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Revision > Interstitial lung disease > Flashcards

Interstitial lung disease Flashcards

1
Q

Where is the abnormality for:
1) Consolidation
2) Reticular
3) GGO

A

1) Air space
2) Interstitium
3) Either or both

Nb. if see GGO, see if dilated airways - if so then know fibrotic process

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2
Q

What is honeycombing?

A

Clustered cystic airways in periphery
3-10mm (but can be larger)

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3
Q

What is typical UIP?

A

Distribution: subpleural & basal (often heterogenous)
Features: reticulation + traction & honeycombing (& no features suggestive of alternative diagnosis)

Probable:
Dist: subpleural & basal (often heterogenous)
Feat: reticulation + traction & NO honeycombing (& no features suggestive of alternative diagnosis)

Indeterminate:
Dist: variable or diffuse
Feat: fibrosis but some features suggestive of non-UIP e.g. GGO, consolidatoin

Not-UIP:
Dist: upper/mid-lung/peribronchovascular predominant
Feat: Prominent consolidation/GGO (w/o acute exacerbation)/mosaic attenuation with sharply defined lobular air trapping on expiration/diffuse nodules or cysts

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4
Q

What is definition of probable UIP?

A

Dist: subpleural & basal (often heterogenous)
Feat: reticulation + traction & NO honeycombing (& no features suggestive of alternative diagnosis)

Definite:
Distribution: subpleural & basal (often heterogenous)
Features: reticulation + traction & honeycombing (& no features suggestive of alternative diagnosis)

Indeterminate:
Dist: variable or diffuse
Feat: fibrosis but some features suggestive of non-UIP e.g. GGO, consolidatoin

Not-UIP:
Dist: upper/mid-lung/peribronchovascular predominant
Feat: Prominent consolidation/GGO (w/o acute exacerbation)/mosaic attenuation with sharply defined lobular air trapping on expiration/diffuse nodules or cysts

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5
Q

What is the definition of indeteminate UIP?

A

Dist: variable or diffuse
Feat: fibrosis but some features suggestive of non-UIP e.g. GGO, consolidatoin

Definite:
Distribution: subpleural & basal (often heterogenous)
Features: reticulation + traction & honeycombing (& no features suggestive of alternative diagnosis)

Probable:
Dist: subpleural & basal (often heterogenous)
Feat: reticulation + traction & NO honeycombing (& no features suggestive of alternative diagnosis)

Not-UIP:
Dist: upper/mid-lung/peribronchovascular predominant
Feat: Prominent consolidation/GGO (w/o acute exacerbation)/mosaic attenuation with sharply defined lobular air trapping on expiration/diffuse nodules or cysts

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6
Q

What is the defintion of not-UIP?

A

Not-UIP:
Dist: upper/mid-lung/peribronchovascular predominant
Feat: Prominent consolidation/GGO (w/o acute exacerbation)/mosaic attenuation with sharply defined lobular air trapping on expiration/diffuse nodules or cysts

Definite:
Distribution: subpleural & basal (often heterogenous)
Features: reticulation + traction & honeycombing (& no features suggestive of alternative diagnosis)

Probable:
Dist: subpleural & basal (often heterogenous)
Feat: reticulation + traction & NO honeycombing (& no features suggestive of alternative diagnosis)

Indeterminate:
Dist: variable or diffuse
Feat: fibrosis but some features suggestive of non-UIP e.g. GGO, consolidatoin

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7
Q

CT shows mosaic attenuation. How can you tell if black or white lung abnormal?

A

Are there fewer/smaller vessels in black lung?
Y (black abnormal)
–> occlusive vascular disease e.g. CTEPH (look for dilation of central PA, RV/LV ratio, subpleural opacities/linear bands, effusions)
–> small airways disease e.g. obliterative bronchiolitis (look for large airway dilatation e.g. bronchiectasis - could ask for expiratory scan if unsure)

N (white abnormal)
–> infiltrative lung disease e.g. GGO

Nb. can have both abnormal - if fewer vessels in black & GGO/fibrosis in white
–> Hypersensitivity pneumonitis OR sarcoid

Nb2. if look similar then probably white lung abnormal

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8
Q

What are CT findings of NSIP?

A

Symmetrical, bilateral GGO
If fibrotic, fine reticulation and volume loss + traction
Bronchovascular, subpleural sparing nb. still often peripheral though
Can have cysts but not honeycombing

Nb. nodules, mosaic attenuation or cysts should make you think of other things

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9
Q

What kinds of NSIP are there?

A

Fibrotic - worse outcome
Cellular

Causes: CTD, autoimmune, drug esp chemo, relapsing OP

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10
Q

What are causes of NSIP?

A

CTD e.g. SLE/scleroderma/myositis
Autoimmune e.g. RA, PBC, antisynthetase
Drugs e.g. chemo
Relapsing OP

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11
Q

What are causes of UIP?

A

IPF
CTD-ILD - RA common, systemic sclerosis (NSIP more common), poly/dermato (UIP/NISP/COP), mixed CTD (UIP/NSIP)
Chronic HP
Asbestosis
Radiation
ANCA vasculitis
Drugs - amidorone

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12
Q

What is histology of UIP?

A
  • Dense fibrosis + architectural distortion (e.g. honeycombing)
  • Predominant subpleural/paraseptal fibrosis with areas of less involved parenchyma
  • Max mild inflammation only (and not lymphocytes >40% = HP)
  • Fibrobastic foci

HP
- Bronchocentric/diffuse interstitial inflammation with thickened alveolar septa
- Lymphocytes >40%, plasma cells +/- occasional multinucleate giant cells
- Poorly formed granuloma
- Tiny foci of OP (scattered plugs of fibroblasts)

Sarcoid
- Lymphatic distribution
- Non-necrotising granulomas
- Central areas of macrophages, epitheliod, multinucleate giant cells, CD4 T-cells
- Surrounded by CD4+8 Tcells, B cells, monocytes, mast cells & fibroblasts

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13
Q

What is the histology of HP?

A
  • Bronchocentric/diffuse interstitial inflammation with thickened alveolar septa
  • Lymphocytes >40%, plasma cells +/- occasional multinucleate giant cells
  • Poorly formed granuloma
  • Tiny foci of OP (scattered plugs of fibroblasts)

Nb.
UIP
- Dense fibrosis + architectural distortion (e.g. honeycombing)
- Predominant subpleural/paraseptal fibrosis with areas of less involved parenchyma
- Max mild inflammation only (and not lymphocytes >40% = HP)
- Fibrobastic foci

Sarcoid
- Lymphatic distribution
- Non-necrotising granulomas
- Central areas of macrophages, epitheliod, multinucleate giant cells, CD4 T-cells
- Surrounded by CD4+8 Tcells, B cells, monocytes, mast cells & fibroblasts

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14
Q

What is the histology of sarcoid?

A
  • Lymphatic distribution
  • Non-necrotising granulomas
  • Central areas of macrophages, epitheliod, multinucleate giant cells, CD4 T-cells
  • Surrounded by CD4+8 Tcells, B cells, monocytes, mast cells & fibroblasts

Nb.
UIP
- Dense fibrosis + architectural distortion (e.g. honeycombing)
- Predominant subpleural/paraseptal fibrosis with areas of less involved parenchyma
- Max mild inflammation only (and not lymphocytes >40% = HP)
- Fibrobastic foci

HP
- Bronchocentric/diffuse interstitial inflammation with thickened alveolar septa
- Lymphocytes >40%, plasma cells +/- occasional multinucleate giant cells
- Poorly formed granuloma
- Tiny foci of OP (scattered plugs of fibroblasts)

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15
Q

What are RFs for IPF?

A

Smoking, GORD, EBV, hep C, fhx of ILD
M>F
<50 years RARE

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16
Q

How is IPF diagnosed?

A

Radiology MDT
- if not definite UIP, then can do lung biopsy (BAL not routinely recommended - main reason would be to r/o HP - lymphocytes >40%)

Histology:
- Dense fibrosis + architectural distortion (e.g. honeycombing)
- Predominant subpleural/paraseptal fibrosis with areas of less involved parenchyma
- Max mild inflammation only (and not lymphocytes >40% = HP)
- Fibrobastic foci

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17
Q

How is biopsy taken for UIP and when is it needed?

A

Only needed if diagnostic uncertainty
Often risk > benefit
Recommend surgical biopsy (or cryobiopsy - 10% PNX, 10% haemorrhage)

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18
Q

What are the main predictors of outcome for IPF?

A

Drop of SATS during 6MWT
TLCO at presentation (<40% = advanced disease)
Drop of FVC 10% or FEV1 15% in first 6-12 months
Overnight oximetry

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19
Q

What is most common mutation associated with IPF?

A

MUC5B (also ass with UIP with RA)

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20
Q

What is treatment for IPF?

A

Criteria: FVC 50-80% for pirfenidone or >50% for nintedanib+ MDT diagnosis
Stop if: FVC decline >10% in 1 year

Pirfenidone SEs. N, decrease appetite, photosensitive rash (30%)
Nintedanib SEs. D

Nb. slow decline in FVC by 50% (and nintedanib increases time to first exacerbation)

Monitor: LFTs at 1/12 for 6/12 then 3/12
- if 3-5xULN then reduce dose or stop but can return when normal (reduced dose and uptitrate)
- if >5ULN then stop (or <5 with symptoms of liver dysfunction)

Nb2. Can consider steroids if lots of GGO suggestive of exacerbation

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21
Q

What are SEs of Pirfenidone? When can it be used and what do you have to monitor?

A

Nausea, decrease appetite, photosensitive rash (30%), wt loss

Indications: FVC 50-80% + MDT diagnosis of IPF –> start low dose and uptitrate
Stop if: FVC decline >10% in 1 year

Monitor: LFTs monthly for 6/12 then three-monthly
–> if 3-5xULN then decrease dose/interrupt and restart when normal
–> >5ULN then stop (or <5 but symptoms of liver dysfunction)

Suggest take with food due to SEs.
Approx 801mg TDS

Contraindications: pregnancy/breast feeding, smoking, eGFR<30, severe hepatic impairment
Caution: mild hepatic/renal impairment

Common interactions: ciprofloxacin (reduce does of pirfenidone and give high dose cipro 750mg)

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22
Q

What are SEs of Nintedanib? What are indications for use? What monitoring is required?

A

Diarrhoea, increased bleeding risk

Indications: FVC >50% + MDT diagnosis of IPF
OR progressive-fibrosing ILD and 10% FVC decline over 24months or 5-10% + symptoms
–> start at full dose (150mg BD)
Stop if: FVC decline >10% in 1 year

Monitor: LFTs monthly for 6/12 then three-monthly
–> if 3-5xULN then decrease dose/interrupt and restart when normal
–> >5ULN then stop (or <5 but symptoms of liver dysfunction)

Nb. only 1% renally excreted therefore can use in patients with very low renal function

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23
Q

What is definition of progressive fibrotic ILD?

A

2/3 of:
- Worsening symptoms
- Radiological progression
- Physiological progression (decrease FVC ≥5% or DLCO ≥10% in 1 year)

All within 1 year in a patient with ILD that isn’t IPF and no other explanation for decline

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24
Q

What radiology patters do you see in CTD-ILD?

A

Chronic fibrosing: NSIP (SSc) or UIP (RA)

Subacute/acute: OP/NSIP/DAD (idiopathic inflammatory myositis)

Nb. if underlying disease quiescent, less likely to be this

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25
Q

What is the most common cause of CTD-ILD? What are the predictors of severity?

A

SSc - tends to present in more chronic way (NSIP)

Severity:
- Increased extent at presentation
- Scl-70, Th/To, U3RNP
- Short term progression in lung function
- ILD in first 4 years of SSc diagnosis

Nb. Anti-centromere Ab = protective (but ass with PH)

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26
Q

What is the typical radiological pattern for SSc-ILD?

A

NSIP - Symmetrical, bilateral GGO, fine reticulation and volume loss + traction, subpleural sparing nb. still often peripheral though

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27
Q

What is the typical radiological pattern for myositis-ILD?

A

OP/NSIP - particularly if subacute/chronic presentation

Can get acute presentation.

Has a good prognosis and CK levels may be normal.

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28
Q

What is the typical radiological pattern for RA-ILD? What are RFs?

A

NSIP but also UIP (NSIP more on radiology, but equal on histology)

RFs: increasing age, smoking, male, anti-CCP

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29
Q

What is the prognosis for RA-ILD with UIP pattern?

A

Very like IPF nb. also ass with Muc5b

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30
Q

What is treatment for CTD-ILD?

A

General:
Prednisolone 0.5-1mg/kg +/- iv/oral cyclophosphamide or azathioprine
–> taper to maintenance <10mg

Dermato/poly - early treatment with the above
SSc - MMF –> use low dose steroids and cyclo if needed to get ression (only use low dose steroids due to risk of renal crisis)

Nintedanib if progressive fibrosing (>10% fibrosis on CT)

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31
Q

What are the CT features of hypersensitivity pneumonitis?

A

Non-fibrotic pattern:
- GGO/mosaic attenuation (suggest parenchymal infiltration)
- Air trapping/ill-defined centirolobular nodules (suggest small airways disease)
- Diffuse distribution +/- basal sparing

Fibrotic:
- reticulation/bronchiectasis/honeycomb (ie. fibrotic features)
+/- centirolobular nodules, mosaic attenuation, 3-density pattern (ie. .small airways involvement)
- Diffuse distribution +/- basal sparing

Nb. BAL very helpful –> >30% lymphocytes (20% in non-smokers) +/- granulomas

32
Q

How does HP present?

A

Very variable presentation and progression

Squawks very helpful but not always present

Nb. is a type 3 hypersensitivity mediated by IgG complexes

33
Q

How is HP classified?

A

Fibrotic
Non-fibrotic

Nb. is a type 3 hypersensitivity mediated by IgG complexes

34
Q

How is HP treated?

A

Avoid exposure (may be sufficient in mild disease)
High dose steroids (0/5mg/kg 2-4 weeks) then taper
MMF/azathioprine/Rituximab to maintain stability or if intolerant to pred

Progressive fibrosing - Nintedanib

35
Q

What are some common drug causes of HP?

A

Amiodarone, nitro, biologics

Other causes: mould, gardening, hot tub (m.avium), farmers (fungi), bird proteins

36
Q

What are histology features of HP?

A

Lymphocytosis on BAL (>20% or 30% in smokers)
BUT may be normal if fibrotic HP

Granulomas - ‘ill defined’ ‘loose forming’

37
Q

How do you define inflammatory non-fibrotic HP on CT?

A

1 of GGO/mosaic attenuation
1 or air trapping/ill-defined centirolobular nodules
Dist: top>bottom

Nb. Resp bronchiolitis in ILD tends to be centirolobular nodules in diffuse distribution

Fibrotic:
1 of reticulation/bronchiectasis/honeyco
1 of centirolobular nodules/mosaic atten/3-density pattern
Dist: top > bottom

38
Q

How is HP diagnosed?

A

Clinical + CT + BAL +/- biopsy

BAL: lympocytes >20% (30% smokers) >50% = highly suggestive
May be normal in fibrotic HP. May see granulomas ‘ill formed’ ‘loose forming’. May see giant cells with cholesterol clefts.

Biopsy (transbronchial if non-fibrotic, transbronchial cryo or surgical if fibrotic): granulomatous, bronchocentric inflammation

Nb. IgG against specific Ag marker of exposure, not disease. Helpful but not diagnostic.

39
Q

What are RFs for mortality with HP?

A

UIP like pattern
Increasing age
Clubbing
Higher severity disease
Declining FVC
Failure to identify trigger
Intense exposure
Smoker
Short-telomeres

40
Q

What causes a lymphocitic BAL? ie. >15%

A

Sarcoid
NSIP
HP (nb. >50% highly suggestive for this)
Drug-induced pneumonitis
Collagen vascular disorders
Lymphocytic interstitial pneumonia
Cryptogenic organising pneumonia
Lymphoproliferative disorders

Nb. >25% highly suggestive of granulomatous disease (sarcoid, HP, berylliosis)

Nb2. Elevated CD4/CD8 ratio suggestive of sarcoid

41
Q

What causes a neutrophilic BAL? ie. >3%

A

IPF
Aspiration
Collagen vascular disease
Infection
Asbestosis
Bronchitis
ARDS

42
Q

What causes an eosinophilic BAL? ie. >1%

A

Eosinophilic pneumonias
Drug-induced pneumonitis
BM transplant
Asthma, bronchitis
Churg-Strauss
ABPA
Infection
Hodgkins

43
Q

What is the difference between a cyst and cavity on CT?

A

Cyst wall <2mm

44
Q

CT shows bizarre-shaped cysts with thick walls. What is the diagnosis?

A

Langerhans cell histiocytosis
- 20-30s
- Strong ass with smoking (but not essential)
- Upper & midzone bizarre shaped cysts with thick walls +/- nodules (become cysts)
- Mixed obstructive/restrictive PFTs
- Can be ass. with cysts in many places e.g. diabetes insipidus and bone cysts
- Might see Bierbeek granules
- CD1a positive cells on biopsy diagnostic

Treat: smoking cessation/cladribine

45
Q

CT shows uniform shaped but variable sized cysts throughout the lungs. What is the diagnosis?

A

Lymphangioleimyomatosis (LAM)
- Female, often young
- Lots of uniformly shaped (all spherical) but variable sized cysts with uniform distribution in lung. Can be large.
- Mixed obstructive/restrictive PFTs
- Ass with tuberous sclerosis (epilepsy, learning difficulties) and renal angiomyolipomas
- Can get chylous effusion
- Might see raised VEGF

46
Q

Pt has basal predominant cysts on CT of irregular shapes. What is most likely diagnosis?

A

Burt-Hogg-Dube
- Irregular shaped cysts (round and elongated), adjacent to interlobular septa, arteries and veins
- Ass with skin folliculoma and renal cysts
- Ass with FLCN gene mutation
- Increased risk of renal and lung cancer

Autosomal dominant

47
Q

What causes nodules in:
1) perilymphatic distribution
2) random
3) centirolobular

A

1) Sarcoid, silicosis
2) Mets, TB, fungal
3) HP, ifx, bronchoalveolar ca, bronchiolitis

48
Q

Pt has ill-defined centirolobar nodultes and scattered thin-walled cysts. What is most likely diagnosis?

A

Lymphocytic interstitial pneumonia
- Female, >50
- Patchy GGO, cysts no zonal prediliction, varying sizes (might not be loads of cysts). Sometimes get calcified nodules associated with the cysts (amyloid deposits)
- Ass with Sjogrens, HIV

BAL lymphocytes
Poly/monoclonal IgM gammopathy

49
Q

What tracheobronchial abnormality is seen with granulomatosis with polyangitis?

A

Subglottic stenosis from granuloma (May see variable extrathoracic obstruction on flow volume loo)

50
Q

What is a flow chart for lung cyst differential?

A

Mimic - bulla, cavity, bronchiectasis
Single - pneumatocele, congenital foregut malformation, normal aging

+ Normal lung parenchyma
—> LAM (smaller cysts but variable size, uniform distribution, ass with TS, young female)
—> BHD (large lentiform/spherical cysts, lower zone/peripheral predominant)

+ nodules
—> LCH (cavitatory nodules, upper zone predominant, bizarre shape, young smoker)
—> LIP (middle age female, GGO, no zonal prediliction, variable size)
—> amyloid

+ GGO
—> PCP (perihilar GGO)
—> LIP

51
Q

What is definition of idiopathic pneumonitis with autoimmune features?

A

2/3 of:
- Clinical extrathoracic feature of autoimmune disease e.g. Raynaud
- Serologic (Ab)
- Radiology or histology

+ not meeting criteria of CTD

52
Q

What is treatment of LAM?

A

Siroliumus + transplant

Avoid OCP.

Young female, cysts all round but of varying size, uniform distribution, ass with tuberous sclerosis

53
Q

What imaging should be done in pt with suspected sarcoid?

A

CXR
+/- CT (may not need CT if typical findings and typical clinical picture)
+/- CMR - if suspicions of cardiac sarcoid and abnormal ECG or echo

Nb. should get ECG, & bloods incl calcium and LFTs annually. Regular lung function.

54
Q

CT and clinical findings not sufficient to diagnose sarcoidosis. What is next test?

A

EBUS if LNs, otherwise TBBx

55
Q

What treatment is needed for sarcoid?

A

Maybe none
10mg pred for longstanding and insiduously progressive disease - trial withdrawal after 6-12months
20-40mg for acute
Can try inhaled steroid for cough

2nd line: methotrexate or azathioprine

Also, leflunomide, infliximab, rituximab

56
Q

What are sarcoid stages?

A

0 - normal CXR
1 - enlarged LNs
2 - enlarged LNs and parenchymal changes
3 - parenchymal changes w/o LNs or fibrosis
4 - fibrosis

57
Q

What is Lofgren’s syndrome?

A

Bilateral hilar lymphadenopathy, erythema nodosum +/- bilateral ankle arthritis

58
Q

What is required to make a definitive diagnosis of sarcoid? When is it not needed?

A

Biopsy

Not needed if Lofgren OR, long-standing pulmonary disease with typical clinical presentation and imaging
+ no obvious alternative

59
Q

What might you see on biopsy in sarcoid? + BAL?

A

Biopsy - non-caeseating granulomas

BAL - raised lymphocytes 15-25%, CD4:CD8 >4

60
Q

How should fatigue be treated in sarcoid?

A

Trial prednisolone only if accompanying disease activity or all other options have been exhausted

61
Q

How long should pt with sarcoid be followed up?

A

Can d/c with Lofgren or stage 1 CXR once resolution confirmed

62
Q

What is the median survival after IPF diagnosis?

A

3 years

Excerbation of IPF: median survival 3 months

63
Q

What is Heerfordt-Waldenstrom syndrome?

A

Sarcoid + fever, parotid gland enlargement, facial nerve palsy and uveitis

64
Q

What is Erasmus syndrome?

A

Progressive scleroderma in response to silica exposure

65
Q

What is desquamative interstitial pneumonia?

A

Smoker
Middle-age
Male

CT - diffuse, peripheral patchy GGO (i.e.non-specific)
Bippsy - Pigment laden macrophages on biopsy

66
Q

What factors are associated with IPF?

A

Age (rare in <60)
Male
Smoking
Family history
Cardiovascular disease & VTE
Occupational - metal, wood, textiles, sand, stone, silica

nb. approx 50% patients are clubbed

67
Q

What factors are associated with poorer prognosis in fibrotic lung disease?

A

TLCO <40% at diagnosis
Decrease FVC ≥10% over 6-12 months
Decrease TLCO ≥15% over 6-12 months
Desaturation on exercise to <88%

68
Q

What is the mechanism of action of nintedanib?

A

Tyrosine kinase inhibitor

69
Q

Radiological patterns of OP?

A

Multifocal peripheral OR peri-lobular OR bronchocentric consolidation

Lymphocytic BAL

nb. eosinophilic pneumonia classically has multifocal peripheral consolidation but will get high eosinophils (eosinophils of BAL >10%)

70
Q

What is pulmonary haemosiderosis?

A

Iron deposition in lung e.g. ass with Goodpastures, idiopathic

Small, ill-defined pulmonary nodules + calcification
Lung parenchymal distortion

Vignette will have haemorrhage

71
Q

What are features of RB-ILD?

A

Need to be current smoker (can also get in RA and scleroderma)

CT: peripheral bilateral GGO & centirolobular nodules. Can get cysts from fibrosis. Tend to also have emphysema.

Pigement-laden macrophages on biopsy

72
Q

What is Goodpasture’s?

A

Anti-GBM disease (type 2 hypersensitivity with Ab adjacent type 4 collagen in renal glomerular basement membrane and cross-reactivity with alveolar membrane)

Pulmonary haemorrhage + glomerulonephritis

Radiology: bilateral GGO –> crazy paving
+/- hilar lymphadenopathy

73
Q

What is granulomatous lymphocytic interstitial pneumonia?

A

ILD seen in CVID

Radiology: bilateral nodules, GGO, lymphadenopathy +/- interlobular septal thickening & bronchiectasis
–> usually mid-lower lobe predominant

Tx: rituximab

74
Q

What is lymphangitis carcinomatosis?

A

Spread of tumour through lymphatics of lung - most commonly secondary to adenoca (breast > lung > stomach)

CT: irregular and nodular interlobular septal thickening + pleural effusion

75
Q

What is classic symptoms for granulomatosis with polyangiitis and how is it treated?

A

Triad of:
- Upper resp tract involvement: hearing loss, gingivitis, oral ulcers, subglottic stenosis
- Lower rep: nodules, infiltrates, cavities, pulmonary haemorrhage
- Glomerulonephritis

Treat
- Life-threatening: plasma exchange, dialysis, immunosuppression
- Organ-threatening: cyclophosphamide + glucocorticoid
- Maintenance after remission: azathioprine or MMF

76
Q

What are features of pulmonary alveolar proteinosis?

A

Crazy paving appearance
Milky BAL
anti-GM-CSF Ab diagnostic

Tx: whole lung lavage

Revision (17 decks)

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