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CT disorder Flashcards

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1
Q

SLE epidermiology

A

F>M

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2
Q

SLE pathogenesis

A

Genetics contributes 30%

  • Provides susceptibility
  • E.g. C1q deficiency (high penetrance for SLE); MHC class (HLADR2, DR3, DRB1), IFN related pathway genes

Environmental

  • UV light, DNA damage, skin damage
  • Infection ?EBV via molecular mimicry
  • Drugs e.g. TNFi, procainamide, hydralazine
  • Heavy metals
  • Smoking

B cell activation and autoantibody production + IFN production + effector T cells (TH17 cells) + problems with phagocytosis (increased apoptotic material serves as autoantigen)

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3
Q

ACR/EULAR classification criteria 2019

A

Does not equal diagnostic criteria. Used in research. But useful to look at it to help reach diagnosis.

Must have positive ANA
Different organs affected
If renal biopsy positive for lupus nephritis, and ANA positive, don’t need other organ manifestations.

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4
Q

Cutaneous manifestations for SLE

A 
Butterfly/malor rash - acute cutaneous lupus 
Subacute cutaneous lupus
Chronic discoid lupus (scarring)
Photosensitive
Bullous
Urticaria
Chill blains
Panniculitis
Alopecia (Rx JAKi)
Painless nasal ulcers

Remember cutaneous lupus does not equal systemic lupus!

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5
Q

MSK manifestations for SLE

A

Arthralgia - symmetrical, migratory, polyarticular

Arthritis (like RA< usually non-erosive but can be deforming = Jaccoud’s arthritis)

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6
Q

Serositis in SLE

A

Pericarditis (big globular heart shadow on CXR)

Also pleuritis

High CRP

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7
Q

Do you get CRP rise in SLE flare?

A

Not usually - must exclude infection!

Unless there is serositis

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8
Q

Pulmonary manifestations in SLE

A

Pleurisy/pleural effusion

Acute pneumonitis

Pulmonary haemorrhage (rare)

ILD: NSIP most common

PE ?APLS

Pulmonary HTN

“Shrinking” lung syndrome

  • Progressive SOB
  • Raised hemidiaphragm, reduced lung volumes
  • RFTs restrictive pattern
  • Unsure mechanism but can respond to immunosuppression
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9
Q

Cardiovascular manifestations in SLE

A 
Pericarditis (most common)
Premature CAD (most common)
Vasculitis
Libman-sacks endocarditis (valvular lesions as a result of microthrombi on heart valves)
Lupus myocarditis
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10
Q

Haematologic manifestations in SLE

A

Anaemia

  • Multifactorial
  • Chronic inflammation (most common), IDA, autoimmune haemolytic anaemia (DAT+), aplastic anaemia, anti-EPO ab

Leucopenia

  • Low lymphocyte count is common but not severe
  • Due to peripheral destruction but the cells are quite normal

Thrombocytopenia

  • Overlap with ITP (10% SLE have ITP; 50% ITP meet SLE criteria)
  • Mainly peripheral destruction
  • Different ab to pure ITP
  • MAHA (mainly TTP)
  • Myelofibrosis

Lymphadenopathy
Splenomegaly

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11
Q

How to differentiate TTP vs DIC?

A

DIC - abnormal coags, abnormal fibrinogen

TTP - normal coags. Platelets and Hb abnormal.

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12
Q

Neurological manifestations in SLE

A

CNS: headache, mood disorder, seizure, cognitive dysfunction, CVA, myelitis etc

PNS: sensory-motor axonal polyneuropathy

Consider catastrophic APLS (seizure, encephalopathy)
Need urgent ICU and immunotherapy and anticoagulation

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13
Q

Ribosomal P abs =

A

Neuro lupus

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14
Q

Immunologic manifestations in SLE

Antibody findings

A

Less specific findings

  • ANA positive >99% (homogenous pattern)
  • Low C3, C4
  • Raised ESR:CRP
  • Positive RF 15-35%

More specific

  • dsDNA 60% (disease activity, renal disease)
  • Anti-smith (most-specific)
  • SSA (Anti-Ro), SSB (anti-La)
  • U1RNP (also in mixed CT disease)
  • Ribosomal P (neuro lupus)
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15
Q

SLE and pregnancy

What are 2 important things to know?

A

Most have successful pregnancies

1) Anti Ro/La positive associated with
- Congenital heart block 1% (increases with subsequent pregnancies if previous babies with CHB)
- Weekly USS
- Consider fluorinated steroids (crosses placenta e.g. dex) +/- IVIG in 2nd degree HB to prevent progression

2) Antiphospholipid status. If positive:
- Asymptomatic: consider low dose aspirin
- Prior obstetric morbidity: low dose aspirin, prophylactic clexane
- Prior thrombosis: therapeutic clexane; continue 6/12 post partum

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16
Q

SLE treatment

A

Non-pharmacologic

  • UV protection
  • Smoking cessation
  • Immunisation
  • Avoid estrogen therapies, sulfonamides (A/W flares)
  • Replete vitamin D
  • CV risk management

Hydroxychloroquine
- Everyone should be on it

Others
Corticosteroids - useful in controlling disease; some stay on small dose lifelong
MTX - useful for polyarthritis, stay away in ILD, renal impairment
Azathioprine 
Leflunomide - stay away in ILD
Mycophenolate - esp renal/pulmonary
Cyclosporin
Cyclophosphamide

Rituximab in refractory disease

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17
Q

Risk of HCQ

A

Retinal toxicity
Accumulative toxicity, dose and duration related
Detected with retinal exam/OCT - “pre maculopathy” may be reversible. Later macular disease “bull’s eye”, visual field loss, often irreversible.

Baseline eye check before starting HCQ
After 5 years, need annual eye checks

Increased risk after 5 years, in older age, renal impairment
Keep dose <5mg/kg Ideal body weight

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18
Q

Biologics in SLE

A

1) Rituximab and veltuzumab (CD20 ab)
- Modest evidence in trials but does work well in the right patients
- Off label use
- Refractory disease, lupus nephritis

2) Belimumab
- Targets B cell activating factor (BAFF) - promotes B cell survival and differential
- FDA approved in lupus nephritis. SAS access only.
- Moderate SLE that has not responded to HCQ/MYC. Not in severe disease or lupus nephritis.

3) Tibulizumab
- Targets BAFF and IL17
- Ongoing trials

4) Anifrolumab
- Anti-IFN therapy
- Trials look promising

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19
Q

APLS presentation

A

Primary or secondary (SLE)

Thrombosis +/- obstetric complications
Also thrombocytopenia, cardiac valve abnormalities livedo reticularis, renal microangiopathy, chorea, myelitis

Associated conditions: HELLP, pre-eclampsia, MAHA

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20
Q

When you see livedo reticularis.. what should you check?

A

APLS ab

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21
Q

APLS ab

A

Anti-cardiolipin ab

Anti-Beta2-glycoprotein1

Lupus anticoagulant - highest risk for thrombosis

“Triple positive” at highest risk of thrombosis
Look out for the prolonged APTT!!

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22
Q

APLS treatment

A

Asymptomatic/primary prevention: no treatment

Secondary prevention:

  • Lifelong anticoagulation with warfarin (INR2-3)
  • DOACS not recommended

Management in pregnancy
Prior thrombosis: therapeutic clexane (continue at least 6/12 post partum) + aspirin
Prior pregnancy loss (meets criteria): low dose aspirin + prophylactic clexane
Asymptomatic: consider low dose aspirin

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23
Q

Pathophysiology Systemic sclerosis

A

Initially, have vascular damage

Autoimmunity - innate, cell mediated and humoral

Tissue fibrosis is the characteristic end result (by the time we see this its too late)

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24
Q

Systemic sclerosis specific ab

A

Anti-centromere = Limited SSc or CREST; PHTN

Anti-topoisomerase I = Anti-Scl-70 = ILD

Anti-RNA polymerase III = severe renal and skin disease

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25
Disease subtypes of Systemic sclerosis
Limited cutaneous Systemic sclerosis (CREST) - Long history of Raynaud's - Distal skin sclerosis, digital ulcers - Major mortality from pulmonary arterial hypertension - Anti-centromere ab Diffuse cutaneous Systemic sclerosis - Short history of Raynaud's - Proximal limb or trunk involvement, with skin sclerosis - Extensive skin disease (contractures) + distal ulcers + more internal organ involvement (lung and kidney) - Tendon friction rubs - Awful morbidity and mortality - Lack of therapy - Anti-Scl-70 (ILD) and RNA polymerase III (scleroderma renal crisis)
26
Pulmonary involvement in Systemic sclerosis
1) Lung fibrosis - Occurs in the first 5 years in dcSSc - Most have lung involvement. Clinically significant in 30%. - Now the major cause of mortality - If >20% lung involvement, they will likely progress - Most prevalent pattern is NSIP - subpleural sparing, ground glass. No honeycombing. - May lead to PAH 2) Pulmonary arterial hypertension - Mostly group 1 - Can occur anytime - Need to keep screening - 1-2% develop per year - Very serious - Present in limited > diffuse - TTE alone may miss up to 30%. BNP is useful.
27
Rx for pulmonary hypertension in systemic sclerosis
Endothelin receptor antagonist - Bosentan, macicentan, ambrisentan - AE: LFT abnormality, tetatrogenic, fluid retention, anaemia NO stimulation - Sildenafil (PDE5), tadalafil (PDE5), Riociguat (GC stimulator) - AE: headache, bleeding, visual disturbance Prostacyclin analogues - IV Epoprostenol (severe SSc-PAH), iloprost, beraprost, trepostanol, selexipag - AE: headache, muscle cramps, diarrhoea Lung transplant * CCBs monotherapy don't work! * Benefits of PAH specific therapies were not as good as for iPAH
28
Cardiac manifestation Systemic sclerosis
Arrhythmias/conduction defects e.g. VT Myocarditis (often with skeletal muscle disease) Cardiac fibrosis (80% in autopsy studies) Valvular heart disease
29
MSK/skin involvement Systemic sclerosis
Puffy fingers Proximal progression of skin thickening Joint contractures +/- arthritis Unable to open mouth due to skin tightening Tendon friction rubs (associated with kidney involvement) - Especially common in diffuse SSc with RNA polymerase III Calcinosis
30
GI involvement Systemic sclerosis
Most frequent internal organ manifestation ~90% Dental disease Oesophageal dysmotility, strictures, candidiasis Reflux Watermelon stomach (GAVE) - poor motility, telangiectasia that bleed Small bowel overgrowth (due to gut wall scarring and motility disturbance) - bloating, diarrhoea, weight loss, high folate Large bowel, diverticular disease Faecal incontinence due to reduced sensation, altered bowel habits, constipation overflow diarrhoea
31
What's an important renal manifestation in Systemic sclerosis?
Scleroderma renal crisis! - Occurs in the first 5 years in dcSSc - Accelerated hypertension (retinal changes, hypertensive encephalopathy, PRES). Normally these people have low BP ~90, so when they raise 20mmHg this is significant. OR new onset BP >150/85. - Renal impairment - Associated with RNA polymerase III, tendon friction rubs - Diffuse subtype - Association with steroids (be careful in using steroids in diffuse subtype) - 40% will need dialysis but recovery can happen up to 2 years after
32
Vasculopathy in Systemic sclerosis | Treatment
1) Raynaud's (universal) - Primary Raynaud occurs in those without CT disease. Negative ab. No pain. Short lasting ~15 min. - Secondary (CT disease) - get tissue damage. Rx: CCB, PDE5 inhibitor, IV prostacyclin (iloprost, epoprostenol) in severe disease after oral therapy 2) >50% have digital ulcers - IV Prostacyclin (iloprost) or PDE5 inhibitor or endothelin receptor antagonist (Bosentan) - IV prostacyclin can be protective for a few months after. Very effective - May need surgical debridement in necrosis
33
Pregnancy in Systemic sclerosis
Limited: generally do well Diffuse: high maternal mortality Increased risk of hypertension, preeclampsia and CS, preterm birth, IUGR, organ complication Dangerous in pulmonary HTN Alot of the drugs can't be used
34
Screening in systemic sclerosis
Screen for ILD and pulmonary HTN Annual ECHO, PFTs Baseline CT. If there are change in PFTs, then repeat CT.
35
Stem cell transplant in systemic sclerosis
Great treatment if patients survive (5-10% mortality) Good for skin and lung involvement, if done early.
36
Therapy for systemic sclerosis-associated ILD?
Nintedanib + mycophenolate (combination therapy) Less drop in FVC over time ``` Others O2 to maintain SpO2 88% and above GORD therapy Quit smoking Vaccinations ```
37
What is Mixed CT disease? | Clinical features
It is an overlap syndrome (doesn't mean we don't know what it is) Features of SLE, scleroderma, rheumatoid, myositis ``` Raynaud's very common Hand oedema (puffy hands) Arthralgia/arthritis Myositis, trigeminal neuralgia ILD Pulmonary HTN (commonest cause of death) ```
38
Mixed CT disease labs
ANA + speckled Characteristic ENA: U1RNP (high titre) Leucopenia, thrombocytopenia Raised ESR 70% RF (more likely to have arthritis). CCP negative. Important negatives - dsDNA, anti-SM
39
"Puffy hands", RNP without dsDNA | Dx?
Mixed CT disease
40
Sjogren's syndrome presentation
Gland involvement - inflammation, fibrosis, lymphocyte infiltration - Dry mouth (dental caries, oral candidiasis), dry eyes - Glandular enlargement occurs in 30% (high rate of lymphoma) Extraglandular - Fatigue, arthralgia/arthritis (universal) - Palpable purpura often on legs - Cystic ILD - Distal renal tubular acidosis/glomerulonephritis - Cryoglobinaemia (renal involvement, rash, mononeuritis multiplex) - Dorsal root ganglionopathy - Peripheral neuropathy - NHL
41
Sjogren's syndrome can be primary or secondary. Which conditions can it be secondary to?
RA >SLE > SSc | HIV
42
Sjogren's syndrome management
Symptomatic ``` Dry mouth Citrus fruit or gum to stimulate saliva Saliva replacement/lubricants Secretagogues (pilocarpine) for both dry mouth and eyes. But side effects. Avoid meds that cause dryness ``` ``` Dry eyes Lubricating eye drops (preservative free) Topical cyclosporin Punctal plugs Secretagogues ``` Extraglandular Exercise NSAIDs HCQ for systemic manifestations Life-threatening: pulsed methylpred +/- plasma X +/- RTX if cryoglobulinaemia
43
DDx of parotid mass
Infections - viral (mumps, EBV, HCV, HIV); bacterial (acute parotitis, TB), fungal Autoimmune - Sjogren's, GPA Inflammatory - IgG4 disease, allergic parotitis, kilmura disease Metabolic - diabetes, bulimia, alcholism, hyperlipoproteinaemia Neoplastic - lymphoma, leukaemia, Warthin tumour Granulomatous - sarcoidosis
44
What's Schirmer's test?
Leave blotting paper under lower lid Then measure distance of moisture Correlate with tear production Useful in Sjogren's
45
Investigations in Sjogren's
Anti-SSA (Anti-Ro60) and/or Anti-SSB - diagnostic Positive RF & ANA titre >1:320 - diagnostic Schirmer's test (tear production) Salivary gland biopsy ``` dsDNA absent Elevated ESR Polyclonal hypergammaglobulinaemia 30% Anaemia, leucopenia (usually neuts) and thromboctopenia Cryoglobulinaemia in 15% ```
46
What are the subtypes of idiopathic inflammatory myopathies?
1) Dermatomyositis 2) Anti-synthetase syndrome 3) Immune-mediated necrotising myopathy (IMNM or NAM) 4) Inclusion body myositis 5) Polymyositis ?does this exist as a distinct entity
47
Presentation idiopathic inflammatory myopathies
3 "Ps" Progressive, painless, proximal weakness BUT all will have extra-muscular manifestations - cutaneous, diaphragmatic and intercostal muscle weakness = T2RF, oesophageal muscle weakness = aspiration, dysphagia, ILD, myocarditis, MI
48
Classic dermatomyositis cutaneous manifestations
Gottren's sign/papules (over extensors of large joints) Shawl sign V sign Heliotrope rash (peri-orbital) Holster sign (lateral thigh where your gun holster would be ) Periungual (around finger nail) erythema Skin findings may precede muscle weakness
49
Myositis specific ab Antisynthetase syndrome Skin disease (dermatomyositis) INMN IBM
Antisynthetase syndrome - 9 ab involved - Jo-1 (most common), PL7, PL12; all 3 are associated with lung disease ``` Skin disease (dermatomyositis) - SAE, Mi-2, MDA5 (ILD), NXP2, TIF1 ``` INMN - SRP, Anti-HMGCR (very specific to stain associated IMNM) IBM - Anti-CN1A
50
Anti-synthetase syndrome | Clinical Presentation
``` Myositis Jo1, PL7, PL12; total 9 ab ( all 3 are associated with lung disease) ILD - most important cause of mortality Mechanic's hands Raynaud phenomenon Inflammatory polyarthritis Oesophageal dysmotility (distal) Fever ```
51
Inclusion body myositis Clinical presentation Treatment
M>F, older demographic 50-60yo Muscle pattern is different to the other myositis ***Asymmetric Distal upper limb (finger flexors, wasting of forearm muscles, watch falling off) Proximal leg weakness (quadricep weakness, frequent falls going downstairs) Mildly elevated CK (but not >10x ULN) Anti-CN1A Less responsive to IS unlike other inflammatory myopathies. Can have limited trial of glucocorticoids.
52
Statin-associated IMNM Clinical Presentation Treatment
1:100,000 statin users Associated with HLADRB1*11:01 Usually after months on treatment, persist after cessation (ongoing immune reaction), CK usually >10x normal Anti-HMGCR ab very specific Treatment Statin cessation won't work Often will need steroids +/- IVIG
53
MDA5+ dermatomyositis Clinical presentation Treatment
May not have muscle disease, or if they have, its subtle Associated with rapidly progressive ILD Very high mortality 50-60% in 6 months Some distinctive features from other DM - ulcerating lesions, inverse gottren's or palm papules (instead of MCP, PIP distribution, gottren's papules are located on the palm), pneumomediastinum Rx: EARLY AGGRESSIVE IMMUNOSUPPRESSION (may survive 2 years if done early)
54
Do we need to avoid statins in idiopathic inflammatory myopathy?
NO | Unless they're anti-HMGCR positive (statin-associated IMNM)
55
Behcet disease | Clinical features
Cardinal features - Relapsing oral and genital ulcers with bilateral posterior or panuveitis Other features - Recurrent papulopustular lesions, erythema nodosa like lesions, non-erosive mono/oligo arthritis - Pathergy (exaggerated skin lesion after minimal trauma) - Vasculitis involving all vessels (thrombotic, pseudoaneurysms)
56
Which genetic factor is associated with Behcet disease?
HLA-B*151
57
What is sarcoidosis characterised by?
Systemic inflammatory disorder characterised by non-caseating granulomas
58
Sarcoidosis presentation
Acute and chronic arthritis (knees and ankles) Muscle involvement common although often asymptomatic Bilateral hilar lymphadenopathy Pulmonary infiltrates Uveitis Also cardiac, neurologic, cutaneous
59
What's Lofgren syndrome?
Acute sarcoidosis Erythema nodosa Acute polyarthritis (typically ankles) Hilar lymphadenopathy Fever
60
What's CREST syndrome?
Type of limited cutaneous sclerosis ``` C - calcinosis R - Raymaud's (years) E - esophageal dysmotility S - skin changes limited to UL, face; gradual onset T - telangectasia ```
61
Does pulmonary hypertension occur in limited or systemic sclerosis?
Both | ~10% in both subtypes (maybe slightly more in limited)
62
ANA with centromere pattern is associated with which disease?
Limited sclerosis
63
ANA with homogenous pattern is associated with which disease?
Lupus (dsDNA, histone +)
64
Main causes of mortality in scleroderma
ILD and pulmonary HTN | Previously was scleroderma renal crisis but ever since the introduction of ACEI, mortality has fallen
65
Who with systemic sclerosis-ILD is likely to progress in their ILD?
Early dcSSc with anti-Scl70 Early dcSSc with high CRP = High risk phenotypes = need treatment
66
ANA with nucleolar pattern is associated with which disease?
Progressive overt systemic sclerosis
67
How do we monitor patients with systemic sclerosis-ILD?
Rapidly progression is likely to occur in the first 5 years Monitor with spirometry and DLCO every 3-4 months for 5 years after disease onset then yearly No advantage in serial HRCTs if PFTs stable
68
Who with systemic sclerosis-ILD should receive immunosuppressive treatment?
Clinical ILD | - FVC% predicted or DLCO% predicted
69
What investigations to do in someone with SSc-ILD and worsening respiratory symptoms?
Repeat - PFTs + DLCO - HRCT ?progressive ILD - ECHO - NT-proBNP - DETECT algorithm (online calc for pHTN) Things to suggest pHTN - FVC/DLCO ratio >0.6 - TR velocity >3.2msec (should = systemic pulmonary pressures) - NT-proBNP >2 fold ULN
70
How to screen for pulmonary HTN in systemic sclerosis?
METHOD ONE Screen every 12 months PFTs - DLCO ≤50% ECHO - sPAP ≥40mmHg = If positive, do RHC = ECHO uses TR jet which is absent in up to 39% of patients = $$$, expertise required, poor image quality = Sensitivity 88%, specificity 83% METHOD TWO Screen every 12 months PFTs - DLCO pred <70% with FVC/DLCO ≥1.8 NT-proBNP ≥210 = If either positive, do RHC = 98% NPV = Cheaper than annual ECHOs *If recent decline in ET, syncope, RHF or ECHO features of Rt heart strain, should do RHC regardless of ECHO/DLCO findings
71
How is iron related to systemic sclerosis?
Iron deficiency in SSc-PAH is associated with worse survival Replace iron!
72
Signs of severe scleroderma renal crisis
``` Microangiopathic haemolytic anaemia and thrombocytopenia HF and flash APO Blurred vision due to retinopathy Headache, fever, malaise Encephalopathy, generalised seizures Pericardial effusion ```
73
Treatment of scleroderma renal crisis
Control BP with ACEI within 72h - Captopril preferred due to short t1/2 - Avoid beta-blockers - Aim 10% reduction in SBP/DBP per day - Can stabilise or improve renal function and survival If CNS involvement: captopril + IV nitroprusside MAHA: consider PLEX
74
When might you consider haematopoietic stem cell transplant in systemic sclerosis?
In those with early progressive SSc at risk of organ failure Idea is to wipe out the existing immune system and replace with non-autoreactive immune system with stem cells High early treatment-related mortality!! Also 1/3 get disease relapse
75
How does drug induced lupus present?
Usually mild Common to get skin and joint manifestations ANA +, dsDNA +, histone ab + Generally resolves with stopping the drug
76
GI manifestations of SLE
Abnormal LFTs (significant liver disease rare) Lupus hepatitis (ribosomal P ab) Ileal/colonic perforation (associated with vasculitis) Acute pancreatitis
77
Renal manifestations of SLE
Glomerulonephritis ``` 6 classes (based on histology) Class 3-4 +/- 5 reflect activate inflammation and warrants prompt immunosuppression ```
78
When does someone with SLE need a renal biopsy?
1) Increased serum Cr without alternate cause 2) Proteinuria ≥1g/24h 3) Proteinuria ≥0.5g/24h AND haematuria 4) Proteinuria ≥0.5g/24hr AND cellular casts
79
Treatment of lupus nephritis
Treat class 3, 4, +/- 5 INDUCTION PHASE IV pulse steroids AND MMF or CYC Refractory disease: rituximab or calcineurin inhibitor (cyclosporin) MAINTENANCE PHASE MMF or AZA
80
Should you continue hydroxychloroquine in lupus during pregnancy?
YES | Reduce risk of cardiac neonatal lupus (CHB)
81
What's overlap myositis?
Combination of myositis and another CT disorder e.g. SLE, scleroderma, Sjogren OR Myositis with overlap features without fulfilling criteria for another CT disorder (clinical feature or antibody)
82
Which subtypes of idiopathic inflammatory myopathy do you get increased risk of malignancy?
Dermatomyositis (x5-7 times) - Colon, lung, breast, ovarian IMNM
83
Empirical therapy for DM, PM, IMNM (idiopathic inflammatory myopathy)
1) high dose glucocorticoids tapering over 1 year 2) steroid sparing agents - AZA, MTX, IVIG, rituximab, PLEX 3) monitor CK, muscle power, PFTs

Rheumatology (5 decks)

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