anwser,s 11

Tuesday, April 11, 2023

Anwser,sDr :ANAS SAHLE

1. Chest xr cases.2. Chest clinical case.

3. Chest ct cases.4. MRCP exam.

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chest xr casesDr :anas sahle

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CXR53a

CXR53bDiagnosis is: Superior Vena Caval Syndrome

Small Cell Cancer Lung

Mass in the region of superior vena cava

CXR54

Sign name is:"Potato" Nodes

"Potato" Nodes Sarcoidosis

Bilateral symmetrical hilar nodesClear space between hilar nodes and heartAP window nodesParatracheal nodesRLL alveolar lung infiltrate

CXR55

Diagnosis is: Silicosis

Bilateral upper lobe diseaseCalcified mediastinal nodes

Egg shell calcificationStable over years

CXR56

Diagnosis is:Progressive Massive Fibrosis

Bilateral upper lobe diseaseCalcified mediastinal nodes in CT

Calcification in the mass like densities in CT

CXR57

Sign name is: 1-2-3 sign1-2-3 sign or Garland triad

is the classic pattern of lymphadenopathy seen in sarcoidosis with •bilateral hilar lymphadenopathy and •right paratracheal nodal enlargement.

http://radiopaedia.org/articles/sarcoidosis-1

http://radiopaedia.org/articles/sarcoidosis-1

http://radiopaedia.org/articles/bilateral-hilar-lymphadenopathy




CXR58a

CXR58b

Diagnosis is: Thyroid Mass

CXR59a

CXR59b

Diagnosis is: Malig Thymoma

CXR60a

CXR60b

Diagnosis is: Fat Pad

chest clinical casesProgressive Dyspnea in an Appalachian Coal MinerSubmitted by

W. Alex Wade MDPulmonary FellowSection of Pulmonary and Critical Care Medicine , Department of MedicineWest Virginia University School of MedicineMorgantown, WVJack L. Kinder, MDChairWest Virginia State Occupational Pneumoconiosis BoardCharleston, WVEdward. L. Petsonk MDProfessor of MedicineSection of Pulmonary and Critical Care Medicine, Department of MedicineWest Virginia University School of MedicineMorgantown, WV


History Physical Exam

• A 32-year-old male initially presented in 1991 complaining of dyspnea on exertion and a non-productive morning cough for two years.

• He was a lifelong nonsmoker and had worked for 15 years as an underground coal miner, transporting coal in a rubber-tired vehicle.

• Five years later, he sought reevaluation due to worsening dyspnea and productive cough.

• His lungs were clear and the cardiovascular examination was normal.


Lab

• The chest radiograph in 1991 was normal (Figure 1.1)

• Five years after initial presentation, blood gases at rest on room air showed mild hypoxia (PaO2 73 mm Hg).

• The radiograph then demonstrated multiple bilateral small opacities, as shown in Figure 1.2.


cxr

(Figure 1.1)

Figure 1.2 .


Question 1• What is the most likely diagnosis for this

patient?• A. Silicosis • B. Asbestosis • C. Lung cancer • D. Coal Workers’ Pneumoconiosis (CWP) • E. Chronic Obstructive Pulmonary Disease

(COPD)


DISCUSSION• CWP is an interstitial lung disease that occurs due to the inflammatory reaction to inhaled coal mine dusts. • When lung clearance mechanisms are overwhelmed, numerous black coal macules develop in the lung parenchyma

adjacent to the respiratory bronchioles (1). • As CWP progresses, the macules enlarge and develop into fibrotic coal nodules with associated emphysema. • Radiographically, the pathologic changes of CWP manifest as small rounded opacities less than 10 mm in diameter.

Historically, the opacities generally have generally appeared after at least 15-20 years of exposure, although there are recent reports of more rapidly progressive disease (2).

• The International Labor Office (ILO) has devised a classification system to describe and quantify the changes of pneumoconiosis on chest radiograph (3).

• The ILO classification scores the profusion (number of small pneumoconiotic opacities per unit area of lung) from 0 to 3. • Early (category 1) CWP may produce few or no symptoms. • However, dust exposure can also lead to chronic bronchitis (even in the absence of smoking tobacco), which results in

cough, sputum production and wheeze. As CWP progresses, dyspnea becomes severe, and affected patients can develop cor pulmonale, respiratory failure and death (4, 5).

• Although silicosis can be a more rapidly developing disease which occurs in underground coal miners, the specific mining job of this patient does not involve activities (e.g., drilling or roof bolting) that typically generate exposure to airborne silica.

• However, mining of thin coal seams can create silica exposures in general mining activities, as performed by this worker. • Asbestosis typically causes interstitial lung changes that are more pronounced in the lower lung zones, and have a more

reticular rather than nodular appearance. • Although both COPD and CWP can cause changes of obstruction and hyperinflation on a chest radiograph, the small

nodules seen on this patient’s chest radiograph would not be typical for COPD. • Lung cancer can cause multiple pulmonary nodules, but the time course and clinical picture in this patient are more

consistent with CWP.


History Continued:• The patient ceased employment in 1997 due to a back

injury, after having worked 21 years in the mines. • He was seen with worsening dyspnea in 2000, at the

age of 41. • He denies any other complaints, such as fevers, chills

or sputum production. • Pulmonary function tests (PFTs) showed an FEV1 of

58% predicted and an FVC of 74% predicted. • A chest radiograph was taken at that time (Figure 1.3).


(Figure 1.3 .)

(Figure 1.3 .)


Question 2• What is the most likely diagnosis to explain

this patient’s new findings?• A. Multiple Arterio-Venous (AV) Malformations • B. Primary Adenocarcinoma of the Lung • C. Active M. tuberculosis infection • D. Progressive Massive Fibrosis (PMF) • E. Metastatic Cancer from an unknown

primary source


DISCUSSION• Both coal and silica dust exposures trigger inflammation of the airways and the interstitium, and pneumoconiosis

can continue to progress for years after termination of all dust exposure (1). • This is one reason why primary prevention through dust control is critical. • Inflammatory nodules can coalesce to form PMF (also called complicated pneumoconiosis), which is recognized on

the chest radiograph as one or more lesions 10mm in diameter or greater. • After PMF develops, the fibrosis and associated emphysema often progress even without further dust exposure, as

was the case with this patient. • Adjacent lung parenchyma is pulled towards the lesions, which most typically occur in the upper lung. • The large airways are distorted as lung volume is lost and lung function may show obstructive and/or restrictive

impairments.• An enlarging PMF lesion can be difficult to distinguish from malignancy, particularly if unilateral. • Silica dust exposure is known to increase the risk of primary lung cancer Also, PMF lesions are frequently PET-

positive, which can add to the diagnostic confusion (6). • However, the bilateral masses on this nonsmoking patient’s chest radiograph are typical of PMF, and his clinical

course makes primary or secondary lung cancer unlikely. • Exposure to silica dusts increases the risk of developing TB and nontuberculous mycobacterial infections (7). • This is likely due to a dysfunction in cellular immunity. • Miners who have inhaled excessive respirable silica and are subsequently exposed to mycobacteria are more likely

to develop active disease. • Although mycobacterial disease should be considered in this patient, there is no cavitation and the radiographic

appearance is more typical of CWP than TB.• Arteriovenous malformations can present as large masses, typically in the lower lung zones. • They are usually accompanied by feeder vessels that can sometimes be identified on a chest radiograph. • Bilateral upper lung zone lesions, as seen in this case, are not suggestive of AV malformations.


History Continued:• Over the next four years, the patient’s

dyspnea progressively worsened, and he died in 2004 at the age of 45 from respiratory failure secondary to coal workers’ pneumoconiosis with PMF.


Question 3• Which of the following measures is/are likely to be

effective in preventing development of PMF among US coal miners?

• A. Decreasing the prevalence of smoking and the number of cigarettes smoked

• B. Decrease the number of infections with M. tuberculosis among coal miners

• C. Decreasing the exposure to inhaled coal mine dust • D. Decrease the work intensity required by miners


DISCUSSION• Advanced CWP, defined as ILO category 2 or greater, is caused by excessive

exposure to respirable coal and/or silica dusts, and greatly increases the risk of development of PMF and important physiologic impairment (8).

• As part of the Federal Coal Mine Health and Safety Act of 1969, coal mine operators are required to observe a permissible exposure limit (PEL) for respirable dust of 2.0 mg/m3 (9) .

• The goal of this dust limit is not only to decrease the overall incidence of CWP, but also to decrease the incidence of advanced CWP to nearly zero, and thus prevent miners from developing PMF.

• However, a small proportion of miners have been observed to develop PMF with an underlying profusion category of 1 or 0 and thus PMF was not completely prevented (10).

• A number of studies have shown that PMF development is not accelerated by tobacco smoking, nor is it dependent on Mycobacterial infection.

• Most operating coal mines are highly mechanized, which generally has reduced work intensity during mine work, but also results in high rates of dust generation.

chest ct cases-10Dr :anas sahle

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HRCT-1

HRCT-1

• 1. Is the disease unilateral or bilateral?• 1. Disease is bilateral. • 2. What is the anatomic location of the linear

structures that reach the pleura?• 2. The structures are in part interlobular septa, but

may also include some intralobular fibrosis. – Note that these lines extend over more than one

lobule. They are referred to as parenchymal or septal bands or long scars.

HRCT-1

• Find 2 examples of architectural distortion--tenting of the pleura--one in each lung.

• Find 2 adjacent centrilobular nodules in the left lung.

• Find 2 examples of subpleural lines, one in each lung.

HRCT-1

HRCT-2

HRCT-2

• Find a group of 3 centrilobular nodules in the right lung.

HRCT-2

Parenchymal Bands and Subpleural Lines

• This lung shows many long, thin lines. The long, non-branching ones correspond to parenchymal bands. Most of the lines form polygons, indicating a patchy fibrosis of interlobular septa. In addition, there are subpleural lines that parallel the pleura, probably representing, in part, interlobular septa bordering partially collapsed lobules. A few centrilobular nodules can be seen.

• Find and follow a parenchymal band.• Find a subpleural line.• Find two centrilobular nodules.

Parenchymal Bands and Subpleural Lines

Histologic Findings

• This view of an entire section shows several long, thin, parenchymal bands, as well as thickening of the bronchovascular interstitium.

• More detail is shown below. • Trichrome stain (collagen is green)

Parenchymal Band

• At higher magnification of the above section, deposition of collagen in a long, thin, parenchymal band can be seen.

• The alveolar parenchyma is mostly normal. Centrilobular interstitium is also fibrotic (see below).

• Find and follow a long, fibrotic parenchymal band that spans several lobules.

Parenchymal Band

Centrilobular Nodules

• At higher magnification of the section above, two regions of centrilobular fibrosis can be seen.

• Find the two regions of centrilobular fibrosis.• In time, this fibrosis and that in the interlobular

septum will radiate in an irregular fashion into the lobule to cause lobular architectural distortion with centrilobular to interlobular septal bridging and lobular shrinkage.

Lobular Remodeling

• This entire section (detailed below) shows more advanced interstitial fibrosis with bridging from interlobular septa to bronchovascular interstitium and distortion of the lobule.

• Note that the more central lung parenchyma is spared.

• (Trichrome stain for connective tissue)

Lobular Remodeling, continued

• This H&E-stained section shows the result of prolonged subpleural, interlobular septal, and centrilobular fibrosis. The fibrosis has distorted the lobular architecture and linked centrilobular and interlobular septal structures. Inflammatory cells are sparse.

• Find an example of a bronchiolovascular bundle. • Note how it is connected to a thickened interlobular septum

to its left.• Find a portion of an interlobular septum with a vein cut

longitudinally. • Note areas of subpleural fibrosis. • The radiating fibrosis in the right lower quadrant (outline it)

represents linked lobular and interlobular septal fibrosis.

Lobular Remodeling, continued

• Here, peribronchiolar fibrosis, which represents a centrilobular nodule on HRCT, is present. Nearby peribronchiolar air spaces have been obliterated, but more distal ones are intact.

• Find the bronchiolar lumen. • Find the pulmonary artery.• Find 2 collections of brown pigment in air

spaces. • What does the pigment represent?• Collections of hemosiderin pigment.

Architectural Distortion

• In this lung, note the marked thickening of the visceral pleura.

• Find where the pleura has folded into the lung parenchyma.

• Find the curved deviation of the interlobar fissure caused by the scar.

• Find the mild deviation of 2 large vessels toward the pleural infolding.

• In HRCT image 1 above, the architectural distortion in the anterior right lung is an example of this pleural infolding.

• Note that there is no honeycombing (see below) in this lung.

Architectural Distortion

More Advanced Disease

• This is an example of a lung with more advanced disease.• Note pleural thickening at the base. • The normally smooth, lateral pleural margin shows

architectural distortion, which is caused by irregular, subpleural fibrosis (causing subpleural nodules on HRCT).

• Find a small subpleural scar (subpleural nodule)• Compare the abnormal parenchyma in the upper lateral,

subpleural region to the more normal parenchyma medially. What is the abnormality?

• Honeycombing, consisting of small cystic spaces with thick walls (more on honeycombing later).

More Advanced Disease

What is it

What is it

• The cause of the changes noted above is shown here. What is it?

• This is an asbestos body, which is a thin asbestos fiber that has been coated with an iron-protein coat within a macrophage.

• The asbestos body is often found in areas of hemosiderin pigment.

Differential diagnosis

• Differential diagnosis of parenchymal bands with architectural distortion on HRCT:–Asbestos-related lung disease, –Atelectasis.– Tuberculosis.– Sarcoidosis.–diffuse pulmonary fibrosis.

Differential diagnosis

• Differential diagnosis of pleural infolding (rounded atelectasis):–Asbestos-related pleuropulmonary disease.– chronic renal failure.–post coronary artery bypass graft surgery.–healed pneumonias.–healed infarcts.

Histologic differential diagnosis:

• Histologic differential diagnosis:• The presence of asbestos bodies and a history

of asbestos exposure distinguish this entity from other fibrosing diseases such as: –usual interstitial pneumonia.– and fibrosis caused by a drug.–organic and other inorganic dusts.– radiation, or collagen vascular diseases.

Diagnosis

Asbestosis

Diagnostic features of asbestosis on HRCT:

• Diagnostic features of asbestosis on HRCT: In a person with a history of asbestos exposure, the diagnosis of asbestosis can be based on the HRCT if three or more of the following abnormalities are present :

• Interlobular septal thickening and centrilobular nodules.

• Parenchymal bands. • Architectural distortion of the lobule. • Honeycombing. • Subpleural lines.

04/11/202371

MRCP EXAMRespiratory


Q1 • Regarding respiratory surfactant:• A- It is produced by alveolar type 2 epithelial cells. • B- It is composed primarily of phospolipids such as

dipalmitoyilelecithin. • C- It reduces lung compliance by changing surface

tension. • D- Production may be enhanced by the administration

of antenatal steroids to mother.• E- At 24 weeks gestation, production is 75% of that at

term.


A1 • Regarding respiratory surfactant:• A- It is produced by alveolar type 2 epithelial cells. (True) • B- It is composed primarily of phospolipids such as

dipalmitoyilelecithin. (True)• C- It reduces lung compliance by changing surface

tension. (False) • D- Production may be enhanced by the administration of

antenatal steroids to mother. (True)• E- At 24 weeks gestation, production is 75% of that at

term. (False)


Q2 • The following syndromes are associated with

respiratory tract abnormalities:• A- CHARGE Syndrome• B- Ciliary dyskinesia• C- Hurler's Syndrome• D- Tay Sachs Disease• E- Cri-du-Chat Syndrome


A2 • The following syndromes are associated with

respiratory tract abnormalities:• A- CHARGE Syndrome(True)• B- Ciliary dyskinesia(True)• C- Hurler's Syndrome(False)• D- Tay Sachs Disease(False)• E- Cri-du-Chat Syndrome(True)


Q3 • Characteristic features of idiopathic diffuse

interstitial fibrosis of the lung (HAMMAN-RICH) include:

• A- Cyanosis on exercise .• B- Inspiratory crackles on auscultation .• C- Hypercapnia .• D- Decreased FEV1/FVC ratio .• E- Decreased gas transfer factor


A3 • Characteristic features of idiopathic diffuse

interstitial fibrosis of the lung (HAMMAN-RICH) include:

• A- Cyanosis on exercise . (True)• B- Inspiratory crackles on auscultation . (True)• C- Hypercapnia . (False)• D- Decreased FEV1/FVC ratio . (False)• E- Decreased gas transfer factor(True)


Q4 • The following conditions are associated with

sleep apnoea:• A- Anorexia nervosa .• B- Large uninflammed tonsils .• C- Guillain-Barre Syndrome .• D- Ondine's Curse .• E- Diencephalic Syndrome


A4 • The following conditions are associated with

sleep apnoea:• A- Anorexia nervosa . (False)• B- Large uninflammed tonsils . (True)• C- Guillain-Barre Syndrome . (True)• D- Ondine's Curse . (True)• E- Diencephalic Syndrome(False)


Q5 • A 7 year old girl presents with acute cough and

wheeze, and is given nebulised salbutamol. The following are indications for admission to hospital:

• A- A peak flow rate of 80% of that predicted for height.

• B- Continuing cough. • C- Respiratory rate of 40/min.• D- Saturation of 90% in air. • E- She looks tired.


A5 • A 7 year old girl presents with acute cough and

wheeze, and is given nebulised salbutamol. The following are indications for admission to hospital:

• A- A peak flow rate of 80% of that predicted for height. (False)

• B- Continuing cough. (False) • C- Respiratory rate of 40/min. (False)• D- Saturation of 90% in air. (True) • E- She looks tired. (True)


Q6 • Chest signs that are reliable diagnostically

are found in:• A- A neonate with meconium aspiration. • B- A 3 month old child following aspiration

pneumonia. • C- A 4 month old child with bronchiolitis. • D- A 6 month old with lobar pneumonia. • E- A 2 year old with inhaled foreign body.


A6 • Chest signs that are reliable diagnostically are

found in:• A- A neonate with meconium aspiration. (False) • B- A 3 month old child following aspiration

pneumonia. (False) • C- A 4 month old child with bronchiolitis. (True) • D- A 6 month old with lobar pneumonia. (False) • E- A 2 year old with inhaled foreign body. (False)


Q7 • In the normal adolescent lung:• A- There is an intrapleural pressure of 30cmH2O

(3kPa) at the end of normal expiration.• B- There is a resting pulmonary blood flow of

10L/min. • C- The V:Q ratio is greater in apical than basal

segments of the lung when upright and at rest.• D- The majority of airway resistance is from large

airways. • E- Cartilage is present in all respiratory bronchioles.


A7 • In the normal adolescent lung:• A- There is an intrapleural pressure of 30cmH2O (3kPa) at

the end of normal expiration. (False)• B- There is a resting pulmonary blood flow of 10L/min.

(False)• C- The V:Q ratio is greater in apical than basal segments

of the lung when upright and at rest. (True)• D- The majority of airway resistance is from large airways.

(False)• E- Cartilage is present in all respiratory bronchioles. (False)

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