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Advanced Immunology > Lupus > Flashcards

Lupus Flashcards

1
Q

lupus is 9x more common in ____

A

women

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2
Q

mortality ratio for SLE is _____ than the general population

A

2-3x higher

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3
Q

______ tend to have more severe disease

A

men and children

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4
Q

_______ patients with lupus nephritis have reduced survival

A

african american

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5
Q

name some effects lupus has on the body

A

unexplained fever, alopecia, chronic fatigue, scalp sores, butterfly rash, anemia/blood clotting, chest pain, Raynaud’s, joint pain, muscle aches, hand and feet swelling, mouth/nose sores, skin changes/sun sensitivity

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6
Q

lupus is a _____ disease with _____ flares

A

chronic disease with acute flares

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7
Q

lupus can mimic what disease?

A

Rheumatoid arthritis

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8
Q

interactions between _____ and _____ result in abnormal immune responses

A

susceptibility genes and environmental factors

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9
Q

who is at higher risk for SLE

A

people with first degree relatives with SLE

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10
Q

etiology of SLE is _____-factorial

A

multi

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11
Q

abnormal clearance of ______ stimulates an immune response

A

apoptotic debris

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12
Q

autoantibodies cause _____

A

tissue destruction

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13
Q

what are some examples of organ damage from SLE

A

renal failure, atherosclerosis, pulmonary fibrosis, stroke

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14
Q

what is drug-induced lupus?

A

lupus-like findings in a patient with no history of SLE/onset at least 1 month after initiation of a drug; improvement within days to months after stopping the drug

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15
Q

true or false: a combo of genetic factors & environment play a role in SLE etiology

A

true

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16
Q

what are some diagnostic criteria used for SLE

A

EULAR/ACR 2019
SLICC 2012

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17
Q

why is SLICC criteria different

A

it does not require the presence of ANA

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18
Q

antinuclear antibodies (ANA) are positive in _____ of patients during the course of disease

A

> 98% (but ANA is not specific to lupus it can mean anything autoimmune)

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19
Q

what antibodies are more specific for SLE?

A

high-tier IgG antibodies to double-stranded DNA and antibodies to the Sm antigen

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20
Q

true or false: the presence of multiple antibodies without clinical symptoms should be considered diagnostic for SLE

A

FALSE

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21
Q

what are some clinical presentation of SLE

A

fever, fatigue, weight loss, neuro, renal, heme, cardiac, skin, MSK

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22
Q

what are the constitutional symptoms present in most lupus patients?

A

fever, fatigue, weight loss

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23
Q

85% of patients with SLE will have ____ and _____

A

arthritis and arthralgias

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24
Q

difference between RA and SLE arthritis/arthralgias?

A

in SLE it is not permanent

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25
Q

characteristics of arthritis/arthralgias in SLE

A

migratory, polyarticular, symmetrical

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26
Q

who more commonly has skin manifestations in lupus

A

women

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27
Q

a ______ usually appears after sun exposure

A

butterfly rash

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28
Q

______ is a common theme for skin lesions and can trigger a skin rash

A

photosensitivity

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29
Q

what are some pulmonary manifestations of SLE

A

pleuritis and pleural effusion, interstitial inflammation leading to fibrosis

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30
Q

what is the leading cause of death in patients with SLE?

A

cardiovascular disease

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31
Q

what is the most common cardiac manifestation of SLE?

A

pericarditis

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32
Q

what are other cardiac manifestations of SLE

A

myocarditis, hypertension, premature atherosclerosis

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33
Q

what are GI manifestations of SLE

A

nausea, vomiting, diarrhea (can be part of a flare, or side effects of medications)

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34
Q

what are hematologic manifestations of SLE?

A

anemia, leukopenia, neutropenia, thrombocytopenia

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35
Q

what are nervous system manifestations of SLE?

A

memory and reasoning difficulties, headache/migraine (flare), seizures, mood disorders (anxiety, depression), psychosis

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36
Q

psychosis in SLE must be distinguished from ____

A

glucocorticoid psychosis: occurs during first few weeks of glucocorticoid therapy

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37
Q

lupus nephritis is more common in who

A

men

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38
Q

lupus nephritis is a significant cause of______

A

morbidity and mortality

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39
Q

selena gomez had a ____ transplant

A

kidney

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40
Q

how does lupus nephritis happen

A

antibodies deposit in kidney; triggers autoimmune response that attacks kidneys— damage leading to proteinuria, albuminuria

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41
Q

what are the 3 antiphospholipid antibodies

A

anticardiolipin, antiB-2-glycoprotein I, lupus anticoagulant

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42
Q

what is antiphospholipid syndrome (APS)

A

systemic autoimmune disorder characterized by thrombosis in presence of antiphospholipid antibodies

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43
Q

APS increases the risk of _____ and _____

A

thrombosis and stroke

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44
Q

immunologic lab tests for SLE

A

ANA +/- anti-dsDNA +/- Anti-sm
antiphospholipid antibodies
ESR and CRP
complement

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45
Q

anemia work up for SLE

A

CBC with diff + BMP

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46
Q

renal work up for SLE

A

SCr, urinalysis with sediment

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47
Q

goals of treatment

A

prevent flares, limit involvement of other organs and prevent damage, reduce disease activity, achieve and maintain remission, reduce use of steroids

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48
Q

pharm treatment consists of _______ AND ______

A

immunosuppression AND symptomatic therapies

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49
Q

self care measures for lupus?

A
  1. hats in the sun
  2. sunscreen always (UVA and UVB, SPF 15 minimum but 30 preferred)
  3. stop smoking
  4. exercise
  5. stress coping
  6. lots of sleep
  7. immunizations (try to give before starting immunosuppressive therapies)
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50
Q

pharm options?

A

anti-inflammatory, anti-malarial, corticosteroids, cytotoxic immunosuppressives

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51
Q

anti inflammatory agents

A

NSAIDs, ASA

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52
Q

antimalarial agents

A

hydroxychloroquine

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53
Q

corticosteroid agents

A

prednisone, methylprednisolone

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54
Q

cytotoxic immunosuppressives

A

azathioprine, methotrexate, mycophenolate, cyclophosphamide, voclosporin, calcineurin inhibitors, JAK inhibitors

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55
Q

biologics

A

rituximab, benlysta, saphnelo

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56
Q

what is the mainstay of lupus treatment

A

hydroxychloroquine

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57
Q

what is cutaneous lupus erythematosus (CLE)

A

skin involvement

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58
Q

first line for CLE

A

topical therapy first line; most commonly topical corticosteroids

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59
Q

for thin skin areas like face and groin, use ____

A

low potency steroids

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60
Q

for trunk and extremities, use ____

A

mid potency

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61
Q

for thick skin areas like scalp, soles, and palms use _____

A

high potency

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62
Q

adverse drug reactions of topical corticosteroids

A

skin atrophy, telangiectasias, steroid-induced dermatitis

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63
Q

use the lowest ___ and ____ for topical corticosteroids

A

potency and duration

64
Q

in addition to topical corticosteroids, you can use ____ for CLE

A

topical calcineurin inhibitors

65
Q

SLE with no specific disease manifestations– what treatment?

A

NSAIDs

66
Q

NSAIDs are first line for what

A

arthritis, musculoskeletal complaints, fever, serositis but no major organ invovement

67
Q

NSAIDs are NOT ____

A

disease modifying; but they do help w/ symptoms

68
Q

try NSAIDs for up to __ weeks and re-assess

A

4

69
Q

potential side effects for NSAIDs

A

GI effects, CV effects, renal

70
Q

hydroxychloroquine dose

A

200-400 mg PO daily (max 5 mg/kg/day)

71
Q

effects of hydroxychloroquine

A

anti-inflammatory, immunomodulatory, antithrombotic

72
Q

counseling for hydroxychloroquine

A

may take 2-8 weeks to see effects and 3-6 months for maximum efficacy.

73
Q

who should receive hydroxychloroquine

A

all patients

74
Q

hydroxychloroquine allows corticosteroid doses to be ____

A

decreased

75
Q

benefits of hydroxychloroquine

A

prevents flares, improves survival, protects against bone mass loss, protects against thrombosis and organ damage, benefits lipids and fasting BG, decreases infections

76
Q

mech of hydroxychloroquine

A

reduces concentrations of inflammatory cytokines; alters antigen presentation and T-cell proliferative responses, decreases activation of TLR

77
Q

hydroxychloroquine elimination

A

renal

78
Q

hydroxychloroquine T1/2

A

40-50 days

79
Q

ADRs of hydroxychloroquine

A

GI and skin reactions (nausea, vomiting, rash, alopecia), QT prolongation, retinal toxicity

80
Q

____ screening required for hydroxychloroquine at baseline and then annually after 5 years

A

eye

81
Q

place in therapy for glucocorticoids

A

monotherapy or adjunct; control flares and maintain low disease activity

82
Q

onset of glucocorticoids

A

rapid

83
Q

dose options for glucocorticoids

A

high IV dose pulse to control flare, high dose oral to control severe disease, low dose oral for maintenance

84
Q

early ADRs for glucocorticoids

A

weight gain, hyperglycemia, infection risk, mood changes, dyspepsia

85
Q

chronic use ADRs for glucocorticoids

A

osteoporosis, infections, cataracts, glaucoma, hyperglycemia/diabetes, fat redistribution, sleep/mood disturbances, thinning of skin (topical)

86
Q

what if no sustained response from NSAIDs, antimalarials, or glucocorticoids?

A

go to immunosuppressives

87
Q

azathioprine MOA

A

purine analog, inhibits nucleic acid synthesis and affects cellular and humoral immune functions

88
Q

what testing to have prior to using azathioprine

A

TPMT testing (if TMPT activity is low, they can’t metabolize the drug= risk for myelosuppression)

89
Q

azathioprine is metabolized to ___

A

mercaptopurine

90
Q

place in therapy for azathioprine

A

for refractory mild disease, mild nephritis, or a steroid-sparing agent
less effective but less toxic

91
Q

ADRs of azathioprine

A

hepatotoxicity, pancreatitis, myelosuppression, N/V, infection

92
Q

monitoring for azathioprine

A

LFTs q6 months, CBC q2 weeks with dose increases then monthly

93
Q

methotrexate MOA

A

inhibition of dihydrofolate reductase, which is needed for DNA synthesis and cell proliferation

94
Q

place in therapy of methotrexate

A

steroid-sparing drug, MSK/skin/serosal disease

95
Q

ADRs of methotrexate

A

bone marrow suppression, increased LFTs, infection, cirrhosis, diarrhea, N/V, mouth sores, GI/pulmonary/nephrotoxicity

96
Q

how to reduce toxicities of methotrexate

A

administer folic acid 1-5 mg daily

97
Q

mycophenolate mofetil (MMF) MOA

A

inhibits IMP dehydrogenase, which results in decreased B and T cell proliferation and decreased antibody production

98
Q

active form of MMF

A

mycophenolic acid

99
Q

onset of MMF

A

3-16 weeks

100
Q

place in therapy for MMF

A

induction, maintenance

101
Q

ADRs of MMF

A

GI complaints most common, infections, leukopenia, anemia, thrombocytopenia

102
Q

evidence suggests that who responds better to MMF

A

hispanic and black patients with lupus nephritis

103
Q

cyclophosphamide MOA

A

alkylating agent, inhibits B and T cell proliferation and antibody production

104
Q

place in therapy of cyclophosphamide

A

induction agent for patients with severe disease or refractory organ involvement including lupus nephritis, neuropsychiatric lupus, severe systemic vasculitis, hematologic disease

105
Q

dosage forms of cyclophosphamide

A

IV or PO, IV is preferred

106
Q

onset of cyclophosphamide

A

3-16 weeks

107
Q

toxicity of cyclophosphamide

A

hemorrhagic cystitis and bladder cancer (greater risk with PO administration)

108
Q

cyclophosphamide is only for ____

A

induction

109
Q

how to prevent bladder toxicity with cyclophosphamide

A

intermittent pulse IV doses, hydration, frequent voiding, or giving with mesna

110
Q

____ and ____ are preferred for maintenance therapy

A

azathioprine and mycophenolate

111
Q

ADRs of cyclophosphamide

A

myelosuppression, increased infection risk, cardiac/hepatic/pulmonary toxicity, decreased fertility, teratogenic, urinary/renal toxicity

112
Q

monitoring for cyclophosphamide

A

baseline and monthly CBCs and urinalysis

113
Q

voclosporin MOA

A

calcineurin inhibitor– blocks activation of T cells, cytokine release, and costimulation of B-cells with release of autoantibodies; helps maintain glomerular filtration barrier in kidneys

114
Q

voclosporin is the first drug to be FDA-approved for _____

A

treatment of active lupus nephritis

115
Q

voclosporin is used in combo with

A

mycophenolate and steroids

116
Q

belimumab brand name

A

benlysta

117
Q

belimumab MOA

A

B-lymphocyte stimulator (BLyS): cytokine that is important for B-cell survival, maturation, and differentiation

118
Q

belimumab is a ________ antibody

A

fully human monoclonal

119
Q

belimumab is FDA approved for ____

A

treatment of autoantibody-positive SLE in addition to standard therapy

120
Q

benefits of belimumab

A

prevents the survival of B- lymphocytes by blocking the binding of BLsY to receptors on B lymphocytes
promotes apoptosis of B-lymphocytes
reduces activity of B-cell mediated immunity and the autoimmune response

121
Q

onset of belimumab

A

8 weeks for action on B cells, 16 weeks for clinical improvement

122
Q

belimumab dosage forms

A

IV or SubQ

123
Q

place in therapy for belimumab

A

decreases flares, disease activity, and steroid use

124
Q

belimumab ADRs

A

nausea, diarrhea, pyrexia, nasopharyngitis, bronchitis, insomnia, pain in extremity, depression, migraine, pharyngitis, injection site reaction

125
Q

limitations for use of belimumab

A

not been evaluated in patients with severe CNS lupus; not recommended

126
Q

data does not support safety and efficacy of belimumab with concomitant use of ____

A

rituximab or other biologics

127
Q

FDA warnings of belimumab

A

mortality (serious and fatal infections reported); progressive multifocal leukoencephalopathy (PML); hypersensitivity reactions (anaphylaxis), depression and suicidality; live vaccines should not be given concurrently

128
Q

rituximab MOA

A

IV chimeric monoclonal antibody directed at the CD20 antigen on B cells

129
Q

rituximab place in therapy

A

use in SLE being investigated, potential for use in refractory lupus nephritis/ severe hematological lupus/ CNS manifestations

130
Q

rituximab ADRs

A

infusion reactions, mucocutaneous reactions, allergy, infection, PML, hepatitis B virus reactivation

131
Q

rituximab FDA warnings

A

fatal infusion reaction within 24 hours of infusion, tumor lysis syndrome, severe mucocutaneous reactions, PML

132
Q

anifrolumab brand name

A

saphnelo

133
Q

anifrolumab MOA

A

fully human IgG1-Kappa monoclonal antibody that blocks type 1 interferons through binding the type I interferon receptor subunit I, leading to reduced inflammation

134
Q

anifrolumab ADRs

A

nasopharyngitis, URTIs, bronchitis, infusion reactions, herpes zoster and cough

135
Q

limitations of use anifrolumab

A

efficacy has not been evaluated in patients with severe active lupus nephritis or severe active CNS lupus; use not recommended for use with other biologic therapies

136
Q

rule of thumb for biologics

A

never use them together

137
Q

FDA warnings anifrolumab

A

serious infections, hypersensitivity reactions, malignancy, avoid use of live or live-attenuated vaccines

138
Q

class I and II lupus nephritis

A

minimal mesangial and mesangial proliferative

139
Q

all patients with nephritis should receive __

A

hydroxychloroquine 200-400 mg/day to reduce damage and flares +/- NSAIDs/glucocorticoids

140
Q

Class III and IV nephritis

A

more severe kidney involvement

141
Q

induction treatment for Class III/IV

A

high dose IV glucocorticoids then PO
+ induction with PO mycophenolate or cyclophosphamide
continue by 6 months

142
Q

maintenance treatment nephritis class III/IV

A

mycophenolate 1-2 g/day or azathioprine 2 mg/kg/day +/- PO low dose glucocorticoids. if no response then belimumab or voclosporin

143
Q

what is nephritis class V

A

membranous lupus nephritis and nephrotic range proteinuria >3 g/day

144
Q

treatment of class V induction

A

PO prednisone + induction with PO mycophenolate continue x 6 months

if no response: switch induction to cyclophosphamide and IV pulse glucocorticoids then prednisone x 6 months

145
Q

maintenance class V nephritis

A

mycophenolate or azathioprine +/- PO glucocorticoids
continue 3-5 years

146
Q

neuropsychiatric lupus treatment

A

hydroxycloroquine is preferred. anticonvulsants, antidepressants, antipsychotics as needed. glucocorticoids alone or in combo for inflammation/neurotoxic damage

147
Q

can you have positive antiphospholipid antibodies without APS?

A

yes

148
Q

what makes you considered to have APS

A

positive antiphospholipid antibodies and a clot/thrombotic event

149
Q

positive antiphospholipid antibodies/no clot: prophylaxis?

A

aspirin 81 mg PO daily
women avoid estrogen
address modifiable risk factors

150
Q

TREATMENT for people that do have APS (antibodies + clot)

A

warfarin with INR goal 2-3, if they are pregnant use LMWH

151
Q

all patients taking prednisone should take

A

calcium and vitamin D

152
Q

hydroxychloroquine in pregnancy _____ recommendent

A

IS

153
Q

highest risk drug-induced SLE

A

procainamide, hydralazine

154
Q

moderate risk drug-induced SLE

A

isoniazid, quinidine, sulfadiazine

155
Q

low risk drug-induced SLE

A

methyldopa, chlorpromazine, carbamazepine, prophylthiouracil, minocycline, captopril

156
Q
A

Advanced Immunology (6 decks)

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