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MS > SLE > Flashcards

SLE Flashcards

0
Q

when does SLE typically prsent

A

20-30 years

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1
Q

hallmark of SLE

A

production of autoantibodies; prototypical immune complex disease

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2
Q

what causes lupus-like disease?

A

hereditary complement deficiency

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3
Q

what organs can SLE effect?

A

renal
pulmonary
cardiac
skin

(one often predominantes)

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4
Q

non-specific symptoms in almost all patients

A

fatigue (80-100%)
fever>80% in patients with active disease
MSK dz: all patients (mostly PIP or MCP, knees, wrists, but any)

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5
Q

to classify lupus you need greater than or equal to ( ) symptoms

A

4

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6
Q

4 skin aspects

A

malar rash
discoid rash
photosensitivty
oral ulcer

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7
Q

2 types of serositis

A

pleuritis

pericarditis

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8
Q

two theroies of how autoantibodies are generated

A

non-specific polyclonal b cell activation

normal immune response, but with some CD4+ t cell responding to autoantigen on MHCII (first signal–second signal co-stim molecules)

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9
Q

mice treated with Cd4 depleting or Cd40/CD40L blocking antibodies..

A

recovered frorm lupus and survived better than untreated mice

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10
Q

once the antibodies are generated…

A

bind directly to cells–>cell dysfunction, cell destruction (anemia, thrombocytopenia)
form immunocomplexes to get stuck places

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11
Q

another issues with immunecomplexes

A

medium sized therefore large enough to activate Complement, but small enough to evade the reticuloendothelial system

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12
Q

malar rash

A

fized erythema, flat or raised sparing nasolabial folds

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13
Q

discoid rash

A

raised patches, adherent kerotoc scaling

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14
Q

RaYNAUDS

A

induced by cold or emotion–change in skin color–white–>blue–>red
digital infarcts, dry gangrene

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15
Q

arthropathy

A

reversible once SLE is controlled without and permanent damage

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16
Q

Jaccoud’s arthropathy

A

hand deformity rare in SLE, but Jaccoud’s that happens- still different frorm RA in that only tendons and ligaments are affected, so patients can actually correct their hand shape

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17
Q

renal disease in lupus

A

extensive subendothelial deposits and everywhere else
full house pattern
wire looping

18
Q

end result of renal disease in lupus

A

glomerular degeneration and fibrosis

19
Q

libman sachs endocarditis

A

pereicardial effusion leads to vegetations on mitral valve

20
Q

types of serositis

A

pleural effusions-loss of costophgrenic angle
pericardial effusion-libman sachs
peritonitis-less common

21
Q

usual SLE CNS

A

bland vasculopathy

22
Q

APS

A

can occur in presence or absence of lupus

23
Q

APL antibodies

A

seen in 25-50% of SLE patients, usually intermittently and at low titer

24
Q

2 important APL tests

A

lupus anticoag- interferes with clotting and increases PTT (not corrected by adding plasma)

anti-cardiolipin ab- targets cardiolipin, an importnat out mito membrane protein

25
Q

major antigen recognized by APA is

A

B2 glycoprotein (B2GP1)-apolipoprotein H (member of C cascade that may be involved in homeostatic regulation)

26
Q

non-pathological abs are

A

IGM and target domain V of BGP

27
Q

pathological ABS

A

domain I-Igg

28
Q

APS shows with

A

thrombosis
recurrent fetal loss in late trimester
thrombocytopenia
livedo reticularis

29
Q

treatment of APS

A

high ontensity warfrain (INR 3-4)

30
Q

3 serological tests for lupus

A

ANA
anti-dsDNA
anti-Smith

31
Q

ANA

A 
diffuse or peripheral rim pattern
high sens (almost all SLE patients have it) but low spec (present in patients with other disease)
*except centromere pattern in specific to CREST
32
Q

anti-dsDNA

A

20-70% SLE

most specific to SLE, esp GNitis

33
Q

anti-smith (antisRNA)

A

only 20-30% of SLE patients, but not seen in any other disease (high spec)

34
Q

treatment of lupus depends on

A

clinical manigestation

35
Q

articular sx

A

NSAID, COX2 inhibs
low dose steroids
plaquenil
dapsone

36
Q

serositis

A

NSAIDS and COX2 inhib

cytotoxin

37
Q

cutaneous disease

A

topical steroids
plaquenil
systemic cytotoxins
dapsone

38
Q

heme disease tx

A

steroids
immunosuppressive
rituximab

39
Q

renal tx

A

systemic steroids
cyclophosphamidde
–good treatment but sideeffects too

40
Q

CNS tx

A

high dose steroids
cytotoxic
antipsychotics

41
Q

future rx directions

A

Benlysta

42
Q

Benlysta

A

inhibits binding of soluble blys to R on b cell
mainly helps skin and arthritis, no nephro or CNS disease
*only mildly helpful

43
Q

late complications in SLE

A

osteonecrosis (avascular b necrosis)
osteoporosis-lumbar spine
early atherosclerosis
pregnancy (APS major factor)–loss in 50% of pregnancies

MS (19 decks)

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