Obstructive lung disease

Question 1

Question 1: What is the primary characteristic of obstructive lung diseases?

Answer 1

Answer: Obstructive Lung Diseases are characterized by an increase in resistance to airflow due to diffuse airway disease.

Question 2

Question 2: How are obstructive lung diseases distinguished from restrictive lung diseases through pulmonary function tests?

Answer 2

Answer: Obstructive lung diseases are distinguished from restrictive lung diseases based on the FEV1/FVC ratio, which is typically less than 0.7.

Question 3

Question 3: Name three examples of obstructive lung diseases.

Answer 3

Answer: COPD, Asthma, Bronchiectasis.

Question 4

Question 4: Define COPD.

Answer 4

Answer: COPD stands for Chronic Obstructive Pulmonary Disease. It’s a common, preventable, and treatable disease characterized by persistent respiratory symptoms and airflow limitation due to airway and/or alveolar abnormalities caused by exposure to noxious particles or gases.

Question 5

Question 5: What are the two major clinicopathologic manifestations of COPD?

Answer 5

Answer: The two major clinicopathologic manifestations of COPD are chronic bronchitis and emphysema.

Question 6

Question 6: What are the common causes of COPD?

Answer 6

Answer: The common causes of COPD include tobacco smoking (90%), environmental pollutants, and alpha-1 anti-trypsin deficiency (specific to emphysema).

Question 7

Question 7: How does chronic exposure to toxic particles/gas lead to COPD pathophysiology?

Answer 7

Answer: Chronic exposure to toxic particles or gases leads to inflammation. Alveolar macrophages detect these particles and release cytokines, triggering an inflammatory process. This process leads to destruction of airway walls, bronchoconstriction, and stimulation of mucus-producing cells.

Question 8

Question 8: How does chronic inflammation caused by toxic particles/gas contribute to irreversible damage in COPD?

Answer 8

Answer: Chronic inflammation results in the release of Transforming Growth Factor beta (TGF-β), which stimulates fibrous tissue deposition. This fibrosis leads to irreversible damage to the airway, distinguishing COPD from asthma.

Question 9

Question 1: How is chronic bronchitis clinically manifested?

Answer 9

Answer:

Chronic bronchitis is clinically manifested by a productive cough that persists for more than 3 months for at least 2 consecutive years.

Question 11

Question 2: What is the key structural difference between chronic bronchitis and emphysema?

Answer 11

Answer: Unlike in chronic bronchitis, emphysema involves irreversible enlargement of the airspaces distal to the terminal bronchiole, along with the destruction of their walls.

Question 12

Question 3: Explain the role of elastic tissue in the pathophysiology of emphysema.

Answer 12

Answer: Elastic tissue within the alveolar and bronchial walls prevents airway collapse. Neutrophilic proteases and elastases destroy this elastic tissue, leading to the destruction of alveolar septa.

This mechanism is specific to emphysema.

Question 13

Question 4: How does the destruction of alveolar septa in emphysema affect the surface area for gas exchange?

Answer 13

Answer:
* The destruction of alveolar septa leads to the formation of larger air sacs with decreased surface area (acinus), resulting in a decreased surface area for gas exchange.

Question 14

Question 5: Differentiate between centrilobular emphysema and panacinar emphysema.

Answer 14

Answer: Centrilobular emphysema occurs in the upper lobes/apices of the lungs and is caused by smoking. Panacinar emphysema, on the other hand, occurs in the lower lobes/bases of the lungs and is caused by alpha-1 anti-trypsin deficiency.

Question 15

Question 6: What is the role of alpha-1 anti-trypsin in the context of emphysema?

Answer 15

Answer: Alpha-1 anti-trypsin is an enzyme that inhibits elastases, which destroy elastic tissue in the lungs. Some patients with a genetic mutation have a deficiency of this enzyme, resulting in increased destruction of elastic tissue in the lungs, particularly in the bases.

Question 16

Question 7: How does alpha-1 anti-trypsin deficiency relate to liver disease?

Answer 16

Answer: Patients with alpha-1 anti-trypsin deficiency may also have underlying liver disease due to the genetic mutation affecting enzyme production.

Question 17

Question 1: What are the key symptoms of asthma?

Answer 17

Answer: Asthma is characterized by chronic airway inflammation and variable expiratory airflow obstruction, leading to symptoms such as wheezing, shortness of breath, chest tightness, and cough.

Question 18

Question 2: Differentiate between asthma and COPD in terms of reversibility.

Answer 18

Answer: Unlike COPD, asthma is a reversible airway disease.

Question 19

Question 3: What is the atopic triad, and how is it related to asthma?

Answer 19

Answer: The atopic triad consists of atopic dermatitis, allergic rhinitis, and asthma.

Patients with atopic dermatitis and allergic rhinitis have an increased risk of developing asthma.

Question 20

Question 4: Name some nonallergic triggers for asthma.

Answer 20

Answer: Nonallergic triggers for asthma include viral upper respiratory tract infections (URTI), cold air, exercise, GERD, and beta-blockers.

Question 21

Question 5: What is Samter’s Triad, and what are its components?

Answer 21

Answer: Samter’s Triad consists of asthma, aspirin hypersensitivity, and nasal polyps.

Question 22

Question 6: Describe the early phase of asthma pathophysiology.

Answer 22

Answer: In the early phase of asthma, dendritic cells present antigens to T helper cells.

This triggers the release of cytokines (interleukin 4 and interleukin 5), activating plasma cells to release IgE antibodies.

These antibodies bind to mast cells, leading to the release of substances such as leukotrienes, prostaglandins, and histamine.

These substances cause bronchial smooth muscle constriction, vasodilation, increased permeability, and bronchial edema, narrowing the airway.

Question 23

Question 7: What role do leukotrienes, prostaglandins, and histamine play in asthma?

Answer 23

Answer: In asthma, these substances released by mast cells act on bronchial smooth muscles, blood vessels, and glands.
Leukotrienes and prostaglandins contribute to bronchospasm and increased permeability of blood vessels, leading to bronchial edema.

Histamine contributes to vasodilation and increased permeability of blood vessels.

Question 24

Question 1: Describe the pathophysiological similarities between the early and late phases of asthma.

Answer 24

Answer:
The pathophysiologic mechanism in the late phase of asthma is similar to that in the early response.
Both involve inflammation, cytokine release, and the release of substances like leukotrienes and prostaglandins that cause bronchospasm, bronchial edema, and narrowing of the airway.

Question 25

Question 2: How does interleukin 5 contribute to the late phase of asthma?

Answer 25

Answer:
Interleukin 5 stimulates the bone marrow to produce eosinophils, which migrate to the airway and release major basic protein (MBP) and cationic peptides.

These substances destroy airway cells, leading to chronic inflammation and hypersensitivity of bronchial smooth muscles.

Question 26

Question 3: What role does mucus production play in the late phase of asthma?

Answer 26

Answer: In the late phase of asthma, mucus glands are stimulated to produce thicker mucus, further narrowing the airway and exacerbating the bronchospasm.

Question 27

Question 4: Define bronchiectasis.

Answer 27

Answer: Bronchiectasis is characterized by the permanent dilation of bronchi and bronchioles due to inflammation stemming from persistent or severe infections. This leads to the destruction of smooth muscle and elastic tissue in the airways.

Question 28

Question 5: How does chronic inflammation contribute to the development of bronchiectasis?

Answer 28

Answer: Chronic inflammation in bronchiectasis results from recurrent infections.
Neutrophils release reactive oxygen species and proteases,
T cells release inflammatory cytokines, and

fibrous tissue deposition occurs due to TGF-β release.

These processes lead to airway damage, narrowing, dilation, excess mucus production, and bronchospasm.

Question 29

Question 6: Explain primary ciliary dyskinesia (PCD) and its connection to bronchiectasis.

Answer 29

Answer:
PCD, also known as Kartagener Syndrome, is a genetic disorder characterized by defective cilia, resulting in chronic infections.
The impaired ciliary function leads to the inability to clear mucus from the airways, contributing to mucus buildup and potential development of bronchiectasis.

Question 30

Question 7: How does cystic fibrosis relate to increased mucus and bronchiectasis?

Answer 30

Answer: Cystic fibrosis is characterized by a defective CFTR, resulting in deficient chloride ion transport and thick, sticky mucus production. The increased mucus contributes to mucus buildup and inflammation, potentially leading to bronchiectasis.

Question 31

Question 8: What are some examples of conditions that can cause mucus buildup and chronic inflammation, leading to bronchiectasis?

Answer 31

Answer: Examples include allergic bronchopulmonary aspergillosis (ABPA), a hypersensitivity reaction to fungi that colonize the airways, and autoimmune diseases like rheumatoid arthritis and systemic lupus erythematosus.

Question 32

Question 1: What are the two primary components of COPD physical features?

Answer 32

Answer: chronic bronchitis and emphysema.

Question 33

Question 2: Describe the “Blue Bloaters” features associated with chronic bronchitis.

Answer 33

Answer: Blue Bloaters with chronic bronchitis have features such as bloating due to lung hyperinflation pushing down the diaphragm, leading to an “obese” appearance.

They also experience right heart failure symptoms like JVD, hepatomegaly, pedal edema, and cyanosis. Productive cough, rhonchi, and wheezing are characteristic, and the cough lasts at least three months for two consecutive years.

Question 34

Question 3: What distinguishes chronic bronchitis from emphysema in terms of cough?

Answer 34

Answer:
the type of cough.
Chronic bronchitis is associated with a productive cough, while emphysema typically leads to a mild cough.

Question 35

Question 4: Explain the “Pink Puffers” features associated with emphysema.

Answer 35

Answer:

Pink Puffers with emphysema exhibit pursed lip breathing to prevent bronchioles from collapsing.

They have a mild cough, reduced breath sounds due to alveolar hyperinflation, dyspnea, tachypnea, cachexia (thinness due to energy expenditure), and a barrel chest caused by lung hyperinflation.

Question 36

Question 5: Why do Pink Puffers engage in pursed lip breathing?

Answer 36

Answer: Pink Puffers use pursed lip breathing to increase airway pressure and prevent bronchioles from collapsing during expiration, compensating for the loss of elastic tissue in emphysema.

Question 37

Question 6: How does alveolar hyperinflation contribute to reduced breath sounds?

Answer 37

Answer:
In emphysema, alveolar hyperinflation results in a significant amount of air trapped within the lungs, making it hard to auscultate for breath sounds.

Question 38

Question 7: What is the mechanism behind the barrel chest in emphysema?

Answer 38

Answer: In emphysema, lung hyperinflation leads to a barrel chest appearance, where the chest diameter from anterior to posterior is enlarged outward.

Question 39

Question 1: How can mucus plugs in the bronchioles affect oxygen and carbon dioxide levels in chronic bronchitis?
.

Answer 39

Answer: In chronic bronchitis, mucus plugs in bronchioles can hinder the movement of oxygen (O2) into the alveoli and the easy passage of carbon dioxide (CO2) out of the alveoli.

This can lead to decreased oxygen getting to the alveoli and increased difficulty removing carbon dioxide.

Question 40

Question 2: Explain the relationship between blood flow and well-ventilated alveoli in chronic bronchitis.

Answer 40

Answer:
Blood flow is increased to well-ventilated alveoli in chronic bronchitis as a compensatory mechanism to avoid bringing hypoxemic (low in O2) hypercapnic (high in CO2) blood to poorly ventilated alveoli.

Question 41

Question 4: What is Cor Pulmonale, and how does it develop in chronic bronchitis?

Answer 41

Answer: Cor Pulmonale is right-sided heart failure (RHF) caused by lung disease.

In chronic bronchitis, decreased oxygen in the alveoli leads to pulmonary vasoconstriction, causing strain on the right side of the heart.

This can result in manifestations such as jugular venous distention (JVD), hepatomegaly, ascites, and pedal edema.

Question 42

Question 5: How does chronic bronchitis increase the risk of pneumonia?

Answer 42

Answer: Mucus plugs in the bronchioles make it harder to clear bacteria from the lungs, increasing the risk of bacterial accumulation and the development of pneumonia.

Question 43

Question 6: What is polycythemia, and how does it relate to chronic bronchitis?

Answer 43

Answer:
Polycythemia refers to an increase in the number of red blood cells (RBCs). In chronic bronchitis, persistent hypoxemia triggers the production of more RBCs as a compensatory mechanism. The kidneys produce erythropoietin (EPO), which stimulates the bone marrow to produce more RBCs, leading to secondary polycythemia.

Question 44

Question 1: Why do patients with early-stage emphysema not exhibit hypoxemia?

Answer 44

Answer:
In early-stage emphysema, patients do not exhibit hypoxemia because excessive mucus production, which leads to hypoxemia in chronic bronchitis, is not a prominent feature in emphysema during the early course of the disease.

Question 45

Question 2: Explain the mechanism of hypoxemia in emphysema.

Answer 45

Answer:
Mild hypoxemia in emphysema is due to a decrease in total surface area (TSA) across the alveoli.

During inspiration, the bronchioles are open, and the alveoli are well-ventilated.

However, decreased TSA leads to reduced area for gas exchange.

Question 46

Question 3: How does the loss of elastic tissue in emphysema contribute to hypercapnia?

Answer 46

Answer:

During expiration in emphysema, the bronchioles collapse due to the loss of elastic tissue.

This collapse makes it difficult for air (and carbon dioxide, CO2) to escape the alveoli, trapping air and CO2 inside.

This trapped CO2 leads to hyperinflation of the alveoli and subsequently, hypercapnia (increased CO2 levels in the blood).

Question 47

Question 4: Why do patients with emphysema experience dyspnea and tachypnea?

Answer 47

Answer:

Air trapping and hyperinflation of the lungs in emphysema make breathing difficult, leading to dyspnea (shortness of breath) and tachypnea (rapid breathing) as the body attempts to obtain more oxygen and expel more carbon dioxide.

Question 48

Question 5: What are bullae or blebs, and how do they relate to pneumothorax?

Answer 48

Answer:
In emphysema, air trapping can cause the formation of bullae or blebs, which are large air spaces where air accumulates.

If these bullae rupture, air can enter the pleural space, leading to pneumothorax—a condition where air accumulates between the lung and the chest wall.

Question 49

Question 6: Which complication is the primary concern in emphysema, and when do hypoxemia and hypercapnia typically develop?

Answer 49

Answer:
* Pneumothorax is the primary complication of emphysema.

• Hypoxemia and hypercapnia typically develop in the later advanced stages of the disease.

Question 50

Question 1: What are the common triggers of asthma?

Answer 50

Answer: Triggers of asthma can be allergic or non-allergic. They include factors like upper respiratory tract infections (URTI), cold air, exercise, beta-blockers, GERD, aspirin (Samter’s triad), and allergens (atopy triad).

Question 51

Question 2: How does bronchospasm and bronchial edema affect breathing in asthma?

Answer 51

Answer:
Bronchospasm and bronchial edema lead to narrowed airways in asthma, resulting in severe wheezing on expiration and making breathing difficult.

Question 52

Question 3: What distinguishes the cough in asthma from the cough in chronic bronchitis?

Answer 52

Answer: Unlike chronic bronchitis, asthma patients often present with a dry cough due to less prominent mucus secretion early in the disease.

Question 53

Question 4: What does a “silent chest” indicate in asthma?

Answer 53

Answer: A “silent chest” is an ominous sign of severe asthma exacerbation. It occurs when the airway is severely obstructed, leading to absent chest sounds on auscultation due to the absence of airflow.

Question 54

Question 5: How does hyperinflation contribute to dyspnea and tachypnea in asthma?

Answer 54

Answer: Hyperinflation of the lungs in asthma makes it difficult for patients to get air in or out. As a compensatory mechanism, patients experience dyspnea (shortness of breath) and tachypnea (rapid breathing), which can lead to hypoxemia and hypercapnia.

Question 55

Question 6: What is “Pulsus paradoxus,” and how does it occur in asthma?

Answer 55

Answer:
Pulsus paradoxus is a condition where the systolic blood pressure (SBP) drops by more than 10 mmHg during inspiration.

In asthma, intense bronchoconstriction and bronchial edema can lead to decreased exhalation of CO2, causing a drop in SBP during inspiration.

Question 56

Question 7: How does increased work of breathing manifest in asthmatic patients?

Answer 56

Answer: Increased work of breathing in asthma involves the use of accessory muscles (such as scalene and sternocleidomastoid), abdominal muscles, and nasal flaring as a compensatory mechanism to facilitate more breathing in case of hypoxemia or hypercapnia.

Question 57

Question 1: How does elastic tissue destruction lead to bronchodilation in bronchiectasis?

Answer 57

Answer: Elastic tissue destruction in bronchiectasis leads to bronchodilation due to the weakening of the bronchial walls. This dilation contributes to the clinical features of the condition.

Question 58

Question 2: What causes the productive, foul-smelling cough in bronchiectasis?

Answer 58

Answer: The excessive mucus production in bronchiectasis leads to a productive, foul-smelling cough.

The accumulated mucus becomes a breeding ground for bacteria, leading to the characteristic odor.

Question 59

Question 3: Explain the connection between chronic hypoxemia and clubbing of the digits in bronchiectasis.

Answer 59

Answer: Chronic hypoxemia, which is a result of bronchial obstruction and decreased oxygen entering the alveoli, can alter the configuration of the nail bed.

This alteration causes the digits to become clubbed, where the nail bed bulges out.

Question 60

Question 4: How does mucus accumulation contribute to hemoptysis in bronchiectasis?
(coughing up blood).

Answer 60

Answer: The excessive mucus production in bronchiectasis can lead to bronchodilation and thinning of the bronchial walls. This can cause blood vessels to be more susceptible to damage, resulting in hemoptysis

Question 61

Question 5: Why does bronchiectasis lead to hypercapnia?

Answer 61

Answer: Mucus accumulation obstructs the bronchial airways, making efficient exhalation of carbon dioxide (CO2) difficult.
This accumulation can lead to hypercapnia (increased CO2 levels in the blood).

Question 62

Question 6: How does mucus accumulation and bronchospasm contribute to hypoxemia in bronchiectasis?

Answer 62

Answer: Mucus accumulation and bronchospasm obstruct the bronchial airways, leading to decreased oxygen (O2) entering the alveoli. This decrease in O2 leads to hypoxemia, which triggers compensatory mechanisms like increased respiratory rate and heart rate, resulting in tachypnea and dyspnea.

Question 63

Question 7: Which common bacteria are often associated with infections in bronchiectasis?

Answer 63

Answer:

In bronchiectasis, Pseudomonas aeruginosa is a common bacteria that can colonize and multiply in the lungs due to the clogged bronchial airways.

Question 64

Question 8: What is cystic fibrosis, and how does it contribute to bronchiectasis?

Answer 64

Answer: Cystic fibrosis (CF) is a genetic disorder characterized by a defect in the transmembrane protein that affects chloride and water transport. This leads to thickened secretions in various parts of the body, including the lungs, resulting in bronchiectasis. CF patients experience bronchodilation, fibrosis, bronchospasm, and other related features.

Question 65

Question 1: What is the common problem in all obstructed lung diseases?

Answer 65

Answer: The common problem in all obstructed lung diseases is difficulty expelling air from the lungs, leading to air trapping and hyperinflation.

Question 66

Question 2: How does hyperinflation affect the lung’s ability to take in additional air?

Answer 66

Answer: Due to hyperinflation, the lungs have limited capacity to take in additional air, leading to a decrease in the Inspiratory Reserve Volume (IRV).

Question 67

Question 3: What happens to the Expiratory Reserve Volume (ERV) in obstructed lung diseases?

Answer 67

Answer: In obstructed lung diseases, due to air trapping, the Expiratory Reserve Volume (ERV) increases significantly.

Question 68

Question 4: How does air trapping affect the Residual Volume (RV) in obstructed lung diseases?

Answer 68

Answer: Air trapping in obstructed lung diseases leads to a significant increase in the Residual Volume (RV).

Question 69

Question 5: What can be observed in the Flow Volume Loop of patients with obstructed lung diseases?

Answer 69

Answer: In the Flow Volume Loop of patients with obstructed lung diseases, the graph shifts to the left due to increased Residual Volume (RV) and Total Lung Capacity (TLC).

Question 70

Question 6: How does the FEV1/FVC ratio change in obstructed lung diseases?

Answer 70

Answer: In obstructed lung diseases, the FEV1/FVC ratio decreases significantly, leading to FEV1/FVC values less than 80%.

Question 71

Question 1: What is a key characteristic of the lungs in restrictive lung diseases?

Answer 71

Answer: In restrictive lung diseases, the lungs are very fibrotic and prone to collapse, leading to reduced lung compliance.

Question 72

Question 2: How does reduced lung compliance affect the Inspiratory Reserve Volume (IRV) in restrictive lung diseases?

Answer 72

Answer: Reduced lung compliance in restrictive lung diseases results in a decrease in the Inspiratory Reserve Volume (IRV).

Question 72

Question 4: How is the Residual Volume (RV) affected in restrictive lung diseases?

Answer 72

Answer: In restrictive lung diseases, the Residual Volume (RV) decreases due to the diminished amount of air remaining in the lungs.

Question 72

Question 3: What is the effect of reduced lung compliance on the Expiratory Reserve Volume (ERV) in restrictive lung diseases?

Answer 72

Answer: Reduced lung compliance leads to a decrease in the Expiratory Reserve Volume (ERV) due to the limited ability of the lungs to exhale air effectively.

Question 72

Question 5: Explain the impact of reduced lung compliance on the Total Lung Capacity (TLC) and Functional Residual Capacity (FRC) in restrictive lung diseases.

Answer 72

Answer:
Reduced lung compliance leads to a decrease in both (TLC) and (FRC), making the lungs hold less air and remaining less expanded.

Question 72

Question 6: What change can be observed in the Flow Volume Loop of patients with restrictive lung diseases?

Answer 72

Answer: In patients with restrictive lung diseases, the Flow Volume Loop shows a smaller loop that is shifted to the right, indicating reduced Residual Volume (RV) and Total Lung Capacity (TLC).

Question 73

Question 7: How does the FEV1/FVC ratio change in restrictive lung diseases?

Answer 73

Answer: In restrictive lung diseases, the Forced Vital Capacity (FVC) is significantly reduced, leading to FEV1/FVC ratios greater than or equal to 80%.

Question 74

Question 8: Compare the FEV1/FVC ratios between obstructive and restrictive lung diseases.

Answer 74

Answer: In obstructive lung diseases, FEV1/FVC < 80% due to reduced FEV1, while in restrictive lung diseases, FEV1/FVC ≥ 80% due to reduced FVC.

Question 75

Question 1: What is the purpose of the DLCO (diffusion capacity of carbon monoxide) test in diagnosing lung diseases?

Answer 75

Answer: The DLCO test measures how efficiently carbon monoxide (CO) diffuses across the alveolar-capillary membrane. It helps assess the total surface area (TSA), pressure gradient, and thickness of the respiratory membranes, providing insights into lung conditions such as emphysema, interstitial lung disease (ILD), and asthma.

Question 76

Question 2: How does DLCO vary in different lung diseases such as emphysema, ILD, and asthma?

Answer 76

Answer: In emphysema, which reduces the total surface area (TSA) of the alveoli, DLCO is decreased. In ILD, thickened respiratory membranes decrease DLCO. In asthma, due to hyperinflated alveoli from bronchoconstriction and edema, DLCO may slightly increase or remain normal.

Question 77

uestion 3: Explain how the bronchodilator test helps differentiate between COPD and asthma.

Answer 77

Answer: The bronchodilator test involves administering a β-agonist and measuring FEV1 before and after. In COPD, which is relatively irreversible, a post-bronchodilator increase in FEV1 is less than 12%. In asthma, which is reversible, an increase in FEV1 after the test is equal to or greater than 12%.