Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MSK/Derm > SM 232: SLE > Flashcards

SM 232: SLE Flashcards

You may prefer our related Brainscape-certified flashcards:
Dermatology Board Prep flashcards
1
Q

What is SLE?

A

A multisystem, inflammatory autoimmune disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does SLE cause damage?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which gender is more at risk for SLE?

A

Women, especially during child-bearing years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which ethnicities are more at risk for SLE?

A

Black, Hispanic, Native American, and Asia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is serological autoimmunity?

A

Autoantibodies and markers of autoimmunity without symptoms of clinical autoimmune disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which single gene defects can lead to SLE?

A

C1q or C4, though it often takes several genetic defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where do the SNP’s that cause SLE occur?

A

Noncoding DNA mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

STAT4 mutations leads to SLE, RA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

To what extent does heritability lead to SLE?

A

Loci mutations lead to 15% of SLE heritability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are environemtnal influences leading to SLE?

A

UV light Medications Viral Infections Cigarette Smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does UV light cause SLE?

A

Causes DNA damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do medications cause drug-induced SLE?

A

Medications cause epigenetic medications such as decreaseed DNA methylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which viral infection is associated with SLE?

A

EBV infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What mechanism does female sex and hormones lead to SLE?

A

Unknown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do autoantibodies and proinflammatory molecules influence the inflammatory resposne?

A

They sustain the inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are ANA?

A

Autonuclear antibodies - the common factor of SLE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

When is the ANA most useful in diagnosing SLE?

A

If tehre’s a high pretest probability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What’s a good antibody for diagnosis of SLE?

A

Anti-dsDNA, which predicts a flare Also Anti-smith

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Which autoantibody correlates with light sensitivity rashes in SLE?

A

Anti-SSA and Anti-SSB

27
Q

Which autoantibodies can cross the placental barrier in pregannt women?

A

Anti-SSA and Anti-SSB causing neonatal lupus

28
Q

When can autoantibodies be detected in the blood of a patient?

A

Up to 5 years before a diagnosis of SLE

29
Q

Can we predict which patients with positive autoantibodies will develop SLE?

A

Nope, monitor anyone with autoantibodies closely over time

30
Q

What are natural autoantibodies?

A

IgM autoantibodies that clear cellular debris in healthy individuals

31
Q

What are pathogenic autoantibodies?

A

IgG antibodies that form circulating immune complexes and can directly target cells via cross-reactivity with other antigens

32
Q

How can circulating IC cause glomerulonephritis?

A

Circulating IC in SLE can deposit int eh glomerular membrane and cause Glomerulonephritis

33
Q

Whan can anti-DNA cause glomerulonephritis?

A

Can directly bind the basement membrane

34
Q

How can anti-DNA cause renal tubular injury?

A

Directly binding and damaging renal tubular cells

35
Q

What do anti-SSA and anti-SSB autoantibodies do to pregnant women with SLE?

A

Crosses placental barrier and causes a temporary rash as well as a risk of complete heart block in utero

36
Q

What do anti-SSA and anti-SSB autoantibodies do to pregnant women with SLE?

A

Crosses placental barrier and causes a temporary rash as well as a risk of complete heart block in utero

37
Q

What are the ACR criteria and how many are needed to diagnose criteria?

A

ACR criteria used for research on Lupus Don’t need them to diagnose SLE in clinic

38
Q

List clinical ACR criteria?

A

Malar Rash Discoid Rash Photosensitivity Painless oral ulcers on the roof of the mouth Glomerulonephritis Neurological Disorder

39
Q

List laboratory ACR criteria?

A

Immunogenic hemolytic anemia Luekopenia/Lymphopenia ANA anti-dsDNA

40
Q

What are non-ACR criteria for SLE?

A

Lots of rashes Lymphadenopathy Low C3/C4 ILD Myocarditis

41
Q

What is the disease activity of SLE?

A

SLE is characterized by periods of flare and remission

42
Q

What is the difference between a flare and remission?

A

Flare = high disease activity Remission = low disease activity

43
Q

What are the flare rates for SLE?

A

Varies by person, regardless of medication use

44
Q

What can be used to predict SLE flares?

A

Rising anti-dsDNA titers Drops in C3/C4 Increases Sed Rate Lymphopenia

45
Q

Why do C3 and C4 drop in SLE?

A

The circulating IC’s in SLE use up complement

46
Q

How does severe SLE mainfest?

A

Abrupt onset of symptoms Increased renal, neuro, hematogolic and serosial involvement Rapid organ damage

47
Q

Why is SLE mortality bimodal?

A

Patients die early or late

48
Q

What are early causes of mortality in SLE?

A

Severe SLE manifestations like stroke or infection from immunosuppression

49
Q

What are late causes of mortality in SLE?

A

CVD like Stroke and MI Organ failure such as Kidneys Infection Malignancy

50
Q

What can cause lupus mortality both early and late?

A

Infection, due to immunosuppression needed to treat SLE

51
Q

What are the goals of therapy in SLE?

A

Induce remission Maintenance therapy to limit end organ damage Supportive therapy to prevent long-term complications from disease and treatment

52
Q

What medications are used for acute, organ threatening flares?

A

Corticosteroids

53
Q

What are the risks of Corticosteroids?

A

With long term use, risk of osteoperosis, diabetes, and HTN/HLD

54
Q

What is the mainstay drug for SLE?

A

Hydroxycloroquine

55
Q

How does Hydroxychloroquine effect SLE?

A

Lowers frequency and severity of flares

56
Q

What immunosuppressants are used for SLE?

A

Methotrexate Mycophenolate Azathioprine Tacrolimus Belimumab

57
Q

What is Belimumab?

A

A bioligicthat targets BAFF, B-cell activiting factor

58
Q

What is Cyclophosphamide?

A

A powerful, last-line immunospupressant for SLE commonly used in cancer

59
Q

What are the toxicities of SLE immunosuppresion?

A

Liver dysfunction Infection Cancer Infertility

60
Q

What supportive treatments exist for SLE?

A

Avoid sunlight

Liver function and blood surveillance

Prophylactic antibiotics

Osteoperosis screening

61
Q

What is this and what does it suggest?

A

Malar Rash on both Cheeks = Lupus

“Butterlfy Rash”

62
Q

What is this and what does it suggest?

A

An oral ulcer

Possibly Lupus

63
Q

What is this and what does it suggest?

A

A Discoid rash effecting the entirety of the scalp

= Lupus

MSK/Derm (46 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions