Paraseptal Emphysema

1. Challenge

54M smoker

Paraseptal Emphysema Axial CT

Part A — Questions

Q1. Major finding(s) visible in the image (select all that apply):

1 Centrilobular emphysema

2 Blebs

3 Panlobular Emphysema

4 Paraseptal emphysema

Additional Information

2. Findings

Paraseptal Emphysema
Subtle Centrilobular Emphysema RUL

Paraseptal Emphysema
Axial CT of the upper lobes demonstrates cystic air spaces representing expanded destroyed peripheral subpleural alveoli. These changes are characteristically located in a subpleural distribution, seen anteriorly along the costal pleura and centrally abutting the mediastinal pleura (white arrowheads).
This pattern is diagnostic of paraseptal emphysema, which involves the distal part of the acinus. While it can be an isolated finding, it is frequently seen in conjunction with centrilobular emphysema in smokers. The most significant clinical complication of paraseptal emphysema is spontaneous pneumothorax, which occurs when these subpleural blebs or bullae rupture into the pleural space
Paraseptal emphysema is characterized by subpleural and perifissural cystic changes and is a primary cause of spontaneous pneumothorax, particularly in young adults.
Ashley Davidoff MD – TheCommonVein.com (b35196-01bL)

Subtle Centrilobular Emphysema

Mixed Paraseptal and Centrilobular EmphysemaAxial CT images demonstrate two distinct patterns of emphysema. There are multiple subpleural, thin-walled air-containing spaces arranged along the lung periphery (white arrowheads, c), consistent with paraseptal emphysema. More centrally, there are numerous well-demarcated, rounded lucencies without visible walls, creating a “Swiss cheese” appearance (white ring, c); the centrilobular artery is characteristically absent within these spaces, defining them as centrilobular emphysema.Centrilobular emphysema, the most common type, is strongly associated with smoking and begins with destruction of the respiratory bronchioles in the center of the pulmonary lobule, with a predilection for the upper lobes. Paraseptal emphysema involves the distal acinus and is notable for its subpleural location and association with spontaneous pneumothorax. The coexistence of these two types is a frequent finding in patients with a significant smoking history.The coexistence of peripheral, subpleural bullae (paraseptal) and central, “wall-less” lucencies (centrilobular) is a classic presentation of mixed emphysema, most commonly seen in smokers.
Ashley Davidoff MD – TheCommonVein.com (b35196-01cL

Part A — Answers

Q1. Major finding(s)
1 ✔	Centrilobular emphysema
2 ❌	Blebs
3 ❌	Panlobular Emphysema
4 ✔	Paraseptal emphysema

Part B — Findings

Comparison of Cystic Air Spaces in the Lung

Title	Details
Paraseptal Emphysema	• Definition: Emphysema characterized by cystic changes at the periphery of the acinus, typically in a subpleural or perifissural location. • Comment: It is a major risk factor for spontaneous pneumothorax due to the rupture of subpleural blebs or bullae. • Citation: Patel, Radiographics 2006
Centrilobular Emphysema	• Definition: The most common type of emphysema, characterized by destruction of the respiratory bronchioles in the center of the pulmonary acinus. • Comment: Strongly associated with smoking, it is typically most severe in the upper lung zones. • Citation: Stern, AJR 1991
Bulla	• Definition: A gas-containing space in the lung measuring more than 1 cm in diameter, with a wall thickness of less than 1 mm. • Comment: Bullae result from the destruction of lung parenchyma and can compress adjacent healthy lung tissue. • Citation: Hansell, Radiology 2008
Bleb	• Definition: A small (typically less than 1 cm) gas-containing space located within the visceral pleura. • Comment: Blebs are distinct from bullae (which are intraparenchymal); their rupture is a classic cause of primary spontaneous pneumothorax. • Citation: Hansell, Radiology 2008
Panlobular Emphysema	• Definition: Emphysema characterized by uniform destruction of the entire pulmonary acinus, from the respiratory bronchiole to the alveoli. • Comment: Classically associated with alpha-1 antitrypsin deficiency, it typically has a lower lobe predominance. • Citation: Patel, Radiographics 2006

Feature	Bleb	Paraseptal Emphysema	Bulla	Lung Cyst	Pneumatocele
Location	Intrapleural (within the visceral pleura)	Intraparenchymal (within lung tissue), subpleural	Intraparenchymal, subpleural	Intraparenchymal, can be anywhere	Intraparenchymal, can be anywhere
Pathology	Air dissects between the layers of the pleura	Destruction of alveolar walls at the periphery of the acinus	Coalescence and expansion of emphysemous spaces	A true epithelial-lined cavity, congenital or acquired	Transient, from a check-valve mechanism after infection or trauma
Wall	Very thin wall formed by the pleura	Often appears “wall-less” or has a very thin wall	Thin wall (< 1 mm) of compressed lung and pleura	Thin (< 2 mm), well-defined, regular wall	Thin, regular wall
Size	Typically < 1 cm	Typically < 1 cm	Defined as being > 1 cm	Variable	Variable, can be large
Permanence	Permanent	Permanent (progressive)	Permanent (progressive)	Permanent	Transient

3. Diagnosis

Definition	Paraseptal emphysema, also known as distal acinar emphysema, is a morphological subtype of pulmonary emphysema. It is pathologically defined by the abnormal and permanent enlargement of airspaces in the most distal part of the acinus, adjacent to the pleura and interlobular septa. This enlargement is accompanied by the destruction of alveolar walls.
Cause	The most common cause is cigarette smoking. Other contributing factors include exposure to environmental pollutants, such as industrial chemicals and dust particles. Certain genetic predispositions like Marfan syndrome are also a factor. Marijuana smoking has been specifically linked to a higher prevalence of paraseptal emphysema compared to tobacco-only smokers, possibly due to barotrauma from inhalation techniques like the Valsalva maneuver. It can also be idiopathic, especially in young adults who present with spontaneous pneumothorax.
Pathophysiology	Chronic inflammation, triggered by irritants like smoke, leads to the recruitment of inflammatory cells (macrophages, neutrophils, T lymphocytes) in the distal airways. These cells release proteases, such as neutrophil elastase, which break down elastin and other components of the alveolar walls. This destruction preferentially occurs in the periphery of the secondary pulmonary lobule. Mechanical forces and higher strain at the pleural interface during ventilation may also contribute to the peripheral distribution. The process results in loss of elastic recoil and alveolar support structures, leading to permanent airspace enlargement.
Structural Result	The primary structural changes include dilated distal acini and the formation of subpleural and paraseptal cystic spaces or lucencies. These can coalesce to form larger air-filled sacs known as bullae (>1 cm in diameter). The condition predominantly affects the subpleural regions, often along the dorsal surface of the upper lobes. While paraseptal emphysema is not typically associated with fibrosis, some mild fibrosis may be present.
Functional Impact	Isolated or mild paraseptal emphysema is often asymptomatic and may not be associated with significant airflow obstruction. However, when more extensive, it can lead to a decrease in the diffusing capacity for carbon monoxide (DLCO) and a reduced FEV1/FVC ratio. The loss of elastic recoil and gas-trapping can cause lung hyperinflation, increasing total lung capacity and residual volume. Clinically, this can manifest as dyspnea, especially on exertion, and reduced exercise tolerance. A major complication is spontaneous pneumothorax due to the rupture of subpleural bullae.
Imaging	High-resolution computed tomography (HRCT) is the definitive imaging modality. It demonstrates subpleural and paraseptal lucencies or cystic spaces, often with visible walls, characteristically located adjacent to the pleura or interlobular septa. These findings are most common in the upper lobes. The formation of bullae appears as well-defined, hypoattenuated airspaces greater than 1 cm. Chest radiography has low sensitivity for mild disease but may show subpleural lucencies or evidence of hyperinflation in more advanced cases.
Labs	Laboratory studies are not typically used to diagnose paraseptal emphysema directly but are part of the overall assessment of a patient with suspected COPD. Arterial blood gas (ABG) analysis may show hypoxemia, and in advanced disease, hypercapnia with compensatory metabolic alkalosis. A complete blood count might reveal polycythemia secondary to chronic hypoxemia. Pulmonary Function Tests (PFTs) are essential. In isolated paraseptal emphysema, PFTs may be normal, but in more severe cases or when coexisting with other emphysema types, they show an obstructive pattern with a reduced FEV1/FVC ratio, increased lung volumes, and a reduced DLCO. Testing for Alpha-1 antitrypsin deficiency may be indicated, especially in younger patients or those with a family history.
Treatment	There is no cure for emphysema, so treatment focuses on slowing disease progression and managing symptoms. Smoking cessation is the most critical intervention. Pharmacologic management includes bronchodilators, inhaled corticosteroids, and antibiotics for infectious exacerbations. For patients with severe symptoms, supportive therapies such as oxygen therapy, pulmonary rehabilitation, and nutritional support are beneficial. In cases of large bullae causing significant compression or recurrent pneumothorax, surgical interventions like bullectomy or bronchoscopic lung volume reduction may be considered.
Prognosis	The prognosis is variable and depends on the extent of the disease, the presence of other types of emphysema, and patient factors like smoking status. Mild, isolated paraseptal emphysema may not significantly impact life expectancy. However, it is a progressive condition, and a higher burden of paraseptal emphysema is associated with increased dyspnea, more frequent exacerbations, reduced lung function, and decreased exercise capacity. It is a significant risk factor for spontaneous pneumothorax and has been associated with an increased risk for lung cancer. Quitting smoking can slow the rate of lung function decline.

4. Medical History and Culture

Etymology	The term emphysema originates from the Ancient Greek word ἐμφύσημα (emphýsēma), meaning “inflation” or “swelling”. This is derived from emphysan, “to blow in” or “inflate,” which combines en (“in”) and physa (“wind, blast”). The term was used in the 1660s to describe a distention with air. René Laennec later applied it to lungs that did not collapse upon autopsy because they were full of air. The prefix para- comes from Greek, meaning “near,” and septal is from the Latin septum, referring to a dividing wall. Thus, “paraseptal” literally means “adjacent to a septum,” accurately describing the condition’s location next to the interlobular septa and pleura.
AKA / Terminology	Paraseptal emphysema is also known as Distal Acinar Emphysema because it affects the most distal part of the pulmonary acinus. It is sometimes referred to as Subpleural Emphysema due to its characteristic location beneath the pleura.
Historical Notes	The understanding of emphysema has evolved over centuries. Early descriptions of what was likely emphysema date back to 1679 by Théophile Bonet, who noted “voluminous lungs,” and in 1769 by Giovanni Battista Morgagni, who described lungs that were “turgid particularly from air”. The first illustrations of emphysematous lungs were made by Frederik Ruysch in 1721. A significant advance came in the 18th century with Leopold Auenbrugger, an Austrian physician who in 1761 introduced the technique of percussion for diagnosing chest diseases. He developed this method by tapping on wine casks in his father’s inn to check the fluid levels, applying the same principle to the human thorax. However, his work was largely ignored for decades. It was René Laennec, the French physician who invented the stethoscope in 1816, who solidified the clinical understanding of emphysema. In his 1821 treatise, he correlated the sounds he heard via auscultation with post-mortem findings, providing the first detailed descriptions of emphysema, bronchiectasis, and pneumothorax. He was the first to define emphysema as tissue damage in the peripheral air passages. The formal definitions for different types of emphysema, including paraseptal, were established much later, with key criteria being agreed upon at the CIBA Guest Symposium in 1959.
Cultural or Practice Insights	The history of emphysema is inextricably linked with the history of tobacco smoking. While early physicians like Laennec identified environmental factors as causes, the overwhelming association with smoking became clear in the mid-20th century. In 1950, British researchers demonstrated a clear link between smoking and lung cancer, with evidence for its role in what is now termed COPD mounting in the following decades. Dr. Charles Fletcher’s work in 1976 was pivotal in scientifically linking smoking to the progression of emphysema and chronic bronchitis, establishing the basis for modern smoking cessation campaigns. The cultural perception of smoking has shifted dramatically, from being a common, even advertised, practice in the mid-20th century to being recognized as the leading cause of preventable death. This has led to widespread public health campaigns and a shift in medical practice, where smoking cessation is now the cornerstone of managing emphysema. The rise in marijuana use has also brought new insights, with studies suggesting a link between cannabis smoking and a higher prevalence of paraseptal emphysema, possibly due to barotrauma from inhalation techniques.
Notable Figures or Contributions	Leopold Auenbrugger (1722–1809): An Austrian physician who invented percussion as a diagnostic technique to assess the chest, drawing an analogy from tapping wine barrels. His book, Inventum Novum (1761), laid the groundwork for physical examination of the thorax. René Laennec (1781–1826): A French physician and the “father of chest medicine,” he invented the stethoscope in 1816. His work, De l’Auscultation Médiate, provided the first descriptions of numerous pulmonary conditions, including emphysema, based on correlating clinical sounds with autopsy findings. He died from tuberculosis, a disease he extensively studied with his own invention. Giovanni Battista Morgagni (1682–1771): An Italian anatomist who, in 1769, provided one of the earliest pathological descriptions of emphysematous lungs as being “turgid… from air”. Charles Fletcher (1911–1995): A British physician whose longitudinal studies on London transport workers, published in “The Natural History of Chronic Bronchitis and Emphysema” (1976), definitively established the causal link between smoking and the progressive decline in lung function seen in COPD.
Quotes and/or Teaching Lines	“Paraseptal emphysema: think peripheral, think subpleural, think pneumothorax.” “The word emphysema is derived from Ancient Greek ἐμφύσημα ‘inflation, swelling’… from ἐμφυσάω emphysao ‘to blow in, to inflate’.” “A new discovery that enables the physician from the percussion of the human thorax to detect the diseases hidden within the chest.” – The English title of Leopold Auenbrugger’s 1761 book, Inventum Novum. “With self-management I have a better understanding of my condition and am able to cope with it in a more positive way.” – A quote from a patient with COPD, highlighting the shift towards patient empowerment.

6. MCQs

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Page 5 — Emphysema (Interactive MCQs)

Part A — Questions

Question	Choices
Q1. Which protease, released by neutrophils in response to chronic inflammation from smoking, is most directly implicated in the breakdown of elastin and subsequent alveolar wall destruction in emphysema?	1 Caspase-3 2 Alpha-1 antitrypsin 3 Neutrophil elastase 4 Matrix metalloproteinase-9 (MMP-9)
Q2. Paraseptal emphysema is morphologically defined by the permanent enlargement of airspaces in which specific portion of the acinus?	1 The respiratory bronchiole 2 The entire acinus (panacinar) 3 The central part of the acinus (centriacinar) 4 The distal part of the acinus
Q3. A young, otherwise healthy adult with extensive isolated paraseptal emphysema is at a significantly increased risk for which of the following acute complications?	1 Spontaneous pneumothorax 2 Cor pulmonale 3 Acute respiratory distress syndrome (ARDS) 4 Pulmonary embolism
Q4. In a patient with severe alpha-1 antitrypsin (AAT) deficiency, which therapy has been proven to slow the rate of emphysema progression as measured by CT lung density?	1 Inhaled corticosteroids 2 Intravenous AAT augmentation therapy 3 Long-term oxygen therapy 4 Pulmonary rehabilitation
Q5. When using quantitative CT (QCT) to assess emphysema, the “density mask” method quantifies the disease by measuring:	1 The fractal dimension of the airways 2 The average lung density in Hounsfield Units (HU) 3 The percentage of lung voxels below a specific HU threshold (e.g., -950 HU) 4 The degree of mosaic attenuation on expiratory scans
Q6. A 35-year-old non-smoking woman presents with a third spontaneous pneumothorax. HRCT reveals numerous, uniform, thin-walled, round cysts scattered diffusely through both lungs, with normal intervening parenchyma. Which diagnosis is most likely?	1 Centrilobular emphysema 2 Langerhans cell histiocytosis (LCH) 3 Lymphangioleiomyomatosis (LAM) 4 Birt-Hogg-Dubé syndrome
Q7. An HRCT of a smoker shows a 4 cm air-filled space with a paper-thin wall in the lung apex. It is located within the lung parenchyma and surrounded by other emphysematous changes. According to the Fleischner Society Glossary, what is the most precise term for this finding?	1 Bulla 2 Cyst 3 Pneumatocele 4 Bleb

Part B — Answers & Explanations

Question	Answer	Explanation
Q1. Which protease, released by neutrophils in response to chronic inflammation from smoking, is most directly implicated in the breakdown of elastin and subsequent alveolar wall destruction in emphysema?	3 — Neutrophil elastase	Key discriminator: protease–antiprotease imbalance with elastase-driven elastolysis underlies smoking-related emphysema. Citation: Shapiro, N Engl J Med 2003
	1 — Caspase-3	Apoptosis mediator; not the primary elastin-degrading enzyme in emphysema.
	2 — Alpha-1 antitrypsin	Protease inhibitor (protective); deficiency predisposes to panacinar emphysema.
	4 — MMP-9	Contributes to matrix turnover; elastase is the principal elastolytic driver.
Q2. Paraseptal emphysema is morphologically defined by the permanent enlargement of airspaces in which specific portion of the acinus?	4 — The distal part of the acinus	Key discriminator: The disease affects the distal acinus (alveolar ducts/sacs). These acini are located at the periphery of the secondary pulmonary lobule, abutting the pleura and interlobular septa. While it’s seen at the lobular periphery, the primary pathological change is within the acinus itself. Citation: Hansell, Radiology 2008
	1 — The respiratory bronchiole	Defines centrilobular emphysema.
	2 — The entire acinus (panacinar)	Definition of panacinar emphysema.
	3 — Central part of the acinus	Centrilobular subtype, common in smokers.
Q3. A young, otherwise healthy adult with extensive isolated paraseptal emphysema is at a significantly increased risk for which acute complication?	1 — Spontaneous pneumothorax	Key discriminator: peripheral subpleural bullae predispose to rupture ⇒ pneumothorax in young adults. Citation: Bintcliffe, Thorax 2015
	2 — Cor pulmonale	Late COPD complication; not typical of isolated paraseptal disease.
	3 — ARDS	Diffuse inflammatory lung injury; not a direct consequence of paraseptal emphysema.
	4 — Pulmonary embolism	Thromboembolic; unrelated to emphysematous airspace changes.
Q4. In a patient with severe alpha-1 antitrypsin (AAT) deficiency, which therapy has been proven to slow the rate of emphysema progression as measured by CT lung density?	2 — Intravenous AAT augmentation therapy	Key discriminator: This is the only therapy that corrects the underlying protease-antiprotease imbalance in AAT deficiency. Randomized controlled trials (e.g., RAPID) have shown it significantly reduces the loss of lung tissue as measured by quantitative CT densitometry. [3, 5] Citation: Chapman KR, Lancet 2015
	1 — Inhaled corticosteroids	Used to reduce inflammation and exacerbations in some COPD patients, but does not address the core AAT deficiency or slow parenchymal destruction.
	3 — Long-term oxygen therapy	A supportive treatment that improves survival in patients with severe chronic hypoxemia, but it does not alter the progression of the underlying emphysema.
	4 — Pulmonary rehabilitation	Improves exercise capacity, symptoms, and quality of life, but does not slow the destruction of lung parenchyma.
Q5. When using quantitative CT (QCT) to assess emphysema, the “density mask” method quantifies the disease by measuring:	3 — The percentage of lung voxels below a specific HU threshold (e.g., -950 HU)	Key discriminator: The density mask technique works by identifying all voxels in the lung with an attenuation value lower than a set threshold (commonly -950 HU for inspiratory scans) and expressing this as a percentage of total lung voxels. This percentage represents areas of parenchymal destruction. [4, 25] Citation: Gevenois, Am J Respir Crit Care Med 1996
	1 — The fractal dimension of the airways	This is a research technique used to assess the complexity of airway branching, not to quantify emphysema.
	2 — The average lung density in Hounsfield Units (HU)	While mean lung density decreases in emphysema, it is a less sensitive measure than the density mask, as it averages areas of emphysema with areas of normal or even fibrotic lung.
	4 — The degree of mosaic attenuation on expiratory scans	This is the method used to quantify air trapping, an indicator of small airways disease, not the parenchymal destruction of emphysema itself.
Q6. A 35-year-old non-smoking woman presents with a third spontaneous pneumothorax. HRCT reveals numerous, uniform, thin-walled, round cysts scattered diffusely through both lungs, with normal intervening parenchyma. Which diagnosis is most likely?	3 — Lymphangioleiomyomatosis (LAM)	Key discriminator: The combination of a young female patient, recurrent pneumothoraces, and diffuse, uniform, thin-walled round cysts is the classic presentation for LAM. [2, 7, 11] Citation: McCormack FX, Am J Respir Crit Care Med 2016
	1 — Centrilobular emphysema	Incorrect patient demographic (non-smoker) and imaging pattern (emphysema is airspace destruction, not well-defined cysts, and is centrilobular/upper-lobe predominant).
	2 — Langerhans cell histiocytosis (LCH)	Typically affects smokers and features bizarrely shaped, often confluent cysts and nodules, with a characteristic upper and mid-lung predominance, sparing the costophrenic angles.
	3 — Birt-Hogg-Dubé syndrome	Another cause of cystic lung disease and pneumothorax, but the cysts are classically irregular, lentiform (oval), and have a lower-lobe and subpleural predominance.
Q7. An HRCT of a smoker shows a 4 cm air-filled space with a paper-thin wall in the lung apex. It is located within the lung parenchyma and surrounded by other emphysematous changes. According to the Fleischner Society Glossary, what is the most precise term for this finding?	1 — Bulla	Key discriminator: A bulla is specifically defined as an intraparenchymal, air-filled space >1 cm with a wall <1 mm thick, resulting from emphysematous destruction. This description fits perfectly. [14, 16] Citation: Hansell (Fleischner Glossary), Radiology 2008
	2 — Cyst	“Cyst” is a general term for any circumscribed air- or fluid-filled space with a well-defined wall. While a bulla is a type of cyst, “bulla” is the more precise term given the context of emphysema. [13]
	3 — Pneumatocele	This term describes a transient, thin-walled, air-filled space that typically develops following pneumonia (e.g., Staphylococcal) or trauma, not as part of chronic emphysema.
	4 — Bleb	A bleb is a collection of air within the layers of the visceral pleura, not within the lung parenchyma itself. It is by definition an extra-parenchymal finding.

Additional Information
see below

7. Memory Page

Mnemonic for the Pathogenesis of Paraseptal EmphysemaThis artistic montage illustrates the key factors in the development of paraseptal emphysema. The sequence begins with a devilish figure representing smoking, whose smoke rises to the lung apices and periphery. This leads release of proteases and elastases. The elastases cause loss of elasticity depicted as a wrinkled man. The proteases cause alveolar destruction and in the case of paraseptal emphysema – destriuction of the peripherally placed subpleural alveoli. The figure pulling on the lung represents an additional mechanical stress an the peripheral alveoli.
A magnified CT image of the consequnces of these chemical and mechanical stresses is shown as a magnified CT image at the bottom
Paraseptal emphysema is defined when these subpleural pathological airspaces measure <1 cm and are bounded by interlobular septa.When they get >1cms they are defined as bulla.
Ashley Davidoff Art, AI-assisted — Memory Image – TheCommonVein.com (b35196-MAD.03.8s)

Artistic Rendering of Paraseptal Emphysema
This diagram depicts the secondary lobule with emphysematous changes along the pleural surface, illustrating the destruction of distal alveolar structures adjacent to the interlobular septa.
Editorial Comment The forces of the pleura during inspiration and expiration translated on to the alveoli below the pleura and in the context of loss of elasticity of the subpleural alveoli they became stretched and create the air spaces of paraseptal emphysema
Ashley Davidoff, MD TheCommonVein.com (lungs-0782)

From Smoke to Cyst – The Unravelling Edge

A devil’s bargain, breath by breath,
The smoke ascends to court its death.
It seeks the edges, climbs the height,
And settles at the lung’s far light.

Two agents follow in its wake,
The enzymes that will stretch and break.
First Elastase, a wicked hand,
That loosens every elastic band,
(The wrinkled man, a truth foretold,
The tissues sag, no longer bold).

Then Protease joins the foul attack,
And tears the walls, with no way back.
The outer sacs, they cannot stand,
And crumble at the foe’s command.
A final force, the pull and tug
Of every breath, a constant drug,
That stretches out the weakened space,
And leaves a void upon its face.

So see the art, the story told,
From devil’s pact to weakened fold.
A tiny cyst, a subpleural tear,
The paraseptal damage clear.
And if it grows beyond one’s ken,
A bulla it is called by men.

The Common Vein

VG Med WF lungs upper lobes bilateral paraseptal emphysema DDx paraseptal emphysema CT 60M smoker

Paraseptal Emphysema

1. Challenge

54M smoker

Part A — Questions

2. Findings

Paraseptal Emphysema
Subtle Centrilobular Emphysema RUL

Subtle Centrilobular Emphysema

Part A — Answers

Part B — Findings

Comparison of Cystic Air Spaces in the Lung

3. Diagnosis

4. Medical History and Culture

6. MCQs

Page 5 — Emphysema (Interactive MCQs)

Part A — Questions

Part B — Answers & Explanations

7. Memory Page

1. Challenge

2. Findings

2. Findings

3. Diagnosis

4. Medical History and Culture

6. MCQs

7. Memory Page

TCV

Paraseptal Emphysema

1. Challenge

54M smoker

Part A — Questions

Related Links

2. Findings

Paraseptal EmphysemaSubtle Centrilobular Emphysema RUL

Subtle Centrilobular Emphysema

Part A — Answers

Part B — Findings

Comparison of Cystic Air Spaces in the Lung

Related Links

3. Diagnosis

Related Links

4. Medical History and Culture

Related Links

6. MCQs

Page 5 — Emphysema (Interactive MCQs)

Part A — Questions

Part B — Answers & Explanations

Related Links

7. Memory Page

Related Links

1. Challenge

2. Findings

2. Findings

3. Diagnosis

4. Medical History and Culture

6. MCQs

7. Memory Page

TCV

Paraseptal Emphysema
Subtle Centrilobular Emphysema RUL