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Hematology-Immunology > SLE, RA, Psoriasis > Flashcards

SLE, RA, Psoriasis Flashcards

1
Q

Definition of SLE

A

Prototypic systemic autoimmune disease characterized by heterogeneous, multisystem involvement and the production of an array of autoantibodies.

Clinical features in individual patients can be quite variable

There is no gold standard test for the diagnosis of SLE.

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2
Q

having the greatest sensitivity-98% for the diagnosis

A

antinuclear antibodies

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3
Q

having the greatest specificity 70%

A

Anti-dsDNA and Anti-Smith antibodies

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4
Q

having the greatest specificity 70%

A

Anti-dsDNA and Anti-Smith antibodies

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5
Q

less photosensitivity, more serositis, an older age at diagnosis, and a higher 1 year mortality compared to women

A

Lupus in men

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6
Q

Tissue damage in SLE is mediated by

A

recruitment of inflammatory cells, reactive oxygen intermediates, production of inflammatory cytokines, and modulation of the coagulation cascade.

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7
Q

Sun exposure in SLE

A

• Definite - UVB Light
• Experimental studies have shown that UV light is a potent inhibitor of DNA methylation in CD4+ cells, causing autoreactivity of T cells.
• Also induces apoptosis of keratinocytes and production of anti-Ro, anti-La, anti-Sm, and other lupus autoantibodies

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8
Q

has been identified as a possible factor in the development of lupus and may reside in and interact with B cells and promotes interferon α (IFNα) production by plasmacytoid dendritic cells (pDCs), suggesting that elevated IFNα in lupus may be—at least in part—due to aberrantly controlled chronic viral infection

A

Epstein-Barr Virus (EBV)

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9
Q

are the main effectors of the onset of disease in SLE.
In humans, they are probably necessary for disease, but not sufficient and are traditionally viewed as essential media- tors of pathology in SLE, particularly when they are in the form of immune complexes

A

Autoantibodies

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10
Q

Probable Cause of SLE

A

-Estrogen and Prolactin
-EBV
-Lupus inducing medications

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11
Q

When to highly consider SLE

A

A woman of childbearing age with:
• Constitutional symptoms of fever, weight loss, malaise, severe fatigue
• Skin rash and/or stomatitis
• Arthritis
• Proteinuria, cylindruria, hematuria
• Cytopenias

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12
Q

Most common clinical features of the disease (SLE):

A

• Constitutional symptoms
• Rash
• Mucosal ulcers
• Inflammatory polyarthritis
• Photosensitivity
• Serositis

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13
Q

is the most common of the potentially lifethreatening manifestations

A

Lupus nephritis

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14
Q

SLICC Classification Requirements

A

> 4 criteria (at leaset 1 clinical and 1 laboratory criteria) or Biopsy-proven lupus nephritis with positive ANA or Anti-DNA

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15
Q

SLICC Classification Requirements

A

> 4 criteria (at leaset 1 clinical and 1 laboratory criteria) or Biopsy-proven lupus nephritis with positive ANA or Anti-DNA

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16
Q

Acute cutaneous lupus erythematosus

A

Localized acute cutaneous lupus erythematosus (malar rash butterfly rash)

This lesion is characterized by macular or papular erythema in a malar distrubution sparing the nasolabial folds

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17
Q

Subacute lupus erthematosus (SCLE)

A
  • Common in Drugs-Induced lupus
  • Subacute lupus erthematosus (papulosquamous variant)
  • Lesions typically involve the back, neck, shoulders, and extensor surfaces of the arms and usually spare the central area of the face
  • Lesions heal without scar
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18
Q

Chronic cutanous lupus erythematosus (CCLE) lesions

A

-Discord lupus erythematosus involving the face and scalp
-Discoid lesions are formed of chronic cutanenous lupus and are commonly found on the scalp, face, and external ears
-If untreated, these lesion can lead to permanent alopecia and disfigurement

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19
Q

Common complication of discoid lupus most frequenly develop on the vertex and parietal areas

A

Scarring alopecia

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20
Q

is characterized by short, irregularly sized hair at the frontal hairline and is associated with active systemic disease

A

Lupus hair

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21
Q

manifests as diffuse hair thinning

A

Telogen effluvium

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22
Q

discrete areas of hair loss and induced by stress

A

Alopecia areata

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23
Q

red macules, palatal erythema or petechiae, erosions, or ulcerations; usually painless

A

Acute oral lupus

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24
Q

red macules, palatal erythema or petechiae, erosions, or ulcerations; usually painless

A

Acute oral lupus

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25
are rare; characterized by welldemaracted, round, red patches
Subacute oral lesions
26
are rare; characterized by welldemaracted, round, red patches
Subacute oral lesions
27
present as painful, well demarcated,round, red lesions with white radiating hyperkeratotic striae; frequently involves the lip and spreads from the vermilion border to the skin of the lip
Oral discoid lesions
28
symmetric, inflammatory arthritis predominantly affecting the knees, wrists, and small joints of the hands
Lupus arthritis
29
symmetric, inflammatory arthritis predominantly affecting the knees, wrists, and small joints of the hands
Lupus arthritis
30
typically small and not as inflammatory as those present in rheumatoid arthritis
Synovial effusions
31
Hand deformities can occur as a result of ligamental and/or joint capsule laxity and joint subluxation
Jaccoud's- like arthropathy
32
very common manifestations of SLE, present in up to 90% of patients at some point during the course of their disease
Arthritis and Arthralgias
33
end result of interruption of the blood supply to bone, leading to reactive hyperemia of adjacent bone, demineralization, and then collapse.
Avascular Necrosis (AVN) - is often bilateral; joint effusions may occur
34
end result of interruption of the blood supply to bone, leading to reactive hyperemia of adjacent bone, demineralization, and then collapse.
Avascular Necrosis (AVN) - is often bilateral; joint effusions may occur
35
Most common affected sites in AVN
-femoral heads -tibial plateaus -femoral condyles
36
Most common affected sites in AVN
-femoral heads -tibial plateaus -femoral condyles
37
Routing screening procedures for SLE with Renal involvement
include inquiring about newonset polyuria, nocturia, or foamy urine and looking for the presence of hypertension or lower extremity edema. It is important to screen at regular intervals for the presence of proteinuria and/or hematuria and a change in serum creatinine; in active SLE patients, screening at 3-month intervals is prudent.
38
Class I - Lupis Nephritis
Minimal mesangial lupus nephritis - Normal glomeruli by light microscopy, but mesangia immune deposit by immunofluorescence
39
Class II - Lupis Nephritis
Mesengial Proliferative Nephritis -Purely mesangial hypercellularity of any degree or mesangial matrix expansion by light microscopy
40
Class III - Lupis Nephritis
Focal Lupus Nephritis - Active or inactive focal, segmental or global endocapulary or extracapillalry gmn involving <50% og all glomeruli
41
Class IV - Lupis Nephritis
DIffuse Lupus Nephritis - Active or inactive diffuse, segmental or endocapillary or extracapillary gmn involving >50% of all glomeruli typically with diffuse subendothelial immune deposit, with or without mesangial alterations
42
Class V - Lupis Nephritis
Membranous Lupus Nephritis - Global or segmental subepithelial immune deposit
43
Class VI - Lupis Nephritis
Advanced Sclerotic Lupus Nephritis - >90% of glomeruli globally sclerosed without residual activity
44
with or without an effusion most common cardiac manifestation of SLE, occurring in more than 50% of SLE patient
Pericarditis
45
Myocarditis in SLE
• Uncommon manifestation • Poor prognosis • should be suspected in a patient presenting with various combinations of the following clinical features: -unexplained heart failure or cardiomegaly -unexplained tachycardia -unexplained electrocardiographic abnormalities
46
Most common ocular manifestation; can occur in the presence or absence of secondary Sjögren’s
Keratoconjunctivitis Sicca (KCS)- Dry eyes
47
Most common ocular manifestation; can occur in the presence or absence of secondary Sjögren’s
Keratoconjunctivitis Sicca (KCS)- Dry eyes
48
Other Optha manifestations in SLE
• Episcleritis and scleritis • Uveitis - extremely rare • Discoid lupus can involve the lower eyelid and conjunctiva • Effects of Glucocorticoids and antimalarial agents
49
Anemia of chronic disease (ACD)
• most common anemia in SLE • normochromic, normocytic anemia • characterized by the presence of low serum iron, low transferrin, and normal to increased serum ferritin
50
Anemia of chronic disease (ACD)
• most common anemia in SLE • normochromic, normocytic anemia • characterized by the presence of low serum iron, low transferrin, and normal to increased serum ferritin
51
Autoimmune hemolytic anemia (AIHA) should be suspected in the setting of the following laboratory abnormalities:
• increased serum unconjugated bilirubin • increased lactate dehydrogenase (LDH) • increased reticulocyte count • reduced serum haptoglobin. • Direct Coombs’ test is typically positive • peripheral blood smear demonstrates spherocytosis
52
Presence of __________ is specific for SLE
Hematoxylin bodies
53
Hydroxychloroquine
• background therapy in most SLE patients - Lupus treatment goals is to suppressed the immune to decrease flares • dose: 200mg/day • Monitor for eye toxicity
54
Corticosteroids
• Used to manage lupus flares • Closely supervised by rheumatologist / specialist • Calcium + vit D to prevent osteoporosis
55
Rheumatoid Arthritis
• is a chronic inflammatory disease of unknown etiology • Characterized by a symmetric polyarthritis, the most common form of chronic inflammatory arthritis • Female predilection
56
Persistent active RA often
results in articular cartilage and bone destruction and functional disability
57
The primary target in rheumatoid arthritis is
synovium as this is the joint structure that is heavily exposed to the inflammatory cells and cytokines present within the joint. In response to the inflammatory process the synovium develops hyperplasia of the lining cells, pannus formation and eventual fibrosis and joint destruction
58
Hyperextension of the Interphalangeal Joints in RA
Z deformity
59
Hyperextension of the Interphalangeal Joints in RA
Z deformity
60
Flexion of the proximal and Hyperextension of the distal interphalangeal joints in RA
Boutonniere deformity
61
DIP flexion and PIP hyperextension in RA
Swan neck deformity - The lesion probably begins with shortening of the interosseous muscles and tendons. - Shortening of the intrinsic muscles exerts tension on the dorsal tendon sheath, leading to hyperextension of the PIP joint
62
Other chronic hand deformities in RA include
-ulnar deviation -MCP subluxation -intrinsic muscle atrophy -rheumatoid nodules.
63
de Quervain’s tenosynovitis of the extensors of the thumb
- causes severe discomfort and yet is easily treated - Finkelstein’s test - ulnar flexion at the wrist after the thumb is maximally flexed and adducted
64
de Quervain’s tenosynovitis of the extensors of the thumb
- causes severe discomfort and yet is easily treated - Finkelstein’s test - ulnar flexion at the wrist after the thumb is maximally flexed and adducted
65
“Trigger” fingers
Frequently, rheumatoid nodules develop within tendon sheaths and may “lock” the finger painfully into fixed flexionor cause trigger fingers
66
RA Monitoring and treament
-Bone densitometry should be performed routinely in patients with RA -treatment with bisphosphonates should be considered as an adjunct to therapy.
67
Felty's syndrome
• seropositive, erosive RA symptoms • Neutropenia • Splenomegaly
68
The initial pathologic change in RA is often seen as inflammatory changes in medium and small blood vessels.
Vasculitis
69
Rheumatoid vasculitis affects a very small subset of patients with established, often severe, RA
• Distal arteritis (including from splinter hemorrhage, nail fold infarcts, and gangrene) • Cutaneous ulceration (including pyoderma gangrenosum) • Peripheral neuropathy (mononeuritis multiplex or sensory stocking-glove neuropathy) • Palpable purpura
70
is commonly found on autopsy of patients with RA, but clinical disease during life is seen less frequently
Pleuritis
71
Disease CVS in RA
• Increased risk of premature death in RA is due largely to an increased incidence of cardiovascular disease, primarily myocardial infarction and congestive heart failure • Atherosclerosis • Pericarditis • Myocarditis • Endocardial Inflammation • Conduction Defects
72
2010 New ACR/EULAR Criteria for RA
Patients are definitively diagnosed RA if score >6 points
73
RA Management
• NSAIDS • Analgesics • Corticosteroids: low dose as “bridge therapy” for DMARDs or biologics • DMARDS (Methotrexate Hydroxychloroquine o Leflunomide, SSZ) • NEW MEDICATIONS (Biologic DMARDs especially anti-TNF Tofacitinib Xeljanz® oral small molecule)
74
RA Management
• NSAIDS • Analgesics • Corticosteroids: low dose as “bridge therapy” for DMARDs or biologics • DMARDS (Methotrexate Hydroxychloroquine o Leflunomide, SSZ) • NEW MEDICATIONS (Biologic DMARDs especially anti-TNF Tofacitinib Xeljanz® oral small molecule)
75
Monitoring for patient with RA
• Hematologic (CBC), lung, liver (avoid alcohol); once a week • Ophthalmologic • GI • Infection, (eg TB. Regular follow up with rheumatologist)
76
Treatment Strategies in RA
1. Early diagnosis / referral to rheumatology 2. Early use of DMARDs eg. MTX 3. Identify a treatment target (remission) 4. Monitor and adjust disease-modifying therapy according to the target 5. Add biological DMARD if target is not achieved
77
Psoriasis
• Hyper-inflammatory skin disease; demarcated, erythematous, scaly plaques • 7 to 42% develop arthritis or PsA • Psoriasis skin lesions may develop after onset of arthritis in ~15% of cases
78
80-90%; Red, scaly plaques in discrete patches. The extent of body surface area covered varies widely from patient to patient
Chronic Plaque Psoriasis
79
<10%; Multiple, small red spots, usually on the trunk and limbs
Guttate psoriasis
80
<10%; Multiple, small red spots, usually on the trunk and limbs
Guttate psoriasis
81
<5%; Very red scale free lesions that form in skin folds
Inverse/flexural psoriasis
82
<5%; White blisters surrounded by red skin, which may be localized to a particular area, but which can also cover the whole body
Pustular psoriasis
83
<5%; White blisters surrounded by red skin, which may be localized to a particular area, but which can also cover the whole body
Pustular psoriasis
84
<2%; Severe red inflammation and skin shedding covering most of the body. This is a rare but DANGEROUS FORM of the disease that can cause patients to lose excessive amounts of heat through the skin
Erythrodermic Psoriasis
85
Psoriasis Skin
• Characterized by epidermal hyperplasia, mononuclear leukocytes in the papillary dermis, neutrophils in the stratum corneum, and an increase in various subsets of dendritic cells. • Epidermis- CD8+ T cells are the predominant T cell subset • Dermis- mixture of CD4+ and CD8+ • Vascular changes are prominent in psoriasis with impressive growth and dilation of superficial blood vessels.
86
Psoriasis Genetic Factors
• 40 percent have a family history in first-degree relatives • HLA susceptibility region for psoriasis is HLA-Cw6 • HLA-B27, chiefly in patients with predominant spinal disease, and with HLA-B38 and HLA-B39
87
Laboratory Parameters in PsA
• No diagnostic laboratory test for PsA • Negative rheumatoid factor (RF) in majority • Elevated ESR/ CRP but nonspecific
88
Radiographic features of PsA
Peripheral PsA 1. DIP involvement - "pencil-in-cup" deformity 2. Marginal erosions 3. Small-joint ankylosis 4. Marked bony resportion and the consequent collapse of soft tissue - TELESCOPING FINGERS
89
Management of Psoriasis/Psoriatic Arthritis
• NSAIDs • DMARDs: Methotrexate, Sulfasalazine, cyclosporine • Topicals, psoralens plus ultraviolet A light (PUVA) for psoriasis lesions • Biologics
90
Mainstay in the management of psoriatic arthritis and other spondyloarthropathies are the
NSAIDs and DMARDs
91
Psoriasis with skin involvement treatment
psoralens plus UVA light should be given. Refer to a trained specialist, like a rheumatologist when handling biologics for these cases.
92
Biological Treatment of PsA
• Anti-TNF-α (Etanercept, Infliximab, Adalimumab, Golimumab • Ustekinumab (a monoclonal antibody that blocks binding of IL-12 and IL-23) - Effective treatment for PsA • Secukinumab (IL-17 inhibitor)

Hematology-Immunology (6 decks)

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