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MSDR > Rheumatology 2 > Flashcards

Rheumatology 2 Flashcards

1
Q

What are possible differentials of monoarticular/oligoarticular (less than 4 joints) arthritis with fever and without fever?

A
  • Monoarticular/Oligoarticular Arthritis (≤ 4 joints)
    • Fever: infection and systemic onset JIA
    • No Fever: trauma, JIA, Lyme arthritis, Psoriatic arthritis
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2
Q

What are possible differentials of polyarticular (5+ joints) arthritis with fever and without fever?

A
  • Polyarticular Arthritis (≥ 5 joints)
    • Fever: infection, SLE, systemic onset JIA
    • No Fever: JIA or other rheumatic disease
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3
Q

What is the umbrella term for most joint pain in juveniles?

A

Juvenile Spondylarthropathies: umbrella term for joint pain in juveniles

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4
Q

For JIA (Juvenile Idiopathic Arthritis), what is the criteria (age and duration), genetics, and pathophysiology?

A
  • JIA (Juvenile Idiopathic Arthritis)
    • Criteria: age at onset is < 16 yo, duration is > 6 weeks, and all other causes are ruled out
    • Genetics: HLA types + environmental factors
    • Pathophysiology is very similar to RA: proliferation of synovium and increase in vascularity
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5
Q

What are some characteristics of oligoarticular JIA?

A
  • Oligoarticular JIA: asymmetric joints, muscles atrophy, and limb-length discrepancy, often ANA positive (also found in SLE)
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6
Q

What are some characteristics of Polyarticular RF JIA?

A
  • Polyarticular RF JIA
    • Can be RF negative or positive
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7
Q

Is RF+ or RF- polyarticular JIA more damaging?

A
  • RF positive can be more damaging because it follows the course of adult RA
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8
Q

What are the symptoms associated with systemic JIA?

What are the lab tests of systemic JIA?

What is the fever pattern associated with systemic JIA?

A
  • Systemic JIA: associated with rash, fever lasting > 2 weeks, and microcytic anemia
    • Elevated WBCs, D dimer, AST/ALT, LDH (tissue damage factors)
    • Quotidian fever pattern: spikes at night
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9
Q

What are the symtoms/features associated with psoriatic arthritis?

A
  • Psoriatic Arthritis: dactylitis (big swollen digits), nail abnormalities, and/or family history of psoriasis
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10
Q

What are the charactersitics of enthesitis related JIA?

A
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11
Q

List 3 extra-articular complications of JIA.

A
  • Uveitis
  • Growth abnormalities
  • Macrophage Activation Syndrome
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12
Q

For Uveitis,

  • What JIA is it usually associated with?
  • What are the general symptoms?
  • What can predict a higher risk?
  • What three things can be caused by uveitis?
A
  • Uveitis
    • Oligoarticular JIA
    • Often asymptomatic
    • ANA positivity predicts higher risk
    • Can lose sight
    • Presentation
      • Posterior synechiae: irregular border of pupil
      • Hypopyon: collection of inflammatory fluid at bottom of iris
      • Band keratopathy: cloudy white band across iris
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13
Q

For growth abnormalties in JIA, what are the two types of growth abnormalities and what JIA are they associated with?

A
  • Growth abnormalities
    • Oligoarticular JIA: limb-length discrepancy
    • Polyarticular JIA: micrognathia – damage to the mandibular growth plate
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14
Q

For Macrophage Activation Syndrome (MAS), what JIA is it associated with? What is the hallmark appearance on a slide?

A
  • Macrophage Activation Syndrome
    • Systemic JIA
    • Hallmark: macrophages ingesting other hematopoietic cells on bone marrow biopsy
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15
Q

What is the general approach to any JIA (3 treatments)?

A
  • NSAIDs
  • Corticosteroids (prednisone)
  • DMARDS
    • Methotrexate
    • Hydroxychloroquine
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16
Q

What are the differential diagnoses/clinical features of acute arthritis (5 of them)?

A
  • Differential Diagnoses
    • Infection: single event with inflammation and fever
      • Accompanied with systemic illness
    • Trauma: possible hemarthrosis (blood in joint)
    • Crystals: may be accompanied with previous episodes and fever
    • Inflammatory arthritis: usually polyarticular, but has to start somewhere
    • Malignancy
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17
Q

What are the two types of crystals found in synovial fluid?

A
  • Monosodium urate (MSU)
    • Negative birefringent
    • Pointed ends of crystals
  • Calcium pyrophosphate dehydrate (CPPD)
    • Positive birefringent
    • Blunt ends of crystals
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18
Q

For synovial fluid analysis, provide the color, viscosity, WBC count, neutrophils, and glucose level for:

  • Normal
  • Non-inflammatory
  • Inflammatory
  • Septic
  • Hemmorrhagic
A
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19
Q

What are the risk factors of gout? There are 4 main ones and know how they generally work.

A
  • Risk factors
    • Ethanol: increased nucleotide catabolism and decreased
    • Diuretics: thiazides enhance tubular reabsorption of uric acid
    • Salicylates: aspirin at low doses blocks excretion of urate
    • Lead: decreases renal excretion
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20
Q

What is the general pathogenesis of gout including the general immune response?

A
  • Increased production or decreased excretion → excess uric acid build-up (product of purine metabolism) → precipitation of MSU crystals into joint from → triggers immune response with IL-1, IL-6, and TNF-alpha
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21
Q

Why is gout considered self-limiting?

A
  • Gout is self-limiting because it is coated with apoprotein B, which decreases inflammatory triggers
22
Q

What occurs in the tophaceous phase of gout? What are tophi and what can they do to bones? How do they appear in x-rays?

A
  • Tophaceous Phase: collections of uric acid in soft tissues (ears, fingers/hands, feet, elbow)
    • Can result in destructive, erosive changes to the joint and bone as tophi eat through
      • Hole punch look to bone
      • “Over-hanging edge”
    • Looks a lot like rheumatoid arthritis, but differentiated by culture
23
Q

Compare gout to rheumatoid arthritis (4 main differences)

A

Gout versus RA

  • RA has symmetric polyarticular and insidious pain
  • RA nodules instead of tophi
  • RA has prolonged morning stiffness
  • RA has +RF antibodiesNext
24
Q

Compare gout to psedogout. 4 main differences

A
  • Pseudogout has CPPD crystals that are tubular/rhomboid shaped
  • Pseudogout has normal serum uric acid levels
  • Pseudogout has chondrocalcinosis on XR (Ca++ buildup on articular cartilage giving rise to “fuzzy” look) - SHOWN IN PIC ATTACHED
  • Pseudogout is treated with the same as acute gout
25
Q

How can you modify the lifestyle of crystal arthritis?

A
  • Risk factor modification: no alcohol, discontinue low dose aspirin
26
Q

What are the acute treatments for crystal arthritis (gout and pseudogout)?

A
  • Acute
    • NSAIDS
    • Steroids
    • Colchicine: mitotic poison that inhibits microtubules of neutrophils
    • ACTH injections (gout only)
27
Q

What are the chronic treatments for crystal arthritis (gout and pseudogout)?

A
  • Chronic
    • Uricosuric agents: increase solubility/excretion of uric acid
      • Probenecid
      • Uricase
      • Lesinurad
    • Allopurinol: xanthine oxidase inhibitor
    • Febuxostat: xanthine oxidase inhibitor
28
Q

What is ankylosing spondylitis?

A
  • Chronic inflammatory disease of the axial skeleton manifested by back pain and progressive stiffness of the spine
    • Can affect peripheral joints
29
Q

List members of the HLA-B27-associated family of diseases (3 of them)

A
  • Psoriatic arthritis, IBD-related arthritis, and reactive arthritis
30
Q

What are the musculoskeletal symptoms of ankylosing spondylitis? 6 total.

A
  • Inflammatory low back pain
  • Improvement with exercise and gets worse with rest
  • Hip, groin, and buttock pain (hip pain is associated with worse prognosis)
  • Enthesitis are inflamed enthuses (areas where tendons and ligaments attach to bones)
  • Peripheral arthritis
  • Dactylitis
31
Q

What are the two main tests that we use to diagnose back deformities (ankylosing spondylitis)?

A
  • Schober Test: forward flexion of lumbar spine
    • The difference in length of the lumbar spine between the standing and flexed position – must be greater than 4cm
  • Occiput to wall: distance of occipital bone to wall when standing against a wall
32
Q

List 3 extra articular manifestations of ankylosing spondylitis.

A
  • Uveitis
  • Psoriasis
  • Cardiovascular disease
33
Q

What is the non-pharmacological (3), pharmacological (3~), and other treatments for ankylosing spondylitis(1)?

A
  • Non-pharmacological: smoking cessation, exercise, PT
  • Pharmacological: NSAIDs, TNF-alpha inhibitors
    • If peripheral arthritis, use sulfasalazine (DMARD)
  • Surgery
34
Q

What are the three different types of manifestations including malignancy risk for Dermatomyositis?

A
  • Cutaneous
  • Muscle
  • Systemic
35
Q

What are the 3 cutaneous manifestations of dermatomyositis and what are their features??

A
  • Periorbital violaceous or heliotrope rash with swelling: rash and swelling around eye
  • Gottron’s Papules: raised scaly and dry skin on extensor surfaces
    • Compared to psoriasis, this has rash on joints of fingers
  • Periungual erythema: abnormal capillaries at base of fingernail
36
Q

What does Periorbital violaceous or heliotrope rash with swelling look like?

A
37
Q

What does Gottron’s Papules look like?

A
38
Q

What does Periungual erythema look like?

A
39
Q

What is the pathology of dermatomyositis?

A
  • Pathology: fatty replacement of muscle tissue, complement deposition, and inflammatory blue muscle cells present
40
Q

What imaging is used for dermatomyositis?

A
  • Imaging: MRI shows inflamed muscle tissue (more water = whiter muscles)
41
Q

What lab tests are used for dermatomyositis? What antibodies do we look for?

A
  • Laboratory tests: creatine kinase (CK), aldolase, and transaminase (AST and ALT but may be mistaken for liver diseases)
    • Anti-Jo1 and Anti-MDA5 – highly specific for certain subsets of myositis
    • Electromyography (EMG) – certain patterns characteristic of myositis
42
Q

Distinguish features of juvenile versus adult dermatomyositis.

A
  • Better prognosis and no cancer
  • Present with vasculitis and soft-tissue calcification (indicators of long-term complications)
43
Q

For dematomyositis, what are the treatments for muscle and skin inovolvement (3 overall)?

A
  • Glucocorticoids
  • Sunblock
  • Immunosuppressants: methotrexate, azathioprine, and B-cell targeting drugs (rituximab)
44
Q

How rare and severe is scleroderma when compared to lupus?

A
  • Scleroderma is rarer than lupus but higher mortality rate
45
Q

What are the physical findings of scleroderma?

A
  • Sclerodactyly: immobile fingers due to collagen accumulation in subcutaneous tissue
  • Raynaud’s phenomenon: reversible perfusion of fingers shown in a change of color (SEE PIC ATTACHED)
  • Gangrene: necrosis of fingers
  • Periungual erythema: abnormal capillaries at base of fingernail
  • Esophageal dysmotility: aspiration due to weakness in peristalsis muscles of esophagus
    • Fluid can’t go down
  • Interstitial lung disease: inflammation of lungs followed by fibrosis
  • Kidney issues: vascular fibrosis with lack of lumen
    • Onion-skinning look
46
Q

What three reasons can be argued for classifying scleroderma as an autoimmune disease?

A
  • Why it might be an autoimmune disease
    • Associated with autoantibodies – ANA positivity
    • Shares susceptibility genes with lupus
    • Treated with immunosuppressive drugs
47
Q

What three reasons can be argued for NOT classifying scleroderma as an autoimmune disease?

A
  • Why it might not be an autoimmune disease
    • It may be made worse by high dose prednisone
    • Tissues show more fibrosis than inflammation
    • Many abnormalities are vascular
48
Q

What are the major clinical manifestations of Sjorgen’s Syndrome (SS)?

A
  • Sicca complex: dry eyes and dry mouth
    • Can get oral infections: candidiasis
49
Q

What are the diagnostic approaches (lab tests and pathology) to investigate for Sjorgren’s?

A
  • Autoantibodies: SSA (Ro) and SSB (La) (SS = Sjorgren’s Syndrome)
  • Lip biopsy: salivary glands will be infiltrated with inflammatory cells
50
Q

What are the non-pharmacological for Sjorgren’s (for dry mouth and eyes)?

A
  • Non-pharmacological treatments
    • Dry-mouth: dental care and water
    • Dry-eyes: artificial tears and occlusion of the lacrimal puncta (blockage of tear duct)
51
Q

What are the pharmacological for Sjorgren’s (for dry mouth and eyes)?

A
  • Pharmacologic treatments
    • Dry-mouth: cholinergic agents to stimulate salivation
    • Dry-eyes: topical cyclosporine

MSDR (7 decks)

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