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1

Features of UIP

Basal and subpleural predominant
Honeycombing/reticular opacities
(+ secondary signs of fibrosis (not part of 'high confidence' criteria))
Absence of;
- extensive groundglass opacity,
- segmental or lobar consolidation,
- Bilateral cysts
- Mosaic perfusion or air trapping
- Profuse micronodules

2

Differential diagnosis of UIP

IPF (most common)
Connective tissue disease (eg RA)
Drug toxicity (rare)
Asbestosis (rare)

3

Difference between UIP and NSIP

NSIP has more secondary signs of fibrosis (traction bronchiectasis, reticulation), and relative sparing of subpleural lung.

4

Traction bronchiectasis without honeycombing (most likely differentials

NSIP
Sarcoidosis
HSP

5

Acute symptoms + groundglass opacity + Intralobular interstitial thickening

Pulmonary oedema
Infection
Diffuse alveolar damage (eg drug toxicity)
Haemorrhage

6

Chronic symptoms + groundglass opacity + intralobular interstitial thickening

HSP
NSIP
UIP (rare to have GGO)

7

Nodular distribution in sarcoidosis

Perilymphatic
Typically peribronchovascular and subpleural
Upper lobe predominant
Galaxy sign

8

Nodular distribution in Lymphangitic carcinomatosis

Perilymphatic
Typically interlobular septa > subplerual/peribronchovascular
May have lower lobe predominance due to increased blood flow.

9

Nodular distribution in silicosis or coal workers pneumoconiosis

Both look similar but have different histology
Usually centrilobular > subpleural/interlobular septa (dust cleared by lymphatics in the alveoli first)
Upper lobe predominant and posterior lung.

10

GGO centrilobular nodules + chronic symptoms

HP (antigen exposure)
RB (smokers)
Follicular bronchiolitis (immunosuppressed)

11

GGO centrilobular nodules + acute symptoms

Atypical (viral/myco) pneumonia (typicals also possible)
Pulmonary oedema
Pulmonary haemorrhage

12

Differentials for perilymphatic nodules

Sarcoidosis
Neoplasm
Silicosis / coal workers lung

13

Differentials for random nodules

Miliary infection
Neoplasm

14

Differentials for centrilobular nodules

Infection
Hypersensitivity pneumonitis
Mucinous adencarcinoma
Respiratory bronchiolitis
Oedema
Haemorrhage

15

Groundglass opacity in acute setting

Infection (atypicals)
Oedema
Acute lung injury
Haemorrhage
Aspiration
Hypersensitivity pneumonitis (acute)
Acute eosinophilic pneumonia

16

Chronic groundglass opacity with peripheral distribution

Interstitial pneumonia
- NSIP (subpleural sparing)
- DIP (smokers)
- UIP

17

Most common differentials for groundglass opacity in chronic setting

Hypersensitivity pneumonitis
NSIP
DIP

18

Differentials of mosaic attenuation

HSP
Asthma
Constrictive Bronchiolitis (bronchiolitis obliterans)
Vasculitis
Chronic PE

19

Differentials of headcheese sign
(Groundglass + mosaic attenuation)

HSP (by far most common)
DIP and RB
Follicular bronchiolitis and lymphoid IP
Sarcoidosis
Atypical infections
2 different processes. (Eg oedema and asthma)

20

Cystic lung disease, top 3 differentials

LAM (lymphangioleiomyomatosis)
LCH (Langerhans cell histiocytosis)
LIP (Lymphoid Interstital pneumonia)

21

Key points about LIP

Associated with connective tissue diseases, most commonly sjögrens disease
Lung bases
Up to a dozen cysts
Adjacent to vessels

22

Key points about LCH

Smoking related disease
Upper lobe predominant
Irregular cysts
Nodules (GGO or solid) may precede

23

Key points about LIP

Associated with connective tissue diseases, most commonly sjögrens disease
Lung bases
Up to a dozen cysts
Adjacent to vessels

24

Key features of immunodeficiency (pulmonary changes)

Includes congenital (agammaglobulinaemia, hypogammaglobulinaemia), acquired (AIDS), ciliary diskinesia
Lower lobe predominant large airways changes.
May have some small airways changes as well (particularly with ciliary diskinesia).

25

What is kartageners syndrome

Primary ciliary diskinesia
Situs inversus.

26

What is Williams-Campbell Syndrome

Absence of cartilage in the 4th-6th order bronchi
Results in cystic bronchiectasis without airways inflammation in the mid-lower lung.
Bronchi may collapse on expiration.

27

Tracheobronchomegaly

Atrophy of portions of the tracheal and bronchial walls.
CT shows severely dilated trachea and central bronchi without inflammatory changes.
Scalloping due to intact cartilage rings.
Rare.

28

What is Williams-Campbell Syndrome

Absence of cartilage in the 4th-6th order bronchi
Results in cystic bronchiectasis without airways inflammation in the mid-lower lung.
Bronchi may collapse on expiration.

29

Differentials of soft tissue attentuation centrilobular nodules

Bronchiolar impaction. Caused by diseases which spread via airways
- Infection
- Tumour (invasive mucinous adeno)
- Aspiration

30

Tree in bud - Differentials

Almost always infection (acute or chronic) (90%)
If chronic consider cause of chronic (immunodeficiency, cliliary diskinesia, CF)

Can also be caused by
Aspiration
Invasive mucinous adenocarcinoma (rarely)
Panbronchiolitis
ABPA.

31

Mosaic perfusion as the predominant finding

Asthma
Hypersensitivity pneumonitis
Constrictive bronchiolitis
Vascular (chronic PE, vasculitis)

32

Tree in bud - Differentials

Almost always infection (acute or chronic) (90%)
If chronic consider cause of chronic (immunodeficiency, cliliary diskinesia, CF)

Can also be caused by
Aspiration
Invasive mucinous adenocarcinoma
Panbronchiolitis
ABPA.

33

Mosaic perfusion as the predominant finding

Asthma
Hypersensitivity pneumonitis
Constrictive bronchiolitis
Vascular (chronic PE, vasculitis)

34

Mosaic perfusion, Air trapping and fibrosis is highly suggestive of...

Hypersensitivity pneumonitis

35

5 categories of pulmonary hypertension

1 - Pulmonary arterial hypertension or veno-occlusive disease
2 - Left ventricular failure
3 - Lung disease/hypoxia
4 - Chronic PE
5 - Unclear/multifactorial

36

Differentials for crazy paving in acute setting

Oedema
Haemorrhage
Diffuse alveolar damage
Atypical infections

37

Systemic causes of diffuse alveolar damage

Sepsis
Burns
DIC
Pancreatitis
Shock
Drugs

38

Pulmonic causes of diffuse alveolar damage

Pneumonia
Aspiration
Trauma
Toxic inhalations.

39

High confidence of UIP (Typical/definite UIP)

- Honeycombing
- Reticulation
- Basal/subpleural dominant
- Absence of features atypical for UIP

40

Intermediate confidence (Possible/probable UIP)

- Absence of honeycombing
- Reticulation
- Basal/subpleural dominant
- Absence of features atypical for UIP

41

Alternative diagnosis with intermediate confidence UIP

- IPF (60-90%)
- HP (most of remainder)
- Connective tissue disease

42

Features of NSIP

Basal and subpleural/peripheral distribution
Subpleural sparing is suggestive of NSIP but only present up to 50% of the time.
Concentric rather than patchy (UIP is more patchy)

Cellular type
- GGO +/- fine reticulation and traction bronchiectasis

Fibrotic type
- Traction bronchiectasis and fine reticulation (honey combing is uncommon)

43

Features of DIP

Basal and peripheral distribution (classically) but can vary.
GGO is the main feature
On the same spectrum as RB so may also have centrilobular GGO nodules, mosaic perfusion, air trapping.

44

Reverse halo sign (Atoll sign)

Central clearing with a rim of consolidation
DDx:
- OP
- Infarction
- Infection (particularly fungal)(Mucormycosis)
- Sarcoidosis
- Vasculitis (GPA)

45

Features of organising pneumonia (OP)

Basal predominant
Peripheral and peribronchovascular
Focal nodular or mass-like consolidation with irregular margins and/or spiculation.
Normal lung in between.

Additionally; Atoll sign, perilobular opacities

Caused by rounded plugs of granulation tissue in the alveoli or respiratory bronchioles (distal airways).

46

Causes of OP

Idiopathic (cryptogenic OP)

Connective tissue disease
Infection
Drugs
Toxic inhalations
Immunologic disorders
Graft-vs-host disease

Secondary to:
Chronic eosinophilic pneumonia (indistinguishable expect for presence of eosinophils)
HP
GPA
DAD

47

Features of Acute Interstitial Pneumonia (same as DAD)

Idiopathic interstitial pneumonia presents with ARDS of unknown cause.

Diffuse GGO or consolidation.
Eventually develop fibrosis in an anterior, subpleural location.

48

Features of lymphoid interstitial pneumonia (LIP)

Patchy GGO (most common)
May also have consolidation
GGO nodules - perilymphatic or centrilobular
Cysts (limited in number, thin-walled)

Features are non-specific so relies on the clinical history to suggest the diagnosis of LIP

49

Causes of LIP

Connective tissue disease (Sjogrens)
Immunodeficiency disorders

50

Features of Pleuroparenchymalfibroelastosis (PPFE)

Apical and subpleural distribution
Consolidation and fibrosis involving both pleura and parenchyma

51

Causes of PPFE

Idiopathic
Chronic infection
Drugs
Connective tissue disease
Bone marrow translant
Chronic rejection of lung transplant.

52

Most common lung presentations in scleroderma

NSIP > UIP > all others (80% have pulmonary disease)

May also have pulmonary hypertension (vascular or pulmonary cause), oesophageal dysmotility, raynauds.
((Scl-70 and anti U3 RNP antibodies are specific))

53

What is CREST

Limited cutaneous scleroderma
Calcinosis
Raynauds
oEsophageal dysmotility
Sclerodactyl
Telangiectasia

Pulmonary vascular disease > fibrotic lung disease.

54

Lung presentations of RA

40% of patients will have pulmonary disease
UIP and NSIP >> LIP/follicular bronchiolitis and OP

May also see rheumatoid nodules (can become large and cavitate - may complicate with bronchopleural fistula)

55

Lung presentations of SLE

- DAD, Diffuse alveolar haemorrhage, pulmonary oedema.
- Serositis (thickening/effusions of pleura/pericardium reflecting exudative effusions)
- Vanishing lung syndrome (restrictive pattern on PFTs with slowly elevating diaphragms, no parenchymal disease)

SLE - rash, oral ulcers, photosensitivity, arthritis, serositis (anti-dsDNA is specific)

56

Lung presentations of polymyositis and dermatomyositis

(Muscle weakness, arthritis (skin changes in dermato-)
(Anti-Jo-1 antibodies specific)
NSIP most common along with OP.
DAD may occur.

57

Sjögrens disease lung presentations

(disease of lacrimal and salivary glands)
(anti-SSA and anti-SSB autoantibodies)
NSIP pattern
LIP - usually up to a dozen rounded cysts, possibility to also have GGO centrilobular nodules

58

What is IPAF

Interstitial pneumonia with autoimmune features
Must meet 2 of 3 criteria
- Clinical - Serological - Morphological (rad or path)
Rad:
- NSIP/OP/LIP
and
- Multicompartment disease (pleural, pericardial, airways, vascular)

59

Features of RB

Upper/central predominant
GGO centrilobular nodules
Mild mosaic perfusion/air trapping

60

Features of DIP

Basal/peripheral predominant (same as UIP/NSIP)
GGO
Focal air density lucencies (cysts or emphysema)

61

Features of LCH

Primarily in smokers, age 30-40yrs. Often asymptomatic until ptx.
Upper lobe predominance. (basal spared)
Soft tissue attenuation nodules that cavitate with time.
Later disease will have irregularly shaped cysts with both thin and thick walls.

62

Differentiating Cystic lung diseases
(LCH, LAM, LIP, Others (septic emboli, fungal, mets, GPA)

LCH - spares the basal lung. No pleural effusion. Irregular and high number of cysts/nodules

LAM - Throughout the lung. Female only. Pleural effusion possible. Regular rounded cysts. No nodules.

LIP - Fewer cysts.

Septic emboli, fungal infection, GPA, cystic mets, tracheobroncial papillomatosis - larger cysts

63

Staging sarcoidosis

Based on CXR not HRCT.
Higher stages = less likely to spontaneously regress
(90% stage 1 vs 20% stage 3)

0 - normal
1 - Hilar LN
2 - Hilar and parenchymal disease
3 - Parenchymal disease only
4 - Fibrosis

64

Perilymphatic nodules differential diagnosis

Sarcoidosis (90% of the time)
Lymphangitic spread of cancer (2nd most common, more in interlobular septa and lower lobe predominant)
LIP
Pneumoconioses (Silicosis/CWP)
Amyloidosis

65

Distribution of sarcoidosis nodules

Perilymphatic
More peribronchovascular and subpleural
Upper/mid zones
Bilateral, symmetric.

66

Features of Hypersensitivity Pneumonitis (HP)

Acute - rare. Findings are likely similar to subacute but more severe

Subacute - Patchy central, mid/upper zone GGO, GGO nodules, Mosaic perfusion. (Consolidation if secondary OP is a feature)

Chronic - Same as subacute but replace GGO with fibrosis.

67

What are some exposures typical of the different acuities of HP

Acute - Rapid onset. Exposure to moldy hay
Subacute - Weeks to months exposure
Chronic - Years of exposure. eg bird fanciers

Smoking is protective but not absolutely.

68

Key points about simple pulmonary eosinophilia

AKA Loeffler syndrome
Rare, unknown cause
Absent or mild symptoms
Migratory consolidation (non-segmental)
Spontaneous resolution after 1 month

69

Features of acute eosinophilic pneumonia (AEP)

Rapid onset (less than 1 week)
Usually in smokers who have increased their number of cigarettes leading up to event
Does not show peripheral eosinophilia (unlike other eosinophilic lung diseases)
Characterised by infiltration of eosinophils - Diffuse GGO/consolidation.
May progress to ARDS

70

Features of chronic eosinophilic pneumonia

Most common idiopathic eosinophilic disease
50% have asthma.
(can be a reaction to drugs or parasites)
Peripheral and upper lobe consolidation (photographic negative of oedema). May have atoll sign.
May be indistinguishable from OP (OP usually lower lobe predominance)

71

Hypereosinophilic Syndrome features

systemic disorder that typically affects CNS and heart
Lung features are usually related to cardiac failure.
Males 20-40yo.

72

Features of Eosinophilic GPA (Churg-strauss syndrome)

Combination of vasculitis and eosinophilia
Involves Lungs, CNS, skin
Migratory consolidation in peripheral distribution (similar to CEP) but in a lobular distribution.

73

Features of ABPA

Seen in asthmatics and CF.
More of a clinical diagnosis.
Predominant central, mid/upper lungs bronchiectasis (thickening, mucoid impaction, dilation).
Often asymmetrical.

74

Potential differentiating features of atypical vs 'typical' infections

Atypical
- viral, chlamydia, M.pneumonia, Legionella, Pneumocystis
- Diffuse, bilateral. GGO significant component

Typical
- Typical bacteria, mycobacteria, fungal
- Patchy, asymmetric, consolidation.

75

Infective causes of TIB

More associated with bacterial and mycobacterial infections with impaction of bronchioles.
Fungal and viral infections are less likely to cause this.
In both acute and chronic settings, TIB is most likely to represent infection (atypical mycobacterium in chronic).

76

What sort of history is found with actinomyces infection?

Normal part of oral flora.
Predisposing factors:
- poor dental hygiene
- alcoholism
- pre-existing lung disease (emphysema, bronchiectasis)

77

Who is affected by nocardia infection

Bacteria found within the soil.
Usually seen in the setting of immunocompromise.

78

Features of acute TB

Solitary nodule (granulomatous reaction)
May have an enlarged draining LN with low attenuation.
Both the nodule and LN may calcify with time.

79

Features of reactivation TB

Consolidation in the upper lobe (highest oxygen tension)
Cavitation
Endobronchial spread (centrilobular nodules of soft tissue attenuation, TIB)
Scarring
Pleural effusions/thickening

80

Features of Miliary TB

Haematogenous spread not limited by an immune response.
Random small nodules.
ddx - fungal disease (coccidio, histo, blasto), metastatic disease

81

Features of MAI

Middle lobe/lingula airways disease
(Bronchiectasis, airway wall thickening, mucous impaction)
May have TIB and centrilobular nodules.

These features are reasonably predictive of MAI in an elderly female.

82

Typical bacteria in community acquired pneumonia

Strep pnuemonia
H. influenzae
S. aureus
Gram -ve organisms

83

Typical bacteria in hospital acquired pneumonia

S. aureus
Pseudomonas (atypical)
E. coli
Acinetobacter
Klebsiella
H. influenzae

84

How do people develop silicosis?

Chronic inhalation of silicon dioxide
- glass manufacturing
- sand blasting
- mining/quarrying
- stone cutting

85

Patterns of simple silicosis

(appearances can be indistinguishable from sarcoidosis)
Posterior upper lobes
Perilymphatic nodules - centrilobular and peribronchovascular
Hilar/mediastinal nodes may have eggshell calcification.

86

Pattern of complicated silicosis

Chronic exposure results in progressive fibrosis.

Fibrosis
Perilymphatic nodules
May develop PMF (confluent areas of fibrosis)

87

Pneumoconioses that look similar to silicosis

CWP (coal mining)
Berylliosis (aerospace and ceramic industries)
Inhaled talcosis (textiles, rubber, paper)

88

Features of acute silicosis/silcoproteinosis

Indistinguishable from Pulmonary Alveolar Proteinosis
Extensive/diffuse GGO + consolidation
May also have crazy paving.

89

Complications of silicosis

Increased risk of Tb
Increased risk of bronchogenic carcinoma (differentiate from PMF with PET or MRI)

90

Early appearances of asbestos exposure

Pleural thickening and pleural effusion (exudative)
Can be unilateral

91

Features of asbestosis + complications

UIP type pattern
Pleural plaques (over the ribs, spare costophrenic angles)

Highest risk of bronchogenic carcinoma and also mesothelioma

92

Complications of asbestosis

Highest risk of malignancy our of all the pneumoconioses
- brochogenic carcinoma
Also at high risk of mesothelioma.

93

How do people develop siderosis

Inhalation of iron oxide
- most commonly with welding

94

Features of siderosis

No significant inflammatory or granulomatous reaction
(May also inhale silica dust so there could be a mixed pattern)
Features similar to subacute HP
- Centrilobular GGO nodules
- Patchy GGO (from the presence of the actual dust)
- Mosaic perfusion

Hard metal pneumoconiosis looks similar to siderosis and is more likely to progress to fibrosis.