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MSK/Derm > SM 232: SLE > Flashcards

SM 232: SLE Flashcards

1
Q

What is SLE?

A

A multisystem, inflammatory autoimmune disease

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2
Q

How does SLE cause damage?

A

Production of autoantibodies which deposit in tissues and fix complement leading to inflammation and tissue damage

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3
Q

Is the course and prognosis of SLE fixed?

A

No, it varies a lot can can be mild to life-threatening leading to irreversible end-organ damage

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4
Q

Which gender is more at risk for SLE?

A

Women, especially during child-bearing years

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5
Q

Which ethnicities are more at risk for SLE?

A

Black, Hispanic, Native American, and Asia

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6
Q

How do genetic and environmental interactions increase risk of autoimmune disease?

A

SLE and other autoimmune disease have a genetic predisposiiton as well as environmental influences that can lead to the development of serological autoimmunity or clinical disease

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7
Q

What is serological autoimmunity?

A

Autoantibodies and markers of autoimmunity without symptoms of clinical autoimmune disease

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8
Q

Which single gene defects can lead to SLE?

A

C1q or C4, though it often takes several genetic defects

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9
Q

Where do the SNP’s that cause SLE occur?

A

Noncoding DNA mutations

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10
Q

What are the common loci that are mutated in autoimmune disease?

A

STAT4 mutations leads to SLE, RA

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11
Q

To what extent does heritability lead to SLE?

A

Loci mutations lead to 15% of SLE heritability

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12
Q

What are environemtnal influences leading to SLE?

A

UV light Medications Viral Infections Cigarette Smoking

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13
Q

How does UV light cause SLE?

A

Causes DNA damage

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14
Q

How do medications cause drug-induced SLE?

A

Medications cause epigenetic medications such as decreaseed DNA methylation

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15
Q

Which viral infection is associated with SLE?

A

EBV infection

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16
Q

What mechanism does female sex and hormones lead to SLE?

A

Unknown

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17
Q

How does impaired apoptosis lead to SLE?

A

Impaired apoptosis leads to abnormally functioning Dendritic, T and B Cells which produce autoantibodies and proinflammatory molecules leading to tissue injury

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18
Q

How do autoantibodies and proinflammatory molecules influence the inflammatory resposne?

A

They sustain the inflammatory response

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19
Q

How do phagocyticic cells relate to SLE?

A

Phagocytic cells like Neutrophils become dysfunctional and cannot clear debris APC pick up debris and present on MHCII to sensitize T and B cells leading to autoinflammation

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20
Q

What are ANA?

A

Autonuclear antibodies - the common factor of SLE

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21
Q

How are ANA detected?

A

Immunoflourescence is the best way to detect ANA in serum Fix patients applied to glass slide with fixed cells where ANA can bind, and worse lupus corresponds with a higher dilution of serum still causing immunofluorescene

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22
Q

Describe the test charactersitics of ANA?

A

ANA is sensitive but not specific for Lupus ANA can be found in Scleroderma, normal patients, autoimmune thyroid disease, and IPF

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23
Q

How should a negative ANA be interpreted if the patient has SLE symptoms?

A

Px probably doesn’t have SLE due to high sensitivity of ANA

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24
Q

When is the ANA most useful in diagnosing SLE?

A

If tehre’s a high pretest probability

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25
What's a good antibody for diagnosis of SLE?
Anti-dsDNA, which predicts a flare Also Anti-smith
26
Which autoantibody correlates with light sensitivity rashes in SLE?
Anti-SSA and Anti-SSB
27
Which autoantibodies can cross the placental barrier in pregannt women?
Anti-SSA and Anti-SSB causing neonatal lupus
28
When can autoantibodies be detected in the blood of a patient?
Up to 5 years before a diagnosis of SLE
29
Can we predict which patients with positive autoantibodies will develop SLE?
Nope, monitor anyone with autoantibodies closely over time
30
What are natural autoantibodies?
IgM autoantibodies that clear cellular debris in healthy individuals
31
What are pathogenic autoantibodies?
IgG antibodies that form circulating immune complexes and can directly target cells via cross-reactivity with other antigens
32
How can circulating IC cause glomerulonephritis?
Circulating IC in SLE can deposit int eh glomerular membrane and cause Glomerulonephritis
33
Whan can anti-DNA cause glomerulonephritis?
Can directly bind the basement membrane
34
How can anti-DNA cause renal tubular injury?
Directly binding and damaging renal tubular cells
35
What do anti-SSA and anti-SSB autoantibodies do to pregnant women with SLE?
Crosses placental barrier and causes a temporary rash as well as a risk of complete heart block in utero
36
What do anti-SSA and anti-SSB autoantibodies do to pregnant women with SLE?
Crosses placental barrier and causes a temporary rash as well as a risk of complete heart block in utero
37
What are the ACR criteria and how many are needed to diagnose criteria?
ACR criteria used for research on Lupus Don't need them to diagnose SLE in clinic
38
List clinical ACR criteria?
Malar Rash Discoid Rash Photosensitivity Painless oral ulcers on the roof of the mouth Glomerulonephritis Neurological Disorder
39
List laboratory ACR criteria?
Immunogenic hemolytic anemia Luekopenia/Lymphopenia ANA anti-dsDNA
40
What are non-ACR criteria for SLE?
Lots of rashes Lymphadenopathy Low C3/C4 ILD Myocarditis
41
What is the disease activity of SLE?
SLE is characterized by periods of flare and remission
42
What is the difference between a flare and remission?
Flare = high disease activity Remission = low disease activity
43
What are the flare rates for SLE?
Varies by person, regardless of medication use
44
What can be used to predict SLE flares?
Rising anti-dsDNA titers Drops in C3/C4 Increases Sed Rate Lymphopenia
45
Why do C3 and C4 drop in SLE?
The circulating IC's in SLE use up complement
46
How does severe SLE mainfest?
Abrupt onset of symptoms Increased renal, neuro, hematogolic and serosial involvement Rapid organ damage
47
Why is SLE mortality bimodal?
Patients die early or late
48
What are early causes of mortality in SLE?
Severe SLE manifestations like stroke or infection from immunosuppression
49
What are late causes of mortality in SLE?
CVD like Stroke and MI Organ failure such as Kidneys Infection Malignancy
50
What can cause lupus mortality both early and late?
Infection, due to immunosuppression needed to treat SLE
51
What are the goals of therapy in SLE?
Induce remission Maintenance therapy to limit end organ damage Supportive therapy to prevent long-term complications from disease and treatment
52
What medications are used for acute, organ threatening flares?
Corticosteroids
53
What are the risks of Corticosteroids?
With long term use, risk of osteoperosis, diabetes, and HTN/HLD
54
What is the mainstay drug for SLE?
Hydroxycloroquine
55
How does Hydroxychloroquine effect SLE?
Lowers frequency and severity of flares
56
What immunosuppressants are used for SLE?
Methotrexate Mycophenolate Azathioprine Tacrolimus Belimumab
57
What is Belimumab?
A bioligicthat targets BAFF, B-cell activiting factor
58
What is Cyclophosphamide?
A powerful, last-line immunospupressant for SLE commonly used in cancer
59
What are the toxicities of SLE immunosuppresion?
Liver dysfunction Infection Cancer Infertility
60
What supportive treatments exist for SLE?
Avoid sunlight Liver function and blood surveillance Prophylactic antibiotics Osteoperosis screening
61
What is this and what does it suggest?
Malar Rash on both Cheeks = Lupus "Butterlfy Rash"
62
What is this and what does it suggest?
An oral ulcer Possibly Lupus
63
What is this and what does it suggest?
A Discoid rash effecting the entirety of the scalp = Lupus

MSK/Derm (46 decks)

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