path respiratory - formatted Flashcards

1
Q
  1. 1.APRIL02 Which of the following best describes the most common macroscopic’ appearance of bronchioalveolar carcinoma of the lung?
  2. Central hilar mass
  3. Peripheral solitary mass favouring the upper lobes
  4. Peripheral mass, usually as multiple diffuse nodules with tendency to coalescence
  5. Central area of ill-defined consolidation
  6. Bilateral ill-defined unresolving multifocal consolidation
A
  • LW: Robbins states “BAC involve peripheral parts of lung as either single nodule, or more often as multiple diffuse nodules that may coalesce to produce pneumonia like consolidation” hence answer 3 is preferred.
    2. Peripheral solitary mass favouring the upper lobes 3. Peripheral mass, usually as multiple diffuse nodules with tendency to coalescence Adenocarcinomas in situ (AIS) of the lung refer to a relatively new entity for a pre-invasive lesion in the lung. This entity partly replaces the noninvasive end of the previous term bronchoalveolar carcinoma. Adenocarcinoma in situ is defined as a localised adenocarcinoma of <3 cm that exhibits a lepidic growth pattern, with neoplastic cells along the alveolar structures but without stromal, vascular, or pleural invasion 1.- < 3 cm- no invasion- lepidic growth
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2
Q
  1. 2.APRIL02 Lung carcinomas are associated with the following paraneoplastic syndromes, with the EXCEPTION of:
  2. Lambert-Eaton syndrome (a myasthenia like syndrome)
  3. Hypocalcaemia
  4. Gynaecomastia.
  5. Low serum sodium
  6. Horner syndrome
A
  1. Horner syndrome (not paraneoplastic syndrome)
  • LW:
  • cushing syndrome –> ACTH
  • carcinoid syndrome –> serotinin and bradykinin
  • Hypocalceamia –> calcitonin
  • hypoglycaemia
  • PTHrP –>hypercalcaemia
  • SIADH –> low Na++
  • Eaton Lambert syndrome
  • limbic encephalitis
  • gynacomasteia –> gonadotrophins.
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3
Q

APRIL02 Concerning mesothelioma, Which of the following statements IS INCORRECT:

  1. Asbestos workers who smoke have a greater risk of developing mesothelioma than those who do not smoke
  2. The epithelial form has a better prognosis than the sarcomatous form
  3. Tumour characteristically extends into the fissures
  4. Tumour can arise from the parietal or the visceral pleura
  5. There is a greater risk of developing the tumour with the crocidolite-type of asbestos fibre than anthophyllite.
A
  1. Asbestos workers who smoke have a greater risk of developing mesothelioma than those who do not smoke
    * *Does not increase risk of mesothelioma in smokers, but smoking+asbestos= 55x lung cancer.**

Mesothelioma, also known as malignant mesothelioma, is an aggressive malignant tumour of the mesothelium. Pleura (visceral and parietal) .

Given the presence of the mesothelium in different parts of the body, mesothelioma can arise in various locations pleural mesothelioma (~90%) peritoneal mesothelioma (~10%) pericardial mesothelioma (<1%) cystic/multicystic mesothelioma, tunica vaginalis, testis mesothelioma (<1%)

Risk factors for mesothelioma:

  • Asbestos-fibre exposure: causes majority of cases erionite-fibre exposure: naturally occurring mineral used in building, particularly in Turkey
  • simian virus 40 (SV40)
  • radiation exposure

Amphibole fibres (needle like): CrocidoLITE (most hazardous), anthophylLITE

Serpentine (curly, more soluble and gets impacted upper airway): ChrysoTILE.

Histology: epithelial: 60%, sarcomatoid: 20% mixed: 20% (or slightly more)

Histologic subtype has significant implications for prognosis, with the poorest outcomes observed for sarcomatoid tumors.

Ddx: Fibrous solitary tumour

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4
Q
  1. 4.APRIL02 Concerning bronchogenic carcinoma, which of the following statements is correct?
  2. Adenocarcinoma has the strongest correlation with smoking.
  3. Squamous cell carcinoma is the histologic sub-type that most often produce para-neoplastic syndrome
  4. Small cell carcinoma is most responsive to chemotherapy
  5. Bronchioloalveolar carcinoma is a sub-type of large cell carcinoma
  6. There is no increased risk of developing the tumour in asbestos workers
A
  1. Small cell carcinoma is most responsive to chemotherapy (Small cell is sensitive to radiotherapy & chemotherapy, with potential cure rates of 15 – 25 % for localized disease)

APRIL02 Concerning bronchogenic carcinoma, which of the following statements is correct?

  1. Adenocarcinoma has the strongest correlation with smoking. (Small cell > Squamous show strongest association with Smoking)
  2. Squamous cell carcinoma is the histologic sub-type that most often produce para-neoplastic syndrome (Small cell)
  3. Small cell carcinoma is most responsive to chemotherapy (Small cell is sensitive to radiotherapy & chemotherapy, with potential cure rates of 15 – 25 % for localized disease. However, most patients with small cell carcinoma have distant metastases at diagnosis. Thus, even with treatment, the mean survival after diagnosis is only about 1 year.)
  4. Bronchioloalveolar carcinoma is a sub-type of large cell carcinoma (F - adenocarcinoma “in situ”)
  5. There is no increased risk of developing the tumour in asbestos workers (F- Asbestos exposure also increases the risk for lung cancer development. The latent period before the development of lung cancer is 10 to 30 years. Lung cancer is the most frequent malignancy in individuals exposed to asbestos, particularly when coupled with smoking. Asbestos workers who do not smoke have a five-fold greater risk of developing lung cancer than do nonsmoking control subjects, and those who smoke have a 55-fold greater risk.)
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5
Q
  1. 13.02.51 The following are not associated with primary TB
  2. Consolidation
  3. Lung disease of secondary TB worse than primary
  4. Ghon complex defined as the pulmonary lesion only
A

Not assoc with primary TB
3. Ghon complex defined as the pulmonary lesion only

Ghon focus = initial tuberculous granuloma formed during primary infection and is not radiologically visible unless it calcifies - this occurs in up to 15% of cases

Ghon complex = parenchymal granuloma (Ghon focus) + ipsilateral mediastinal LN

Ranke = Calcified Gohn focus + calcified LN (ie a progression of Ghon complex)

ref: Radiopaedia

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6
Q
  1. 5.APRIL02 Concerning pulmonary tuberculosis, which of the following statements IS INCORRECT?
  2. Primary infection is usually asymptomatic
  3. The Ghon focus is characteristic of post-primary (secondary) tuberculosis
  4. Cavitation is characteristically seen in reactivation of tuberculosis
  5. In miliary tuberculosis, grey-white nodules are scattered throughout the lung parenchyma and the pleura
  6. Bronchial stenosis is a complication
A
  1. The Ghon focus is characteristic of post-primary (secondary) tuberculosis (Initial focus of 1° infection = Ghon complex)

*LW:
Gohn Focus = primary infection of bacilli causing small inflammatory consolidation focus.
Gohn compex = Combination of parenchymal lung lesion (Gohn focus) and nodal involvement.
Ranke complex = Progressive fibrosis of Gohn complex, becoming radiologically calcified.

  1. 5.APRIL02 Concerning pulmonary tuberculosis, which of the following statements IS INCORRECT?
  2. Primary infection is usually asymptomatic (Usually progresses to fibrosis & calcification (asymptomatic)
  3. The Ghon focus is characteristic of post-primary (secondary) tuberculosis (Initial focus of 1° infection = Ghon complex)
  4. Cavitation is characteristically seen in reactivation of tuberculosis (Erosion into a bronchiole & drainage of caseous focus → CAVITY)
  5. In miliary tuberculosis, grey-white nodules are scattered throughout the lung parenchyma and the pleura
  6. Bronchial stenosis is a complication
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7
Q
  1. 6.APRIL02 A patient with known coal worker’s pneumoconiosis has a CXR. They have increased risk of all of the following conditions WITH THE EXCEPTION of:
  2. Tuberculosis
  3. Bronchogenic carcinoma
  4. Progressive massive fibrosis
  5. Chronic bronchitis
  6. Emphysema
A
  1. Bronchogenic carcinoma
    Note- increased risk of -> TB-> Copd, emphysema-> PMFdetabatable regarding cancer

**LJS - Robbins 9th ed says no increased risk of TB either

Robbins:
The spectrum of lung findings in coal workers is wide, varying from asymptomatic anthracosis, to simple coal workers’ pneumoconiosis with little to no pulmonary dysfunction, to complicated coal workers’ pneumoconiosis, or progressive massive fibrosis, in which lung function is compromised.
Coal workers may also develop emphysema and chronic bronchitis independent of smoking.
Unlike silicosis, there is no convincing evidence that coal dust increases susceptibility to tuberculosis. There is also no compelling evidence that coal workers’ pneumoconiosis in the absence of smoking predisposes to cancer.

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8
Q
  1. 7.APRIL02 Concerning bacterial pneumonia, which of the following statements IS INCORRECT?
  2. Klebsiella pneumoniae causes lobar pneumonia with abundant inflammatory exudate
  3. Streptococcus pyogenes is the commonest cause of community-acquired pneumonia
  4. Haemophilus influenzae causes round pneumonia
  5. Staphylococcus aureus pneumonia is associated with abscess formation
  6. Haemorrhagic oedema of hilar and mediastinal lymph nodes is characteristic of inhalational anthrax
A
  1. Streptococcus pyogenes is the commonest cause of community-acquired pneumonia (46% Pneumococcus pneumoniae, 29% Gram negatives, 23% Staph. Aureus)
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9
Q
  1. 8.APRIL02 A patient with known asbestos exposure has an abnormal CXR. Which of the following conditions IS NOT asbestos related?
  2. Pleural effusion
  3. Non calcified pleural plaques
  4. Laryngeal carcinoma
  5. Bronchogenic carcinoma
  6. Pulmonary microlithiasis
A
  1. Pulmonary microlithiasis
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10
Q
  1. 9.APRIL02 Which of the following statements concerning asbestos exposure IS LEAST correct?
  2. There is an increased incidence of carcinoma in families of asbestos workers
  3. Histologically asbestosis is characterised by a diffuse basal pulmonary fibrosis with visible asbestos fibres encased in an ironcontaining proteinaceous coating.
  4. The pulmonary fibrosis begins around the respiratory bronchioles and alveolar ducts.
  5. Macroscopic nodule formation may occur in patients with rheumatoid disease
  6. While the risk is markedly increased the overall lifetime incidence of mesothelioma with heavy asbestos exposure remains low – in the order of 1 in 1000.
A
  1. While the risk is markedly increased the overall lifetime incidence of mesothelioma with heavy asbestos exposure remains low – in the order of 1 in 1000. (Lifetime risk with high exposure ~10% i.e. 1 in 10) 10.
  2. APRIL02 Which of the following statements concerning asbestos exposure IS LEAST correct?
  3. There is an increased incidence of carcinoma in families of asbestos workers
  4. Histologically asbestosis is characterised by a diffuse basal pulmonary fibrosis with visible asbestos fibres encased in an ironcontaining proteinaceous coating.(Asbestos bodies = fibres coated with iron-containing proteinaceous material)
  5. The pulmonary fibrosis begins around the respiratory bronchioles and alveolar ducts.
  6. Macroscopic nodule formation may occur in patients with rheumatoid disease (Large parenchymal nodules may appear in patients with concurrent rheumatoid arthritis (Caplan syndrome)) *LW varying defintions of Caplan syndrome, originally just CWP with Rh nodules, but recently extended to involve all pneumoconioses inlcuding asbestos, so likely true.
  7. While the risk is markedly increased the overall lifetime incidence of mesothelioma with heavy asbestos exposure remains low – in the order of 1 in 1000. (Lifetime risk with high exposure ~10% i.e. 1 in 10)
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11
Q
  1. 10.APRIL02 A 68-year-old man has a suspected primary left bronchogenic carcinoma. Which of the, following aspects of a radiological report HAS NO OR LEAST relevance to staging?
  2. Tumour size greater or less than 5 cm
  3. Involvement of regional intrapulmonary nodes (separate to hilar or mediastinal nodes)
  4. Side of any mediastinal node enlargement
  5. Distance from the carina
  6. Presence of lobar collapse
A
  1. Involvement of regional intrapulmonary nodes (separate to hilar or mediastinal nodes) +/- involvement means that it goes from N0 to N1 can’ remember this as a part of staging system

**LJS - intrapulmonary nodes = N1, so does have relevance. Old question, previously distance to carina was important, now only involvement of carina is (8th edition staging). If this were asked now, distance from carina would be least true

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12
Q
  1. 13.02.06 Coal workers pneumoconiosis on 6 months follow up chest x-ray least likely finding ? Rob p269
  2. TB
  3. PMF
  4. Bronchial Ca
  5. Caplan’s syndrome
  6. Pulmonary HT
A
  1. TB: *LW: robbins states unlike silicosis, there is no convincing evidence that coal dust increases susceptibility to TB: so this is also false
  2. Bronchial Ca (No ↑ risk of lung cancer)
    * LW agrees.
  3. 13.02.06 Coal workers pneumoconiosis on 6 months follow up chest x-ray least likely finding ? Rob p269

Previous answers:
1. TB (Incidence of TB increased)

  1. PMF
  2. Bronchial Ca (No ↑ risk of lung cancer)
  3. Caplan’s syndrome (Occurs in patients with Rheumatoid Arthritis & pneumoconiosis)
  4. Pulmonary HT (Involvement of pulmonary vasculature by scarring → pulmonary hypertension & cor pulmonale)
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13
Q
  1. 13.03.02 Patient with suspected C. psittacosis for HRCT ? Rob p310-311, 483
  2. Inflammation – histiocytes/lymphocytes confined to alveolar walls
  3. Neutrophilic exudate within alveoli
  4. Grey/white slough on bronchial walls
  5. Mucous plugging and areas of atelectasis
A
  1. Inflammation – histiocytes/lymphocytes confined to alveolar walls
  • C. psittaci is excreted from infected birds and inhaled with dust particles.
  • Although human infection may be asymptomatic or mild, C. psittaci also causes a severe pneumonia, also known as ornithosis.
  • Lethal generalized disease, most frequent during epidemics, is marked by focal areas of necrosis in the liver and spleen and diffuse mononuclear infiltrates in the kidneys, heart, and (sometimes) brain.
  • The alveolar septa are widened and edematous and usually have a mononuclear inflammatory infiltrate of lymphocytes, histiocytes, and occasionally plasma cells.
  • In acute cases, neutrophils may also be present.
  • The alveoli may be free from exudate, but in many patients there are intra-alveolar proteinaceous material, a cellular exudate, and characteristically pink hyaline membranes lining the alveolar walls, similar to those seen in hyaline membrane disease of infants.
  • These changes reflect alveolar damage similar to that seen diffusely in ARDS.
  • Subsidence of the disease is followed by reconstitution of the native architecture
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14
Q
  1. 13.03.41 In pure emphysema VS pure chronic bronchitis? Rob p459
  2. Emphysema occurs younger
  3. Chronic bronchitis more likely to have cardiomegaly
  4. Elastic recoil is preserved in emphysema
  5. bronchitis earlier and more short of breath
  6. cor pulmonale more common in emphysema
A
  1. Chronic bronchitis more likely to have cardiomegaly (Emphysema small heart vs Bronchitis large heart)
  2. 13.03.41 In pure emphysema VS pure chronic bronchitis? BRob p459
  3. Emphysema occurs younger (Emphysema 50-75 vs Bronchitis 40-45)
  4. Chronic bronchitis more likely to have cardiomegaly (Emphysema small heart vs Bronchitis large heart)
  5. Elastic recoil is preserved in emphysema
  6. bronchitis earlier and more short of breath (Dyspnoea - Emphysema severe:early vs Bronchitis mild late)
  7. cor pulmonale more common in emphysema (Emphysema Rare: terminal vs Bronchitis common)
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15
Q
  1. 13.03.42 DEFINITION of chronic bronchitis is ? Rob p463

1. Productive cough in 3 consecutive months over for 2 consecutive years

A
  1. Productive cough in 3 consecutive months over for 2 consecutive years
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16
Q
  1. 5.03.40 Young female with tufts of capillary formation? Rob p130
  2. Primary pulmonary hypertension
  3. Goodpastures
  4. SLE
  5. Recurrent thromboemboli
A
  1. Primary pulmonary hypertension

• Plexogenic pulmonary arteriopathy in primary pulmonary hypertension.
Plexogenic arteriopathy has been a term used to describe a constellation of vascular changes occurring in those with pulmonary arterial hypertension. It is considered the histologic hallmark of idiopathic pulmonary arterial hypertension; it is seen in approximately 75% of cases

The term for the clinical situation has not been largely replaced by idiopathic pulmonary hypertension.

chest CT, may been seen as small, tortuous peripheral arteries without a significant connection to pulmonary veins.
Features of background pulmonary hypertension may also be present.
features of pulmonary hypertension on CT- dilated pulmonary trunk- peripheral pruning and tortuousity of pulmonary arteries- right ventricular dilation and/ or hypertrophy- interventricular septal flattening/ bowing- right atrial dilation

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17
Q
  1. 13.02.10 Definition of Bronchiectasis ? Rob 464
  2. Permanent dilatation bronchus and bronchioles > accompanying arterioles
  3. Permanent dilatation bronchus and bronchioles > 1.1 accompanying arterioles
  4. Chronic Permanent dilatation of the bronchi and bronchioles caused by destruction of the muscle and elastic supporting tissue, resulting from or associated with necrotizing infection of bronchus and bronchioles
  5. Chronic infection of bronchus and bronchioles
  6. Cylindrical saccular, varicose dilation of bronchus and bronchioles
A
  1. Chronic Permanent dilatation of the bronchi and bronchioles caused by destruction of the muscle and elastic supporting tissue, resulting from or associated with necrotizing infection of bronchus and bronchioles
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18
Q
  1. 13.03.38 ARDS takes a long time to resolve because Rob p466
  2. Usually associated with bacterial superinfection
  3. Always goes on to fibrosis
  4. Abnormality is due to endothelaial damage and increased capillary permeability.
  5. Takes a long time for Type II pneumocytes to recover
A

*LW quoting Robbins:
Organising stage, type 2 pnuemocytes undergo proliferation to try and regenerate the alveolar lining damaged. Resolution is unusual, more commonly there is organisation of the fibrin exudate with resultant intra alveolar septa fibrosis, and marked thickening of alveolar septa, due to proliferation of interstitial cells and collagen deposition.
Fatal cases often have superimposed broncho-pneumonia.
Initial injury is to capillary endothelium most commonly, progressing to both endothelium and alveolar epithelium.
Acute consequences of damage to alveolar capillary membrane include increased vascular permeability, and alveolar flooding, loss of difusion capacity, surfactant abnormalities due to type 2 cell injury, Exudate and diffuse tissue destruction cannot be easily resolved, resulting in organisation with scarring –> chronic disease.

Thus:
1. Usually associated with bacterial superinfection: not always (tend to be fatal cases), so less correct

  1. Always goes on to fibrosis: commonly goes onto fibrosis, so partially correct, but term ‘always’ makes me dubious.
  2. Abnormality is due to endothelaial damage and increased capillary permeability: TRUE.
  3. Takes a long time for Type II pneumocytes to recover: semi true.

Previous answer:
• the exudate and diffuse tissue destruction that occur with ARDS cannot be easily resolved, and the result is generally organization with scarring, producing severe chronic changes, in contrast to the transudate of cardiogenic pulmonary edema, which usually resolves

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19
Q
  1. 7.02.55 Hyaline Membrane Disease (‘mild’ form) Rob p466
  2. Child typically breathless at birth
  3. Child becomes breathless a short time after birth
  4. Various durations for recovery
A
  1. Child becomes breathless a short time after birth
  • At birth may require resuscitation but usually quickly establishes spontaneous breathing + normal colour
  • Shortly after (30mins)develops respiratory distress + cyanosis requiring ventilation
  • In uncomplicated cases recovery begins in 3 – 4 days
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20
Q
  1. 13.02.08 Desquamative interstitial pneumonitis ? Rob p468
  2. Hamman-Rich syndrome
  3. Desquamative lymphocytic interstitial pneumonitis
  4. Chronic interstitial pneumonitis
  5. Treatable condition and can progress to UIP
  6. Chronic form of UIP
A
  1. Treatable condition and can progress to UIP
    * LW: confusing question with terminology used…
  2. Hamman-Rich syndrome: False –> Acute interstitial pneumonitis.
  3. Desquamative lymphocytic interstitial pneumonitis: False - macrophages predominate = smokers macrophages.
  4. Chronic interstitial pneumonitis: is a broad umbrella term for interstitial pneumonias of chronic duration, although not radiologically descriptive it tends not to include ground glass appearacnes which DIP is…..
    Differing line of thought…symptoms are usually insideous and thus suggest chronicity, and micro shows mild chronic inflammatory changes….
  5. Treatable condition and can progress to UIP: most correct option (sub set can progress to fibrosis with continued smoking).
  6. Chronic form of UIP: False, DIP minimal if any fibrosis, and is usually non progressive (subset can progress to fibrosis with continued smoking).
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21
Q
  1. 13.03.94 Sarcoid – which is TRUE? Rob p470
  2. Relapsing/ remitting course
  3. Complete recovery in 60-80%
  4. Residual pulmonary/ visusal impairment in 30%
A
  1. Complete recovery in 60-80%

Course → either
(1) Progressive Chronicity Or
(2) Periods of activity interspersed with remissions
• 70% recover with no/minimal residual manifestations
• 20% have permanent loss of some lung function / visual impairment
• 10% have progressive pulmonary fibrosis & cor pulmonale

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22
Q
  1. 13.03.31 Sarcoid which is MOST ATYPICAL ? Rob p470
  2. Afro-american
  3. South East Asian
  4. Ashkenzai Jew
  5. Living in tropics
  6. Male
A
  1. South East Asian (rare in Asians – from B&H)
  2. 13.03.31 Sarcoid which is MOST ATYPICAL ? Rob p470
  3. Afro-american (Most common)
  4. South East Asian (rare in Asians – from B&H)
  5. Ashkenzai Jew (no mention of this)
  6. Living in tropics (no mention of this)
  7. Male (more prevalent in females, but race more important overall)
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23
Q
  1. 13.02.07 Sarcoid What is true answer? Rob p470
  2. Hypogammaglobulinemia
  3. Subpleural interstitial fibrosis
  4. Bone lesion distal and proximal femur
  5. 50% affect spleen and liver
A
  1. Subpleural interstitial fibrosis true
  2. 13.02.07 Sarcoid What is true answer? Rob p470
  3. Hypogammaglobulinemia (Increased ACE level in 2/3, Hypercalciuria 2/3, Hypercalcaemia 2%-15%, hypergammaglobinemia 50%)
  4. Subpleural interstitial fibrosis true
  5. Bone lesion distal and proximal femur ( 5%- circumscribed (punched out ) areas of bone resorption in phalanges)
  6. 50% affect spleen and liver (microscopically involved in 75% of cases)
    • microscopically involved in 75% of cases
    • splenomegaly in 20% (hepatomegaly less freq. ~5% - scattered granulomas in portal triads)
    • Nodules & Nodular thickening in a perilymphatic distribution
    o Perihilar bronchovascular
    o Subpleural inc. fissures
    • nodules 3mm – 1cm

*LW:
Additional facts:
–> Approximately, 50 to 65 percent of patients with sarcoidosis have granulomas on liver biopsy, but symptomatic hepatic sarcoid occurs in 5 to 15 percent
–> The frequency of splenic involvement in sarcoidosis has been reported to be 10% to 50%, depending on whether it is detected on physical examination (5% to 14%), a radiological test (33% to 53%), or a tissue biopsy (24% to 59%)

–> 3 main patterns of sarcoid fibrosis described corresponding to pulmonary function testing results:
1) central bronchial distortion or bronchiectasis featuring air trapping, with predominantly obstructive physiology.
2) peripheral honeycombing, with predominantly restrictive physiology and low DLCO:
usually a minor feature and present only in severe fibrosis, subpleural, mainly the middle and upper lung zones, lower lobes predominance resembling UIP is rare
3) diffuse linear fibrotic pattern, with more mild effect on respiratory function: typically radiate away from hila in all directions

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24
Q
  1. 13.02.09 Young girl with moderate to several sarcoid presents with sudden death – cause? (Normal Calcium Score) Rob p470
  2. Renal failure
  3. Pulmonary HT
  4. Ruptured berry aneurysm
  5. Hypertensive cerebral haemorrhage
  6. Cardiac sarcoid
A
  1. Cardiac sarcoid
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25
Q
  1. 13.02.27 What disease is characterised by non caseating granuloma? Rob p470
  2. TB
  3. Chronic Crohn’s
  4. EG
  5. Sarcoid
A
  1. Sarcoid • In Sarcoid - All involved tissues show classic noncaseating granulomas – composed of aggregate of tightly clustered epithelioid cells, often with Langhans or foreign body-type giant cells
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26
Q
  1. 13.03.46 In Goodpatures syndrome ? Rob p473
  2. Lung involvement occurs later than renal
  3. Lung involvement characterized by necrotizing haemorrhagic pneumonitis
  4. may avert pulmonary disease with renal treatment
  5. minimal, same type (pulm/renal disease)
  6. severe pulmonary disease secondary to vasculitis
  7. pulmonary disease secondary to granulomatosis
A
  1. Lung involvement characterized by necrotizing haemorrhagic pneumonitis true

• A condition characterized by the simultaneous appearance of

  1. Proliferative gomerulonephritis
  2. Necrotizing haemorrhagic interstitial pneumonitis

• Characteristic findings of focal proliferative glomerulonephritis in early cases, or rapid progressive/crescentic GN (RPGN) in rapidly progressive cases

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27
Q
  1. 13.03.39 In pulmonary emboli – which is TRUE? Rob p475
  2. Haemorrhage implies infarction
  3. Always infarct as vessels are end-arteries
  4. With haemorrhage underlying parenchyma is preserved
A
  1. With haemorrhage underlying parenchyma is preserved
    • Smaller emboli can travel out into the more peripheral vessels, where they may or may not cause infarction.
    • In patients with adequate cardiovascular function, the bronchial artery supply can often sustain the lung parenchyma despite obstruction to the pulmonary arterial system.
    • Under these circumstances, hemorrhages may occur, but there is no infarction of the underlying lung parenchyma.
    • Only about 10% of emboli actually cause infarction.
    • Although the underlying pulmonary architecture may be obscured by the suffusion of blood, hemorrhages are distinguished by the preservation of the pulmonary alveolar architecture; in such cases, resorption of the blood permits reconstitution of the preexisting architecture
    • Pulmonary embolism usually causes infarction only when the circulation is already inadequate, as in patients with heart or lung disease.
    • For this reason, pulmonary infarcts tend to be uncommon in the young.
    • About ¾’s of all infarcts affect the lower lobes, and in more than ½ multiple lesions occur
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28
Q
  1. 13.03.47 Incidence of lung cancer ? Rob p498
  2. Squamous and adeno 20-40%,small 20%, large 10%
  3. Squamous and small 20-40%,large 20%, adeno 10%
  4. All 30%
A
  1. Squamous and adeno 20-40%,small 20%, large 10% non-small cell lung cancer (NSCLC) (80%)adenocarcinoma (35%)most common cell type overallmost common in womenmost common cell type in non-smokers but still most patients are smokersperipheralsquamous cell carcinoma (30%)strongly associated with smokingmost common carcinoma to cavitatepoor prognosislarge-cell carcinoma (15%)peripherally located very large, usually more than 4 cmsmall cell carcinoma (20%)almost always in smokersmetastasises earlymost common primary lung malignancy to cause paraneoplastic syndromes and SVC obstructionworst prognosis
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29
Q
  1. 13.03.48 Small cell carcinoma, WHICH IS BEST? Rob p498
  2. Also known as oat cell
  3. Neuroendocrine granules and most likely to have paraneoplastic syndrome
  4. Treatment is with lobectomy and chemotherapy
  5. Ususally peripheral but has hilar nodes
  6. Not associated with smoking
A
  1. Neuroendocrine granules and most likely to have paraneoplastic syndrome
  2. 13.03.48 Small cell carcinoma, WHICH IS BEST? Rob p498
  3. Also known as oat cell (Epithelial cells have little cytoplasm & are round or oval = Oat Cell)
  4. Neuroendocrine granules and most likely to have paraneoplastic syndrome
  5. Treatment is with lobectomy and chemotherapy (Small cell is sensitive to radiotherapy & chemotherapy, with potential cure rates of 15 – 25 % for localized disease)
  6. Ususally peripheral but has hilar nodes (Central, almost never cavitate)
  7. Not associated with smoking ( Sqaumous and Small Cell show strongest association with Smoking; only 1% in non-smokers)
  • Carefull with the wording in the exam on this one, see below!!
  • This highly malignant tumor has a distinctive cell type. The epithelial cells are generally small, have little cytoplasm, and are round or oval and, occasionally, lymphocyte like (although they are about twice the size of a lymphocyte LW - smaller than neighbouring resting Lymphocytes).
  • This is the classic oat cell, which is a specific subtype. (not all Small cell are oat cell!!) true

• Other small cell carcinomas have
o spindle-shaped
o polygonal cells
o and may be thus classified (spindle or polygonal small cell carcinoma).
The cells grow in clusters that exhibit neither glandular nor squamous organization.
• Electron microscopic studies show dense-core neurosecretory granules in some of these tumor cells. The granules are similar to those found in the neuroendocrine argentaffin (Kulchitsky) cells present along the bronchial epithelium, particularly in the fetus and neonate.
• 3-10% of lung cancers develop a paraneoplastic syndrome

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30
Q
  1. 13.02.03 52 year old female, non smoker, 3cm pulmonary mass- query cause? Rob p499
  2. Primary adenocarcinoma
  3. Primary SCC
  4. Primary small cell Ca
  5. Primary bronchoalveolar
  6. Metastatic from breast
A
  1. Primary adenocarcinoma

• Solitary Metastatic Lung Nodule
o A solitary lung nodule represents a primary lung tumor in 62% in patients with known Hx of neoplasm
o 5% of all solitary nodules are metastatic; most likely origin: colon carcinoma (30-40%), osteosarcoma, renal cell carcinoma, testicular tumor, breast carcinoma

*LW: useful pathological marker is TTF-1: thyroid transcription facot, which is positive in primary lung adenocarcinoma and negtive in pulmonary metastatic disease from extra thoracic adenocarcinoma.

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31
Q
  1. 13.02.04 67 year old man, 4cm small cell lung Ca, hilar lymph node, no mets- query survival (without treatment)? Rob p499
  2. 40% 5 years
  3. 20% 5 years
  4. 50% 1 year
  5. 50% 6 months
  6. 6-18 months
A
  1. 20% 5 years?? or5. 6-18 months?? (?weeks) • untreated survival of small cell is 6 - 17 weeks • Even with treatment mean survival after diagnosis is about 1 year
    * LW: Robbins states untreated small cell survival time 6 -17 WEEKS. While mean survival with Tx is 1 year.
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32
Q
  1. 13.03.49 Laryngeal cancer ? Rob p507
  2. Associated with alcohol, smoking and irradiation
  3. Polyps and nodules are associated with increase risk of cancer
  4. Usually arises from false cords
  5. Polyps and nodules usually involve false cords
A
  1. Associated with alcohol, smoking and irradiation
  2. 13.03.49 Laryngeal cancer ? Rob p507
  3. Associated with alcohol, smoking and irradiation
  4. Polyps and nodules are associated with increase risk of cancer (virtually never give rise to cancers)
  5. Usually arises from false cords (true vocal cords)
  6. Polyps and nodules usually involve false cords (true vocal cords)
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33
Q
  1. Asbestos plaques – least associated with ?
  2. asbestos bodies
  3. pleural effusions
  4. anterior/posterolateral site
  5. diaphragm
A
  1. asbestos bodies macrophage ingest asbestos fibre-> collage prolfieration-> stained with haemosiderin and iron
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34
Q
  1. 13.02.01 Pleural fibroma. Unusual finding
  2. Slightly mobile and on pedicle
  3. 1-2 cm in size
  4. 8-10 cm in size
  5. associated with pulmonary effusion
  6. cystic formation with the mass
A
  1. associated with pulmonary effusion (NO PLEURAL EFFUSION)
  2. 13.02.01 Pleural fibroma. Unusual finding
  3. Slightly mobile and on pedicle (50% attached by a pedicle)
  4. 1-2 cm in size (Variable size (small to enormous) but always remains confined to lung surface)
  5. 8-10 cm in size
  6. associated with pulmonary effusion (NO PLEURAL EFFUSION)
  7. cystic formation with the mass
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35
Q
  1. Sep03.01 Alpha feto-protein is least likely to be associated with:
  2. colonic ca
  3. lung ca
  4. pancreatic ca
  5. ?smoking
  6. nonseminiferous tumour of testes
  7. GIST
  8. Uncomplicated cirrhosis
A
  1. GIST

alpha-fetoprotein
Liver cell cancer, nonseminomatous germ cell tumors of testis
Less regularly in CA of colon, lung and pancreas
Non-neoplastic : cirrhosis, toxic liver injury, hepatitis and pregnancy (especially when there is foetal distress or death), smoking

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36
Q
  1. Sep03.30 Alpha 1 antitrypsin deficiency in a 20 year old. Preoperative assessment for lung transplant. The most likely finding on CT is:
  2. Hepatic cirrhosis
  3. Pancreatic…
  4. Adrenal…
A
  1. Hepatic cirrhosis
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37
Q
  1. Sep03.31 Emphysema

1. centriacinar emphysema constitutes 95% of cases

A

True

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38
Q
  1. Sep03.48 Laryngeal carcinoma

1. associated with asbestos exposure and smoking

A

risk factors- smoking- alcohol- coffee- asbest

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39
Q
  1. Sep03.XX Laryngeal Tumour most correct statement
  2. singers nodules on false cords
  3. carcinoma on false cords
  4. carcinoma above true cord
A

Pathology
Squamous cell carcinoma (SCC) accounts for 98% of laryngeal tumors.
Classification The tumor is classified according to its relation to the glottis, which affects the treatment options: supraglottic carcinoma (20-30%)glottic carcinoma (50-60%)subglottic carcinoma (5%)transglottic carcinoma: involving two or more of these spaces
Supraglottic carcinoma
SCC arises from the epiglottis, aryepiglottic fold, false vocal fold, as well as the deep pre-epiglottic and paraglottic space. It metastasises early to cervical lymph nodes.
Glottic carcinoma
SCC arises from the true vocal fold. It manifests early due to hoarseness of voice and rarely metastasises due to the poor lymphatic drainage of the glottis.
Subglottic carcinoma
SCC arises from anywhere below the true vocal fold to the inferior edge of the cricoid cartilage. It produces minimal symptoms, which is responsible for its late diagnosis, which coupled with early lymph node metastasis, means a poor prognosis.

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40
Q
  1. Sep03.49 Asbestos fibres most likely to be found in :
  2. Malignant mesothelioma
  3. Pleural fluid
  4. Pleural plaque
  5. Parenchymal biopsy
  6. Bronchial washings
A
  1. Parenchymal biopsy
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41
Q
  1. Sep03.52 Silicosis vs Coal Workers Pneumoconiosis
  2. lung cancer
  3. lower vs upper
  4. lymph node calcification
A
  1. lung cancer

carcinoma and tuberculosis are potential serious complications of silicosis.

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42
Q
  1. Sep03.74 Paragangliomas
  2. paraganglioma, chemodectoma and carotid body tumours can be used interchangeably
  3. often adherent to vessels resulting in incomplete excision and recurrence of 10%
A
  1. often adherent to vessels resulting in incomplete excision and recurrence of 10% (frequently recur after incomplete resection)
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43
Q
  1. 13.02.05 Bronchial carcinoid ? Rob p504
  2. 0.1-0.05 % lung tumors
  3. 5th –6th decade of life
  4. 2-3:1 male:female
  5. 10% atypical (of which will get carcinoid recurrence in 50%)
  6. histology keratin pearls
A
  1. 10% atypical (of which will get carcinoid recurrence in 50%)
  • Bronchial carcinoids represent 1 to 5% of all lung tumors
  • Most patients with carcinoid tumors are younger than 40 years of age
  • incidence is equal for both sexes
  • The reported 5- to 10-year survival rates for typical carcinoids are 50 to 95%.
  • A minority (10%) of tumors show cytologic atypia, necrosis, and aggressive behavior (50% recurrence or metastasis after 2 years) and are designated atypical carcinoids. (note: Adelaide notes say 25%!!)
  • Histologically the tumor is composed of nests, cords, and masses of cells separated by a delicate fibrous stroma. In common with the lesions of the gastrointestinal tract, the individual cells are quite regular and have uniform round nuclei and infrequent mitoses - note central vs peripheral- typical and atypical
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44
Q
  1. PATH2004 FAT EMBOLISM..describe
A
  • after fractures of long bones, or rarely in the setting of soft tissue trauma and burns.
  • occurs in 90% of individuals with severe skeletal injuries, but less than 10% of such patients have any clinical findings.
  • syndrome typically begins 1 to 3 days after injury, with sudden onset of tachypnea, dyspnea, and tachycardia.
  • Besides pulmonary insufficiency, the syndrome is characterized by neurologic symptoms, including irritability and restlessness, which can progress to delirium or coma.
  • diffuse petechial rash in nondependent areas (occurring in the absence of thrombocytopenia) is seen in 20 to 50% of cases and is useful in establishing a diagnosis.
  • Patients may also present with thrombocytopenia, presumably caused by platelets adhering to the myriad fat globules and being removed from the circulation
  • anemia may result as a consequence of erythrocyte aggregation and hemolysis
  • fatal in up to 10% of cases.
  • The pathogenesis of fat emboli syndrome probably involves both mechanical obstruction and biochemical injury (free fatty acids)
  • platelet activation and recruitment of granulocytes
  • Because lipids are dissolved out of tissue preparations by the solvents routinely used in paraffin embedding, the microscopic demonstration of fat microglobules (i.e., in the absence of accompanying marrow) typically requires specialized techniques, including frozen sections and fat stains.
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45
Q
  1. PATH2004 Emphysema – correct

1. Dilatation of airway distal to terminal bronchioles + distension of airspaces

A

• Abnormal permanent enlargement of the airspaces distal to the terminal bronchiole with destruction of their walls, and without obvious fibrosis

46
Q
  1. PATH2004 All of the following are pneumoconioses except:
  2. Silicosis
  3. Asbestosis
  4. Heavy metal lung
  5. Berylliosis
  6. Bird fanciers lung
A
  1. Bird fanciers lung
  • The term pneumoconiosis was originally coined to describe the non-neoplastic lung reaction to inhalation of mineral dusts (e.g., coal dust anthracosis, silica silicosis, asbestos asbestosis, and beryllium berylliosis) commonly encountered in the workplace
  • Some have now broadened the term to include the organic dusts though
47
Q
  1. PATH2004 a1-ATdefic – incorrect
  2. A Recessive
  3. Von Meyenberg complexes
  4. End stage get cirrhosis + cholestasis
A
  1. Von Meyenberg complexes

Von Meyenberg complexes
- multiple biliary harmatomas

Alpha 1 antitrypsin deficiency:
• alpha1 -Antitrypsin deficiency is an autosomal recessive disorder marked by abnormally low serum levels of this protease inhibitor (Pi)
• However, homozygotes for the PiZZ protein have circulating alpha1 -antitrypsin levels that are only 10% of normal levels
• Neonatal hepatitis with cholestatic jaundice appears in 10% to 20% of newborns with the deficiency. In adolescence, presenting symptoms may be related to hepatitis or cirrhosis. Attacks of hepatitis may subside with apparent complete recovery, or they may become chronic and lead progressively to cirrhosis.
• Hepatocellular carcinoma develops in 2% to 3% of PiZZ adults, usually but not always in the setting of cirrhosis

48
Q
  1. PATH2004 Most diagnostic of asbestosis
  2. Asbestos bodies
  3. Interstitial fibrosis
A
  1. Asbestos bodies
    • Asbestos bodies appear as golden brown, fusiform or beaded rods with a translucent center and consist of asbestos fibers coated with an iron-containing proteinaceous material
    • There are two distinct geometric forms of asbestos: serpentine (curly and flexible fibers) and amphibole (straight, stiff, and brittle fibers).
    • The serpentine chrysotile chemical form accounts for most of the asbestos used in industry.
    • Amphiboles include crocidolite, amosite, tremolite, anthophyllite, and actinolyte.
    • amphiboles, even though less prevalent, are more pathogenic particularly with respect to induction of malignant pleural tumors (mesotheliomas).
    • Some studies of mesotheliomas have shown the link is almost always to amphibole exposure.
    • The relatively few cases of mesotheliomas arising in chrysotile workers are in all likelihood due to contamination of chrysotile with the amphibole tremolite.
    • The greater pathogenicity of straight and stiff amphiboles is apparently related to their aerodynamic properties and solubility.
    • Chrysotiles, with their more flexible, curled structure, are likely to become impacted in the upper respiratory passages and removed by the mucociliary elevator. Furthermore, once trapped in the lungs, chrysotiles are gradually leached from the tissues because they are more soluble than amphiboles.
    • In contrast, the straight, stiff amphiboles may align themselves in the airstream and thus be delivered deeper into the lungs, where they can penetrate epithelial cells and reach the interstitium.
    • The length of amphibole fibers also plays a role in pathogenicity, those longer than 8 mm and thinner than 0.5 mm being more injurious than shorter, thicker ones. • Nevertheless, both amphiboles and serpentines are fibrogenic, and increasing doses are associated with a higher incidence of all asbestos-related disease except that only amphibole exposure correlates with mesothelioma.
49
Q
  1. PATH2004 Ca lung – most correct
  2. Small cell better prognosis than squamous
  3. Squamous commonest
  4. Large cell = “scar carcinoma”
A

non correct

• None of these are correct, correct option absent

• Adenocarcinoma 40%
o Most common form in M & F, and in nonsmokers
• Squamous cell 30%
• Small cell 20%
• Large cell 10-15%
• Scar cancers are usually adenocarcinomas

50
Q
  1. PATH2004 Which of the following does not show neuroendocrine differentiation
  2. Small cell tumour
  3. Typical Carcinoid
  4. Tumorlets
  5. bronchioloalveolar cell carcinoma
  6. atypical carcinoid
A
  1. bronchioloalveolar cell carcinoma

• Neoplasms of neuroendocrine cells in the lung include benign tumorlets, small, inconsequential hyperplastic neuroendocrine cells seen in areas of scarring or chronic inflammation; carcinoids; and the (already discussed) highly aggressive small cell carcinoma of the lung.

51
Q
  1. PATH2004 Characteristic features of Rh nodule

1. Central fibrinoid necrosis surrounded by palisading histiocytes

A

• Microscopically, they have a central zone of fibrinoid necrosis surrounded by a prominent rim of epithelioid histiocytes and numerous lymphocytes and plasma cells

52
Q
  1. PATH2004 Most characteristic of TB
  2. Caseous necrosis
  3. Acid fast bacilli
  4. fibrinoid necrosis
A
  1. Caseous necrosis

• Acid fastness is not specific for Mycobacterium tuberculosis, as all species of mycobacteria possess this characteristic (i.e. acid fastness should not be equated with tuberculosis).

53
Q
  1. PATH2004 Lung mets commonest cause
  2. Colorectal
  3. Renal
  4. Breast
  5. Gastric
  6. Head and neck
  7. Thyroid
A
  1. Breast
54
Q
  1. PATH2004 Immune reaction to tuberculosis is an example of
  2. Antibody mediated immunity
  3. Delayed hypersensitivity reaction
  4. Immune complex mediated
  5. Immunosuppression
A
  1. Delayed hypersensitivity reaction
55
Q
  1. PATH2004 Secondary TB can occur in all of these settings except
  2. reactivation
  3. reinfection
  4. Ghon complex
  5. Immune suppression
  6. Silicosis
A

. Ghon complex F – ghon complex is the initial focus of primary infection consisting of a parenchymal subpleural lesion close to interlobar fissure and hilar lymph nodes

56
Q
  1. PATH2004 Characteristic histology features of asbestos fibres (LOTS on)
A

• curled & flexible (serpentine) = chrysotile (90%)
– most common type used in industry

• brittle, straight amphiboles = crocidolite / amosite (10%)
– less prevalent, but more pathogenic

  • Amphiboles fracture → smaller (longer than 8 mm and thinner than 0.5 mm) fragments which reach the airways, and penetrate epithelium to reach interstitium
  • Chrysotiles → deposit in the upper tracheobronchial tree & are cleared, because more flexible & more soluble
  • N.B. all types are fibrogenic but crocidolite is the most carcinogenic (particularly w.r.t. mesothelioma)

• Asbestos bodies = fibres coated with iron-containing proteinaceous material, which arise when macrophages attempt to phagocytose fibres
– iron derived from phagocyte ferritin
o Golden brown, fusiform or beaded rods with translucent centre
• Ferruginous bodies = similar iron protein coated inorganic particles, with no asbestos core
• Focal pleural plaques and mesothelioma do not have asbestos bodies

57
Q
  1. PATH2004 Differential diagnosis of malignant mesothelioma includes all of the following except:
  2. solitary fibrous tumour
  3. metastatic adenocarcinoma
  4. pleural fibrosis
  5. pleural plaques
  6. haemangioblastoma
A
  1. haemangioblastoma
58
Q
  1. PATH2004 Emphysema is defined as:
  2. dilation of airspace distal to terminal bronchioles with destruction of walls
  3. destruction of airspaces proximal to distal bronchioles with no destruction of walls
  4. dilated bronchioles
  5. subpleural fibrosis
A
  1. dilation of airspace distal to terminal bronchioles with destruction of walls • Abnormal permanent enlargement of the airspaces distal to the terminal bronchiole with destruction of their walls, and without obvious fibrosis
59
Q
  1. PATH2004 Regarding pulmonary emboli and infarcts, which of the following is MOST CORRECT:
  2. Majority (>50%) result in white infarcts because it is an end circulation
  3. 75% are in the lower lobes
  4. Pulmonary haemorrhage suggest infarction
  5. The presence of viable alveoli pneumocytes/endothelium in an area of haemorrhage is against a diagnosis of PE
  6. > 50% of infarcts are solitary
A
  1. 75% are in the lower lobes
60
Q
  1. PATH2004 Which of the following is least likely associated with mesothelioma
  2. Exposure to chrysotile fibres
  3. exposure to amphibole fibres
  4. latency period between exposure and tumour
  5. pulmonary fibrosis
A
  1. Exposure to chrysotile fibres
serpentine = chrosytile - shallow infiltration - less phathogenic
amphibole = crocidolite - deep respiratory infiltration - more pathogenic

**LJS - agree that serpentine is lower risk. Though could also be testing the fact that only 20% mesothelioma pt have concurrent pulmonary asbestosis

61
Q
  1. Patient with suspected psittacosis for HRCT:
  2. Inflammation- histiocytes /lymphocytes confined to alveolar walls
  3. Neutrophilic exudate within alveoli
  4. Grey / white slough on bronchial walls
  5. Mucous plugging and areas of atelectasis
A
  1. Inflammation- histiocytes /lymphocytes confined to alveolar walls T Psittacosis is an infection caused by the obligatory intracellular bacterium Chlamydia psittaci; assocd with birds & poultry. Predominant manifestation is respiratory tract infection with constitiutional symptoms. May also have CNS, skin, spleen, renal, haematologic, joint involvement… The most common imaging finding is unilateral, LL dense infiltrate/consolidation. May present in a bilateral, nodular, miliary, or interstitial pattern. Histo findings may include tracheobronchitis and interstitial pneumonitis with air-space involvement and predominant mononuclear cell infiltration. Findings may also include macrophages that contain cytoplasmic inclusion bodies (ie, Levinthal-Coles-Lillie [LCL] bodies), focal necrosis of hepatocytes along with Kupffer cell hyperplasia in the liver, and hepatic noncaseating granulomata. [eMedicine]
62
Q
  1. Patient with HIV with normal CD4 count, patchy pulmonary opacities on CXR, which is most likely:
  2. CMV
  3. Toxoplasmosis
  4. Kaposi’s
  5. Cryptococcus
  6. PCP
A
  1. Cryptococcus T - preferentially infects immunosuppressed individuals, occurs in up to 155 of AIDS patients. Pulmonary infection is usually associated with brain / meningeal disease, but this scenario implies that the patient is immunocompetent. CXR: patchy infiltrates/pneumonitis (affecting any part of lung; bilateral/unilateral, mulitlobar/lobar). May manifest as granulomas 2-7mm, or miliary disease (similar to TB). [Cryptococcosis, eMedicine]

**LJS - all these occur in immunosuppressed. ?Kaposi in least suppressed? Typically seen at CD4 < 200 but nowadays seen with higher CD4 (since AART)
RP says cryptococcus causes asymptomatic disease in lung only in immunocompetent, so maybe this is true?

  1. Patient with HIV with normal CD4 count, patchy pulmonary opacities on CXR, which is most likely: (GC)
  2. CMV F - occurs in those with CD4 counts <100.
    CXR: bilateral hazy infiltrates, focal nodules, masses, bronchiectasais.
  3. Toxoplasmosis F - cerebral toxoplasmosis occurs in those with CD4 counts <150.
  4. Kaposi’s F - usually develops in the setting of a low CD4 count (<150-200 according to RG, Dahnert gives <400). CXR: mid-lower zone pulmonary opacities and parenchymal nodules (peribronchovascular distribution).
  5. Cryptococcus T - preferentially infects immunosuppressed individuals, occurs in up to 155 of AIDS patients. Pulmonary infection is usually associated with brain / meningeal disease, but this scenario implies that the patient is immunocompetent. CXR: patchy infiltrates/pneumonitis (affecting any part of lung; bilateral/unilateral, mulitlobar/lobar). May manifest as granulomas 2-7mm, or miliary disease (similar to TB). [Cryptococcosis, eMedicine]
  6. PCP F - occurs in those with CD4 counts <200. CXR: bilateral perihilar interstitial infiltrates, diffuse alveolar infiltrates, often associated with pneumatocoeles, apical predominance in pts on prophylactic aerosolised pentamidine). [Dahnert]

Despite the emphasis on opportunisitic infections, remember that ‘typical’ bacterial lower respiratory tract infections are one of the most serious disorders in IV infection (S.pneumoniae, S.aureus, H.influenzae, GNB). [Robbins]

63
Q
  1. In patient with multiple positive blood cultures for Candida, which would be atypical:
  2. Empyema
  3. Osteomyelitis
  4. Tricuspid valve lesions
  5. Splenic lesions
  6. Kidney lesions
A
  1. Empyema F - rare… only a few case reports of candida empyema (eg. Indian J Pathol Microbiol 2008). A Taiwanese study (Chest 2000) looked at 67 patients with fungal empyema (of which 18 were immunocompromised); found that Candida was the most commonly encountered species (64%).
  2. In patient with multiple positive blood cultures for Candida, which would be atypical: (GC)
  3. Empyema F - rare… only a few case reports of candida empyema (eg. Indian J Pathol Microbiol 2008). A Taiwanese study (Chest 2000) looked at 67 patients with fungal empyema (of which 18 were immunocompromised); found that Candida was the most commonly encountered species (64%).
  4. Osteomyelitis T - originates either exogenously (direct inoculation) or endogenously (candidaemia or disseminated infection). Mostly due to haematogenous seeding, involves the vertebral discs and often progresses to discitis with contiguous extension to the vetebral body. Other bones include wrist, femur, scapula, proximal humerus. Can also cause arthritis, costochondritis, myositis.
  5. Tricuspid valve lesions T ? - however, endocarditis most commonly involves the aortic and mitral valves. Infrequently involves tricuspid valve and rarely the pulmonary valve (Scand J Infect Dis 2007).
  6. Splenic lesions T - splenic abscess and hypersplenism - both are manifestations of disseminated candidiasis and are usually simultaneously associated with liver invovlement.
  7. Kidney lesions T - manifestation of candidaemia or disseminated candidiasis.
64
Q
  1. Patient with cystic fibrosis- long term survival is associated with:
  2. No increased risk of malignancy
  3. Increased risk of malignancy only if has transplant
  4. Increased risk of GIT and lymphoma
  5. Increased risk of GIT, pancreas, biliary and lymphoma
  6. Increased risk of cholangiocarcinoma
A

*LW:
–> People with CF have an increased risk of digestive tract cancers, including cancers of the small bowel, colon, pancreas, and biliary tract. This risk is increased in people with CF who have had organ transplantation.
Agree lymphomatous malignancy, i.e. PTLD is a possibility, but would depend on transplantation, so based out of the options provided - option 4 is my preferred option.

  1. Increased risk of GIT and lymphoma T - see options 1 & 2.
  2. Increased risk of GIT, pancreas, biliary and lymphoma T - GIT (esp. colon Ca), pancreatic carcinoma (uncommon but there is an increased risk), biliary (if we agree on option 5 rationale), and PTLD.
  3. Patient with cystic fibrosis - long term survival is associated with: (GC) ** opinions **
  4. No increased risk of malignancy F - there is a 20:1 odds ratio for GIT malignancy in CF patients aged 20-29yo.
  5. Increased risk of malignancy only if has transplant F - see above. Post transplant lymphoproliferative disorder occurs in up to 9% of lung transplant recipitents overall. CF is a recognised risk factor for PTLD, which can range from mild lymphoid hyperplasia to malignant lymphoma. [High incidence of PTLD in paed pts with CF, Am J Respir Crit Care Med 200].
  6. Increased risk of GIT and lymphoma T - see options 1 and 2.
  7. Increased risk of GIT, pancreas, biliary and lymphoma T - GIT (esp. colon Ca), pancreatic carcinoma (uncommon but there is an increased risk), biliary (if we agree on option 5 rationale), and PTLD.
  8. Increased risk of cholangiocarcinoma T? - but it appears exceedingly rare!! Biliary complications include cholelithiasis (12-24%), cholecystitis, microgallbladder (up to 30%), focal or multilobular biliary cirrhosis from inspissated bile, strictures/beading/dilatation (similar to sclerosing cholangitis). Hepatolithiasis is a rare but serious complication (<20 cases in the literature). A few case reports of cholangiocarcinoma exist [Hepatolithiasis & Cholangio in CF, Dig Dis Sci 2007]. [also used Dahnert; Review of abdo manifestations of CF, RG 2006]
65
Q
  1. Patient A has dissection involving ascending aorta, Patient B has dissection involving the descending aorta:
  2. Both have type A.
  3. Both have type B.
  4. Patient A has type A and patient B has type B.
  5. Patient A has DeBakey III and patient B has type B.
  6. Patient A has DeBakey I and patient B has DeBakey III
A
  1. Patient A has type A and patient B has type B T
Stanford type A (60%) - involves at least ascending aorta (DeBakey types I and II), surgical management. 
Stanford B (40%) - limited to descending aorta (De Bakey III), medical treatment.

De Bakey pnemonic - BAD (both, ascending, descending - I, II, III)

66
Q
  1. Sarcoid, which is most atypical:
  2. Afro-American
  3. Southeast Asian
  4. Ashkenazi Jew
  5. Living in tropics
  6. Male
A
  1. Southeast Asian T - almost unknown among Native Indians, Aussie aboriginals, or southern Asians (eg Koreans). [eMedicine]
  2. Sarcoid, which is most atypical: (GC)
  3. Afro-American F - 10 times more prevalent in US Afro-Americans than in US cauasians. [Robbins]
  4. Southeast Asian T - almost unknown among Native Indians, Aussie aboriginals, or southern Asians (eg Koreans). [eMedicine]
  5. Ashkenazi Jew - Jews have incidence rates of around 2 in 100,000. [Respirology 2006]
  6. Living in tropics - incidence in Africa, SE Asia, India, central & south America is <10 per 100,000. [eMedicine] 5. Male - females are more often affected than males, but only by 3:1. [Dahnert]
67
Q
  1. ARDS takes a long time to resolve because:
  2. Usually associated with bacterial superinfection
  3. Always goes on to fibrosis
  4. Abnormality is due to endothelial damage, as well as increased capillary permeability
  5. Takes a long time for type II pneumocytes to recover
A

*LW quoting Robbins:
Organising stage, type 2 pnuemocytes undergo proliferation to try and regenerate the alveolar lining damaged. Resolution is unusual, more commonly there is organisation of the fibrin exudate with resultant intra alveolar septa fibrosis, and marked thickening of alveolar septa, due to proliferation of interstitial cells and collagen deposition.
Fatal cases often have superimposed broncho-pneumonia.
Initial injury is to capillary endothelium most commonly, progressing to both endothelium and alveolar epithelium.
Acute consequences of damage to alveolar capillary membrane include increased vascular permeability, and alveolar flooding, loss of difusion capacity, surfactant abnormalities due to type 2 cell injury, Exudate and diffuse tissue destruction cannot be easily resolved, resulting in organisation with scarring –> chronic disease.

Thus:
1. Usually associated with bacterial superinfection: not always (tend to be fatal cases), so less correct

  1. Always goes on to fibrosis: commonly goes onto fibrosis, so partially correct, but term ‘always’ makes me dubious.
  2. Abnormality is due to endothelaial damage and increased capillary permeability: TRUE.
  3. Takes a long time for Type II pneumocytes to recover: semi true.

Previous notes:
controversy: some answer had 2 and some had 3

  1. Abnormality is due to endothelial damage, as well as increased capillary permeability T - integrity of the alveolar-capillary membrane is compromised by either endothelial or epithelial injury, or usually both.
    * Exudative stage: - endothelial - increased vascular permeability (oedema, inflammation, haemorrhage), leads to fibrin exudation and formation of hyaline membranes. - epithelial - damage to type II pneumocytes, resulting in widespread reduction in surfactant production (with subsequent decreased lung compliance and alveolar collapse).
    * Proliferative (organising) stage: type II pneumocytes attempt to regenerate the alveolar lining, organisation of fibrin exudate.
    * Fibrotic stage: variable scarring and cyst formation.
  2. ARDS takes a long time to resolve because: (GC)
  3. Usually associated with bacterial superinfection F - sepsis is the most common risk factor for ARDS. But as far as having ARDS, with secondary bacterial superinfection as the cause of delayed resolution… ** can’t find much on this. **
  4. Always goes on to fibrosis F - the acute (exudative) phase usually resolves completely. Less commonly, residual pulmonary fibrosis occurs, in which the alveolar spaces are filled with mesenchymal cells and new blood vessels. This process seems to be facilitated by IL-1. [eMedicine]
  5. Abnormality is due to endothelial damage, as well as increased capillary permeability T - integrity of the alveolar-capillary membrane is compromised by either endothelial or epithelial injury, or usually both.
    * Exudative stage: - endothelial - increased vascular permeability (oedema, inflammation, haemorrhage), leads to fibrin exudation and formation of hyaline membranes. - epithelial - damage to type II pneumocytes, resulting in widespread reduction in surfactant production (with subsequent decreased lung compliance and alveolar collapse).
    * Proliferative (organising) stage: type II pneumocytes attempt to regenerate the alveolar lining, organisation of fibrin exudate.
    * Fibrotic stage: variable scarring and cyst formation.
  6. Takes a long time for type II pneumocytes to recover F - type I pneumocytes are more vulnerable than type II. Hyperplasia of type II pneumocytes occurs around 5-7 days. [Dahnert, Robbins]
68
Q
  1. In pulmonary emboli, which is true:
  2. Haemorrhage implies infarction
  3. Always infarct as vessels are end arteries
  4. With haemorrhage underlying parenchyma is preserved
  5. Breast carcinoma is the most common cause of tumour embolism
A
  1. With haemorrhage underlying parenchyma is preserved
  2. In pulmonary emboli, which is true: (GC)
  3. Haemorrhage implies infarction F - infarction resulting from pulmonary haemorrhage is the exception rather than the rule, occurring as few as 10% of cases. It occurs only if there is compromise in cardiac function or bronchial circulation, or if the region of the lung at risk is underventilated as a result of underlying pulmonary disease.
  4. Always infarct as vessels are end arteries F - see above.
  5. With haemorrhage underlying parenchyma is preserved
  6. Breast carcinoma is the most common cause of tumour embolism F - gastric Ca most common. Other solid malignancies that may form emboli in the IVC: breast, prostate, lung, HCC, ovarian, osteosarcoma, lymphoma, choriocarcinoma.
69
Q
  1. Definition of Thymoma:
  2. Any benign thymic tumour
  3. Benign tumour of epithelial cells
  4. Any tumour of thymic epithelial cells
  5. Any tumour of thymus
  6. Benign tumours of epithelial and mesenchymal origin
A
  1. Any tumour of thymic epithelial cells = the term “thymoma” is restricted to tumours in which epithelial cells constitute the neoplastic element [Robbins]. Divided into “invasive” and “non invasive” (cf. benign and malignant, as in Robbins) because invasive thymoma may lack the histologic features of malignancy [RG].
70
Q
  1. Young female with tufts of capillary formation with dilated thin walled arteries implies:
  2. Primary pulmonary hypertension
  3. Goodpasture’s
  4. SLE
  5. Recurrent thromboemboli
A
  1. Primary pulmonary hypertensionT - plexogenic pulmonary arteriopathy (see Robbins) is seen in PPH or congenital heart disease with left to right shunts - tuft of capillary formations that spans the lumens of dilated thin-walled arteries
71
Q
  1. Coal workers pneumoconiosis, which is not true:
  2. 2-5 x risk of lung cancer independent of smoking
  3. <10% go on to Progressive massive fibrosis
  4. Characterised by coal macules and coal nodules
  5. PMF tends to progress even in the absence of further exposure
  6. Increased incidence of TB
A
  1. 2-5 x risk of lung cancer independent of smoking F - once smoking-related risk is taken into account, there is no increased frequency of bronchogenic carcinoma (distinguishes from silicosis and asbestosis).
    * LW: Robbins states no increased incidence of TB, unlike silicosis, thus also false.
  2. Coal workers pneumoconiosis, which is not true: (GC)
  3. 2-5 x risk of lung cancer independent of smoking F - once smoking-related risk is taken into account, there is no increased frequency of bronchogenic carcinoma (distinguishes from silicosis and asbestosis).
  4. <10% go on to Progressive massive fibrosis T - fewer than 10% of cases of simple CWP progress to PMF, a generic term that applies to a confluent fibrosing reaction in the lung (complication of any of the fibrogenic pneumoconioses - CWP, silicosis, asbestosis). Generally takes many years to develop. PMF in CWP is a fibrotic mass of haphazardly arranged collagen with numerous pigment-laden macrophages and with abundant free pigment, +/- necrosis, cholesterol clefts, chronic inflam infiltrate. Hx differs from silicosis of PMF: central hyalinised collagen surrounded by a rim of macrophages, focal necrosis common +/- granulomatous inflammation.
  5. Characterised by coal macules and coal nodules T - macules are dust laden macropahges, 1-2mm. Nodules are slightly larger (still <5mm), and have additional delicate network of collagen fibres. Lesions are scattered throughout, but predominantly in upper lobes and upper zones of lower lobes. Radiographically indistinguishable from silicosis.
  6. PMF tends to progress even in the absence of further exposure T
  7. Increased incidence of TB T - as in silicosis. [Robbins; Pneumoconiosis RG 2006] Added options 4 and 5.
72
Q
  1. In benign asbestos pleural plaques, which would be most atypical:
  2. Pleural effusion
  3. Predominant anterior and posterior plaques
  4. Diaphragmatic involvement
  5. Parietal pleura
  6. Golden brown nodes with iron containing proteinaceous material
A
  1. Golden brown nodes with iron containing proteinaceous material - no asbestos bodies
73
Q
  1. Which does not cause Bronchiolitis Obliterans
  2. Tuberous sclerosis
  3. GVHD
  4. Collagen vascular disorders
  5. Viral infections
  6. Bleomycin
A
  1. Tuberous sclerosis F - 1-4% have lung involvement - LAM. CRITTSCOPRAInfectionTBTransplantSewyer james/sarcoid
74
Q
  1. Patient with Hodgkin’s disease stage IIIES, which is not true:
  2. Nodes above diaphragm
  3. Nodes below diaphragm
  4. Involvement of extra nodal sites
  5. Involvement of spleen
  6. Involvement of liver
A
  1. Involvement of liver

lugano modified ann arbor
stage 1 - one nodal group
stage 2 - two nodal group
stage 3 - on both side of diaphragm. Or one nodal group above hemidiaphragm and spleen involvement

stage III(1): involvement of the spleen or splenic, hilar, coeliac, or portal nodes

stage III(2): involvement of the para-aortic, iliac, inguinal, or mesenteric nodes

stage 4 - extra nodal met-> cannot be irradiated in same radiation field
a - no systemic symptoms
b - systemic symptom involvement
e - extra nodal contiguous extension that can be encompassed by radiation field

75
Q
  1. In Goodpasture’s syndrome:
  2. Lung involvement precedes renal involvement
  3. Lung involvement occurs later than renal
  4. Lung involvement characterised by necrotizing haemorrhagic pneumonitis
  5. Usually mild
A
  1. Lung involvement characterised by necrotizing haemorrhagic pneumonitis T - acute focal necrosis of alveoli, intra-alveolar haemorrhage, fibrous thickening of septa etc = necrotising haemorrhagic interstitial pneumonitis
  2. In Goodpasture’s syndrome (JS)
  3. Lung involvement precedes renal involvement T (??) - glomerulonephritis and pneumonitis occur simultaneously but it begins clinically with respiratory symptoms (haemoptysis) and focal pulmonary consolidation
  4. Lung involvement occurs later than renal F
  5. Lung involvement characterised by necrotizing haemorrhagic pneumonitis T - acute focal necrosis of alveoli, intra-alveolar haemorrhage, fibrous thickening of septa etc = necrotising haemorrhagic interstitial pneumonitis
  6. Usually mild F - used to have a dismal prognosis but plasma exchange has improved outcomes Goodpasture syndrome, also referred as antiglomerular basement membrane (anti-GBM) antibody disease, is an autoimmune disease characterised by damage to the alveolar and renal glomerular basement membranes by a cytotoxic antibody (type 2 hypersensitivity). It is a type of pulmonary-renal syndrome.Goodpasture syndrome is defined by:- pulmonary haemorrhage- glomerulonephritis- circulating antiglomerular basement membrane antibodiesM> FPulmonary : non-specific opacityCT : crazy paving, consolidation, LN. Resolve in 2 weeksPrognosis : poor. may need plasmophoresis and immunosuppressant
76
Q
  1. What is most controversial subgroup in Hodgkin’s lymphoma classification:
  2. Nodular sclerosis
  3. Lymphocytic predominant
  4. Lymphocytic rich
  5. Lymphocyte depleted
  6. Mixed cellularity
A
  1. Lymphocyte depleted - rare and somewhat controversial. Most cases prove to be large cell lymphoma. Older male patients with disseminated disease, HIV patients, developing countries.
  2. What is most controversial subgroup in Hodgkin’s lymphoma classification: (GC)
  3. Nodular sclerosis - most common, young adults M=F. Hx: lacunar variant of RS cell, collagen bands with formation of nodules, CD30/CD15+. Excellent prognosis. 2. Lymphocytic predominant - young adult males. Hx: L+H (popcorn) variant of RS cell, panB-cell markers +. Excellent prognosis; 3-5% transform into DLBCL.
  4. Lymphocytic rich - rare.
  5. Lymphocyte depleted - rare and somewhat controversial. Most cases prove to be large cell lymphoma. Older male patients with disseminated disease, HIV patients, developing countries.
  6. Mixed cellularity - older men. Hx: lots of RS cells and heterogeneous infiltrate. Usually disseminated disease + B symptoms. Changed option 3 from “lymphocyte proliferative”. [Robbins]
77
Q
  1. Sarcoid, which is true:
  2. Relapsing/ remitting course
  3. Complete recovery in 60-80%
  4. Residual pulmonary/ visual impairment in 30%
  5. Parenchymal involvement only has a better prognosis than nodes + lung changes
  6. Eyes are involved in 75% of cases
A
  1. Complete recovery in 60-80% T - 70% recover with no or minimal residual disease
  2. Sarcoid, which is true: (GC)
  3. Relapsing/ remitting course F - majority recover, 10% develop progressive pulmonary fibrosis and cor pulmonale.
  4. Complete recovery in 60-80% T - 70% recover with no or minimal residual disease
  5. Residual pulmonary/ visual impairment in 30% F - 20%
  6. Parenchymal involvement only has a better prognosis than nodes + lung changes F - stage 3 versus stage 2 disease (Silzbach classification on CXR: Stage 0 - normal, 1 - adenopathy, 2 - LN + lung, 3 - lung only, 4 - pulmonary fibrosis).
78
Q
  1. Definition of chronic bronchitis:
  2. Clinical + micro/ macro
  3. Reid index >0.5
  4. Histo defined
  5. Histo which was bronchiectasis
A

*AJL - Robbins says: Chronic bronchitis is defined clinically as persistent cough with sputum production for at least 3 months in at least 2 consecutive years in the absence of any other identifiable cause.
I would therefore favour 1. to be the best answer in this question.

  1. Reid index >0.5 T - Normally 0.4. Ratio of submucosal gland layer (b-c) to that of the bronchial wall (a-d). Increased in chronic bronchitis. But this is an “old” method (still quoted in Robbins); the other method is to measure the mucus gland area in a given area of mucosa (eMedicine).
  2. Definition of chronic bronchitis: (GC)
  3. Clinical + micro/ macro F - diagnosis is made on clinical grounds. Some people with symptoms of chronic bronchitis may have no demonstrable histologic abnormality in their airways. However, there is a strong tendency for the presence of mucus gland hyperplasia in bronchial walls. This accounts for the increased sputum production (bronchial glands produce ~98% of total airway mucus production).
  4. Reid index >0.5 T - Normally 0.4. Ratio of submucosal gland layer (b-c) to that of the bronchial wall (a-d). Increased in chronic bronchitis. But this is an “old” method (still quoted in Robbins); the other method is to measure the mucus gland area in a given area of mucosa (eMedicine).
  5. Histo defined F - clinical definition: perisistent cough productive of sputum for >= 3 months in >= 2 consecutive years.
  6. Histo which was bronchiectasis F - Hx: 1. enlargement of mucus-secreting glands (hallmark) 2. increased goblet cells (mainly involves bronchioles)
  7. bronchiolar obstruction (mucus plugging, inflam, fibroisis) 4. bronchiolitis. Bronchiolitis obliterans in severe cases. [Adelaide notes]
79
Q
  1. Man does not want surgery, hilar mass, oncologist wants to know if small cell, does CT – most likely bit of hx that would help:
  2. CXR 1 year ago, hilar mass, lost to follow up
  3. Normal CXR 9 months ago
  4. hyponatraemia
  5. Peripheral location
  6. Mediastinal widening
A
  1. Hyponatraemia T - secondary to SIADH; main features of the syndrome consist of hyponatremia and hypotonicity (< 280mOsm/kg), absence of fluid volume depletion, inappropriate urinary osmolality (> 100 mOsm/kg), increased urinary sodium excretion (>40mmol/L) while on normal salt and water intake, and absence of thyroid, adrenal, pituitary or renal dysfunction. SIADH results from 3 factors: 1. inappropriate stimulation from pulmonary pathology (bacterial pneumonia, TB, lung abscess) or drugs (eg. cytotoxics); 2. uncontrolled secretions from virtually any CNS disorder (including trauma, surgery); 3. ectopic ADH elaboration by tumours, particularly small cell (oat cell) lung carcinoma, duodenum and pancreatic cancers, olfactory neuroblastoma and lymphomas. [Hyponatremia and SIADH, CAMJ 2002].
  2. Man does not want surgery, hilar mass, oncologist wants to know if small cell, does CT – most likely bit of hx that would help: (GC)
  3. CXR 1 year ago, hilar mass, lost to follow up F - 5YS with therapy is 25% for limited stage disease (disease confined to one hemithorax, including mediastinal/supraclavicular nodes); extensive stage (beyond definition of limited stage, or malig. pleural effusion) is rapidly fatal. Most have spread at presentation.
  4. Normal CXR 9 months ago F - non discriminatory.
  5. Hyponatraemia T - secondary to SIADH; main features of the syndrome consist of hyponatremia and hypotonicity (< 280mOsm/kg), absence of fluid volume depletion, inappropriate urinary osmolality (> 100 mOsm/kg), increased urinary sodium excretion (>40mmol/L) while on normal salt and water intake, and absence of thyroid, adrenal, pituitary or renal dysfunction. SIADH results from 3 factors: 1. inappropriate stimulation from pulmonary pathology (bacterial pneumonia, TB, lung abscess) or drugs (eg. cytotoxics); 2. uncontrolled secretions from virtually any CNS disorder (including trauma, surgery);
  6. ectopic ADH elaboration by tumours, particularly small cell (oat cell) lung carcinoma, duodenum and pancreatic cancers, olfactory neuroblastoma and lymphomas. [Hyponatremia and SIADH, CAMJ 2002].
  7. Peripheral location F - usually perihilar surrounding large bronchi, but peripheral location is non discriminatory.
  8. Mediastinal widening F - non discriminatory.
80
Q
  1. Mesothelioma, which is true:
  2. Involves visceral pleura in <1%
  3. Smoking
  4. Lag time variable 5-15 years
  5. EM to differentiate from adenoCa
  6. Heavy exposure does not increase risk
A

r. EM to differentiate from adenoCa 4.

Mesothelioma, which is true: (JS)

a. Involves visceral pleura in <1% F – can involve either visceral or parietal pleura – can’t find exact percentages.
b. Smoking F – no increased risk in asbestos workers who smoke
c. Lag time variable 5-15 years F – latency period is 25-45 years
d. EM to differentiate from adenoCa T – epithelial mesothelioma can be difficult to differentiate from adenocarcinoma with distinguishing features including positive staining for acid mucopolysaccharide, lack of staining for CEA, staining for keratin and EM showing presence of long microvilli and tonofilaments e. Heavy exposure (asbestos???) does not increase risk F – lifetime risk of heavy exposure is 7-10% Mesothelioma:- aggressive neoplasm of the mesothelium- occur : pleura 90 > peritoneum 10 > pericardium1- cause: SEARsimbian viruserionite : industrial metal dustasbestosradiation- hits type : epitheliod 60mixed 25sarcomatoid 15 - stage :1 - parietal pleura2 - parietal pleura + visceral pleura / or - lung - diaphragm involvement3 - endothoracic fascia, mediastinal fat, pericardium4 - extension through structures (chest wall, mediastinum, peritoneum, diaphragm)( note 1 -3 resectable )N - similar to lung

81
Q
  1. Silicosis – least likely. Hx of retired miner:
  2. Upper fibrosis
  3. Pulmonary Alveolar Proteinosis
  4. Increased risk of TB
  5. Cancer
  6. Infection
A

they are all true. Silicosis -> increase risk of cancer as well. used to be controversial

  1. Silicosis – least likely. Hx of retired miner: (GC)
  2. Upper fibrosis T
  3. PAP T - Acute silicoproteinosis produces identical changes to those seen in PAP [Adelaide path notes], and is included as a cause of secondary PAP [Dahnert]. Heavy exposures to silica dust, particularly in sandblasters, exposure times as short as 6-8mths and generally <3yrs. Results in filling of the airspaces with proteinaceous material (PAS +ve), thus giving a diffuse bilateral alveolitis, lower zone predominance. HRCT: patchy centrilobular GGO and consolidation; with intralobular reticulations may give a crazy paving appearance.
  4. Increased risk of TB T - concomitant primary TB occurs in 25% of pts with acute or classic (chronic simple) silicosis. Men with silicosis have a RR of TB that is 2.8 times that for men without. Increased susceptibility is due to impaired macrophage function.
  5. Cancer F (recalled answer) - but apparently still controversial. In 1997 the International Agency for Research on Cancer concluded that crystalline silica from occupational sources is carcinogenic in humans [Robbins 8th ed, 2007]. Meta-analysis (Japan 2004) showed that silicosis has a RR of 2.37. Also showed that smoking strongly increases the risk in silicotic patients, with RR 4.47. This is true, and it’s the last fucking time im going to say it - SG
  6. Infection T - TB and atypical mycobacteria. Cavitation predisposes to aspergilloma.
82
Q
  1. Community acquired pneumonia – least correct:
  2. Viral
  3. Mycoplasma + Chlamydia
  4. Px with symptoms of dyspnoea, haemoptysis, effusion
  5. Bronchial ulceration means bacterial superimposed infection
A
  1. Bronchial ulceration means bacterial superimposed infection F - causes include HSV, radiation, drugs, TB, malignancy, Wegener’s, post transplant lymphoproliferative disease.
  2. Community acquired pneumonia – least correct: (GC)
  3. Viral T - community acquired atypical pneumonias include viral infections (RSV, parainfluenza (kids); influenza A & B (adults); adenovirus (military reccruits).
  4. Mycoplasma + Chlamydia T
  5. Px with symptoms of dyspnoea, haemoptysis, effusion T - onset is usually abrupt, with high fever, shaking chills, pleuritic chest pain, productive mucopurulent cough; occasionally haemoptysis. Parapneumonic effusion.
  6. Bronchial ulceration means bacterial superimposed infection F - causes include HSV, radiation, drugs, TB, malignancy, Wegener’s, post transplant lymphoproliferative disease.
83
Q
  1. Carcinoid of the lung:
  2. All benign
  3. Rarely deviates the bronchus or invades it
  4. Involves Type 1 pneumocytes
  5. Difficult to make diagnosis on FNA
  6. Small cell lung cancer
A
  1. Small cell lung cancer T - KCC 3
  2. Carcinoid of the lung: (GC)
  3. All benign F - KCC2 (atypical carcinoid) and KCC 3 (small cell Ca) may metastasise to liver
  4. Rarely deviates the bronchus or invades it F - typically demonstrates endobronchial growth; the other growth pattern is peribronchial in which tumour penetrates the bronchial wall and fans out into the peribronchial tissue (collar button lesion)
  5. Involves Type 1 pneumocytes F
  6. Difficult to make diagnosis on FNA F - I assume dx is easy as micorscopically these are small uniform cells with fine stippled nuclear chromatin; IHC staining is positive for neuron-specific enolase; EM shows dense core neurosecretory granules.
    * *LJS sounds like easy to dx as NET but difficult to ddx from atypical and small cell carcinoma - would require histological evidence e.g. invasion, necrosis
  7. Small cell lung cancer T - KCC 3
84
Q
  1. TB, which is most correct:
  2. Organ involved can be CNS or kidney in isolation
  3. Type 1 hypersensitivity reaction
  4. Ghon focus is parenchymal + LN
  5. Biopsy caseous region verses non necrotic region for dx of bacilli for treatment
A
  1. Organ involved can be CNS or kidney in isolation This is true -SG11.

TB, which is most correct: (GC)

  1. Organ involved can be CNS or kidney in isolation This is true -SG
  2. Type 1 hypersensitivity reaction F - type IV immune reaction.
  3. Ghon focus is parenchymal + LN F - GF is the parenchymal scar (may calcify); Gohn complex includes the hilar node.
  4. Biopsy caseous region verses non necrotic region for dx of bacilli for treatment
85
Q
  1. Alcoholic and cachetic patient with Bacteroides:
  2. Aspiration from mouth organism
  3. Commensal from mouth
  4. Aspiration from stomach bug
  5. Bowel diverticulitis
  6. Osteomyelitis
A
  1. Aspiration from mouth organism T - bacteroides is one of the anaerobic oral flora that is implicated in aspiration pneumonia (others: prevotella, fusobacterium, peptostreptococcus), admixed with aerobic bacteria (S.pneumonia, S.aureus, H.influenza, P.aeruginosa). Resultant pneumonia is partly chemical (irritant gastric acid), and partly bacterial; often necrotizing and may lead to abscess formation in survivors. Abscess would contribute to cachexia - symptoms include clubbing, anaemia, weight loss. Secondary amyloidosis may develop. [Robbins]
86
Q
  1. Concerning fat embolism, which of the following is least correct:
  2. Over 80% of fat emboli are asymptomatic
  3. Features of fat embolism include hypoxia, thrombocytopenia and CNS symptoms
  4. Symptoms are usually established within 6 hours of trauma / fracture
  5. Neurological manifestations include irritability, restlessness, confusion, and coma
  6. 20-50% of cases are associated with a purpuric rash
A
  1. Symptoms are usually established within 6 hours of trauma / fracture F - syndrome typically begins 1 to 3 days after injury, with sudden onset of tachypnea, dyspnea, and tachycardia.
  2. Concerning fat embolism, which of the following is least correct: (GC)
  3. Over 80% of fat emboli are asymptomatic T - occurs in 90% of individuals with severe skeletal injuries, but less than 10% of such patients have any clinical findings. Fatal in up to 10% of cases.
  4. Features of fat embolism include hypoxia, thrombocytopenia and CNS symptoms T - thrombocytopenia is presumably caused by platelets adhering to the myriad fat globules and being removed from the circulation. Anemia may result as a consequence of erythrocyte aggregation and hemolysis. 3. Symptoms are usually established within 6 hours of trauma / fracture F - syndrome typically begins 1 to 3 days after injury, with sudden onset of tachypnea, dyspnea, and tachycardia.
  5. Neurological manifestations include irritability, restlessness, confusion, and coma T - besides pulmonary insufficiency, the syndrome is characterized by neurologic symptoms, including irritability and restlessness, which can progress to delirium or coma.
  6. 20-50% of cases are associated with a purpuric rash T - diffuse petechial rash in nondependent areas (occurring in the absence of thrombocytopenia) is seen in 20 to 50% of cases and is useful in establishing a diagnosis. [see Eric’s answer 04.48]
87
Q
  1. 35yo outpatient HRCT request ‘Late onset asthma’ worsening dyspnoea, initially episodic and now chronic. Biopsy shows granuloma. Which of the following is most likely with this history:
  2. Silicosis
  3. TB
  4. Hypersensitivity pneumonitis
  5. Sarcoid
  6. Histoplasmosis
A
  1. Hypersensitivity pneumonitis - immunologically mediated response to an extrinsic antigen that involves both immune-complex (type III) and delayed-type (IV) hypersensitivity reactions. Clinically: acute reaction (large loadfever, cough, SOB 4-8hrs post exposure), subacute (acute episodes, background of progressive respiratory deterioration - chronic cough and SOB), or chronic disease. Non caseating granulomas in >2/3 of cases.
  2. 35yo outpatient HRCT request ‘Late onset asthma’ worsening dyspnoea, initially episodic and now chronic. Biopsy shows granuloma. Which of the following is most likely with this history: (GC)
  3. Silicosis - occupational exposure. Hx: silicotic nodule of whorled collagen fibres, silica particles are weakly birefringent.
  4. TB - reactivation (secondary) TB either from reactivation (due to weakened host resistance) or exogenous reinfection (in areas of high contagion). <5% of those with primary disease develop secondary TB. May be asymptomatic if localised; or insidious onset of low-grade fever, night sweats, sputum production, haemoptysis, pleuritic pain; extrapulmonary manifestations.
  5. Hypersensitivity pneumonitis - immunologically mediated response to an extrinsic antigen that involves both immune-complex (type III) and delayed-type (IV) hypersensitivity reactions. Clinically: acute reaction (large loadfever, cough, SOB 4-8hrs post exposure), subacute (acute episodes, background of progressive respiratory deterioration - chronic cough and SOB), or chronic disease. Non caseating granulomas in >2/3 of cases.
  6. Sarcoid - multisystemic disease of unknown aetiology; non caseating granulomas. 50% may be asymptomatic; 2/3 of symptomatic cases present with gradual onset of SOB, dry cough, vague substernal discomfort, or constitutional symptoms (fever, wt loss, anorexia, fatigue, night sweats).
  7. Histoplasmosis - H.capsulatum, endemic in Ohio and central Mississippi region. 3 clinical forms: acute (primary), chronic (cavitary), disseminated miliary (in immunocompromised, infants). Symptoms resemble a flu-like syndrome, most often self-limited. Cavitary disease occurs in vulnerable host (upper lobe, similar to secondary TB) - symptoms of cough, haemoptysis, SOB and chest pain may occur. Hx: granulomas, strikingly similar to TB, differentiation requires identification of yeast forms (PAS or silver stains).
88
Q
  1. Concerning centrilobular emphysema, which of the following is most correct:
  2. The acini are uniformly enlarged from level of terminal bronchiole to terminal alveoli
  3. Proximal part of acini is enlarged, relative or complete sparing of distal acini
  4. Proximal portion of acinus normal or near normal, with dominant involvement of distal portion
  5. Whole acini destroyed leaving irregular lined spaces >1cm in diameter
  6. Acini uniformly involved but disease effects central zone of secondary pulmonary lobules
A

b Proximal part of acini is enlarged , relative or complete sparing of distal acini.

  1. Concerning centrilobular emphysema, which of the following is most correct: (JS)
    a The acini are uniformly enlarged from the level of terminal bronchioles to terminal alveoli. F - Panacinar/panlobular
    b Proximal part of acini is enlarged , relative or complete sparing of distal acini. T
    c Proximal part of the acinus normal or near normal with dominant involvement of distal portion. F - Paraseptal/distal acinar
    d Whole acini destroyed leaving irregular spaces > 1cm in diameter. F - can occur with both panacinar and centrilobular - if severe
    e Acini uniformly involved but disease effects central zone of secondary pulmonary lobule. F
89
Q
  1. Pulmonary adenocarcinoma vs squamous cell carcinoma. Which of the following is most correct:
  2. The 2 are macroscopically similar
  3. Adenocarcinomas are more likely to show cavitation
  4. Adenocarcinoma is more likely to be peripheral and affect women, rather than SCC
  5. Adenocarcinoma have a stronger association with emphysema, chronic bronchitis
  6. Adenocarcinoma is more likely to show massive lymphadenopathy and extrathoracic disease compared with SCC
A
  1. Adenocarcinoma is more likely to be peripheral and affect women, rather than SCC T - 75% are peripheral, most common tumours to affect women and non smokers (but also seen in smokers). SCCs tend to be central, more common in male smokers.
  2. Pulmonary adenocarcinoma vs squamous cell carcinoma. Which of the following is most correct: (GC) 1. The 2 are macroscopically similar F - adenocarcinoma usually peripheral, may be associated with scarring, 80% contain mucin. SCC appears as grey-white infiltrative tumour, usually associated with larger, more central bronchi, cavitation in 30%.
  3. Adenocarcinomas are more likely to show cavitation F - cavitating tumours = 4/5 SCC, followed by BAC. [Dahnert]
  4. Adenocarcinoma is more likely to be peripheral and affect women, rather than SCC T - 75% are peripheral, most common tumours to affect women and non smokers (but also seen in smokers). SCCs tend to be central, more common in male smokers.
  5. Adenocarcinoma have a stronger association with emphysema, chronic bronchitis F - implies a heavy smoking history, thus small cell and SCC would have a stronger association.
  6. Adenocarcinoma is more likely to show massive lymphadenopathy and extrathoracic disease compared with SCC ?? T - SCC typically a large central mass that spreads to local hilar nodes, but disseminates outside thorax later than other types. Adeno’s metastasise widely at an early stage.
90
Q
  1. Patient with markedly thickened pleura encasing one lung. Which of the following statements is most correct?
  2. Only approximately 10-20% with patients with mesothelioma will have associated lower lobe fibrosis
  3. Mesothelioma and metastatic adenocarcinoma have markedly different appearances on light microscopy
  4. Presence of asbestos bodies on pleural biopsy suggest change is more likely reactive / fibrosis
  5. Granuloma in pleural tissue suggests chronic irritation rather than neoplastic infective etiology
  6. Apical lung lesion suggests it is most likely infective in nature
A
  1. Only approximately 10-20% with patients with mesothelioma will have associated lower lobe fibrosis T - 90% of malig. mesotheliomas are related to asbestos but only 10% have asbestosis. As opposed to peritoneal mesothelioma, where 50% have asbestosis. [Robbins]18.

Patient with markedly thickened pleura encasing one lung. Which of the following statements is most correct? (GC)

  1. Only approximately 10-20% with patients with mesothelioma will have associated lower lobe fibrosis T - 90% of malig. mesotheliomas are related to asbestos but only 10% have asbestosis. As opposed to peritoneal mesothelioma, where 50% have asbestosis. [Robbins]
  2. Mesothelioma and metastatic adenocarcinoma have markedly different appearances on light microscopy F - differentiated by antigenic keratin positivity, CEA stain negative, presence of long microvilli on EM.
  3. Presence of asbestos bodies on pleural biopsy suggest change is more likely reactive / fibrosis F - diffuse pleural thickening is rare, involves visceral pleura (cf. pleural plaques - parietal). Neither of theses entities (or mesothelioma) contain asbestos bodies on histology.
  4. Granuloma in pleural tissue suggests chronic irritation rather than neoplastic infective etiology F
  5. Apical lung lesion suggests it is most likely infective in nature F
91
Q
  1. A chest CT request states ‘pulmonary carcinoid’. Which of the following findings would be least expected:
  2. Bronchiectasis
  3. 1cm endobronchial mass confined to a mainstem bronchus
  4. 8cm cystic mass
  5. Pneumonia
  6. Hilar lymphadenopathy
A
  1. 8cm cystic mass F - carcinoid tumours are usually 2-5cm; typical (classic) <2.5cm and atypical >2.5cm.
  2. A chest CT request states ‘pulmonary carcinoid’. Which of the following findings would be least expected: (GC)
  3. Bronchiectasis T - post obstructive.
  4. 1cm endobronchial mass confined to a mainstem bronchus T - typical (classic) carcinoids usually central and manifest as an endobronchial nodule or hilar/perihilar mass close to the bronchus.
  5. 8cm cystic mass F - carcinoid tumours are usually 2-5cm; typical (classic) <2.5cm and atypical >2.5cm.
  6. Pneumonia T - post obstructive.
  7. Hilar lymphadenopathy T - mets to regional lymph nodes in 25%. [Dahnert; Bronchial carcinoid RG 2002]
92
Q
  1. Concerning PE, which of the following is most correct:
  2. Approximately 40% lead to infarction
  3. Emboli affect upper, mid and lower zones equally but not all lobes equally
  4. In the young, PE more frequently leads to infarction
  5. In the presence of a predisposing cause, secondary episodes may occur in up to 30%
  6. Pulmonary haemorrhage in PE implies reperfusion of an infarct
A
  1. In the presence of a predisposing cause, secondary episodes may occur in up to 30% - T - 30% develop a second embolus
  2. Concerning PE, which of the following is most correct: (TW)
  3. Approximately 40% lead to infarction - F - 10% (path notes)
  4. Emboli affect upper, mid and lower zones equally but not all lobes equally - F - 75% affect lower lobes (path notes). Dahnert says (about) 25% each LL, about 15% for ULs and ML.
  5. In the young, PE more frequently leads to infarction - F - May potentially be seen more in young cf old as usually due to abnormal bronchial supply, usually assoc with underlying heart-lung disease, but still as a whole only accounts for 10% of cases.
  6. In the presence of a predisposing cause, secondary episodes may occur in up to 30% - T - 30% develop a second embolus
  7. Pulmonary haemorrhage in PE implies reperfusion of an infarct - F - collateral circulation of lung - dual pulmonary blood supply and only pulmonary arteries involved in PE. Haemorrhage results without lung infarction. Inadequate bronchial artery supply usually results in lung infarct
93
Q
  1. 57yo male has non specific pulmonary fibrosis. Which of the following is least likely to be related:
  2. Past employment as a stone mason
  3. Hx of erosive arthropathy
  4. Hx of chlamydial infection
  5. Hx of previous chemotherapy
  6. Muscle biopsy – non caseating granuloma
A
  1. Hx of chlamydial infection F - C.psittaci (psittacosis: inhaled dust particles of infected bird excreta; most commonly a single lower lobe consolidation). C.pneumoniae (10-20% of adult CAP; usually a single subsegmental lower lobe infiltrate, ARDS has been reported). Can’t see that either causes fibrosis. NB. C.trachomatis infection is seen in infants (vertical transmission from infected mum).
  2. 57yo male has non specific pulmonary fibrosis. Which of the following is least likely to be related: (GC) 1. Past employment as a stone mason - chronic silicosis may occur in these patients 20-40yrs after exposure (inhalation of crystalline silica dusts). HRCT findings include nodules, interstitial thickening, subpleural curvilinear lines, GGO, parenchymal fibrous bands, traction bronchiectasis, honeycombing.
  3. Hx of erosive arthropathy - Rheumatoid lung occurs in up to 50% of patients with RA, lower lobe predominance.
  4. Hx of chlamydial infection F - C.psittaci (psittacosis: inhaled dust particles of infected bird excreta; most commonly a single lower lobe consolidation). C.pneumoniae (10-20% of adult CAP; usually a single subsegmental lower lobe infiltrate, ARDS has been reported). Can’t see that either causes fibrosis. NB. C.trachomatis infection is seen in infants (vertical transmission from infected mum).
  5. Hx of previous chemotherapy - chemotherapeutic agents such as methotrexate, bleomycin, cylcophosphamide and carmustine may cause diffuse lung disease and fibrosis.
  6. Muscle biopsy – non caseating granuloma - sarcoidosis may cause myopathy in 25%; fibrosis occurs in 20% of those with pulmonary involvement. End stage sarcoidosis may appear as upper zone fibrosis.
94
Q
  1. FNA of a 52 yo hilar lung mass shown abdundant cells with eosinophilic cystoplasm and intercellular bridges, together with minor necrotic tissue, most characteristic of:
  2. Bronchial carcinoid
  3. Nodal involvement with Sarcoidosis
  4. Bronchogenic cysts
  5. SCC
  6. Small cell carcinoma of the lung
A
  1. SCC - T - production of keratin and intercellular bridges in well-differentiated forms. Pathoutlines: Pink cytoplasm with distinct cell borders and intercellular bridges characteristic for squamous cell carcinoma.
  2. FNA of a 52 yo hilar lung mass shown abdundant cells with eosinophilic cystoplasm and intercellular bridges, together with minor necrotic tissue, most characteristic of: (TW)
  3. Bronchial carcinoid - F - nests, cords, and massess of cells separated by a delicate fibrous stroma. Regular cells, uniform round nuclei.
  4. Nodal involvement with Sarcoidosis - F - noncaseating granulomas, each composed of an aggregate of tightly clustered epithelioid cells, often with Langerhans or foreign body-type giant cells. Laminated concretions (Schaumann bodies), stellate inclusions (asteroid bodies).
  5. Bronchogenic cysts - F - lined by bronchial type epitleium and are usually filled with mucinous secretions or with air.
  6. SCC - T - production of keratin and intercellular bridges in well-differentiated forms. Pathoutlines: Pink cytoplasm with distinct cell borders and intercellular bridges characteristic for squamous cell carcinoma.
  7. Small cell carcinoma of the lung - F - small epithelial cells, little cytoplasm, round or oval and, occasionally, lymphocyte like (but about 2x size of lymphocyte) - “classic oat cell”. KCC type 3 (Kulchitsky cell carcinoma, where type 1 is “classic carcinoid”, type 2 is “atypical carcinoid).
95
Q
  1. 62 yo smokers CXR is introduced at a clinical meeting as showing ‘occupational asbestos exposure with complications’. Which of the following is least likely to be an associated finding:
  2. Focal non calcified pleural thickening
  3. Pleural effusion
  4. Mediastinal lymphadenopathy
  5. Lobar collapse
  6. Progressive massive fibrosis
A

*LW: favored answer is PMF.

**LJS - I think PMF least likely. Abestosis causes UIP type fibrosis - basal distribution, not PMF (think lower lobes b/c they are needles and shoot there - Prometheus). Lobar collapse probably referring to increased risk of lung carcinoma in asbestos exposure)

  1. Focal non calcified pleural thickening - T - commonest manifestation. 6% of general population.
  2. Pleural effusion - T - earliest asbestos related pleural abnormality. Latent period 8-10y after exposure.
  3. Mediastinal lymphadenopathy: radiopedia states hilar or mediastinal lymphadenopathy by its self is unusual for asbestos, thus when seen warrant search for malignancy, so in light of the wording og the question of ‘complications’, i would say this is true albeit it a two step thought process. - T - related to malignancy / MM / bronchogenic Ca.
  4. Lobar collapse: cannot find lobar collapse as a direct cause by asbestos, and asbestos related lung malignancy usually presents as a mass, with no mention of lobar collapse. Extrapolating as the pleural fibres tend to get stuck at the distal ends of the bronchioles, hence peripherally located, thus eventual cancer mass development but not be central enough to cause lobar collapse (this is stretching the argument logic here though)
    - Atelectais does occur, espicially round atelectasis or contraction atelectasis due to asbestos, but unlikely to be an entire lobe…..
    - May be secondary to compressive atelectasis in setting of large effusion with established mesothelioma.
  5. Progressive massive fibrosis - Majority of resources discuss asbesotosis which is the interstitial fibrosis of asbestos disease, resembling UIP, but not progressing to progressive massive fibrosis, thus favoured to be less likely to occur, in agreement with- eMed: unlike other pneumoconioses, progressive massive fibrosis tend not to occur. Also says lymphadenopathy tend not to occur too.

Previous answers:
Lobar collapse - F - ?as for 3.I prefer this over 5 GL23.
62 yo smokers CXR is introduced at a clinical meeting as showing ‘occupational asbestos exposure with complications’. Which of the following is least likely to be an associated finding: (TW)

  1. Focal non calcified pleural thickening - T - commonest manifestation. 6% of general population.
  2. Pleural effusion - T - earliest asbestos related pleural abnormality. Latent period 8-10y after exposure.
  3. Mediastinal lymphadenopathy - T - related to malignancy / MM / bronchogenic Ca.
  4. Lobar collapse - T - ?as for 3.
  5. Progressive massive fibrosis - ?F - eMed: unlike other pneumoconioses, progressive massive fibrosis tend not to occur. Also says lymphadenopathy tend not to occur too.
96
Q
  1. Least likely to have associated pulmonary findings on HRCT:
  2. SLE
  3. Progressive systemic sclerosis
  4. RA
  5. PAN
  6. Dermatomyosistis – polymyositis
A
  1. PAN - F - PAN typically affects small to medium system arteries, resulting in a necrotizing vasculitis. Involvement of bronchial arteries has been described in PAN, however, the presence of capillaritis or other lung parenchymal involvement by vasculitis strongly suggests another disease process (eg microscopic polyangiitis, Wegener’s, or Churg-Strauss).
  2. Least likely to have associated pulmonary findings on HRCT: (TW)
  3. SLE - T - a variety of pulmonary abnormalities may be seen in SLE. Pneumonia, lupus pneumonitis, diffuse pulmonary haemorrhage, COP/OP, pulmonary fibrosis (uncommon in SLE compared with other CVDs).
  4. Progressive systemic sclerosis - T - Only 1% present with pulmonary symptoms, but up to 75% have evidnce of pulmonary disease at some point in their disease. HRCT findings of interstitial fibrosis in PSS are similar to those of IPF, including: GGO, consolidation, fine reticular opacities, coarse or irregular reticulation, traction bronchietasis, and honeycombing.
  5. RA - T - Commonly associated with thoracic abnormalities, including interstitial pneumonia and fibrosis. Histologically NSIP or UIP. HRCT - range of possible findings from GGO to fine reticulation and coarse reticulation with honeycombing. COP / OP may also occur in patients
  6. PAN - F - PAN typically affects small to medium system arteries, resulting in a necrotizing vasculitis. Involvement of bronchial arteries has been described in PAN, however, the presence of capillaritis or other lung parenchymal involvement by vasculitis strongly suggests another disease process (eg microscopic polyangiitis, Wegener’s, or Churg-Strauss).
  7. Dermatomyosistis – polymyositis - T - PM-DM is less commonly associated with pulmonary involvement than other connective tissue diseases. Reported incidence of pulmonary function abnormalities is 30%, and 5% show chest radiographic abnormalities. Pattern of involvment is typically that of COP / NISP / or UIP. HRCT findings of PM-DM include GGO, fine reticular opacities indicating fibrosis, consolidation, honeycombing (TI and UTD)
97
Q
  1. CXR report states ‘right hilar mass invading mediastinum associated with hilar, mediastinal lymphadenopathy but no subcarinal disease. NO other metastases seen’ What else would be necessary for TNM staging:
  2. Size of lung lesion
  3. Sides of hilar and mediastinal nodes involved
  4. Size of mass and presence / absence of pleural effusions
  5. Size of mass and presence of distal lung collapse
  6. Distance of the lung hilar mass from the carina
A

*AJL edit
Depending on interpretation of the question, ‘No other mets’ could mean it is M0. (and there is no pleural effusion). Also that answer has size of lesion in the answer which isn’t required maybe giving a hint that’s not the correct option.
In order to give an N stage (which is only important if it is M0) the side of the hilar LN is required so perhaps 2. is the answer.

**LJS - agree. Mass is invading mediastinum so T4 by definition, I interpret M0 as they say no mets, N stage is unclear: ipsilateral would be N1/N2, contralateral N3

*LW: agree with above logic

Previous answer:
3. Size of mass and presence / absence of pleural effusions
Presence of effusion would make it M1a disease

  1. CXR report states ‘right hilar mass invading mediastinum associated with hilar, mediastinal lymphadenopathy but no subcarinal disease. NO other metastases seen’ What else would be necessary for TNM staging:
  2. Size of lung lesion
  3. Sides of hilar and mediastinal nodes involved
  4. Size of mass and presence / absence of pleural effusions
  5. Size of mass and presence of distal lung collapse
  6. Distance of the lung hilar mass from the carina
98
Q
  1. Recent decrease in Kaposi sarcoma. Main reason for this:
  2. Decreased incidence of EBV
  3. Increased proportion of heterosexuals getting HIV
  4. New retroviral treatment
  5. ?Community education
  6. Prophylactic treatment
A
  1. New retroviral treatment T - AIDS-associated (epidemic) KS was originally found in 1/3 of AIDS patients, particularly male homosexuals. However, with current regimens of intensive antiretrovrial therapy, the incidence is now <1% (although still the most prevalent malignancy in AIDS pts in the US).
    Four forms of KS:
  2. Classic KS - typically older men of Eastern European or Mediterranean descent, red-purple skin plaques/nodules esp. on the distal extremities, tumours tend to remain localised to skin and subcutaneous tissue.
  3. Endemic KS (aka lymphadenopathic or African) - children of subsaharan Africa (same geographic distribution as Burkitt’s), present with lymphadenopathy, occ. involves viscera, extremely aggressive.
  4. Transplant- assocd KS - solid organ transplant recipients on long-term immunosuppression, aggressive with nodal, mucosal, and visceral involvement.
  5. AIDS-assocd (epidemic) KS [Robbins]
99
Q
  1. Primary TB which is the most not incorrect
  2. Only 1/10, 000 primary infection is clinically significant
  3. 80% of patients asymptomatic
  4. Progressive primary disease most commonly causes middle or lower lobe consolidation
A
  1. Progressive primary disease most commonly causes middle or lower lobe consolidation
  • *LJS - Robbins says only 5% have clinically significant infection. Robbins also: in contrast to apical disease with cavitation in secondary disease, primary progressive resembles bacterial pneumonia with lobar consolidation etc. RP/radiographics it says favours lower and middle lobes in adults. I would choose this as more correct
    https: //pubs.rsna.org/doi/10.1148/rg.275065176
  • AJL - I agree with LJS.
100
Q
  1. 2 years ago lung Bx showed BOOP. Likely evolutionary changes on HRCT:
  2. Resolved
  3. 30% worse, 30% improvement, 40% static
  4. Progression of fibrotic changes and honeycombing
A
  1. Resolved - T - likely appearance if treated.
  2. 2 years ago lung Bx showed BOOP. Likely evolutionary changes on HRCT: (TW)
  3. Resolved - T - likely appearance if treated.
  4. 30% worse, 30% improvement, 40% static - F - the majority of patients recover completely after Rx corticosteroids, but replaces occur frequently within 3 months after Rx is stopped or reduced (Radiographics 2007). Dahnert: 30% persistent disease, 10% mortality due to preogressive / recurrent disease. 84% improve with Rx. UTD: 1/3 demonstrate persistent disease, and recovery, usually with complete clinical and physiologic improvement and normalization of chest film occurs in 2/3 Rx with glucocorticoids.
  5. Progression of fibrotic changes and honeycombing - F
101
Q

31.TB, which is false:

a. Primary TB characterized by the ghon focus
b. TB bronchopneumonia characterized by 3-5 mm yellow nodules
c. Cavitation is characteristically seen in reactivation of tuberculosis s

A

b. TB bronchopneumonia characterized by 3-5 mm yellow nodules - F - in the highly susceptible, highly sensitized individual, the TB infection may spread rapidly throughout large areas of lung parenchyma “galloping consumption”. Sometimes, with such overwhelming disease, well-developed tubercles do not form. (remember centrilobular nodules and tree in bud appearance)

102
Q
  1. 67 year old man, 4cm small cell lung Ca, hilar lymph node, no mets - query survival (without treatment)?

a. 20% 5 years
b. 50% 1 year
c. 50% 6 months
d. 6-18 months (weeks?)

A

d. 6-18 weeks - T - this is prob the correct answer - Robbins says Untreated, the survival time for patients with small cell cancer is 6 to 17 weeks. Even thought SCLC is particularly sensitive to radiation and chemoTx with the potentiazl for cure, most patients hav edistant mets at Dx. At presentation 60-70% of SCLC have extensive stage, 30-40% have limited stage disease. (limited staged get Rx combined modality therapy; extensive stage get chemotherapy alone). From time of Dx - median survival ranges: limited disease 15-20months, extensive 8-13 months. 20-40% limited stage and less than 5% of extensive stage survive two years. 10-13% limited stage and 1-2% extensive stage survive 5y. (UTD) Changed option d. to 6-18weeks. Initial option had 6-18months (?weeks).

103
Q
  1. DIP, which is true:
  2. Aka Hamman rich
  3. Chronic interstitial pneumonitis.
  4. Treatable, but may progress to UIP
A

*LW: confusing options,
Favoured option is of treatable but may progress to UIP as per previous repeat…
Chonic interstitial pneumonitis is an umbrella term, which could be argued either way….

  1. Chronic - T - progressive cough and dyspnoea. DIP = numerous macrophages filling alveoli, mild inflammation of alveolar walls, and minimal fibrosis. More than 90% of patients with DIP are cigarette smokers
  2. DIP, which is true: (TW)
  3. Aka Hamman rich - F - = AIP (fulminant disease. Histologic pattern of diffuse alveolar damage with alveolar hyaline membranes and diffuse, active interstitial fibrosis).
  4. Chronic - T - progressive cough and dyspnoea. DIP = numerous macrophages filling alveoli, mild inflammation of alveolar walls, and minimal fibrosis. More than 90% of patients with DIP are cigarette smokers.
  5. Treatable, but may progress to UIP - F - path notes say some develop major fibrosis (UIP like) and some ?earliest phase of UIP. However UTD says “one review of HRCT findings found no evidence of progression from DIP to UIP, further supporting the concept that DIP and UIP are separate and distinct entities, with important differences in prognosis.
104
Q
  1. Emphysema – correct

a. Dilatation of airway distal to terminal bronchioles + distension of airspaces
b. Destruction of airspaces proximal to distal bronchioles with no destruction of walls
c. Dilated bronchioles
d. Subpleural fibrosis

A

a. Destruction of the airspace distal to the terminal bronchioles with destruction of their walls T - Definition according to Robbins – abnormal permanent enlargement of the airspaces distal to the terminal bronchiole, accompanied by destruction of their wall and without obvious fibrosis

105
Q
  1. Which lung cancer is least associated with smoking?
  2. Small cell carcinoma
  3. Large cell carcinoma
  4. Squamous cell carcinoma
  5. Adenocarcinoma
  6. Bronchoalveolar carcinoma
A

Bronchoalveolar carcinoma - no association with smoking. .

Which lung cancer is least associated with smoking? (GC)

  1. Small cell carcinoma T - strong association.
  2. Large cell carcinoma T - common in male smokers. 3. Squamous cell carcinoma T - strong association.
  3. Bronchoalveolar carcinoma - no association with smoking.
106
Q
  1. Patient with myasthenia gravis for CT chest. What should you look for?
  2. Thymic neoplasm
  3. Thymic mass + hilar mass
A
  1. Thymic neoplasm - T - Thymus is intimately involved in the pathogenesis of MG.

Patient with myasthenia gravis for CT chest. What should you look for? (TW)

  1. Thymic neoplasm - T - Thymus is intimately involved in the pathogenesis of MG.
  2. Thymic mass + hilar mass - F - however we would normally review the entire CT of the chest for abnormalities anyway as we’re not like “CTCA and cardiologists”. It is postulated that all patients with MG have B cells that produce AChR-Ab in the thymus. In addition, 75% of patients with MG have thymic abnormalities - thymic hyperplasia is most common (85%), but various tumors (primarily thymoma) are present in up to 15%. The thymic tumors are usually noninvasive cortical thymomas, but invasive carcinoma can occur. Important to image mediastinum of any patient with MG. MG can be considered a paraneoplastic effect of thymoma, but not of extrathymic tumors. Nonetheless, MG has been assoc with extrathymic tumors, such as small cell lung cancer (?hilar mass) and Hodgkin lymphoma. It is uncertain from these studies whether this co-occurrence represents a true association. The data DO NOT warrant an extensive search for malignancy, other than thymoma, in myasthenics, even in older patients.
107
Q

Neuroendocrine neoplasm of the lungs – FALSE

a. Small foci of neuro endocrine cells in a scar are inconsequential
b. Carcinoid occur in alveolar cells and deviates rather than invading adjacent bronchi
c. Mitotic rate, lymph node invasion and differentiation important to differentiate between typical and atypical carcinoid but this is difficult with a FNA
d. Small cell is neuroendocrine tumour

A

Carcinoid occur in alveolar cells and deviates rather than invading adjacent bronchi - F - arise from K cells of bronchial mucosa and penetrate the bronchial wall to fan out producing the collar-button lesions

  1. Neuroendocrine neoplasm of the lungs – FALSE (JS)
    a. Small foci of neuro endocrine cells in a scar are inconsequential - T - can have benign tumorlets in areas of scarring or chronic inflammation
    b. Carcinoid occur in alveolar cells and deviates rather than invading adjacent bronchi - F - arise from K cells of bronchial mucosa and penetrate the bronchial wall to fan out producing the collar-button lesions
    c. Mitotic rate, lymph node invasion and differentiation important to differentiate between typical and atypical carcinoid but this is difficult with a FNA - T - I presume but can’t find anything about FNA diagnosis…
    d. Small cell is neuroendocrine tumour - T - contain neurosecretory granules similar to those found in Kulchitsky cells
108
Q

. Associated with sarcoidosis….

a. Hypertrophic cardiomyopathy
b. Proliferative glomerulonephritis
c. Erythema marginatum
d. Diabetes mellitus
e. Loeffler’s syndrome

A

Proliferative glomerulonephritis - T - see below.

  1. Associated with sarcoidosis…. (GC)
    a. Hypertrophic cardiomyopathy - F - dilated CMP. Other cardiac manifestations: arrhythmia, heart block, failure.
    b. Proliferative glomerulonephritis - T - see below.
    c. Erythema marginatum - F - erythema nodosum (multiple bilateral tender erythematous nodules mostly on anterior tibia). EM occurs in rheumatic fever (Jones criteria).
    d. Diabetes mellitus - F - diabetes insipidus from HPA involvement. Other CNS manifestations: basal leptomeningeal involvement (diffuse or nodular), periventricular and deep WM T2 hyperintensities, cranial nerve palsies (7th>8,2,5), spinal cord granuloma.
    e. Loeffler’s syndrome - F - Lofgren’s syndrome (acute sarcoidosis) = fever + malaise + bilateral hilar lymphadenopathy, erythema nodosum, large joint arthralgia, occ. uveitis/parotitis.

Renal manifestations of sarcoidosis are commonly related to nephrocalcinosis, which results from hypercalcemia.
On occasion, the granulomatous process can directly involve the kidney, producing interstitial nephritis and glomerulonephritis. The major histological findings of renal sarcoid that have been described are: FSGS, membranous GN, mesangial proiferative GN, IgA nephropathy, and cresenteric GN. Most patients have proteinuria, clinical nephritic syndrome, and/or HTN. [RG 2004; Atlas of sarcoidosis 2005; Dahnert]

109
Q

. Which is true regarding Churg Strauss Disease?

a. c-ANCA
b. Not associated with eosinophilia
c. Allergic rhinitis and gastroenteritis
d. Lower frequency of cardiac involvement than Wegener’s

A

. Allergic rhinitis and gastroenteritis - T - ? hypersensitivity response to inhaled agent. Allergic rhinitis or asthma (phase 1); periph/tissue eosinophilia (phase 2); systemic small vessel granulomatous vasculitis (phase 3) usually develops within 3yrs of onset of asthma. Eosinophilic tissue infiltration causes eo pneumonia and gastroenteritis. GIT involvement occurs in 20% - ulceration, haemorrhage, perforation, bowel wall thickening. Can also get extravascular “allergic” granulomas / eosinophilic abscesses.

Which is true regarding Churg Strauss Disease? (GC)

a. c-ANCA - F - p-ANCA in 70%
b. Not associated with eosinophilia - F - peripheral blood + tissue eosinophilia with Loeffler syndrome.
c. Allergic rhinitis and gastroenteritis - T - ? hypersensitivity response to inhaled agent. Allergic rhinitis or asthma (phase 1); periph/tissue eosinophilia (phase 2); systemic small vessel granulomatous vasculitis (phase 3) usually develops within 3yrs of onset of asthma. Eosinophilic tissue infiltration causes eo pneumonia and gastroenteritis. GIT involvement occurs in 20% - ulceration, haemorrhage, perforation, bowel wall thickening. Can also get extravascular “allergic” granulomas / eosinophilic abscesses.
d. Lower frequency of cardiac involvement than Wegener’s - F - higher; heart involved in up to 47% (coronary vasculitis, myocarditis, pericardial tamponade accounts for 50% of deaths). [Dahnert p484]

110
Q
  1. Oat cell cancer is a subset of which cancer?

a. Small cell
b. Large cell
c. Adenoca
d. Squamous cell

A

a. Small cell - T - WHO classified small cell lung cancers into 3 subcategories: oat cell carcinoma, intermediate cell type, and combined oat cell carcinoma. This subclassification has been difficult to reproduce, however, even by expert lung cancer pathologists, and in 1988, the International Association for the Study of Lung Cancer recommended dropping the intermediate cell type from the classification and adding the category of mixed small cell carcinoma and large cell carcinoma. [eMedicine]