Rheum I and II Flashcards

1
Q

cause of RA

A
  • autoimmune
  • triggered by T cell activation
  • causes deformities and disability
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2
Q

synovitis and RA

A
  • swollen, warm, stiff joints
  • ALWAYS multiple joints
  • symmetrical
  • low back NOT involved
  • tethering of tissues -> decreased ROM and erosion of joints -> deformity and loss of function
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3
Q

rheumatoid nodules

A
  • usually found on pressure points
  • elbow, heel, MCP joint
  • nodule has central area of fibroid necrosis
  • less fluid filled than cysts
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4
Q

common joints involved in RA

A
  • c spine
  • shoulders
  • elbows
  • hands and wrists (DIP spared)
  • hip (later in disease)
  • knee
  • foot and ankle
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5
Q

boutonniere deformity

A
  • assoc with RA
  • flexion of PIP
  • hyperextension of DIP
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6
Q

swan neck deformity

A
  • assoc with RA
  • hyperextension of PIP
  • flexion of DIP
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7
Q

other organs impacted by RA

A
  • lungs
  • eyes
  • skin
  • heart
  • NS
  • blood
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8
Q

heart complications of RA

A
  • often see pericardial effusions
  • MI
  • stroke
  • atherosclerosis
  • pericarditis
  • endocarditis
  • LVHF
  • vasculitis
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9
Q

what causes NS issues with RA

A
  • c spine instability (usually at C1-2)

- causes peripheral nerve entrapment and vasculitis -> mononeuritis multiplex

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10
Q

blood sx associated with RA

A
  • hypochromatic microcytic anemia
  • also have low serum ferratin or normal Fe binding capacity
  • seen in almost all RA pts
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11
Q

common PE findings in RA

A
  • warm, erythematous joints
  • commonly involves hands and wrists
  • DIP excluded
  • ulnar deviation of digits
  • nodules
  • baker cysts
  • general decreased ROM
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12
Q

serology for RA

A
  • ANA- not diagnostic and doesnt follow disease activity
  • RF- often seroneg in first year of disease
  • anti-CCP- highly specific, associated with shared epitope
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13
Q

diagnostic criteria for RA

A
  • joint involvement (5 pt max)
  • serology (3 pt max)
  • duration (1 pt max)
  • acute phase reactants (1 pt max)
  • need 6 points for definitive RA dx
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14
Q

other considerations for RA dx

A
  • family hx
  • joint tap for synovial fluid
  • x ray
  • MRI or bone scan
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15
Q

clinical course of RA

A
  • damage occurs early in most pts
  • 50% show joint space narrowing in first 2 years
  • 50% disabled after 10 years
  • early death
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16
Q

what is the DOC for RA?

A
  • methotrexate
  • works by inhibiting DNA synthesis through inhibition of dihydrofolate reductase
  • requires monitoring of blood, liver, lungs, kidneys
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17
Q

treatment of RA

A
  • NSAIDS
  • steroids
  • mtx/ DMARDS
  • tumor necrosis inhibitors
  • if newly dx use steroids until mtx takes effect
  • steroids for flares
  • intra-articular triamcinolone
  • hydroxychloroquine and sulfasalazine often in combo with mtx
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18
Q

felty’s syndrome

A
  • RA + neutropenia + splenomegaly
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19
Q

polymyalgia rheumatica (PMR)

A
  • idiopathic inflammatory disorder
  • proximal muscle pain
  • abrupt onset, self limited
  • sx worse in AM
  • “trouble getting dressed”
  • highly associated with temporal arteritis
  • dx of exclusion, get ESR
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20
Q

treatment of PMR

A
  • PO steroids
  • app pts should be biopsied for temporal arteritis or consult optho
  • no imaging
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21
Q

reactive arthritis

A
  • autoimmune reaction after infections (GI or GU)
  • associated with HLA- B27 halotype
  • triad of urethritis, arthritis, conjunctivitis
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22
Q

common infections associated with reactive arthritis

A
  • chlamydia
  • campylobacter
  • salmonella
  • shigella
  • yersinia
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23
Q

diagnosis of reactive arthritis

A
  • based on hx/ PE
  • cultures to det infection
  • CBC, CRP, UA, urine culture
  • echo
  • HIV pts higher risk
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24
Q

treatment of reactive arthritis

A
  • based on sx
  • treat infection
  • NSAIDs
  • steroids
  • DMARDS if NSAIDs and steroids are ineffective
  • 2/3 recover spontaneously
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25
Q

anterior uveitis

A
  • occurs in pts with reactive arthritis
  • one of leading causes of preventable vision loss
  • progresses over a few hours
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26
Q

si/sx of anterior uveitis

A
  • red eye
  • pain worse with reading
  • blurred vision
  • photophobia
  • excessive tear production
  • abnormally shaped pupil
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27
Q

juvenile idiopathic arthritis (JIA)

A
  • kids < 16 y/o
  • chronic inflammation of connective tissue
  • pain and swelling
  • can impact one or many joints
  • duration > 6 weeks
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28
Q

si/sx of JIA

A
  • often have fever and rash that is similar to SLE
  • joint inflammation
  • contractures
  • joint damage
  • leads to decreased mobility, strength, endurace
  • episodic- go from sx free to extreme pain quickly
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29
Q

subtypes of JIA

A
  • systemic onset arthritis
  • polyarticular arthritis
  • oligoarticular arthritis
  • enthesis
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30
Q

systemic onset arthritis

A
  • subtype of JIA
  • arthritis and fever > 103
  • fluctuating rash
  • inflammation of internal organs and joints
  • anemia and leukocytosis
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31
Q

polyarticular arthritis

A
  • subset of JIA
  • arthritis in 5 or more joints
  • constant pain
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32
Q

oligoarticular arthritis

A
  • subset of JIA
  • arthritis in 4 or fewer joints
  • if dx before 7 have best chance of disease subsiding
  • high risk uveitis
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33
Q

enthesis related arthritis

A
  • subtyle of JIA
  • involves ligaments as well as spine
  • aka sondyloarthritis
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34
Q

treatment for JIA

A
  • refer to rheum
  • sx control
  • intra-articular steroid injection if only a few joints involved
  • PO prednisone
  • DMARDS +/- biologics
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35
Q

polymyositis

A
  • immune mediated
  • inflammation of muscles and associated tissues in response to cell damage
  • bilateral muscle weakness
36
Q

associated diseases with polymyositis

A
  • raynauds
  • RA
  • SLE
  • Sjorgens
  • CV disease
  • cancer
37
Q

sx of polymyositis

A
  • proximal muscle weakness
  • dysphagia
  • bloating, constipation
  • arrythmias and conduction defects
  • pulmonary and kidney involvement
38
Q

diagnosis of polymyositis

A
  • CBC, ESR, elevated CK and LDH
  • elevated liver enzymes
  • ANA
  • EMG
  • muscle biopsy
39
Q

treatment of polymyositis

A
  • steroids 4-8 weeks
  • monitor CK lev and muscle strenth
  • immunosuppressives if no response to steroids or extra-skel manifestations
  • IVIG
  • TNF inhibitors
  • consult
40
Q

dermatomyositis

A
  • heliotrope rash and grotton papules
  • muscle weakness
  • capillary loops at base of fingernails- “dirty look”
41
Q

heliotrope rash

A
  • sx of dermatomyositis
  • purple discoloration on upper eyelids
  • flat red rash on cheeks and trunk
42
Q

gottron papules

A
  • sx of dermatomyositis

- scaly rash on knuckles

43
Q

muscle biopsy for dermatomyositis

A
  • shows perivascular and perimysial inflammation
44
Q

inclusion body myositis

A
  • asymmetrical distal muscle weakness
  • more common in older men
  • falls common
  • facial muscle weakness
  • dysphagia and choking
  • progresses slowly so may be confused with MD
45
Q

treatment of inclusion body myositis

A
  • resistant to immunotherapy

- axathioprine + prednisone often tried for a few months

46
Q

treatment of dermatomyositis

A
  • same as polymyositis
47
Q

livedo reticularis

A
  • reticular/ lace like pattern on skin
  • cyanotic discoloration of skin
  • found mainly on arms and legs
  • d/t altered flow in BV feeding skin -> dilation of other vessels to compensate
48
Q

giant cell arteritis

A
  • aka temporal arteritis
  • large vessel disease
  • most common of systemic vasculitis
  • in older adults
  • strong association with PMR
49
Q

clinical manifestations of giant cell arteritis

A
  • new onset HA and temporal tenderness
  • jaw claudication
  • abrupt onset visual disturb
  • thoracic aortic aneurysm possible
50
Q

classification criteria for giant cell arteritis

A
  • need at least 3 of the following 5:
  • age > 50
  • new onset localized HA
  • tenderness or decreased pulse of temporal artery
  • ESR > 50 (often >70)
  • biopsy of temporal artery with necrotizing arteritis and giant cells
51
Q

diagnosis of giant cell arteritis

A
  • gold standard= temporal a. biopsy
  • scheduling biopsy should not interfere with tx
  • color doppler US, CT, MRI
52
Q

treatment of giant cell arteritis without vision loss

A
  • prednisone as single dose
  • taper to d/c steroids- drop by 10%
  • treatment can last 12-16 months
  • also give low dose ASA
53
Q

treatment of giant cell arteritis with vision loss

A
  • methylprenisolone IV X 3 days then PO prednisone
  • taper to d/c steroids- drop by 10%
  • treatment can last 12-16 months
  • also give low dose ASA
54
Q

Takayasu Arteritis

A
  • large vessel disease
  • inflammation of aorta and its branches
  • mainly females, usually younger
  • classically asian woman in 40s
55
Q

clinical presentation of takayasu arteritis

A
  • look chronically ill with constitutional sx
  • pulselessness
  • extremities are cool, dev arm or leg claudication
  • subclavian steel syndrome
  • myalgias and lg joint synovitis
  • bruits
  • HTN
  • elevated ESR and CRP
  • HA and vision loss
56
Q

dx of takayasu arteritis

A
  • elevated ESR and CRP
  • MRI, CT, angiogram
  • normochromic normocytic anemia
57
Q

treatment of takayasu arteritis

A
  • acute- steroids

- chronic- surgical bypass once arterial stenosis has occured

58
Q

polyarteritis nodosa (PAN)

A
  • necrotizing vasculitis of medium +/- sm vessels
  • systemic sx: kidneys*, skin, joints, muscles, nerves, GIT
  • NO lung involvement*
  • not associated with ANCA
  • middle aged/ older men
  • associated with HBV and HCV
59
Q

clinical manifestations of PAN

A
  • nonspecific constitutional sx
  • often have HTN d/t renal disease
  • skin rash/ ulcers: purpura, livedo reticularis
  • peripheral neuropathies
  • renal sx
  • GIT sx
60
Q

diagnosis of PAN

A
  • elevated ESR
  • UA shows proteinuria
  • biopsy if skin, muscle, or nerve involvement
  • nerve conduction study if nerve involvement
61
Q

classification criteria for PAN

A
  • need at least 3 of the following:
  • unexplained wt loss > 4 kg
  • myalgias/ weakness
  • mono or polyneuropathy
  • new onset diastolic > 90 mmHg
  • elevated BUN
62
Q

treatment for mild PAN

A
  • prednisone PO X 4 weeks

- taper to d/c

63
Q

treatment for mod-severe PAN

A
  • prednisone PO plus cyclophosphamide Q 2 weeks for three doses
64
Q

treatment for severe PAN

A
  • methylprednisolone IV X 3 days then PO steroids
65
Q

kawasaki disease

A
  • medium vessel disease
  • most common in kids*
  • fever > 5 days*
  • coronary artery involvement -> aneurysm if untreated
66
Q

clinical presentation of kawasaki disease

A
  • fever > 5 days
  • bilat bulbar conjuctival injection
  • oral mucous membrane changes
  • polymorphous rash
  • cervical LD
  • peripheral extremity changes
  • need at least four of five listed plus fever to dx
67
Q

diagnosis of kawasaki

A
  • fever plus 4/5 of sx
  • get baseline echo + every 2-6 weeks
  • no labs
68
Q

treatment of kawasaki

A
  • IVIG single infusion over 8-12 hours
  • ASA 30-50 mg/kg X 4 doses until fever is gone for 48 hours
  • continue with low dose ASA
  • postpone live vaccines for at least 11 mo if pt has had IVIG
69
Q

microscopic polyangiitis

A
  • small vessel disease
  • necrotizing vasculitis with few/no immune deposits
  • +/- medium vessels
  • most common cause of pulmonary renal syndrome
70
Q

clinical presentation of microscopic polyangiitis

A
  • purpura
  • pulmonary hemorrhage*
  • interstitial lung fibrosis
  • ulcers
  • splinter hemorrhages
71
Q

diagnosis of microscopic polyangiitis

A
  • elevated ESR
  • positive ANCA
  • UA- hematuria, proteinura, RBC casts
  • CT
72
Q

treatment of microscopic polyangiitis

A
  • cyclophosphamide PO plus prednisone for 3-6 mo
  • key to good outcome is early dx
  • recurrence possible
73
Q

granulomatosis with polyangiitis

A
  • aka wegner’s disease
  • necrotizing vasculitis of small vessels
  • +/- medium vessels
  • common in 40s/50s
  • ANCA associated
74
Q

clinical presentation of granulomatosis with polyangiitis

A
  • triad of upper and lower respiratory sx and glomerulonephritis
  • constitutional sx
  • crusting, ulceration, bleeding, and perf of nasal septum
  • proptosis, ptosis, opthalmoplegia
  • scleritis
75
Q

upper RT sx associated with granulomatosis with polyangiitis

A
  • nasal congestion
  • sinusitis
  • otitis media
  • mastoiditis
76
Q

lower RT sx associated with granulomatosis with polyangiitis

A
  • cough
  • dyspnea
  • hemoptysis
77
Q

diagnosis of granulomatosis with polyangiitis

A
  • elevated ESR and CRP
  • slight anemia and leukocytosis
  • UA shows proteinura and red cell casts
  • CXR followed by chest CT
78
Q

treatment of granulomatosis with polyangiitis

A
  • cyclophosphamide plus prednisone

- continue for 3-6 mo

79
Q

IgA vasculitis

A
  • aka Henoch-Schonlein
  • small vessel disease
  • affects skin, GIT, kidneys
  • found in kids**
  • generally self limited, cause unknown
80
Q

clinical presentation of IgA vasculitis

A
  • purpura (all)
  • arthralgia/arthritis in lower extremity large joints
  • abdominal pain- possible intussusception
  • renal disease- hematuria without RBC
81
Q

classification of IgA vasculitis

A
  • MUST have purpura and at least one of the following:
  • abdominal pain
  • arthritis
  • renal involvement
  • leukocytoclastic vasculitis or proliferative glomerulonephritis with IgA deposition
82
Q

diagnosis of IgA vasculitis

A
  • clinical

- based on purpura plus at least one other cardinal sx

83
Q

treatment of IgA vasculitis

A
  • supportive/ symptomatic
  • oral hydration
  • NSAIDs (naproxen) for joint/ abdominal pain
  • if severe abdominal pain and decreased PO intake give them prednisone
84
Q

behcet disease

A
  • variable vessel disease
  • triad of aphthous ulcers, genital ulcers, recurrent eye inflammation
  • HLA-B51 risk factor
85
Q

clinical presentation of behcet disease

A
  • aphthous ulcers- numerous, frequent, more painful
  • genital ulcers
  • anterior and/or posterior uveitis
  • lungs- aneurysms
  • GIT ulcers
86
Q

treatment of behcet disease

A
  • steroids
  • colchicine and thalidomide for mucocutaneous findings
  • cyclophosphamide if severe ocular or CNS sx