Lung Disease of Vascular Origin Flashcards
(17 cards)
Pulmonary Embolism Cause Key Features Clinical Consequences
Deep vein thrombus Blockage of pulmonary arteries Sudden death or infarction
Pulmonary Hypertension Cause Key Features Clinical Consequences
Primary or secondary Increased pulmonary pressures Cor pulmonale
Pulmonary Congestion/Oedema Cause Key Features Clinical Consequences
Hemodynamic or microvascular Fluid accumulation in alveoli Pink sputum, hypoxia
ARDS Cause Key Features Clinical Consequences
Infection, sepsis, toxins Diffuse alveolar damage, hyaline membranes Severe hypoxemia, high mortality
COVID-19 Lung Injury Cause Key Features Clinical Consequences
Viral infection + cytokine storm Epithelial & endothelial injury, thrombosis ARDS, multi-organ failure
Explain the pathogenesis and potential outcomes of pulmonary embolism.
✅ Model Answer:
* Pathogenesis:
o Typically results from thrombotic emboli originating in the deep veins of the legs.
o Embolus lodges in a pulmonary artery, blocking blood flow.
o Despite the blockage, lungs are double supplied (pulmonary and bronchial arteries), offering some protection.
* Outcomes:
o Large embolus (e.g., saddle embolus): sudden death from obstructed pulmonary circulation.
o Small emboli:
If pre-existing lung disease exists, may lead to pulmonary infarction.
Without disease, may be asymptomatic or cause minor infarcts.
o Chronic embolism: fibrosis and remodeling of pulmonary vessels.
Define pulmonary hypertension and differentiate between its primary and secondary causes.
✅ Model Answer:
* Definition:
o Pulmonary hypertension is when pulmonary artery pressure exceeds 25% of systemic aortic pressure (normal is ~12.5%).
* Primary Pulmonary Hypertension:
o Idiopathic, rare.
o Likely due to autoimmune endothelial or smooth muscle dysfunction.
* Secondary Pulmonary Hypertension:
o Chronic Obstructive Airways Disease (COAD) or restrictive lung diseases (loss of vascular area).
o Heart diseases, like mitral stenosis.
o Recurrent pulmonary emboli.
o Pulmonary fibrosis, reducing vascular compliance.
* Progression & Outcome:
o Leads to cor pulmonale (right-sided heart failure) if untreated.
List and explain the haemodynamic causes of pulmonary congestion and oedema.
✅ Model Answer:
* Increased hydrostatic pressure (fluid overload into alveoli):
o Left-sided heart failure.
o Mitral valve stenosis.
o Pulmonary vein obstruction.
o Volume overload.
* Decreased oncotic pressure (reduced fluid reabsorption):
o Hypoalbuminemia.
o Nephrotic syndrome.
* Pulmonary consequences:
o Fluid accumulation predominantly in basal lung regions.
o Engorged vessels, microhaemorrhages.
o Haemosiderin-laden macrophages (“heart failure cells”) seen.
o Pink frothy sputum typical clinically.
Describe how microvascular injury leads to Acute Respiratory Distress Syndrome (ARDS).
✅ Model Answer:
* Microvascular Injury:
o Inflammatory destruction of the alveolar-capillary barrier.
o Increased vascular permeability → exudation of protein-rich fluid.
* Histology:
o Formation of hyaline membranes composed of fibrin and necrotic debris.
o Type II pneumocyte proliferation as a repair attempt.
o If unresolved, progresses to fibrosis.
* Causes:
o Sepsis.
o Viral infections (e.g., COVID-19).
o Inhalation injuries (toxins, near drowning).
o Oxygen toxicity.
* Clinical Result:
o Bilateral lung consolidation.
o Hypoxemia, stiff lungs (↓ compliance), and V/Q mismatch.
Explain the unique features of COVID-19-related lung injury (COVID-ALI/CALI) compared to classical ARDS.
✅ Model Answer:
* Initiation:
o SARS-CoV-2 first infects alveolar epithelial cells.
o Subsequently triggers an innate immune response.
* Progression:
o In severe disease, endothelial injury becomes prominent.
o Leads to cytokine storm → systemic inflammation.
* Consequences:
o Pulmonary oedema.
o Pneumonia.
o Multi-organ failure (due to systemic endothelial dysfunction).
* Unique Features:
o Extensive microthrombosis (COVID thrombopathy).
o High levels of extracellular vesicles (EVs), contributing to vascular injury and coagulation abnormalities.
* Berlin Definition of ARDS Applied:
o Acute onset.
o Hypoxemia.
o Bilateral lung opacities.
o Decreased lung compliance.
What are extracellular vesicles (EVs) and what is their role in ARDS?
✅ Model Answer:
* Definition:
o EVs are membrane-bound particles released by cells, including exosomes, microvesicles, and apoptotic bodies.
* Role in ARDS:
o EVs act as mediators of intercellular communication.
o They can amplify inflammatory responses.
o In COVID-19, EVs from platelets, neutrophils, and monocytes contribute to endothelial injury and thrombosis (“COVID thrombopathy”).
* Clinical Implication:
o EVs are a potential target for therapeutic intervention in ARDS and severe COVID-19.
Explain the interaction between the lung’s vascular system and the air spaces, and its importance for gas exchange.
✅ Model Answer:
* Integration:
o The alveolar spaces (air-filled) and the capillary networks (blood-filled) are closely juxtaposed at the alveolar-capillary membrane.
o This thin barrier allows for rapid and efficient gas exchange — oxygen moves into blood, and carbon dioxide moves into alveoli.
* Importance:
o Disruption of either side (vascular or airspace) severely impairs gas exchange.
o In vascular injuries (e.g., ARDS), increased permeability leads to proteinaceous edema in alveoli, impairing oxygen transfer.
o In airspace diseases (e.g., pneumonia), exudate fills alveoli, again impairing diffusion.
* Clinical Examples:
o ARDS shows both alveolar flooding and endothelial injury.
o COVID-19 demonstrates profound interaction disturbance, leading to ventilation-perfusion (V/Q) mismatch and hypoxemia.
Describe the unique features of the lung’s vascular supply and their clinical significance.
✅ Model Answer:
* Double Blood Supply:
o Pulmonary arteries: Deliver deoxygenated blood from the right heart to alveoli for oxygenation.
o Bronchial arteries: Arise from the systemic circulation (aorta), providing oxygenated blood to lung tissues themselves.
* Significance:
o Protective redundancy: Even if a pulmonary artery is blocked (e.g., pulmonary embolism), bronchial arteries may prevent full infarction — unless pre-existing lung disease compromises bronchial circulation.
* Clinical Implications:
o In large embolism, sudden death occurs if the embolus prevents enough blood from reaching the lungs.
o In chronic lung disease (fibrosis, emphysema), loss of vascular reserve increases infarct risk even with small emboli.
Outline how the lung vasculature and the heart interact functionally, and what happens when this relationship is disrupted.
✅ Model Answer:
* Normal Relationship:
o The right ventricle pumps blood into the low-pressure pulmonary circulation (~12.5% of systemic pressure).
o The lung acts as a low-resistance vascular bed, allowing smooth blood flow with minimal right ventricular strain.
* Pathological Disruptions:
o Pulmonary Hypertension: Increases pulmonary vascular resistance.
Right ventricle faces higher afterload → Right ventricular hypertrophy → Cor pulmonale (right heart failure).
o Pulmonary Embolism: Acute rise in pulmonary vascular resistance → sudden right heart strain → potentially fatal.
* Summary:
o Healthy lungs = right heart’s best friend.
o Diseased lungs = right heart’s burden.
Pulmonary Embolism Effect on Lungs Effect on Heart
Blocks blood flow, causes infarcts or sudden ventilation-perfusion mismatch Acute right heart strain; possible acute cor pulmonale
Pulmonary Hypertension Effect on Lungs Effect on Heart
Chronic vascular remodeling; reduced perfusion; V/Q mismatch Chronic right ventricular hypertrophy → right-sided heart failure
ARDS (e.g., COVID-19-related) Effect on Lungs Effect on Heart
Severe capillary leak; alveolar flooding; impaired oxygenation; decreased lung compliance Indirect stress due to hypoxia and increased pulmonary vascular resistance
