Pulmonary diseases Flashcards

1
Q

What are pulmonary function tests (PFTs) and how do they help diagnose restrictive and obstructive pulmonary diseases?

A

PFTs measure lung function, including oxygen levels, tidal volume, and airflow rates. In obstructive diseases (e.g., COPD, asthma), FEV1 is reduced, and the FEV1/FVC ratio is decreased. In restrictive diseases (e.g., pulmonary fibrosis), both FEV1 and FVC are reduced, but the FEV1/FVC ratio is typically normal or increased.

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2
Q

What is the etiology of Chronic Obstructive Pulmonary Disease (COPD)?

A

COPD is most commonly caused by smoking and second most common is hereditary deficiency in α1-antitrypsin (AAT).

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3
Q

What is the pathophysiology of COPD

A

It involves chronic inflammation and immune response that leads to lung tissue damage, including emphysema and chronic bronchitis. In emphysema, alveolar walls are destroyed, reducing gas exchange, while chronic bronchitis results in airway obstruction due to inflammation and excessive mucus production.

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4
Q

What are the two types of obstructive airway diseases included in COPD?

A

Emphysema, which involves enlargement of airspaces and destruction of lung tissue, and chronic bronchitis, characterized by increased mucus production and airway obstruction.

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5
Q

What is the pathology of Emphysema in relation to the two main causes of COPD (smoking and ATT )

A

Smoking: Increases protease activity (e.g., elastase), breaking down elastin and destroying alveoli, causing air trapping and loss of elasticity.
AAT Deficiency: Low AAT means less protease inhibition, leading to uncontrolled elastin breakdown and early-onset emphysema (especially in the lower lobes).

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6
Q

What is the pathology of Chronic bronchitis in relation to the two main causes of COPD (smoking and ATT )

A

Smoking: Causes inflammation, mucus hypersecretion, and airway narrowing, leading to persistent cough and blockage.
AAT Deficiency: Amplifies inflammation and mucus buildup, worsening airflow obstruction.

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7
Q

What are the clinical manifestations of COPD?

A

People with predominant emphysema are classically referred to as pink puffers, loss of lung elasticity and hyperinflation of the lungs. Airways often collapse during expiration because pressure in surrounding lung tissues exceeds airway pressure

People with a clinical syndrome of chronic bronchitis are classically labeled blue bloaters, due to cyanosis

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8
Q

How can the second most common cause of COPD can be treated?

A

(Human) AAT is available for replacement therapy in people with a hereditary deficiency of the enzyme.

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9
Q

What is asthma, and what are its causes?

A

Asthma is a chronic inflammatory disease of the airways, leading to reversible bronchospasms and airway obstruction. It can be triggered by allergens (extrinsic) or non-allergic factors such as respiratory infections or exercise (intrinsic).

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10
Q

What are the risk factors of Asthma?

A

Genetic predisposition for the development of an immunoglobulin E (IgE)-mediated response to (common) allergens. Other risk factors for (childhood) asthma include family history of asthma, allergies, (antenatal) exposure to tobacco smoke and pollution.

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11
Q

What is the pathophysiology of asthma?

A

Asthma involves airway inflammation and Obstruction, bronchoconstriction, increased mucus secretion, and airway remodeling. Mast cells release inflammatory mediators (e.g., histamine), causing smooth muscle tightening and narrowing of airways.

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12
Q

What are the role of cytokines in Asthma

A

Cytokines, including tumor necrosis factor (TNF)-α and interleukin 4 (IL-4) and IL-5, contribute to the pathogenesis of bronchial asthma by affecting bronchial epithelial and smooth muscle cells. TNF-α, for instance, increases migration and activation of inflammatory cells and contributes to airway remodeling. IL-4 and IL-5 are involved in the proinflammatory response and allergic reactions in asthma.

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13
Q

What are the clinical manifestations of asthma?

A

Symptoms include wheezing, shortness of breath, chest tightness, and coughing, often triggered by allergens or irritants.

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14
Q

What are the clinical manifestations during a prolonged asthma attack

A

During a prolonged attack, air becomes trapped behind the occluded and narrowed airways, causing hyperinflation of the lungs.

As a result, more energy is needed to breath and the (accessory) muscles are required to maintain ventilation and gas exchange. Dyspnea and fatigue occur

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15
Q

What changes are found in the small airways leading to airway obstruction during an acute asthma attack

A

During an asthmatic attack, the airways narrow because of bronchospasm, edema of the bronchial mucosa, and mucus plugging. Expiration becomes prolonged because of progressive airway obstruction

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16
Q

How does respiratory infections impact asthma?

A

Frequent viral respiratory infections can exacerbate asthma or even lead to its development. These infections, especially when frequent at an early age, may exaggerate the T2H response, predisposing the airways to allergic responses and IgE production. Additionally, viral infections are known triggers for asthma exacerbations.

17
Q

What is influenza, and what are its causes?

A

Influenza is a viral infection of the upper respiratory tract caused by the influenza virus, with types A, B, and C affecting humans. The viruses are single-stranded ribonucleic acid (RNA) genome.

18
Q

What is the transmission route of influenza?

A

Influenza is (more) contagious (than bacterial respiratory tract infections). Transmission occurs by inhalation of droplets.

19
Q

What is the pathophysiology of influenza?

A

Influenza infects the upper respiratory tract, damaging mucous-secreting epithelial cells, leading to fluid leakage and a runny nose. It can progress to pneumonia and bacterial infections as complications.

There are 3 types of infections
1. An (uncomplicated) upper respiratory infection (rhinotracheitis),
2. (viral) pneumonia
3. respiratory viral infection followed by a bacterial infection.

20
Q

What are the clinical manifestations of influenza?

A

Symptoms include fever, chills, muscle aches, headache, sore throat, non-productive cough, and nasal discharge.

In severe cases, pneumonia may develop.

21
Q

Who is at higher risk for severe influenza?

A

Elderly, young children, and people with weakened immune systems are at higher risk for complications like pneumonia.

22
Q

What is a pulmonary embolism, and what causes it?

A

A pulmonary embolism is a blockage in the pulmonary arteries, usually caused by a blood clot (embolus) originating in the legs (deep vein thrombosis). It can also be caused by fat, air, or amniotic fluid emboli.

23
Q

What are the 3 main contributing factors in the formation of thrombosis in the venous system (also described in the Virchow’s triad)?

A
  1. alterations in blood flow (venous stasis)
  2. factors in the vessel wall (vascular injury)
  3. factors affecting the properties of the blood (hypercoagulability)
24
Q

What are the risk factors of pulmonary embolism?

A
  • Immobility
  • Orthopedic surgery at or below the hip
  • Cancer (due to secretion of pro-coagulants)
  • Pregnancy
  • Obesity
  • Long-haul flight
25
Q

What is the pathophysiology of pulmonary embolism?

A

The embolus blocks blood flow to the lungs, leading to decreased oxygenation and increased pressure in the pulmonary arteries, causing right-sided heart failure. It also reduces gas exchange in the lungs.

26
Q

Describe the hemodynamic (pressures in the heart, blood pressure, heart rate) and respiratory (pO2, pCO2, respiratory rate) consequences of an acute severe pulmonary embolism

A
  • Increase in the right ventricular pressure and drop in peripheral blood pressure (hypotension) and rise in heart rate (tachycardia)
  • Reduction in pO2 (hypoxemia), no change or increase in pCO2 (hypocapnia), increase in respiratory rate (tachypnea)
27
Q

What are the clinical manifestations of pulmonary embolism?

A

Symptoms include shortness of breath, pleuritic chest pain, tachypnea, hypoxia, and in severe cases, hypotension, hemoptysis, and collapse.

28
Q

Through which heart valves does a venous embolism travel before it causes a pulmonary embolism (state the respective heart valves in the correct order)?

A

1.) Tricuspid valve -> 2.) Pulmonary valve

29
Q

What is the treament for pulmonary embolism?

A

Treatment is mainly based on the dissolving /removal of the thrombus
- Anticoagulation
- Thrombolysis
- Surgery

30
Q

What are restrictive pulmonary diseases, and what causes them?

A

Restrictive lung diseases, such as pulmonary fibrosis and interstitial lung diseases, are characterized by stiff lungs that cannot fully expand. Causes include autoimmune diseases, occupational exposures, and drug-induced lung disease.

31
Q

What are the clinical manifestations of restrictive pulmonary diseases?

A

Symptoms include dyspnea, tachypnea, and eventual cyanosis. Unlike obstructive diseases, FEV1/FVC may increase as lung compliance decreases.

32
Q

What are the most common bacterial causes of pneumonia?

A

The most common cause is Streptococcus pneumoniae. Other bacterial pathogens include Haemophilus influenzae, Staphylococcus aureus, Klebsiella pneumoniae, and Mycoplasma pneumoniae.

33
Q

What are the clinical manifestations of bacterial pneumonia?

A

Symptoms include high fever, productive cough (often with rust-colored sputum), pleuritic chest pain, and difficulty breathing. Severe cases may lead to bacteremia and sepsis.

34
Q

What is Respiratory Distress Syndrome (RDS) and its cause?

A

RDS is a condition in premature infants due to insufficient surfactant production, leading to alveolar collapse, impaired gas exchange, and hypoxia. It is common in infants born before 28 weeks of gestation.

35
Q

What are the clinical manifestations of RDS?

A

Symptoms include central cyanosis, difficulty breathing, retractions, and grunting sounds during expiration. Oxygen therapy and incubators are used to manage the condition.

36
Q

What causes cystic fibrosis?

A

Cystic fibrosis is an autosomal recessive disorder. CF is caused by mutations in the CFTR gene, and its protein product cause excessive thick mucus that obstructs lungs and the pancreas.

It leads to an impaired Cl- transport due to the mutated gene, and affects the NaCl reabsorption

37
Q

What are the main pathophysiological effects of CF?

A

Lungs: Airway obstruction, chronic infections, and inflammation, leading to bronchiectasis and respiratory failure.
Pancreas: Obstruction of ducts, causing malabsorption and steatorrhea.
Other organs: Liver damage, intestinal obstruction, and male infertility.

38
Q

What are the clinical manifestations of cystic fibrosis?

A

Respiratory: Chronic cough, wheezing, recurrent lung infections. Pulmonary inflammation
Pancreatic function is often abnormal, Gastrointestinal: Failure to thrive, malabsorption, abdominal distension. Which can lead to diarrhea,
Sweat glands: Saltier sweat, electrolyte imbalances.
Reproductive: Male infertility, female fertility issues.

39
Q

Which agegroup is primarily affected by Cystic fibrosis

A

Cystic fibrosis primarily affects children and young adults.