RD respiratory formatted Flashcards
- Dyspnea on exertion, weight loss, clubbing. CT chest shows nodular septal thickening, asymmetric. What is the most likely diagnosis? (also recalled as beading along bronchovascular bundles, lymphadenopathy & pleural effusions)
a. Sarcoid
b. Lymphangitic carcinomatosis
c. Extrinsic allergic alveolitis
d. Idiopathic pulmonary fibrosis
b. Lymphangitic carcinomatosis = classic findings
- Dyspnea on exertion, inspiratory crackles. CT chest shows bilateral ground glass and centrilobular nodules. What is the most likely diagnosis
a. Pulmonary oedema
b. Hypersensitivity pneumonitis
c. Pneumocystis pneumonia
b. Hypersensitivity pneumonitis T upper>lower zone, centrilobular nodules, patchy GGO, headcheese sign
- Dyspnea on exertion, inspiratory crackles. CT chest shows bilateral ground glass and centrilobular nodules. What is the most likely diagnosis
a. Pulmonary oedema T possible, esp. if perihilar & LZ predominance. Usually no abnormal physical findings when purely interstitial oedema.
b. Hypersensitivity pneumonitis T upper>lower zone, centrilobular nodules, patchy GGO, headcheese sign
c. Pneumocystis pneumonia F centrilobular nodules less common
- Which of the following is not a recognised feature of primary pulmonary amyloidosis:
a. Nodules in tracheobronchial tree
b. Bronchopleural fistula
c. Peripheral parenchymal nodules
d. Adenopathy
b. Bronchopleural fistula
Pulmonary amyloidosis
• Nodules in tracheobronchial tree
• Parenchymal nodules – peripheral/subpleural
• Adenopathy[Dahnert]
[SK – added a, c & d – only one option recalled]
- Lung disease, which does not cavitate.
a. Small cell cancer
b. Sarcoidosis
c. Wegeners granulomatosis
d. Squamous cell carcinoma
e. Tuberculosis
f. Coccidoidomycosis
a. Small cell cancer F does not normally cavitate (“distinctly rare” – StatDx) – usually central, rapid growth, early mets
4. Lung disease, which does not cavitate.
a. Small cell cancer F does not normally cavitate (“distinctly rare” – StatDx) – usually central, rapid growth, early mets
b. Sarcoidosis T cavitation of occasional nodule (atypical though)
c. Wegeners granulomatosis T cavitation occurs commonly
d. Squamous cell carcinoma T most common lung Ca to cavitate; cavitation occurs commonly in the peripheral form (although SCC more frequently)
e. Tuberculosis T cavitation is a hallmark of secondary TB
f. Coccidoidomycosis T, esp. with more chronic forms
- Most likely location of a pulmonary sequestration
a. Right upper lobe
b. Right middle lobe
c. Left upper lobe
d. Right lower lobe
e. Left lower lobe
e. Left lower lobe
- Typical appearances of PCP (which is true?)
a. Apical location (superior lobe involvement)
b. 25% associated with pleural effusion
c. Usually have associated hilar adenopathy
d. Associated with CMV pneumonia
e. A gallium scan will only become positive once the radiographic findings are clearly evident
d. Associated with CMV pneumonia T CMV has similar predisposition (cell-mediated immunodeficiency); Most common associated infection with PCP; also DDx for PCP; Bilateral diffuse ground-glass opacities most frequent finding
6. Typical appearances of PCP
a. Apical location (superior lobe involvement) ?T typically perihilar progressing to diffuse, often with peripheral sparing. However upper lobe distribution may occur, esp. with aerosolized pentamidine prophylaxis. Cysts, when they occur, are usually upper lobe distribution.
b. 25% associated with pleural effusion F pleural effusion very unusual (< 5%), suggests alternate Dx
c. Usually have associated hilar adenopathy F hilar adenopathy uncommon (10%), more common with other fungal or bacterial infections
d. Associated with CMV pneumonia T CMV has similar predisposition (cell-mediated immunodeficiency); Most common associated infection with PCP; also DDx for PCP; Bilateral diffuse ground-glass opacities most frequent finding
e. A gallium scan will only become positive once the radiographic findings are clearly evident F bilateral & diffuse Ga-67 uptake without mediastinal involvement prior to radiographic changes (Dahnert)
- PCP Radiographic findings: McLoud p125/130-1, B&H p476o Initially bilateral, perihilar or diffuse, symmetric interstitial pattern – may have a finely granular, reticular/reticulonodular or ground-glass appearanceo Untreated progresses over 3-5 days to a homogeneous, diffuse alveolar consolidationo Hilar adenopathy & pleural effusion very unusual (< 5%), suggests alternate Dxo Typically diffuse perihilar with peripheral sparing – less commonly upper lobe distribution, may be assoc/ w/ aerosolised pentamidine prophylaxis
- HRCT findings: may be positive when CXR is normalo Symmetric/bilateral with a central, perihilar or upper lobe predominance*
o Patchy or diffuse GGO*
• May result in a mosaic pattern (normal lung b/w focal GGOs)
• May progress to consolidation
o Cystic changes
• Thin or thick walls, may coalesce to form multiseptated cysts (upper lobe predominance)
• Present in 20-35% of AIDS patients, uncommon in non-AIDS patients
• May cause PTX
o Reticulation & interlobular septal thickening (resolving disease) – may produce a crazy-paving pattern (superimposed on GGO)
o Less common findings incl. focal consolidation (10% of AIDS patients), bronchiectasis or bronchiolectasis, centrilobular or diffuse nodules, pleural effusion & lymphadenopathy
- Which is most correct regarding the typical features of ARDS (LAS recall – ‘false regarding ARDS’)
a. 10% have residual lung changes
b. Changes are typically anterior and non-dependent (LAS – ‘residual CXR’ are in anterior non-dependent portions of lungs)
c. CXR changes often precede clinical respiratory failure
d. Diffuse thromboembolism is a recognized complication
most true A
most false C
- Which is most correct regarding the typical features of ARDS (LAS recall – ‘false regarding ARDS’) (StatDx)
a. 10% have residual lung changes T – mild chronic fibrosis & low lung volumes in 10% (80% return to normal)
b. Changes are typically anterior and non-dependent (LAS – ‘residual CXR’ are in anterior non-dependent portions of lungs) F for acute setting, T for chronic setting. Acute = Dependent intense pulmonary opacification and more nondependent ground-glass opacities (GGO) (like oil and water in a glass). Chronic = Mild reticular pattern in anterior lung (85%), residual GGO (60%), lobular hyperinflation (50%) &/or emphysema (33%).
c. CXR changes often precede clinical respiratory failure F radiographs typically are normal for the first 12-24 hours after the acute injury, despite the presence of dyspnoea. This latent period is suggestive of ARDS
.d. Diffuse thromboembolism is a recognized complication T? = presumably have ↑ risk of thromboembolism (? Can’t find a reference)
- Patient with ascites and splenomegaly (LAS – chronic liver disease). Enhancing (vivid) round structure above the right hilum.
a. Enlarged pulmonary vein
b. Enlarged pulmonary artery
c. Azygos vein
d. Bronchogenic carcinoma
c. Azygos vein
Could represent an enlarged azygos vein in RHF, in the setting of CLD/portal HTN.“Azygos vein enlargement can be detected in congestive heart failure, portal hypertension, inferior vena cava thrombosis, right atrial mural thrombosis, a pulmonary embolism, congenital azygos continuation to the inferior vena cava, and the arteriovenous fistula.” Clinical Imaging July 1999.
If enlarged “hilum”, rather than “above hilum” would think of hepatopulmonary syndrome, a triad of:
• Chronic liver disease (usually cirrhosis)
• Increased alveolar-arterial oxygen gradient on room air (> 15 mmHg)
• Intrapulmonary vascular dilatation Also think of TB (increased risk in chronic liver disease)
40 yo man. ill defined centrilobular nodules. Non-productive cough. Thickened septal.
a. HP
b. lymphangitis
c. RA
d. asbestosis
A = T = hypersensitivity = centrilobular fuzzy nodules; interstitial pattern late (fibrosis)
40 yo man. ill defined centrilobular nodules. Non-productive cough. Thickened septal.
a. HP
b. lymphangitis
c. RA
d. asbestosis
A = T = hypersensitivity = centrilobular fuzzy nodules; interstitial pattern late (fibrosis)
B = F = lymphangitis = perilymphatic distribution (which incl. centrilobular, but typically perihilar; also not usually ill-defined); fissural thickening is present
C = RA = would be atypical
D = Asbestosis = no centrilobular nodules
smoker. 7mm nodule on CT. fisher follow up. what is it?
depends on what type of nodule and risk factor (low, high - only for solid lesions)
solid single
- low : f/u 6- 12mth. Then consider 18-24 mth.
- high : f/u 6- 12 mth. Then 18- 24 mth
Partial solid- 3-6 mth.
Then every 2 years.
if solid > 6 mm is suspicious.
Ground glass - f/u 6 - 12 mth. then every 1 year. If bigger consider resection
which is classically associated with expansion of a lobe?
BAC is a cause of lobar consolidation with bulging fissures.
Also think of Klebsiella pneumonia.
Patient had pneumonia. Treated with antibiotics and then develops thin walled cysts with fluid level. most likely
a. pneumatoceles
b. caveatting pneumonia
c. abscess
A = pneumatocele = produced by virulent organisms (esp. S. aureus) – thin walled cysts filled with air or partially with fluid; thin & smooth-walled
A = pneumatocele = produced by virulent organisms (esp. S. aureus) – thin walled cysts filled with air or partially with fluid; thin & smooth-walled
B = cavitating pneumonia = thick & irregular walls, often with air-fluid level
C = abscess = thick-walled with shaggy inner lining
Drug related lung change. which is false
a. amiodarone and interstitial infiltrates
b. cyclosporine and mass
c. methotrexate and pneumatoceles
d. pneytoin and pleural effusions.
e. an antibiotic and hypersensitivity pneumonia or something like that
C = methotrexate ?F = NSIP is the most common pattern of methotrexate-induced lung disease; also common is hypersensitivity reaction; usually cause diffuse reticulonodular opacities with lower zone predominance; usually subacute allergic response
A = amiodarone T = 18% get lung toxicity, esp. chronic interstitial pneumonitis; upper zones. *LW - pneumonitis and fibrosis.
B = cyclosporine T = drug-induced lymphoproliferative disorder which may appear as solitary mass, multiple lung nodules & hilar nodes
C = methotrexate and pneumatoceles ?F = NSIP is the most common pattern of methotrexate-induced lung disease; also common is hypersensitivity reaction; usually cause diffuse reticulonodular opacities with lower zone predominance; usually subacute allergic response. *LW - hypersensitivity pneumonitis
D = phenytoin = vasculitis, drug-induced SLE; Pleural effusion is a rare complication of phenytoin use that usually occurs early in the course [Chest 2009].
E = hypersensitivity reaction T: cromolyn sodium, erythromycin, nitrofurantoin, isoniazid, penicillin, sulfonamides, bleomycin, methotrexate, procarbazine, penicillamine; features incl. Interstitial and/or alveolar opacities, patchy peripheral airspace opacities, basilar reticulonodular interstitial opacities (opacities may be fleeting)
Patient who you’ve done a CT guided chest biopsy on. small apical pneumothorax post procedure and 4 hrs post has not increased. Next appropriate management:
a. repeat x-ray in 24 hours
b. immediate chest tube
c. repeat car in 4 hrs
d. oxygen
ANS = A ? repeat CXR in 24 hours
Kandarpa V&IR p482
• Small, asymptomatic PTX, stable
o No Tx needed
• Treat PTX if: SOB, acute CP, size > 30% or continues to increase in size
o Aspiration by 18G angiocath; Place biopsy side down position; Serial CXR
o Small (11 Fr) thoracic catheter into pleural space. Can remove several hours later if air leak has ceasedJMIRO 2006In much of the published work with regard to needle lung biopsy carried out as an outpatient procedure, it is commonly cited that patients are discharged when there is no pneumothorax detected after biopsy on a chest radiograph obtained 1–3 h after biopsy. Some researchers recommend a shorter observation period of 30 min from lung biopsy to discharge of patients without pneumothorax. However, in cases complicated by pneumothorax, management thereafter has not been fixed and varies widely. Also, criteria for hospitalization after pneumothorax vary.When pneumothorax detected on CT immediately after lung biopsy is too small to provide a space for insertion of a needle for aspiration or if a detected pneumothorax completely or almost completely disappears after manual aspiration, the required observation period would be short, that is, approximately within 2 days. In such cases, the likelihood of need for a chest tube is slight and early discharge would be a strong possibility. However, in cases when the size of the pneumothorax does not change or increases despite manual aspiration, the requirement of both chest tube placement and hospitalization would be highly possible, as is suggested by the fact that all eight patients belonging to category C of the present study required chest tube placement. In addition, when the pneumothorax tends to decrease after manual aspiration but remains, chest tube placement may be required. Thus, these patients must be carefully observed until confirmation of disappearance of pneumothorax, as suggested by the three patients belonging to category B who required chest tube placement. Also supporting this suggestion is that although 23 category B cases did not require a chest tube, the period until disappearance of pneumothorax was significantly longer than category A patients or those not necessitating aspiration.
- Regarding bronchogenic cysts, which is the LEAST correct?
a. Communicate with the bronchial tree
b. Occur in the mediastinum more than the lung
c. Are part of a spectrum of foregut cysts
d. When have a thick contrast enhancing wall indicate infection
e. High T2 signal
a. Communicate with the bronchial tree F Do not communicate with bronchial tree & thus do not contain air – however, may become infected, when they may gain communication with the tracheobronchial tree. Note – CCAMs do communicate with bronchial tree, while BPS does not communicate.
b. Occur in the mediastinum more than the lung T 65-90% in1.
Regarding bronchogenic cysts, which is the LEAST correct?
a. Communicate with the bronchial tree F Do not communicate with bronchial tree & thus do not contain air – however, may become infected, when they may gain communication with the tracheobronchial tree. Note – CCAMs do communicate with bronchial tree, while BPS does not communicate.
b. Occur in the mediastinum more than the lung T 65-90% in middle mediastinum; less commonly in lung parenchyma esp. lower lobes
c. Are part of a spectrum of foregut cysts T (= foregut duplication cyst)
d. When have a thick contrast enhancing wall indicate infection T wall may enhance with surrounding consolidation if infected
e. High T2 signal T
- Thoracic outlet syndrome, least likely finding on arteriography and venography.
a. Subclavian artery dissection
b. Subclavian artery aneurysm
c. Subclavian artery stenosis
d. Subclavian artery thrombosis
e. Subclavian vein thrombosis
a. Subclavian artery dissectionoracic outlet syndrome, least likely finding on arteriography and venography.a. Subclavian artery dissection
b. Subclavian artery aneurysm T – SCA aneurysm
c. Subclavian artery stenosis T – narrowing of SCA which is positional (abduction)
d. Subclavian artery thrombosis T – mural thrombi
e. Subclavian vein thrombosis T – may be occlusive or non-occlusive
- 25 year old is treated with antibiotics for RLL pneumonia. 1/52 later a RLL cavity with an air fluid level is demonstrated. (LAS Victoria – thick-walled)
a. Infection of bronchogenic cyst
b. Bronchiectasis
c. Cavitary pneumonia
d. Pulmonary abscess
e. Pneumatocoele
**LJS - I would go cavitary pneumonia. Lots of overlap and inconsistency btw terms cavitary pneumonia, necrotising pneumonia, and lung abscess. Lung abscess often due to aspiration in immunocompromised/alcoholic etc. Seems less likely in 25yo
d. Pulmonary abscess – T rounded, focal; thick-walled with shaggy inner lining; typically caused by Staph., Klebsiella, Pseudomonas & Proteus.
25 year old is treated with antibiotics for RLL pneumonia. 1/52 later a RLL cavity with an air fluid level is demonstrated. (LAS Victoria – thick-walled) (SK, JA agree)
a. Infection of bronchogenic cyst – T 10-35% are parenchymal, usually in lower lobes medially. Presence of air indicates infection. Wall thickening may also be seen with infection (StatDx).
b. Bronchiectasis – T cystic bronchiectasis can have air-fluid levels. Least likely answer in this case though.
c. Cavitary pneumonia – T may occur due to S. aureus, gram negatives, anaerobes & TB; thick irregular walls; air-fluid level often present
d. Pulmonary abscess – T rounded, focal; thick-walled with shaggy inner lining; typically caused by Staph., Klebsiella, Pseudomonas & Proteus
e. Pneumatocoele – ?F thin-walled cyst which has thin & smooth walls & may be partially fluid-filled; more common in kids with virulent bugs (S. aureus)If thick-walled, best answer is D.
- 81 year old man presents with a pneumothorax. Which finding is MOST relevant in deciding to insert a chest drain?
a. Complete collapse of the lung
.b. Ipsilateral mediastinal shift.
c. Air fluid level.
d. Visceral pleura has a sharp outline.
e. Lung markings are seen peripherally
**LJS opinion:
Hx does not state there is a haemothorax or hx of trauma/surgery to make you suspect one (and even if there were, you wouldn’t stick in a drain without knowing why they were bleeding). Common for ptx to have reactive effusion - not an indication for chest drain.
e. lung markings seen peripherally - i.e. it’s not a ptx?? If this is what is meant then this would be most relevant in deciding whether to insert a drain!
Otherwise I would say a. (unlikely to re-inflate without drain if complete collapse)
*LW:
Tricky wording, agree with LJS re peripheral lung markings imply no PTx and hence no chest drain should be inserted, while conversely the question states he presents with a PTx….
Also not enough info to decide if primary spontaneous or secondary spontaneous and clinical condition as below guidelines favour put heavy weighting on clinical stability…..
UpToDate guidelines for primary spontaneous:
–> https://www.uptodate.com/contents/image?imageKey=PULM%2F121366&topicKey=PULM%2F117232&source=see_link
- Clinically stable patients with PSP who fail observation or aspiration, patients who are unstable due to pneumothorax, and patients with recurrent PSP should have a tube or catheter thoracostomy placed.
- Thoracostomy is also appropriate in centers without expertise for aspiration as well as in patients with bilateral or very large pneumothoraces (eg, complete collapse), severe symptoms, concurrent hemothorax or pleural effusion necessitating drainage, complex loculated pneumothorax (unusual in PSP).
UpToDate guiedlines for secondary spontaneous:
- Unstable patients should undergo chest tube thoracostomy.
- Stable patients, most should be treated with chest tube as underlying lung disease more likely to increase likelihoof of aspiration failure and development of tension.
BTS 2010 guidelines:
- decision tree is based on wheter Ptx is >2cm or breathless, neither of which are supplied in above question.
- In a Patient > 50yrs with a spontaneous Ptx, > 3cm or breathless, chest drain recommended with admission. If less 1cm and not breathless - admit for observation.
- Selected patients with large PTx who are asymptomatic may be managed with observation alone.
- To add further confusion, recent NEJM paper states conservative management no inferior in outcomes….. (https://www.nejm.org/doi/full/10.1056/NEJMoa1910775)
Previous answer
c. Air fluid level. T all patients with PTX and concurrent haemothorax should undergo chest tube insertion, then thoracoscopy (UTD)
Original answer:
4. 81 year old man presents with a pneumothorax. Which finding is MOST relevant in deciding to insert a chest drain? (SK – from UTD & BTS guidelines 2003)
a. Complete collapse of the lung. ?F Degree of lung collapse not a reliable predictor – total collapse may be prevented by underlying lung disease
b. Ipsilateral mediastinal shift. ¬F contralateral mediastinal shift may indicate tension PTX, however it does not invariably indicate tension & often does not occur if on PPV
c. Air fluid level. T all patients with PTX and concurrent haemothorax should undergo chest tube insertion, then thoracoscopy (UTD)
d. Visceral pleura has a sharp outline. F a sign of PTX
e. Lung markings are seen peripherally. F
Bilateral perilymphatic/bronchovasuclar nodules. lymphadenopathy. no effusion. centrilobular nodules. most likely.
a. sarcoid.
b. lymphangitis carcinomatosis.
A = T = ticks all the boxes, classic; pleural effusion uncommon but can occur (StatDx)
B = certainly possible; 50% have an effusion
young woman. miliary nodular pattern with relative dense nodules. black pleura.
a. alveolar microlithiasis.
b. secondary haemosiderosis
c. sarcoid
A = alveolar microlithiasis = dense lungs; dense miliary calcifications with “sandstorm” appearance; “black pleura” due to small subpleural cysts; average age 35, Turkish people
B = secondary haemosiderosis = nodular interstitial thickening, often with nodular calcification (esp. longstanding mitral stenosis)
C = sarcoid = can have diffuse micronodular pattern; no black pleura though
man with cough not responding to antis. Subpleural shifting consolidation. most likely a. COP
Considerations in migratory consolidation
• Eosinophilic pneumonia
• COP
• Aspiration
• WegenerCOP
• Resembles bronchopneumonia – patchy air space consolidation
• Fails to clear with Abs! Corticosteroids may cause clearing
• Normal lung volumes
pneumothorax post trauma with fractured ribs. biggest reason to worry.
a. dropped lung
b. air /fluid leve
lc. other options that are definition of pneumothorax
***LJS opinion:
dropped lung probably means fallen lung sign - as indication of tracheobronchial injury - rare high mortality injury with high likelihood of other significant injury. I think this is a bigger reason to worry than a haemothorax (could just be bleeding intercostal vessel), might not be terrible given that we know nothing about their haemodynamic state
*LW: agree with above, if referring to fallen lung, this indicates signifcant lung injury with associated mortality, vs relatively common haemopneumothorax…fallen lung - lacerated tracheobronchial tree requires immediate surgical intevention, vs drain for large haemopneumothoraces…
previous answer
B = indicates haemopneumothorax, so needs chest tube & thoracoscopy
25) 25yo female. Ran marathon the previous day and presents with left sided pleuritic chest pain. Low probability VQ scan result. ED reg concerned about ?PE. Asks which imaging test is most appropriate. Which of the following is most appropriate in this clinical setting?:
i) CTPA CTCA triple rule ou
ii) CTPA
iii) Lower limb Doppler
iv) Venous Angiogram
v) Home
*AJL - CTPA - There is a 20% chance of having a PE with a low probability V/Q therefore CTPA is required to rule out PE.
(Previous answers)
CTPA T according to WA imaging pathways
iii) Lower limb Doppler T/F Possibly, according to UTD/PIOPED pathway, although as per UTD “Many patients with PE are likely to be missed. In one report, only 29 percent of patients with PE (determined by V/Q scan or pulmonary angiogram) had venous thrombosis detected by compression ultrasound”1)
25yo female. Ran marathon the previous day and presents with left sided pleuritic chest pain. Low probability V/Q scan result. ED reg concerned about ?PE. Asks which imaging test is most appropriate. Which of the following is most appropriate in this clinical setting?:
i) CTPA CTCA triple rule out F.
ii) CTPA T according to WA imaging pathways
iii) Lower limb Doppler T/F Possibly, according to UTD/PIOPED pathway, although as per UTD “Many patients with PE are likely to be missed. In one report, only 29 percent of patients with PE (determined by V/Q scan or pulmonary angiogram) had venous thrombosis detected by compression ultrasound”
iv) Venous Angiogram F
v) Home
2) 25yo female. Known asthmatic. Chest pain and SOB. Wells score 1. D-dimer –ve. ED reg concerned about ?PE. Asks which imaging test is most appropriate. Which of the following is most appropriate in this clinical setting?:
i) VQ Scan
ii) CTPA
iii) Lower limb Doppler
iv) Venous Angiogram
v) Home
v) Home
Lol this would never happed in chch, CTPA…
Negative D-dimer and low-risk (PE unlikely) clinically = PE excluded. According to WA pathways still need a CXR though