Rheumatoid Arthritis and Lupus Flashcards

1
Q

Rheumatoid Arthritis (RA)

A

systemic, autoimmune disease
Type III hypersensitivity
inflammatory disease of synovium

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2
Q

RA: Etiology

A

not well understood
environmental and genetic factor
-genetic link + triggering event
-inappropriate immune response to joint injury

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3
Q

RA: Other Risk Factors

A

age: 40’s-60’s
women
tobacco use
family history (genetic link)

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4
Q

RA: Pathogenesis

A

-immune cells attack synovial tissue
(immune cells: lymphocytes and macrophages)
-produce rheumatoid factor (RF)
-antibody against the body’s own antibodies (IgG)
-formation of immune complexes

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5
Q

RA: A Progressive Disease

A

-intensifying inflammatory response
-cartilage destroyed by osteoclasts
-pannus develops: inflammation and exuberant proliferation of synovium (hypertrophied synovium)
-pannus leads to:
-bone erosion
-bone cysts
-fissure development

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6
Q

RA: Early CM

A

very little, maybe joint pain/discomfort

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7
Q

RA: Eventual Joint Manifestations

A

symmetrical
pain, stiffness, motion limitations
inflammation: heat, swelling, tenderness

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8
Q

RA: Advanced Disease CM

A

deformity and disability
joint subluxation

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9
Q

RA: Systemic Involvement

A

fatigue and malaise
potentially affects any and all body systems (depending on severity)
MOST common:
-Sjorgren’s Syndrome
-Rheumatoid Nodules

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10
Q

Sjorgren’s Syndrome

A

destruction of moisture-producing gland (salivary and lacrimal)
-gritty, dry, itchy eyes
-fissured, dry tongue

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11
Q

Rheumatoid Nodules

A

immune mediated granulomas; develop around inflamed joints, subcutaneous and firm, sometimes painful
-common sites: around elbow and knuckles

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12
Q

RA: Goals for Pharm

A

relieve pain and swelling
slow or stop progression of disease
-long-term drug therapy requires pt. adherence
-NSAIDs
-glucocorticoids (short-term)
-disease-modifying anti-rheumatic drugs
-DMARDs slow/stop progression

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13
Q

Corticosteroids in RA

A

usually prednisone
rapid suppression of inflammation
use ONLY when symptoms NOT controlled with NSAIDs
not best choice for long term therapy
-usually small doses less than 10mg/day (seen as small as 2.5mg)

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14
Q

Systemic Lupus Erythematosus (Lupus): Pathogenesis

A

B-lymphocytes are hyperactive and produce autoantibodies
-ANA: antinuclear
antibody
Activated against DNA
Formation of: immune COMPLEXES
Can impact all major organ systems!
Inflammatory response destroys tissue

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15
Q

Lupus: Predisposing Factors (8)

A

genetic factors
gender: female
age: 20-40
race: Black/African Americans higher likelihood
environmental triggers (SUN exposure)
allergy to antibiotics
hormonal factors
tobacco use

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16
Q

Lupus: CM (8)

A

extreme fatigue (most common)
photosensitivity
butterfly rash
fever
weight changes
unusual hair loss
edema (legs or eyes)
Raynaud’s Phenomena

17
Q

Lupus: More CM

A

CNS: HA, dizziness, seizures, stroke
Lungs: Pleuritis, pleural effusions
Heart: myocarditis & endocarditis
Kidneys: nephritis
Blood Vessels: vasculitis
Blood: anemia, leukopenia, thrombocytopenia, blood clots
Joints: arthritis

18
Q

SLE Flares

A

clinical course: exacerbations and remissions
a flare is: an acute exacerbation of symptoms
warning SIGNS of a flare:
-fatigue
-pain
-h/a

19
Q

SLE Flares: Prevention

A

recognize warning signs and avoid triggers
-sunlight exposure
-infection
-abruptly stopping a medication
-stress

20
Q

SLE: Pharmacotherapy

A

therapeutic goal: control symptoms
which agents are used depends on systems involved:
NSAIDs: h/a, musculoskeletal, pleuritis, pericarditis
High dose corticosteroids: severe kidney dz, CNS
Low dose corticosteroids: arthritis
Antimalarials (hydroxychloroquine): skin, musculoskeletal; prevention of kidney and CNS organ damage
Immunosuppressives (methotrexate): severe organ involvement

21
Q

Commonalities btwn RA and SLE- Rheumatoid Disorders

A

Similarities:
-autoimmune diseases
-systemic inflammation
-multiple body system
-pharmacotherapy

MAJOR Difference:
RA= focus on JOINTS (sometimes organs)
SLE= MULTISYSTEM (sometimes joints)