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AA ST2 > Chest > Flashcards

Chest Flashcards

1
Q

what is mosaicism

A

Mosaicism is defined as patchy difference in attenuation of the lung parenchyma. The crucial factor is the amount of air that is found in each voxel.

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2
Q

what is interstitial thickening?

A

infiltration of the interstitium by inflammatory tissue, fibrous tissue, cellular infiltrates or fluid, expand the interstium dispacing air from the voxel and increasing the density of the voxel.

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3
Q

what is air space filling?

A

partial filling of the air spaces with either cells, blood or fluid, displaces air, causing an increase in voxel density. Complete filling of the air spaces leads to consolidation which is not a component of mosaicism.

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4
Q

what is vascular constriction?

A

vascular constriction, secondary to small airways disease or pulmonary embolic disease, results in a reduction of size of the intralobular interstitium, causing an increase in the amount of air within the voxel. As a result, the density of the voxel decreases.

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5
Q

First question to riase when seeing mosaicism?

A

is it due to increased or decreased lung density?

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6
Q

how are mosaicism and GGO related?

A

GGO is a type of mosaicism from high attenuation lung.

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7
Q

How to differentiate types of GGO.
Interstital infiltrate
Partial air space filling
overferfusion

A

No change to vessels
No change to vessels
Minor increase to vascularity

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8
Q

With lower attenuation lung - work out the difference from

emphysema
pulmonary emboli
small airways disease

A

emphysema - blood vessels destroyed with lung

PE - vessels attenuated to no flow

Airway disease - reflex vasoconstriction

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9
Q

Why is it important on mosaicism to review the blood vessles of lung parenchyma

A

if blood vessels are present in normal amounts then you know the parenchyma is more opacified. GGO

if blood vessels are absent in the darker areas then you know it is the darker areas that have lower blood and more likely low attenuation mosaicism and so small airways disease

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10
Q

why does emphysema cause low attenuation of the lung?

A

due to destruction of lung tissue. As a result there are fewer vessels.

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11
Q

how to differentiate emphysema from small airways disease?

A

vascular pattern in emphysema becomes disorganised

small airways disease retains a branching pattern but is less obvious

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12
Q

features of a secondary pulmonary lobule?

A

2-3cm
supplied by a single bronchiole
central artery

venous drainage accumulate in the septa (edges)

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13
Q

what is crazy paving associated with? How sure are we of the association?

A

associated with alveolar proteinosis

but it is a non specific sign

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14
Q

what happens in the lung during alveolar proteinosis to cause the crazy pave pattern?

A

proteinacous fluid accumulates in the air spaces and interstitium causing geometric areas of higher attenuation lung (the paving stones - shaded on the image) interspersed with thickened inter and intralobular septa (the gaps between the paving stones - the lines on the image)

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15
Q

other causes of crazy paving pattern?

A

anything that causes GGO and thickened septa

eg. heart failure, lymphangitis carcinomatosa and non-specific interstitial pneumonitis

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16
Q

what does tree in bud describe?

A

endobronchial pathology on CT. Multiple centrilobular nodules are seen in a linear branching pattern

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17
Q

how many acini to a secondary lobule?

A

4 - 8

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18
Q

how big are acini?

A

6 - 10mm

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19
Q

what do the linterlobular septa contain?

A

lymphatics
connective tissue
septal veins

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20
Q

Interlobular septal thickening is seen in what conditions?

A

Lymphagnitis carcinomatosis
pulmonary oedema
aleveolar proteinosis
lipoid pneumoniasarcoidosis
asbestosis
pneumoconiosis
fibrosing alveolitis

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21
Q

how can setpal thickening be characterised?IST

A

smooth

irregular

modular / beaded

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22
Q

There is a background of fine scattered granuloma nodules. Beading along the oblique fissure is seen (Fig 1a) and is typical of the perifissural distribution, irregualar pattern of IST seen in ……..

A

sarcoid.

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23
Q

Pulmonary alveolar proteinosis is a rare condition in which…..

A

the alveoli fill with a lipid rich, periodic acid-Schiff (PAS) positive proteinaceous fluid. The lung interstitium itself remains relatively normal

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24
Q

Lymphangitis carcinomatosis refers to the spread of tumour through the lymphatic system within the lungs. It most commonly occurs in

A

adenocarcinoma

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25
Q

treein bud should make you think of what?

A

small airways disease

accumulation of mucus / secretions

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26
Q

how to distinguish tree in bud from normal arteriole?

A

larger than arteriole, doesn’t taper, irregular appearance. Patchy areas

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27
Q

which infections can cause bronchiolitis?

A

viruses, especially mycoplasma in children and adults alike, or haemophilus influenzae, atypical mycobacterium and fungi in adults

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28
Q

which infections calssically cause tree in bud?

A

TB and non tuberculous mycobacterium

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29
Q

What lies within the intersitital septum space?

A

a potential space with the pulmonary veins

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30
Q

where are interstitial tissues found?

A

peribronchovascular (hila)
centrilobular (within the pulmonary lobule)
subpleural (periphery of the lung)
interlobular
intralobular

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31
Q

why is knowing about different interstitial tissues important?

A

leads to diagnosis

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32
Q

What are the four main patterns of pathology to look for on thin section CT?

A

Reticular opacities
Nodular opacities
Increased lung density
Reduced lung density

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33
Q

Reticular opacities are also called what?

A

linear opacities

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34
Q

what conditions can cause interstitial septal thickening?

A

carcinomatosa lymphangitis.
interstitial fibrosis
alveolar proteinosis
interstitial pulmonary oedema

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35
Q

What are the three types of nodular opacity pattern in the lung?

A

Centrilobular distribution
Perilymphatic distribution
Random distribution

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36
Q

with a nodular opacity in a centrilobular distribution can get tree in bud. Why?

A

Centrilobular beonchiole - plugged with material due to inflammation from infection (TB/bronchiolitis)

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37
Q

Centrilobular nodular opacity pattern happens because of what relating to the anatomy?

A

centrally there is artery and bronchiole. usually pathology of the bronchiole causing inflammation

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38
Q

Perlymphatic distribution of norular opacities exist becuase of what anatomy?

A

seen in relatin to the lymphatic vessels. Nodules along the bronchovascular bundles, centre of the lobule, septa and the subpleural interstitium.

Seen along the fissues.

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39
Q

Perilymphatic nodular appearance seen in what ocnditions?

A

Sarcoidois and silicosis

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40
Q

Random distribution of nodular opacities? Seen where and why?

A

blood borne disease like miliar metastases. Have no relatin to the lobule anatomy.

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41
Q

What are two forms of increased lung density?

A

Ground glass and consolidation

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42
Q

Ground glass vs consolidation?

A

partial filling vs full fillling of air space. Ground glass can also be interstitium.

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43
Q

What are the main conditions considered for low lung density?

A

emphysema, small airways disease, Langerhand cell histiocytosis, lymphangioleiomyomatosis (LAM) and bronchiectasis.

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44
Q

What is centrilobular emphysema closely related to and why?

A

smoking. Earliest changes occur adjacent to bronchiole at the centre of the pulmonary lobule and go outwards

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45
Q

What is panlobular emphysema assocaited with?

A

alpha 1 antitrypsin deficiency

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46
Q

What are the features of panlobular emphysema?

A

extensive areas of low density in the lung bases.

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47
Q

Low density lungs - small airway disease happens how?

A

Results in difficulty emptying the alveolae resulting in poor gas exchange
low oxygen tension which in turn leads to reflex vasoconstriction

a reduction in perfusion. The combination of retained air and reduced perfusion causes a decrease in lung parenchymal density

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48
Q

crazy paving pattern is associated with?

A

alveolar proteinosis but also lipoid pneumonia. Smoking related ILD

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49
Q

hilar point is the point where…..

A

the lateral margin of the superior pulmonary vein crosses the lateral margin of the basal pulmonary artery:

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50
Q

Two groups of asbesotos?

A

Amphiboles -crocidolite dangerous - straight needles
Serpentines - curved needles

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51
Q

How does crocidolite cause mesothelioma?

A

Fragment, deposit in the small airways and airspaces. Get into the lung interstitum and cause the inflammation / fibrosis.

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52
Q

Which conditions are assocaited with asbesotos BENIGN

A

Pleural plaques
Pleural effusion
Diffuse pleural thickening
Folded lung/round atelectasis
Interstitial lung fibrosis - asbestosis

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53
Q

How to differentiate pleural plaque from thickened pleura?

A

Well defined lateral edge for plaque

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54
Q

What is the earliest asbestos related sign that may be seen?

A

Pleural effusion

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55
Q

Diffuse pleural thickening is said to exist when ….

A

a smooth uninterrupted layer of thickened pleura extends over at least one quarter of the chest wall

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56
Q

How to differentiate diffuse pleural thickening from mesothelioma?

A

In DPT there should not be anything on the mediastinum

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57
Q

Causes of pleural thickening?

A

Post TB empyema, haemothroax, asbestos exposure

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58
Q

What is folded lung?

A

Same as round atelectasis. collapsed lung party surrounded by thickened visceral pleura - forms a mass.

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59
Q

CT appearance of folded lung?

A

Whirpool appearance of vessels and bronchi drawn in
Volume loss.

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60
Q

Abestos ILD pattern

A

Reticular shadowing at the lung bases extending upwards

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61
Q

Sub-pleural small round or branching opacities are seen in what conditions?

A

earliest changes seen in ILF interstitial change, lying a few millimetres from thepleura and they represent peri-bronchiolar fibrosis.

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62
Q

What are Sub-pleural curvilinear opacities

A

lie parallel to the chest wall in the lower zones. They may be seen in early disease, but can represent plaque related atelectasis, or be associated with honeycomb change in more advanced disease.

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63
Q

What are parenchymal bands?

A

linear opacities between 2 and 5 cm in length running through the lung, often ‘joining’ an area of pleural thickening. They represent thickened fibrotic interlobular septa, and are associated with distortion of lung parenchyma. They are more common in asbestosis than in any other form of pulmonary fibrosis.

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64
Q

Pneumoconiosis is caused by the

A

inhalation and deposition of fine particles of inorganic dust in the lungs

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65
Q

inhaled dust may be classified as

A

non-fibrogenic or fibrogenic, depending on how the body reacts to the inhaled particles

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66
Q

Pneumoconiosis can also be classified as simple or complicated. Depedning on….

A

This has nothing to do with the type of dust involved, but depends on whether or not pulmonary massive fibrosis (PMF) is present

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67
Q

Non-fibrogenic dust are what

A

biologically inert, causing minimal fibrosis in the lungs and very few clinical symptoms. Examples include:

Iron oxide causing siderosis
Barium sulphate causing baritosis
Tin oxide causing stannosis

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68
Q

fibrogenic dust are what

A

Coal dust (coal worker’s pneumoconiosis (CWP))
Silica (silicosis)
Asbestos (which is a silicate) – see session in Module 1b Thoracic-Respiratory/Benign Asbestos Related Disease (300-0045)
Beryllium (berylliosis)
Talc (talcosis)

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69
Q

Pure coal dust causes very little fibrous reaction - why does it cause issues?

A

but it is often contaminated with silica and is therefore classified with the fibrogenic dusts. Pulmonary massive fibrosis (PMF) is also seen in CWP.

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70
Q

simple pneumoconiosis findings

A

Characteristic pathological finding is the coal macule which is a deposit of coal pigment in lung parenchyma, 1 to 5 mm in size, without any associated fibrosis

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71
Q

Pulmonary massive fibrosis (PMF) occurs in CWP is defined as what?

A

area of fibrosis containing coal pigment exceeding 1 cm in diameter. PMF opacities can be very large, and when present, the term complicated pneumoconiosis is used.

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72
Q

e characteristic chest radiograph finding in simple CWP is

A

multiple small round opacities, 1-5 mm diameter, in the upper and mid zones. Hilar lymph node enlargement occurs in up to 30% of cases and the nodes are usually calcified (although the eggshell pattern of calcification seen in silicosis is uncommon).

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73
Q

PMF mass migrates centrally towards the hilum, leaving WHAT KIND OF EFFECT ON THE LUNG

A

emphysematous lung between the mass and the chest wall.

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74
Q

how to speerate PMF from a lung cancer?

A

PMF should have background lung nodularity

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75
Q

PMF is seen as

A

PMF develops as a peripheral mass greater than 1cm in diameter with a well-defined lateral border.

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76
Q

What is Caplans syndrome?

A

a manifestation of rheumatoid lung disease and is more commonly seen in CWP than silicosis. Large nodules that are necrobiotic

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77
Q

What are the two diseases from exposure to silica dust?

A

Classic silicosis

Silicoproteinosis

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78
Q

What is classic silicosis

A

This is caused by relatively low exposure to silica dust over a prolonged period of time, resulting in pulmonary nodules and fibrosis (simple silicosis).
silicotic nodule - dense concentric layers of collagen.

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79
Q

What is silicoproteinosis

A

exposed to high concentrations of silica dust particles over a relatively short period of time, e.g. sand blasters.

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80
Q

d eggshell calcification of hilar nodes is virtually pathognomic of

A

silicosis.

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81
Q

CWP apperance is similar to silicoproteinosis or silicosis?

A

Silicosis. Similar pathology type of filling thealveoli and nodules

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82
Q

CT features of silicoproteinosis vs silicosis?

A

silicoproteinosis CT appearances consist of bilateral centrilobular ground glass nodules, multi focal ground glass opacities and areas of consolidation. On high resolution CT thickening of the interlobular, septae may be seen as a crazy paving pattern.

Silicosis small, sharply defined nodules, typically perilymphatic in location, scattered throughout the upper and mid zones of the lungs.

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83
Q

signs of TB in silicoprteinosis

A

cavitation with PMF
rapid progression of lung changes

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84
Q

Siderosis is a condition caused by inhalation of

A

iron oxide particles.

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85
Q

Siderosis chest xr signs?

A

reticulo nodular opacities

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86
Q

Stannosis caused by?

A

Tin

Benign but striking chest radiograph

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87
Q

UIP is also called

A

Idiopathic pulmonary fibrosis

UIP is the histopathological diagnosis - but similar path appearance to
Collagen Vascular disease
Drug toxicicty
Chronic hypersensitivity pneumonias

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88
Q

IPF is common in what demographics?

A

males, 40 - 70 . rare in kids

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89
Q

Increased risk of what in IPF?

A

Bronchogenic carcinoma (x7(
Right heart failure

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90
Q

histological hallmark of UIP is a

A

heterogeneous involvement of lung tissue with alternating areas of normal lung, interstitial inflammation, fibrosis and honeycombing

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91
Q

IPF appearance on CT?

A

subpleural bibasal reticular pattern.
Cystic air spaces (honeycomb destruction)
lymphadenopathy

Mid zone predominance, starts in the lung bases

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92
Q

Non specific interstitial pneumonias (NSIP) - what is it?

A

inflammatory and fibrosing process going on.

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93
Q

How many groups is NSIP divided into and on what basis?

A

3 groups
relative amounts of inflammation and fibrosis. No fibrosis then T1, lots T3

94
Q

HRCT findings for NSIP

A

Symmetrical bilateral GGO at bases

95
Q

what is RB ILD stand for ?

A

Respiratory Bronchiolitis - Interstitial lung disease.

96
Q

What is RB ILD?

A

More severe RB.
Young patients who smoke heavily.

chronic inflammatory cell infiltrate and alveolar lining cell hyperplasia

CENTRED ON THE SMALL AIRWAYS.

97
Q

How to differnetiate RB ILD form DIP?

A

RB ILD is small aiways
DIP is air spaces

98
Q

What is DIP?

A

Desuamative interstitial penumonia - though its macrophages in the distal air spaces

99
Q

DIP HRCT pattern of GGO

A

Lower
peripheral
patchy

100
Q

Phases of diffuse alveolar damage?

A

DAD has an acute exudative phase and a subsequent organising and fibrotic phase.

101
Q

Features of acute interstital pnuemonia on HCRT ?

A

Ground-glass opacification
Air space consolidation
Bronchial dilatation
Architectural distortion

102
Q

Why is cryptogenic organising pneumonia included in IIPs?

A

not intersititial but could be confused with other IIPS.

103
Q

COP on HRCT

A

Consolidation
GGO
NOdules
Band opacities
perilobular pattern

104
Q

How would you describe Lymphocytic intersitital pneumonia

A

widespread interstitial lymphoid infiltrate of the lung, resembling lymphoma but with a clinical course more in keeping with a chronic interstitial pneumonia.

105
Q

Features of LIP?

A

Dense lymphoid interstitial infiltrate.
Intra-alveolar organisation and macrophage accumulation represent minor components in LIP and some architectural distortion, including microscopic honeycomb changes and non-necrotising granulomas may be seen.

106
Q

subpleural Honeycombing should consider?

A

IPF

107
Q

air trapping and centrilobular nodules?

A

RB ILD

108
Q

LIP mainly found in which dmeographic

A

HIV

109
Q

Which IIPs are the rearest

A

DIP and AIP`

110
Q

hypersensitivity pneumonitis (HP ) also called

A

Extrinisic allergic alveolitis

111
Q

Pulmonary function test in HP?

A

Restrictive

112
Q

HP phasez

A

acute, subacute (BOOP), chronic will fibrosis

113
Q

mosaic perfusion happens becuase of what?

A

differences in blood flow within the lung.

114
Q

Classic mosaicism conditions?

A

HP and Bornchiolitis obliterans

115
Q

centriblocular nodules? Causes non infectious

A

Non infectious

Hypersensitivity pneumonitis
Follicular bronchiolitis
Diffuse panbronchiolitis
Respiratory bronchiolitis associated intestitial lung disease (RBILD)
Langerhans cell histiocytosis
Cryptogenic organising pneumonia
Asbestosis
Silicosis
Pneumonconiosis
Lymphocytic interstial pneumonia
Sarcoid

116
Q

centriblocular nodules? Causes infectious

A

Endobronchial TB
Bronchopneumonia
Cystic fibrosis
Infectious bronchiolitis
Allergic bronchopulmonary aspergillosis (ABPA)

117
Q

Which drugs are associated with causing HRCT appearances of ground glass opacity with areas of consolidation similar to acute HP?

A

Bleomycin
Methotrexate
Cyclophosphamide
Sulfonamides

118
Q

gold and amiodarone typically show radiological signs more like So, a good history is important.

A

usual interstitial pneumonia (UIP) or non-specific interstitial pneumonia (NSIP).

119
Q

The nodules are perilymphatic with non-dependent nodular thickening of the interlobular septae and with nodules on the oblique fissures. This pattern is most commonly associated with

A

sarcoid.

120
Q

Sarcoid is the formation of what?

A

formation of multiple non-caeseating granulomas in the involved organs.

121
Q

Triggers for sarcoid?

A

Mycobacteria
Pollen
Inorganic dusts

122
Q

sarcoid presentation

A

Presentation is with symptoms of fatigue, malaise, weakness, weight loss and fever.

123
Q

Sarcoid presentation in caucasions

A

Erythema nodosum (which is uncommon in black patients)
Respiratory illness
Ocular symptoms

124
Q

What are sarcoid garnulomas made out of

A

Monocytes, macrohpages and lymphocytes

125
Q

Do sarcoid granulomas necrotise?

A

rare

126
Q

Where are sarcoid grnulomas distributed?

A

Along bronchovascular bundles, interlobular setpa and pleura

127
Q

Sarcoid markers

A

Raised serum ACE
increased radioactive gallium uptake
abnormal calcium metabolism

128
Q

Which immune complexes and CD4 are circulated around in sarcoid

A

Circulating immune complexes
Depressed cutaneous delayed type hypersensitivity
Increased helper cell (CD4) to suppressor cell (CD8) ratio at the site of involvement

129
Q

What disweases mimic the imaging of sarcoid?

A

Tuberculosis (TB)
Fungal infection
Hypersensitivity pneumonitis
Lymphoma

130
Q

How to diagnose sarcoid?

A

Exclusion of other pathology. With clinical input. More than one organ

131
Q

what kind of prognostic marker is having lung parenchymal change alone?

A

poor

132
Q

what other nodes are involved in sarcoid?

A

para tracheal
aortpulmonary window

133
Q

sarcoid - lung abnormality pattern

A

The lung abnormality is typically bilateral and symmetrical and involves the mid and upper parts of the lung on each side.

134
Q

sarcoid - lung abnormality pattern

A

The lung abnormality is typically bilateral and symmetrical and involves the mid and upper parts of the lung on each side.

reticulonodular is most common in sarcoid

135
Q

Sarcoid - consolidation appearance caused by

A

clustering of granulomas

136
Q

Cystic lung conditions as the main pathology

A

Pulmonary Langerhans’ cell histiocytosis (PLCH)
Lymphangioleiomyomatosis (LAM)
Tuberous sclerosis

137
Q

define a lung cyst

A

A round parenchymal space with a well-defined wall, usually air-containing when in the lung, but without associated pulmonary emphysema.

138
Q

Cyst vs cavity?

A

cavity has a thick or irregular wall.

but a thin walled lesion which has devloped through cavitation can also be a cavity

139
Q

Pulmonary Langerhans’ cell histiocytosis (PLCH)

what is it?

A

group of diseases of unknown pathogenesis, characterised by proliferation of Langerhans’ cells in one or more body systems.

140
Q

On a histopath level why do PLCH form ?

A

disease begins with cellular infiltrate involving Langerhans’ histiocytes leading to granuloma formation.

These form irregular peribronchiolar nodules which then fibrose and may cavitate to form cysts.

141
Q

In PLCH there is preserved lung volume. What other conditions have preserved lung volumes

A

Lymphangioleiomyomatosis
Tuberous sclerosis
Neurofibromatosis-related lung disease (this is covered later in this session)

142
Q

PLCH linical features

A

It is seen in young adults
There is an equal sex distribution
There is a strong association with cigarette smoking
It takes a more benign course than other diffuse cystic diseases

143
Q

Lymphangioleiomyomatosis aetiology

A

exclusively affecting women and specifically those of childbearing age, usually presenting between 17 and 50 years of age (mean 30-35 years).

144
Q

Lymphangioleiomyomatosis pathology

A

smooth muscle cells near small bronchioles, small pulmonary vessels and near lymph nodes/lymphatics

145
Q

why do people get plerual effusion in Lymphangioleiomyomatosis

A

cellular proliferation around mediastinal and hilar lymph nodes and the thoracic duct, leads to lymphatic obstruction, with chylous pleural effusion seen in approximately 60-75% of patients.

146
Q

What is the aetiology of tuberous sclerosis

A

Tuberous sclerosis is an autosomal dominant neurocutaneous syndrome with equal sex distribution.

147
Q

Tuberous sclerosis triad

A

seizures,
mental retardation
adenoma sebaceum

but also
Renal angiomyolipomata
Cardiac rhabdomyomas
Sclerotic bone lesions

148
Q

Neurofibromatosis aetiology

A

Neurofibromatosis (Fig 1) is a relatively common autosomal dominant neurocutaneous syndrome with an incidence of approximately 1:3000

149
Q

NF clinical features

A

Café au lait spots
Peripheral nerve tumours (neurofibromas and schwannomas)
Skin nodules (fibromas)
Hamartomas of the iris

150
Q

NF chest abnormalities

A

Notching and ribbon ribs
Intercostal nerve tumours
Kyphoscoliosis
Cutaneous nodules - fibroma molluscum, which can give the impression on a CXR of lung nodules
Neural tumours
Meningocoeles

151
Q

Lymphocytic interstitial pneumonia has what associations>

A

Sjögren’s syndrome
Acquired immunodeficiency syndrome (AIDS)
Primary biliary cirrhosis

152
Q

Lymphocytic interstitial pneumonia imaging findings

A

bilateral ground-glass opacification, reflecting infiltration of the parenchymal interstitium, and poorly-defined centrilobular nodules, resulting from peribronchial infiltration.

153
Q

Causes of honeycombing

A

Idiopathic pulmonary fibrosis (particularly usual interstitial pneumonia (UIP), in which honeycombing is a characteristic feature)
Collagen vascular disease-related lung fibrosis
Asbestosis
Chronic hypersensitivity pneumonitis
Drug-related interstitial lung disease

154
Q

bilateral basal cystic change is pathognomic of what

A

advanced pulmonary fibrosis

155
Q

Preserved Lung Volume in Diffuse cyst pattern Lung Disease

differentials

A

Tberous sclerosis
NF
PLCH
Lymphangioleiomyomatosis

156
Q

Which diseases have cyst pattern as a secondary feature?

A

Honycombing in ned stage fibrosis

pneumatoceles in pneumonia

LIP

157
Q

What are the differentials for primary cystic diseases

A

PLCH
LAM
Tuberous sclerosis

158
Q

What diseases are mimics of cystic disease?

A

Emphysema

Cystic bronchiectasis

159
Q

In LAM shape of cysts is usually WHAT?

A

round and uniform

160
Q

What does CREST stand for?

A

Calcinosis
Raynauds
Esophageal dysmotility
Scleroderma
Telangiectasia

161
Q

What are the autoimmune rheumatic disorders ? List

A

SLE
Rheum Arthritis
Scleroderma
Polymyositis
Dermatomyositis
Sjogrens

162
Q

What is the mixed picture for mixed connective tissue disorder?

A

SLE
Systemic sclerosis
Polymyositis

163
Q

How is rheumatoid arthritis charachterised?

A

symmetric arthritis
stiffness in morning
rheumatoid factor

164
Q

What is the disease process fo scleroderma?

A

systemic sclerosis is an uncommon disease of connective tissue, characterised by the deposition of excessive extracellular matrix and vascular obliteration. It has approximately 3:1 female predilection.

165
Q

How do dermatomyositis and polymyositis differ?

A

Polymyositis is an autoimmune inflammatory myopathy, characterised by symmetric weakness of the limb girdle and anterior neck muscles.

Dermatomyositis is similar to polymyositis except for the presence of a characteristic skin rash.

166
Q

What is the sjogrens triad?

A

dry eyes
dry mouth
arthritis.

167
Q

What are the SLE antibodies?

A

Anti double stranded DNA
Anti Sm
Anti nuclear
anti phosphlipid

168
Q

What are the scleroderma antibodies?

A

anticentromere
scl 70

169
Q

Polymyositis / dermatomyositis antibodies ?

A

anto jo

170
Q

Sjogrens antibodies

A

anti SS - A (Ro)
La

171
Q

What are the CXR review areas once you see septal lines?

A

Joints
Oesophageal dilation
pulmonary artery dilatation
soft tissue calc (dermatoyositis)
Diaphragm position (myostis)

172
Q

Supine HRCT
Spiral CT
CT pulmonary angiogram
Prone scans
Expiratory scans

Why are all these used in ILD imaging ?

A

Supine and sprial are standard.
CTPA for pulmonary hypertension emboli
Prone removes dependant oedema.
Expiratory used for air trapping in obliterative bronchiolitis

173
Q

what is the pulmonary manifestation of rheumatoid arthritis?

A

rheumatoid nodules

174
Q

Rheumatoid nodule vs malignancy?

A

if single lesion difficult to discern.

Nodule will uptae Fl18 on FDG PET.

Normally need surger

175
Q

What is caplans syndrome?

A

Caplan’s syndrome is the combination of rheumatoid arthritis with pneumoconiosis related to mining dust.

176
Q

How does ILD relate to rheumatoid diseases?

A

can be a direct link or secodnary to the drugs used

177
Q

Which ILD pattern is typically linked to rheumatoid arthritis?

A

UIP

178
Q

ARDS vs diffuse alveolar damage?

A

ARDS is clinical

diffuse alveolar damage is what is seen on imaging

179
Q

Acute pulmonary haemorrhage is seen in which condition

A

SLE

180
Q

Acute interstitial pneumonitis may occur in 1-5% of patients treated with WHAT

A

methotrexate

181
Q

Lung side effect of Asprin (excessive)

A

lung oedema

182
Q

xLung side effect of NSAIDS

A

organising pneumonia pattern

183
Q

Lung side effect of gold

A

Organising pneumonia pattern

184
Q

Lung side effect of methotrexate

A

NSIP

185
Q

Lung side effect of penicillamine

A

Constrictive bronchitis

186
Q

Lung side effect of cytotoxic drugs

A

opportunistic infection

187
Q

type of bronchiectasis seen in rheumatoid arthritis?

A

Cylindrical

188
Q

Obliterative bronhiolitis is assocaited with which treatments?

A

penicillamine, gold, and sulfasalazine treatment

189
Q

what is pulmonary haemorrhage?

A

bleeding from the pulmonary microvasculature

haemosiderin laden macrophages in alveolar spaces and interstitium

190
Q

pulmonary haemorrhage can be divided into two -

A

diffuse pulmonary haemorrhage

focal pulmonary haemorrhage

191
Q

DPH - Immunologically-mediated conditions

A

Goodpastures
SLE
Gran polyangitis,
polyarrteritis nodosa

192
Q

cuases of focal pulmonary haemorrhage

A

Chronic bronchitis
Tumours
Infection
Bronchiectasis
Local trauma (or biopsy)
Pulmonary embolism (PE)
Vascular erosion

193
Q

What is alveolar proteinosis?

A

accumulation within the alveoli of excess PAS-positive material (positive to periodic acid-Schiff stain) that consists of surfactant (phospholipids), proteins and cellular debris.

194
Q

why is there crazy paving pattern in PAP

A

thickened septa and consoldiation with normal liung in between

195
Q

what is secondary PAP associated with?

A

acute and chronic ML
lymphoma
SCID
AIDS

196
Q

Differentials for causes of crazy paving

A

PAP

Lepidic-type adenocarcinoma and lipoid pneumonia

PCP

Sarcoid

NSIP
ARDS
pulmonary haemorrhage

197
Q

Lab test in PAP

A

An elevated serum lactate dehydrogenase (LDH) and
Elevated serum surfactant proteins A and D (SP-A and SP-D)

198
Q

Eosinophilic lung diseases of unknown cause

A

Simple pulmonary eosinophilia (SPE)
Acute eosinophilic pneumonia (AEP)
Chronic eosinophilic pneumonia (CEP)
Idiopathic hypereosinophilic syndrome (IHS)

199
Q

Eosinophilic lung diseases of known cause

A

Allergic bronchopulmonary aspergillosis (ABPA)
Bronchocentric granulomatosis
Parasitic infections
Drug reactions

200
Q

Eosinophilic vasculitis diseases

A

Allergic angiitis
Granulomatosis (Churg-Strauss syndrome)

201
Q

Charcot-Leyden crystal

A

bipyramidal crystals whose presence in sputum and tissues is a hallmark of eosinophilic related disease

202
Q

what are the differentials for Eosinophilic penumonia

A

Pulmonary haemorrhage
Pulmonary vasculitis
Cryptogenic organising pneumonia
Recurrent aspiration

203
Q

what is Loffler syndorme

A

Simple eosinophilic pneumonia

204
Q

Acute eosinophilic pneumonia

criteria

A

Hypoxaemia
Diffuse alveolar or mixed alveolar/interstitial opacities on radiographs

BAL fluid consisting of more than 25% eosinophils

Absence of parasitic, fungal or other infections

Prompt and complete response to cortical steroids with no relapse after discontinuation

blood eosinophil count normal

205
Q

what are the differentials for acute esopinophilic pneumonia

A

Pulmonary oedema
Adult respiratory distress syndrome (ARDS)
Acute interstitial pneumonia
Atypical bacterial or viral pneumonias

206
Q

What is Allergic bronchopulmonary aspergillosis

A

seen in patients with long-standing asthma or cystic fibrosis. It is thought to be mediated by Aspergillus-specific IgE-type I and IgG-type III hypersensitivity reactions.

207
Q

Which disease should be considered with gloved finger appearance on CT / CXR

A

ABPA

208
Q

ABPA differentials

A

Endobronchial lesions
Bronchial atresia
Asthma

209
Q

What is Bronchocentric granulomatosis

A

tissue eosinophilia and tend to have asthma, peripheral eosinophilia and positive sputum cultures for Aspergillus. ONeutrophils present in the lungs

210
Q

CHurg Strauss needs 4 of the following 6 conditions

A

Asthma
Eosinophilia >10% WBC differential count
Neuropathy
Migratory or transient pulmonary opacities
Paranasal sinus abnormalities
Extravascular eosinophils revealed at biopsy

211
Q

CEP is characterised by

A

peripheral non-segmental air space consolidation

212
Q

ABPA manifests with

A

bilateral central bronchiectasis with or without mucoid impaction and fleeting area of consolidation

213
Q

Mild central bronchiectasis can be seen in asthma secondary to chronic inflammation and does not necessarily indicate the presence of ???

A

ABPA

214
Q

On CT, SPE and IHS are characterised by single or multiple nodules with a surrounding ????

A

ground glass halo

215
Q

AEP mimics radiologically

A

hydrostatic pulmonary oedema

216
Q

The relatively late patient age at onset distinguishes the asthma in patients with ?????? from that in the general population

A

Churg-Strauss syndrome

217
Q

Churg-Strauss radiologically is shown by

A

subpleural ground-glass opacity or consolidation with a lobular distribution

218
Q

Bronchocentric granulomatosis differs from the other pulmonary granulomatosis in that it is localised to the ???? and is centred around ????/

A

Lungs

the airways rather than the vessels

219
Q

non-specific symptoms such as shortness of breath, which may be worse on exertion or lying flat, or a non-productive cough.

A

bronchial stenoses

220
Q

Conditions that can stenose the airway

external and intrinsic

A

External
GOitre
Fibrosing mediastinitis

INtrinsic
Focal - tracheal stricture
Diffuse- ampyloid

221
Q

differnetial for massive thyroid goitre

A

thyroiditis
thyorid carcinoma

222
Q

Causes of fibrosing mediastinitis

A

Idiopathic

TB
Fungi

223
Q

causes of tracheal stricture

A

normally trauma of some kind

224
Q

what is Tracheobronchomalacia

A

weakness of the tracheal or bronchial walls and the supporting cartilage

weak cough so infections

225
Q

What percentage of tracheal neoplasms are benign

A

less than 10%

226
Q

Example of benign tracheal neoplasms

A

Squamous cell papilloma – this is the commonest and is secondary to human papilloma virus infection
Hamartoma
Chondroma
Haemangioma
Schwannoma
Leiomyoma

227
Q

Examples of intrinsic tracheal diseases causing stenoses

A

Amyloid
Relapsing polychondritis
Sabre-sheath trachea
Tracheobronchopathia osteochondroplastica
Tuberculosis
Wegener’s granulomatosis

228
Q

material stains red with Congo red, showing apple-green birefringence under polarised light.

A

amyloidosis

229
Q

Differentials for amyloid tracheal disease

A

tracheobronchopathia osteochondroplastica.

230
Q

Sabre sheath trachea diagnostic mesurement relationship

A

The diagnosis is made when the coronal (side-to-side) diameter of the trachea is less than half the sagittal (AP) diameter.

231
Q

tracheobronchopathia osteochondroplastica, calcification spares the posterior tracheal membrane

this is different to its differential of what?

A

Amyloidosis

AA ST2 (14 decks)

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