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COM MOD > Chapter 6- SLE > Flashcards

Chapter 6- SLE Flashcards

1
Q

Epidemiology of SLE

A

women of african american and hispanic descent

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2
Q

What organs are involved in SLE (4)

A

skin, joints, kidney, serosal membrane

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3
Q

What autoantibodies are always present in SLE

A 
antinuclear autoantibodies (ANAs)
*these are not specific to SLE
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4
Q

Mechanism of injury in SLE

A

deposition of immune complexes and binding of antibodies to cells and tissues

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5
Q

11 Common Criteria for SLE

A 
IM DAMN SHARP
immunologic disorder
malar rash
discoid rash
antinuclear antigens 
mucositis (oral or nasal ulcers)
neurologic disorder
serositis (pleuritis or pericarditis)
hematologic  disorder
arthritis
renal disorder
photosensitivity
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6
Q

Most common autoantibodies in SLE

A

double-stranded DNA antigen
anti-smith antigen
ANA

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7
Q

Most common autoantibodies in Sjogren syndrome

A

Ro/SS-A

La/SS-B

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8
Q

4 categories of antinuclear antigens (ANA)

A

antibodies against DNA, histones, nonhistone proteins bound to RNA, and nucleolar antigens

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9
Q

How to detect ANAs

A

indirect immunofluorescence that shows 4 basic patterns

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10
Q

4 basic immunofluorescent patterns for ANAs

A

diffuse, speckled, anti-centromeric, nucleolar

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11
Q

SLE and Antiphospholipid antibodies

A

cause false-positive test result for syphilis

can interfere with clotting tests (PTT)

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12
Q

PTT test and SLE

A

+ PTT test should mean the person has a problem clotting but with SLE it is actually the opposite and the person is prone to more clots

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13
Q

Genetic factors of SLE (4)

A

increased risk in family members, monozygotic twins, HLA-DQ allele, inherited complement deficiency

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14
Q

SLE and MHC molecule involvement

A

has implications with MHC and non-MHC genes

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15
Q

Result of susceptible loci in SLE

A

proteins involved in lymphocyte signaling are at risk

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16
Q

Environmental factors of SLE (4)

A

Exposure to UV light, gender bias (X chromosome), drugs, microbiome

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17
Q

UV light and SLE

A

exacerbates disease

stimulate keratinocytes to produce IL-1 and cause inflammation

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18
Q

Drugs that influence SLE

A

hydralazine, procainamide, and D-penicillamine

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19
Q

Morphology of SLE

A

blood vessels, joints, and kidneys*

20
Q

Blood vessel morphology and SLE

A

acute necrotizing vasculitis of capillaries, small arteries, and arterioles

21
Q

Joint morphology and SLE

A

non-erosive synovitis with little deformity

22
Q

Kidney morphology and SLE

A

renal involvement
6 patterns
glomerular lesions from immune complex deposition

23
Q

Most common glomerular disease in SLE

A

Class IV- diffuse lupus nephritis

24
Q

Least common glomerular disease in SLE

A

Class I- minimal mesangial lupus nephritis

25
Q

Skin morphology in SLE

A

butterfly rash
exposure to sunlight accentuates the erythema
deposition of immunoglobulin and complement along dermal-epidermal junction

26
Q

Serosal Involvement and SLE

A

inflammation of serosal lining membranes
acute and chronic stages
pleuritis and pericarditis may be present

27
Q

Acute stage in serosal involvement in SLE

A

mesothelial surfaces covered with fibrinous exudate

28
Q

Chronic state in serosal involvement in SLE

A

thickened, opaque and coated with fibrous tissue

29
Q

Cardiovascular system and SLE

A

any layer of the heart can be damaged

myocarditis, coronary artery disease, valvular abnormalities, and valvular endocarditis

30
Q

Myocarditis in SLE

A

leads to tachycardia and ECG abnormalities

31
Q

Coronary artery disease in SLE

A

angina and myocardial infarction

32
Q

Valvular abnormalities in SLE

A

mitral and aortic involvement

stenosis and/or regurgitation

33
Q

Valvular endocarditis in SLE

A

Libman-Sacks

big lesions of the heart where bacteria is not present

34
Q

CNS and SLE

A

neuropsychiatic symptoms

35
Q

Spleen and SLE

A

splenomegaly, capsular thickening, follicular hyperplasia

36
Q

Lungs and SLE

A

pleuritis
chronic interstitial fibrosis
secondary pulmonary hypertension

37
Q

Signs of renal involvement in SLE (4)

A

hematuria, red cell casts, proteinuria, classic nephrotic syndrome

38
Q

Why do SLE patients have increased numbers of infection?

A

underlying immune function and treatment with immunosuppressive drugs

39
Q

How to treat disease flares for SLE

A

corticosteroids and immunosuppressive drugs

40
Q

Causes of death in SLE (3)

A

renal failure, infection, coronary artery disease

41
Q

Primary characteristic of Chronic Discoid Lupus Erythematosus

A

skin manifestations on face and scalp
skin plaques to varying degrees- edema, erythema, scaliness, skin atrophy surrounded by elevated erythematous border
*rarely systemic

42
Q

Subacute Cutaneous Lupus Erythematosus

A

mild version of lupus
predominant skin involvement
mild systemic symptoms consistent w SLE

43
Q

How to distinguish subacute cutaneous lupus erythematosus from systemic lupus erythematosus?

A

skin rash tends to be widespread, superficial and nonscarring

44
Q

Drugs that induce Drug Induced Lupus occur?

A

hydralazine, procainamide, isoniazid, and D-penicillamine

anti-TNF therapy

45
Q

What organs does drug induced lupus not affect?

A

renal and CNS

46
Q

How can drug induced lupus be resolved?

A

withdrawal of the drug

COM MOD (21 decks)

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