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100 Cards in this Set
- Front
- Back
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What is SLE
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autoimmune disorder leading to inflammation and tissue damage involving multiple organ systems
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what does the pathophysiology of SLE involve
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1. autoantibody production
2. deposition of immune complexes 3. complement activation 4. tissue destruction/vasculitis |
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Types of SLE
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1. Spontaneous SLE
2. Discoid lupus (skin lesions w/o systemic dz) 3. drug induced lupus 4. ANA-negative lupus |
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Findings associated ANA- negative lupus
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1. Arthritis- Raynaud's phenomenon, subacute cutaneous lupus
2. Serology- Ro (anti-SS-A) antibody positive, ANA negative 3. Risk of neonatal lupus in infants of affected women |
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SLE epidemiology
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1. women childbearing age (90%)
2. African Americans more common 3. very mild in elderly; more severe in children 4. appears in late childhood or adolescence |
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Clinical findings associated with neonatal lupus
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1. skin lesions
2. cardiac abnormalities (AV block, transposition of great vessels) 3. valvular and septal defects |
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Clinical course of SLE
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1. A chronic dz characterized by exacerbations and remissions
2. Malar rash, joint pain and fatigue are the most common initial findings 3. With more advanced dz, renal, pulmonary, cardio and nervous sys are affected |
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Criteria for diagnosing SLE
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4 of 11 must be present
Mucocutaneous sign (1. butterfly rash, 2.photosensitivity, 3.oral or nasopharyngeal ulcers, 4.discoid rash) 5. Arthritis 6. Pericarditis, pleuritis 7. Hematologic dz- hemolytic anemia w/ reticulocytosis, leukopenia, lymphopenia, thrombocytopenia 8. renal dz-proteinuria>.5g/day, cellular casts 9. CNS-seizures, psychosis 10. Immunologic manifestations- positive LE preparation, false-positive test result from syphilis, anti-ds DNA, anti-Sm-Ab 11. ANAs |
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Conditions in which ANAs are elevated
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1. SLE
2. RA 3. scleroderma 4. Sjogren syndrome 5. Mixed CT dz 6. Polymyositis and dermatomyositis 7. drug induced lupus |
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Treatment for SLE
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1. avoid sun exposure bc it can exacerbate cutaneous rashes
2. NSAIDS- for less symptoms 3. Local or systemic corticosteroids- for acute exacerbations 4. systemic steroids for severe manifestations 5. antimalarial agents such as hydroxychloroquine- for constitutional, cutaneous, and articular manifestations |
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What is scleroderma
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chronic CT disorder that can lead to widespread fibrosis
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Pathophysiology of scleroderma
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cytokines stimulate fibroblasts, causing an abnormal amount of collagen deposition
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Clinical features of scleroderma
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1. raynaud's phenomenon
2. cutaneous fibrosis 3. GI involvement 4. Pulmonary involvement 5. cardiac: pericardial effusions, CHF, arrhythmias 6. renal - renal crisis-rapid malignant HTN |
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differential diagnosis of raynaud's phenomenon
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1. Primary
2. scleroderma 3. SLE 4. Mixed connective tissue disease 5. vasculitis 6. medications (beta blockers, nicotine, bleomycin) 7. disorders that disrupt blood flow or vessels, such as thromboangiitis obliterans |
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Scleroderma diagnosis
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1. elevated ANAs
2. anticentromere antibody 3. antitopoisomerase I 4. barium swallow (esophageal dysmotility) and pulmonary function test are used to detect complications |
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Scleroderma treatment
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1. NSAIDS-for musculoskeletal pains
2. H2 blockers or proton pump inhibitors for esophageal reflux 3. raynaud's phenomenon-avoid cold and smoking, keep hands warm; if severe use calcium channel blockers 3. |
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what is Sjogren syndrome
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an autoimmune disease most commonly seen in women. Lymphocytes infiltrate and destroy the lacrimal and salivary glands.
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Patients with sjogrens have an increase risk of what
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non Hodglins lymphoma
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Primary versus secondary Sjogren's syndrome
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Primary - dry eyes and dry mouth, along with lymphocytic infiltration of the minor salivary glands
Secondary- dry eyes and dry mouth along with a CT disease (RA, systemic sclerosis, SLE) |
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Clinical features of Sjogren
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1. dry eyes- burning, redness, blurred vision
2. dry mouth 3. Arthralgias, arthritis, fatigue 4. extraglandular manifestations such as chronic arthritis, interstitial nephritis and vasculitis |
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Treatment for Sjogren Syndrome
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1. Pilocarpine (enhance secretions)
2. Artificial tears for dry eyes 3. Good oral hygiene 4. NSAIDS, steroids for arthralgias, arthritis |
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Diagnosis for Sjogren
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1. ANAs are present in 95% of patients. RF is present in 50-75%
2. Ro (SS-A) present in 55%, La (SS-B) Abs present in 40% of patients 3. Nonspecific findings: increased ESR, normocytic normochromatic anemia, leukopenia |
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what is RA
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chronic inflammatory autoimmune disease involving the synovium of joints. the inflamed synovium can cause damage to cartilage and bone
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Etiology of RA
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uncertain; may be caused by infection (most likely viral), genetic predisposition is necessary
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clinical features of RA
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1. symmetrical joint swelling (can involve every joint except DIP joints)
2. constitutional symptoms 3. cervical spine involvement is common at C1-C2 4. cardiac -pericarditis, pericardial effusions, conduction abnormality, valvular incompetence 5. Pulmonary- pleural effusions, interstitial fibrosis 6. ocular - episcleritis or scleritis 7. soft tissue swelling 8. drying of mucous membrane: Sjogren xerostomia 9. subcutaneous rheumatoid nodules over extensor surfaces |
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characteristic RA hand deformity
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1. ulnar deviation of the MCP joints
2. Boutonniere deformitiesof the PIP joints 3. Swan neck contracture of the fingers |
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Diagnostic Lab finding for RA
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1. RF present in 80% of patients
2. Elevated ESR, C-reactive protein 3. Normocytic normochromic anemia (anemia of chronic disease) |
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Diagnostic radiographs for RA
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1. loss of juxtaarticular bone mass (osteoporosis) near finger bones
2. narrowing of the joint space (due to thinning of the articular cartilage) 3. bony erosions at the margins of the joint |
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Treatment for RA
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1. exercise helps maintain range of motion and muscle strength
2. symptomatic treatment- a. NSAIDS drug of choice for pain control. important for contolling inflammation b. Corticosteroids (low dose)- use if NSAIDS do not provide enough relief |
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2 Variants of RA
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1. Felty's syndrome- anemia, neutropenia, splenomegaly, and RA
2. Juvenile RA- begins before 18. Extra-articular manifestations may predominate (Still's disease), or arthritis predominate |
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Disease modifying drugs for RA
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1. Methotrexate- most popular
2. Hydroxychloroquine 3. sulfasalazine second line agents- gold compounds, penicillamine, azathioprine, cyclosporine |
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what is gout
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inflammatory monoarticular arthritis caused by crystallization of monosodium urate in joints
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Hallmark of gout
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hyperuriccemia
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Demographics of gout
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90% are men over 30 yrs of age. Women not affected until after menopause
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Pathogenesis of gout
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1. increased production of uric acid
2. decreased excretion of uric acid (90% of cases) -renal dz, NSAIDS, diuretics, acidosis |
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Pathophysiology of inflammation in gout
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1. neutrophils play role in acute inflammation of gout
2. inflammation develops when uric acid crystals collect in synovial fluid as extracellular fluid becomes saturated with uric acid. 3. IgGs coat monosodium urate crystals, which are phagocytized by neutrophils, leading to release of inflammatory mediators and proteolytic enzymes from the neutrophils, which then results in inflammation |
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Causes of acute gouty attack
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1. decrease in temperature
2. dehydration 3. stress (emotional or physical) 4. excessive alcohol intake 5. starvation |
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Time course of acute gouty attack
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lasts 7-10 days and then resolves.
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Clinical features of gout
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1. asymptomatic hyperuricemia
2. acute gouty arthritis 3. intercritical gout 4. chronic tophaceous gout |
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Diagnosis of gout
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1. joint aspiration and synovial fluid analysis (needle shaped and negatively birefringent urate crystals)
2. radiographs reveal punched out erosions with an overhanging cortical bone |
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Gout treatment
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1. acute gout- NSAIDS (indomethacin DOC)
2. Colchicine 3. Corticosteroids |
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What should be avoided in all stages of gout? Give examples
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avoid secondary causes of hyperuricemia
1. medications that increase uric acid levels (thiazide and loop diuretics) 2. obesity 3. reduce alcohol intake 4. reduce dietary purine intake |
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Complications of gout
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1. nephrolithiasis
2, degenerative arthritis |
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what is pseudogout
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calcium pyrophosphate crystals deposit in joints, leading to inflammation
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Pseudogout risk factors
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1. deposition increases with age and with OA of the joints ( common in elderly w/ degenerative joint dz)
2. Hemochromatosis, hyperparathyroidism, hypothyroidism, Bartter's syndrome |
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clinical features of pseudogout
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1. most common joints affected are knees and wrists
2. classically monoarticular, but can be polyarticular |
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Pseudogout diagnosis
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1. joint aspirate - weakly birefringent, rod shaped and rhomboid crystals
2. radiographs- chondrocalcinosis (cartilage calcification) |
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Treatment for pseudogout
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1. treat underlying disorder
2. symptomatic managment (NSAIDS, colchicine, steroid injections) 3. total joint replacement if appropriate |
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What is the cause of myopathies
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genetically susceptible individual plus an environment trigger lead to immune activation, which results in chronic inflammation
1. dermatomyositis- humoral immune mechanisms 2. polymyositis and inclusion body myositis- cell mediated process |
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Clinical features common to both polymyositis and dermatomyositis
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1. symmetrical proximal muscle weakness
2. myalgia (33%) 3. dysphagia (30%) |
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Clinical features unique to dermatomyositis
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1. Heliotrope rash (butterfly)
2. Gottron's papules, erythematous, scaly lesions over the knuckles 3. V sign- rash on the face, neck and anterior chest 4. Shawl sign- rash on shoulders and upper back, elbows and knees 5. Periungal erythema w/ telangiectases 6. Subcutaneous calcifications in children- can be extremely painful |
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How do you treat myopathies
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1. corticosteroids are the initial treatment (continue until symptoms improve and then taper very slowly)
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Diagnosis for myopathies
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LAB
1. elevated CK ( corresponds to degree of muscle necrosis) 2. LDH, aldolase, AST, ALT elevated 3. Anti-Jo 1 antibodies 4. Abnormal EMG (90%) 5.mm biopsy |
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Cause and course of Polymyalgia Rheumatica
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unknown cause, but an autoimmune process may be responsible. Self limited dz (duration 1-2 yrs)
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Epidemiology of Polymyalgia Rheumatica
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women with mean age of 70
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How is Polymyalgia rheumatica diagnosed
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1. essentially a clinical diagnosis
2. ESR always >50 |
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Treatment for Polymyalgia rheumatica
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Corticosteroids suppress inflammation until dz resolves itself
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Clinical features of Polymyalgia rheumatica
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1. Hip and shoulder mm pain (bilateral)
2. constitutional symptoms ( malaise, fever, depression, weight loss, fatigue) 3. Joint swelling 4. sign and symptoms of temporal arteritis |
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Epidemiology of Fibromyalgia
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adult women (85%)
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What is Fibromyalgia
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chronic nonprogressive course with waxing and waning in severity
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cause of fibromyalgia
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unknown
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What is the key to diagnosis fibromyalgia
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multiple trigger points (pts that are tender to palpation)
1. symmetrical 2. eighteen locations haven been identified |
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treatment for fribromyalgia
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1. stay active and productive
2. medications are generally not effective . SSRI and TCAs have shown some effect. Avoid narcotics |
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Clinical features of Fibromyalgia
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1. stiffness
2. sleep patterns are disrupted ans sleep is unrefreshing 3. anxiety and depression is common |
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Diagnosis of fibromyalgia
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1. widespread pain for atleast 3 mths
2. pain in atleast 11 of 18 tender pt locations |
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Treatment of Ankylosing spondylitis
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1. NSAIDs (indomethacin) for symptoms
2. Physical therapy 3. surgery |
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clinical features of Ankylosing Spondylitis
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1. low back pain stiffness
2. neck pain 3. Enthesitis -inflammation at tendinous insertions into bone 4. chest pain and diminished chest expansion 5. shoulder and hip pain 6. constitutional symptoms 7. extra- articular manifestations 8. loss of normal posture as dz advances |
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Ankylosing Spondylitis diagnosis
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1. imaging of lumbar spine and pelvis reveal sacroiliitis
2. eventually vertebral column fuse producing bamboo spine 3. Elevated ESR 4. HLA-B27 |
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Epidemiology of Fibromyalgia
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adult women (85%)
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What is Fibromyalgia
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chronic nonprogressive course with waxing and waning in severity
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cause of fibromyalgia
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unknown
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What is the key to diagnosis fibromyalgia
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multiple trigger points (pts that are tender to palpation)
1. symmetrical 2. eighteen locations haven been identified |
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treatment for fribromyalgia
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1. stay active and productive
2. medications are generally not effective . SSRI and TCAs have shown some effect. Avoid narcotics |
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Clinical features of Fibromyalgia
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1. stiffness
2. sleep patterns are disrupted ans sleep is unrefreshing 3. anxiety and depression is common |
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Diagnosis of fibromyalgia
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1. widespread pain for atleast 3 mths
2. pain in atleast 11 of 18 tender pt locations |
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Treatment of Ankylosing spondylitis
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1. NSAIDs (indomethacin) for symptoms
2. Physical therapy 3. surgery |
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clinical features of Ankylosing Spondylitis
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1. low back pain stiffness
2. neck pain 3. Enthesitis -inflammation at tendinous insertions into bone 4. chest pain and diminished chest expansion 5. shoulder and hip pain 6. constitutional symptoms 7. extra- articular manifestations 8. loss of normal posture as dz advances |
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Ankylosing Spondylitis diagnosis
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1. imaging of lumbar spine and pelvis reveal sacroiliitis
2. eventually vertebral column fuse producing bamboo spine 3. Elevated ESR 4. HLA-B27 |
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Epidemiology of Ankylosing spondylitis
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1. three times more common in males than females
2. Strong HLA B27 association |
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what is reactive arthritis
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1. asymmetric inflammatory oligoarthritis of lower extremities. Arthritis preceded by infection (usually enteric or urogenital)
2. occurs in HLA- B27 positive individuals 3. Reiters syndrome 4. salmonella, shigella, campylobacter, chlamydia, Yersinia |
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Diagnosis of Reiter's syndrome
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send synovial fluid for analysis (to rule out infection or crystals)
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Treatment for Reiters syndrome
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1. NSAIDS are first line
2. sulfasalazine and immunosuppressive agents like azathioprine |
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Clinical features of Reiters Syndrome
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1. Evidence of infection 1-4 weeks before symptoms
2. Fatigue, malaise, weight loss, and fever 3. Joint pain can persist or recur over long-term period |
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Psoriatic Arthritis distribution
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asymmetric and polyarticular
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causes of polyarticular joint pain
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1. RA
2. SLE 3. viral arthritis 4. reiter's syndrome 5. rheumatic fever 6. lyme disease 7. gonococcal arthritis 8. drug-induced arthritis |
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causes of monoarticular joint pain
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1. osteoarthritis
2. gout 3. pseudogout 4. trauma 5. septic arthritis 6. hemarthrosis |
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Epidemiology of temporal arteritis
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>50 y/o, twice as common in women as men
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Diagnosis of temporal arteritis
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1. elevated ESR
2. biopsy of the temporal artery |
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Temporal arteritis treatment
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1. use high dose steroids early to prevent blindness
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Keys to diagnosing temporal arteritis
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1. Age >50 y/o
2. new headache 3. tender/palpation temporal artery 4. high ESR 5. jaw claudication |
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Treatment for Takayasu's Arteritis
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1. steroids may relieve symptoms
2. treat hypertension 3. surgery or angioplasty |
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what is Takayasu Arteritis
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1. vasculitis of aortic arch and it major branches- potentially leading to stenosis or narrowing of vessels
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Clincal features of Takayasu's arteritis
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1. constitutional symptoms- fever, night sweats, malaise, arthralgias, fatigue
2. signs and symptoms of ischemia develop 3. pain and tenderness over involved vessels 4. absent pulses in carotid, radial, or ulnar arteries; aortic regurg may be present |
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What is Churg-Strauss Syndrome
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vasculitis involving many organ systems
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Diagnosis of Churg Strauss
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made by biopsy of lung or skin tissue (prominence of eosinophils). It is associated with p-ANCA
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Clinical features of Churg Strauss
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1. constitutional findings (fever, fatigue, wtloss)
2. respiratory- asthma, dyspnea 3. skin lesions- subcutaneous nodules and palpable purpura |
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what is Wegener's
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vasculitis predominately the kidneys and upper and lower respiratory tract
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treatment of Wegener's
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cyclophosphamide and corticosteroids
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Diagnosis of Wegener's
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1. chest radiograph (nodules or infiltrates)
2. lab findings: elevated ESR; anemia, hematuria; positive c-ANCA in 90% of patients 3. open lung biopsy confirms diagnosis |
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Clinical features of Wegener's
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1. upper respiratory symptoms (sinusitis); purulent or bloody nasal discharge
2. oral ulcers 3. pulmonary symptoms (cough, hemoptysis, dyspnea) 4. renal involvement 5. eye disease 6. musculoskeletal 7. tracheal stenosis 8. constitutional findings |
