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Connective tissue diseases > SLE > Flashcards

SLE Flashcards

1
Q

Autoantibody in neuro lupus

A

Ribosomal P Abs

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2
Q

Most specific antibody in SLE

A

Anti smith -most specific (renal and CNS disease)
Others -anti ds DNA, SSA,SSB
U1RNP- MCTD, myositis, Raynauds

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3
Q

Risk factors for poor outcome in pregnancy

A 
Active disease in last 6-12 months
Serological activity (ds-dna,complements)
Lupus nephritis
Anti SSA,SSB
aPL serology
Organ damage
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4
Q

Autoantibody associated with congenital heart block in neonate

A

Anti- SSA/anti Ro (1-3% risk)

Risk in subsequent pregnancy -13-17%

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5
Q

Role of HCQ in SLE

A

Decreases flares, progression to renal and CNS lupus
Decreases end organ damage,doubles response to MMF
Protects against CHB in SSA positive mothers

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6
Q

Monoclonal antibody in refractory SLE

A

Belimumab
MOA- blocks the B lymphocyte stimulator (BLyS), a soluble protein that binds to B cells. This molecule is overexpressed in people with lupus

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7
Q

Highest risk of thrombosis in SLE

A

Triple positive- B2 microglobulin, anti Cardiolipin, lupus anticoagulant
Of these highest risk - lupus anticoagulant (look for prolonged APTT)

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8
Q

Anticoagulation in APLS

A

Asymptomatic /primary prevention -No RX/low dose aspirin
Secondary prevention - Warfarin INR 2-3, indefinitely
Pregnancy
Prior thrombosis -therapeutic LMWH+Aspirin
Prior pregnancy loss -low dose daily LMWH+aspirin

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9
Q

Lupus nephritis features

A

30-50% of SLE
Worse prognosis in Asians, African -American and Hispanic
Glomerular hematuria, proteinuria/NS, AKI
Renal biopsy gold standard

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10
Q

Histopathological features in lupus nephritis

A

Subendothelial immune deposits(wire loops), hypercellularity
Leukocyte infiltration
Fibrinoid necrosis, hyaline thrombi
Deposits -IgG, IgA,Ig M, C1q, C3

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11
Q

Poor prognostic features in proliferative lupus nephritis

A

High Cr at presentation
Failure to achieve remission
High chronicity index on Bx
Ethnicity -African -American, Hispanic

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12
Q

Cyclophosphamide vs MMF in induction Rx for lupus nephritis

A

Cyclophosphamide preferred with severe disease

as higher risk of relapse and ESRF with MMF

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13
Q

Cause of deaths in SLE

A

Early deaths -active disease, infection

Late - coronary atherosclerosis, SLE, treatment complications

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14
Q

Genetic mutations predisposing to SLE

A

Deficiencies of complement componenets C1q,C4A,B,C2
TREX1 gene mutations -encodes 3’repair endonuclease1
required to degrade DNA
MHC -hla-dr2,dr3,drb10301/1501
INF related pathway genes -IRF5,IRAK-1,TLR7,STAT4
T/B cell signalling/survival pathway, Immune complex clearance

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15
Q

MOA of drug induced lupus

A

DNA hypomethylation -procainamide, hydralazine

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16
Q

Epigenetic changes in SLE

A

Hypomethylation of DNA including IFN related genes
Aberrant expression of certain miRNAs in peripheral blood
Hypo or hyperacetylation of histones in pro-inflammatory genes (TNF alpha, IL-6)

17
Q

Immunopathogenesis of LSE

A

Loss of self tolerance to auto antigens
Increased apoptotic material serving as auto ags due to decreased phagocytosis and increased cellular apoptosis
Autoag form IC with autoab and trigger inflammatory cascade

18
Q

Enviornmental factors in SLE

A

UV light -> inf cytokine release from keratinocytes ->T cell DNA hypomethylation
Infection -EBV
Smoking
Pollutants -silica

19
Q

Drugs causing lupus

A

Procainamide, Hydralazine,diltiazem, INH, Methyldopa,chlorpromazine, INF-alpha
Serious manifestations rare (renal,CNS)
Anti histone ab -associated with certain drugs (procainamide, hydralazine, INH)
Resolves with withdrawal of drug
TNF inhibitors -cause autoabs, clinical lupus rare

20
Q

Hormonal abnormalities in lupus

A

Decreased DHEA, androgen, hyper prolactinemia

21
Q

Arthritis features in SLE

A

Arthralgias more than arthritis
Symm, polyarticular, migratory
Site- knee, wrist, finger joints
Morning stiffness less prominent
Non deforming, non erosive
Rhupus -RA/SE overlap, antiCCP associated with erosive disease
Avascular necrosis can occur in hip/kneeupto 40%

22
Q

Cardiovascular manifestation in SLE

A

Pericarditis is the MCC cardiac SLE manifestation
Myocardial -arryth, conduction abnorm
Valvular - Mitral>aortic, regur>stenosis
Libman Sacks endocarditis -rare
CAD - Increased risk, occurs at earlier age

23
Q

Pulmonary manifestations in SLE

A

PLeurisy
Parenchymal -rare
Pulmonary HTN , shrinking lung syndrome -rare

24
Q

GI manifestations

A

Deranged LFT
Auto immune hepatitis, acute pancreatitis
Intestinal pseudo obstruction

25
Q

Hematological manifestations

A

Anemia, AIHA, leucopenia, Thrombocytopenia(ITP can occur before SLE onset), TTP
Evans syndrome -AIHA+ITP
LNE
Splenomegaly

26
Q

Neuropsychiatric manifestation

A

Aseptic meningitis, CVD,Seizure,Myelitis

Peripheral -GBS, autonomic neuropathy, MG, plexopathy

27
Q

Renal lupus

A 
Class I-Minimal mesangial
Class II -Mesangial proliferative
Class III- Focal (<50% of glomeruli) (hematuria, pnuria,low GFR, +/-nephrotic syndrome)
Class IV- Diffuse(nephrotic syndrome)
Class V- Membranous (nephrotic syndrome)
Class VI-Advanced sclerosing
28
Q

Auto ab in SLE

A

Mostly ANA positive

Dense fine speckled ANA pattern -less probablity of AI disesea

29
Q

Disease activity markers

A

ESR>CRP
Increased anti-ds DNA ab
Low C3,C4

30
Q

Management of disease

A

Minor disease -HCQ, NSAIDS, steroids
Major -Steroids, Aza, Mtx, leflu,Cycloph,Cyclosp,Tac,MMF
Rituximab for refractory disease

31
Q

Indications for renal biopsy in SLE

A

–Increased Serum Cr without alt cause
–Confirmed pnuria>1gm/24hrs
–Combinations of pnuria>0.5g/24hrs and hematuria>5RBC
OR proteinuria>0.5gm/24hrs plus cellular casts

32
Q

Poor prognosis indicators in renal lupus

A

Disease severity( higher Cr at presentation,pnuria)
Class, activity,chronicity scores
Interstitial fibrosis and crescents
Delay in diagnosis/treatment
HTN, Low hematocrit, black race
Socioeconomic class
Differential gene expression on Bx -BAFF/APRIL,NFKB,IL-6

Improvement in pnuria to<0.7-0.8g/day at 12months predicts better long term outcome

33
Q

Treatment of lupus nephritis

A 
Class I,II,VI -No immunosuppression
Class III, IV(+/- V) - immunosuppression
  Induction(Pulse steroids+ MMF/Cycloph), maintainance(MMF/ Aza) , serological monitoring
ACEI if pnuria>0.5g/day
Target BP< 130/80
Statins if LDL >2.6mmol/L
PLEX for thrombotic microangiopathy
34
Q

Targeted therapy in SLE

A

RITUXIMAB

BELIMUMAB
Human mAb- binds to soluble BAFF/BLyS preventing binding to its receptor on B cells
S/E -depression, suicide
Efficacy in musculoskl,mucocut, hematological domains and QOL

Anti-IFN receptor Ab -Anifrolumab

35
Q

Pregnancy in SLE

A

Plan pregancy when SLE quiscent for 6 months(esp lupus nephritis)
Flares can occur any trimester, post partum.
Risk factors -active disease 6months prior to conception, h\o lupus nephritis, discontinuation of HCQ

36
Q

Contraindications to pregnancy in lupus

A 
Severe pulm HTN (Sys PAP>50mmHg)
Severe restrictive lung disease
Advanced renal insufficiency
Advanced HF
Previous severe pre eclampsia /HELLP despite Rx
CVA within 6 months
Severe disease flare within 6 months
37
Q

Differentiating features bet pre-eclampsia and lupus nephritis

A

Hematuria/Active urinary sediment -> LN
Complement levels ->Low in LN, N/H in PE
Anti-ds DNA levels - > Increased in LN, N in PE
PE - Elevated liver enzymes, high uric acid

38
Q

Antiphospholipid Ab ab and pregnancy

A

Asymptomatic pt - consider low dose aspirin (LD ASA)
Prior obst morbidity - LD ASA+ Prophylactic LMWH
Prior thrombosis -therapeutic LMWH until 6/12 post partum

Connective tissue diseases (5 decks)

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