difference between an “early stage” allergic response and a “late stage” allergic response.

f.) Discuss the significance of avoiding exposure to asthma “triggers” in asthma & identify some common triggers of asthma.

23. Compare and contrast the pathophysiology of chronic bronchitis and emphysema. 

a.) Differentiate the pathophysiologic changes of the airways in each disorder and how the mechanisms of air trapping are different in these 2 disorders.

c.)  Compare and contrast the clinical manifestations of chronic bronchitis and emphysema. 

d.) Why does polycythemia commonly occur during the early stages of chronic bronchitis (triggered by the adaptive mechanism of increased erythropoiesis) but does not typically occur until the later stages of emphysema.

e.) Differentiate the pathphysiology of centriacinar (centrilobular) emphysema versus panacinar emphysema (including discussing the role of alpha-1-antitrypsin in panacinar emphysema). 

24. Differentiate the pathophysiology and clinical manifestations of cystic fibrosis (including the genetic pathophysiology, diagnostic testing, and pathophysiologic effects on the GI tract, pancreas and skin in addition to pulmonary pathophysiology). 

25. Describe the pathophysiology of idiopathic pulmonary fibrosis (as a case model of interstitial lung disorders).  

26. a.) Describe the meaning of the term “Ventilation/Perfusion ratio” (or V/Q ratio). 

b.) How does a “V/Q mismatch” affect pulmonary gas exchange?

c.) What types of pathophysiologic alterations would cause a low V/Q ratio?

d.) What types of pathophysiologic alterations would cause a high V/Q ratio?  

27. Discuss the pathophysiology of pulmonary embolism (a pulmonary vascular disorder).  

a.) Discuss why a patient with deep vein thrombosis is at risk to develop pulmonary embolism.

b.) Other than blood clots, identify 3 additional substances which can gain access to the blood stream and cause pulmonary embolism.  Describe pathophysiologic conditions or clinical treatments that place a patient at risk for embolizing these substances.

c.) Differentiate between the clinical presentations of a patient with a massive pulmonary

  embolus and a patient with multiple small pulmonary emboli.  Which is the most immediately life-threatening?

28. a.) Discuss the pathophysiology of pulmonary hypertension (a pulmonary vascular disorder).  

b.) Differentiate the pathophysiology of primary pulmonary hypertension (i.e., originating from pathophysiologic changes in the pulmonary arteries themselves) and secondary pulmonary

  hypertension (i.e., originating from hypoxia-induced pulmonary vasoconstriction that occurs in response to pulmonary disease). 

29. (a) Describe the pathophysiologic process of “hypoxia-induced pulmonary vasoconstriction.”  (Note that it is alveolar hypoxia that triggers the pulmonary vasoconstriction, and it is the pulmonary arterial blood vessels that are vasoconstricting in response to the alveolar hypoxia.) 

(b) What is the adaptive purpose of this pulmonary vasoconstriction in response to alveolar hypoxia?

(c) Consider how hypoxia-induced pulmonary vasoconstriction affects the resistance to blood flow through the pulmonary vessels.  Is the resistance to flow increased or decreased?  How would that change in resistance to flow influence the workload of the right ventricle of the heart?

30. Describe the pathophysiology of “cor pulmonale” (a pulmonary vascular disorder). Consider the how the hypoxia-induced pulmonary vasoconstriction associated with chronic lung disease can cause “cor pulmonale.”