This occupational exposure is the most common cause of pleural plaques.
What is asbestos?
Fibroblasts lay down collagen and extracellular matrix, forming dense fibrous plaques.
This murmur at the left lower sternal border suggests dysfunction related to pulmonary hypertension.
What is a systolic murmur of tricuspid regurgitation?
This law states that flow is proportional to the pressure difference over resistance.
What is Ohm's Law?
This type of gas exchange abnormality improves significantly with 100% oxygen because some alveoli are still ventilated and perfused, just not well.
What is V/Q mismatch?
In V/Q mismatch (like pulmonary edema), certain lung areas have low ventilation relative to perfusion (low V/Q), leading to hypoxemia. However, these alveoli still receive some oxygen, so increasing FiO₂ raises PAO₂ and improves oxygen diffusion into the blood. This makes V/Q mismatch highly responsive to supplemental oxygen.
This lung function pattern is seen in asbestosis.
What is restrictive?
Asbestosis increases the risk for these two malignancies.
What are bronchogenic carcinoma and mesothelioma?
The risk of bronchogenic carcinoma is greater than that of mesothelioma
This heart sound becomes louder with elevated pulmonary artery pressure.
What is P2?
According to Poiseuille’s Law, resistance is most affected by this vessel property.
What is radius?
Patients with this cause of hypoxemia, such as in interstitial lung disease or COPD, usually improve with oxygen due to preserved alveolar-capillary gradient.
What is diffusion limitation?
Fibrosis or alveolar wall thickening (as in ILD) slows O₂ diffusion, especially during exertion. Increasing PAO₂ via supplemental oxygen steepens the diffusion gradient, helping oxygen cross the thickened barrier more effectively. CO₂ diffusion is typically preserved due to higher solubility.
This PFT value is reduced due to impaired gas exchange.
What is DLCO?
This histologic finding is pathognomonic for asbestos exposure.
What are ferruginous bodies (asbestos bodies)?
Asbestos (ferruginous bodies) are golden-brown fusiform rods resembling dumbbells, found in alveolar sputum sample, visualized using Prussian blue stain, often obtained by bronchoalveolar lavage. They are created by macrophages phagocytosing asbestos.
This physical exam finding indicates right-sided heart failure.
What is jugular venous distension (JVD) and bilateral lower extremity edema?
If the radius is halved, the resistance increases by this factor.
What is 16 times?
This type of hypoxemia shows little to no improvement with 100% oxygen because blood bypasses the ventilated alveoli entirely.
What is a right-to-left shunt?
In a shunt, blood flows through the lungs (or heart) without contacting oxygenated alveoli. Even if FiO₂ is 100%, this blood remains deoxygenated and mixes with arterial blood, lowering total PaO₂. This is the only mechanism of hypoxemia that does not correct with oxygen therapy.
Examples: ARDS, lobar pneumonia, AVMs, congenital defects like VSD/ASD with reversal
This physical finding, heard at the lung bases, is classic for pulmonary fibrosis.
What are fine inspiratory crackles?
List the classic imaging findings for Silicosis, Asbestosis, Coal miner’s lung (must get at least 1 each)
What are Eggshell calcifications of lymph nodes (Silicosis), Calcified pleural plaques (Asbestosis), and Small, rounded, nodular opacities (coal miners lungs)?
Inhaled silica particles (highly toxic) are phagocytosed by macrophages which causes macrophage apoptosis and chronic inflammation. This leads to fibrosis and granuloma formation in lung and lymphatic tissue. Over time, dystrophic calcification occurs, beginning at the periphery of lymph nodes → creating a thin “eggshell” pattern.
Inhaled asbestos fibers can migrate to the pleural surfaces via lymphatics. Fibers trigger chronic inflammation in the pleura, leading to fibrosis and eventually calcification. These plaques do not impair lung function, but they are a marker of asbestos exposure.
Inhaled coal dust (carbon) is phagocytosed by macrophages. This triggers chronic inflammation and macrophage accumulation, especially around bronchioles. Leading to focal fibrosis and nodule formation, classically in the upper lobes due to dust deposition patterns.
This law explains how pressure in the pulmonary circulation increases when vascular resistance rises, such as in interstitial lung disease, placing more afterload on the right side of the heart.
What is Ohm's Law?
ΔP=Q×R; pressure = flow × resistance
Q = (pulmonary artery pressure - left atrial pressure) / pulmonary vascular resistance
This physiologic condition in interstitial lung disease increases pulmonary vascular resistance.
What is hypoxic vasoconstriction?
This pathophysiologic mechanism causes hypoxemia by delivering air to alveoli that receive no blood flow, and thus, even 100% oxygen may not help.
What is dead space ventilation?
Dead space is ventilation without perfusion - air enters alveoli that are not receiving blood, so no gas exchange occurs. This contributes to wasted ventilation and inefficiency. Supplemental oxygen doesn’t help unless perfusion is restored, as in early PE.
This echocardiographic finding indicates increased pressure in the pulmonary vasculature.
What is right ventricular hypertrophy or elevated pulmonary artery pressure?
List the common environmental toxin exposures (5) relevant to the USMLE and their Major Complications. There are 5.
What are:
Silica - TB risk and fibrosis.
Coal dust - chronic bronchitis -> massive pulmonary fibrosis.
Asbestos - lung cancer.
Bird waste particles - Hypersensitivity pneumonitis (chronic inflammation, fibrosis).
Smoke - (COPD, asthma, lung cancer)
This law shows that a slight decrease in pulmonary vessel radius, due to fibrosis or vasoconstriction, leads to a significant increase in resistance, raising pulmonary artery pressure and straining the right ventricle
What is Poiseuille’s Law?
R= 8ηL / πr^4
Pulmonary Hypertension Mechanism:
This variable in Poiseuille’s Law would increase if pulmonary vessels become fibrotic.
What is length (L)?
Fibrosis stretches and makes it longer
This is the physiological reason why patients with hypoventilation (e.g., opioid overdose or neuromuscular disease) respond well to oxygen therapy despite having elevated CO₂.
What is decreased alveolar ventilation with intact diffusion and perfusion?
In hypoventilation, alveolar oxygen drops (low PAO₂) because not enough fresh air is reaching the alveoli. But once oxygen is delivered, diffusion and perfusion are normal, so oxygen easily crosses into blood. CO₂ rises due to low ventilation, but O₂ therapy quickly improves PaO₂.
Draw a detailed flowchart for the pathophysiology of asbestosis from inhalation and finish with its complications.
What are Inhaled asbestos fibers reach the alveoli → taken up by macrophages, which can't digest them → Macrophages release inflammatory cytokines and ROS → which recruit fibroblasts -> deposit collagen and extracellular matrix activation and collagen buildup → results in interstitial fibrosis, especially in the lower lungs → fibrosis causes stiff lungs, thickens alveolar walls, and decreases lung compliance → leads to impaired gas exchange and hypoxemia → pulmonary vasoconstriction and eventually pulmonary hypertension → chronic pressure overload causes right heart strain (cor pulmonale). Some fibers also reach the pleura, forming plaques or causing mesothelioma.