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Bloc H - Movement > May28 M1-Rheumatoid Arthritis > Flashcards

May28 M1-Rheumatoid Arthritis Flashcards

1
Q

(imp) location and charact of pain in RA

A
  • wrist, MCPs (hands) and MTPs (toes), PIPs (hands and toes)
  • pain (with the inflammation) is symmetrical (many joints affected on both sides) but doesn’t have to be the exact same joint
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2
Q

charact of the painful joints in RA

A

synovitis

  • swelling (focal) around the joint
  • shiny skin over joint
  • is an inflammatory disease so may expect to see the 5 signs of inflammation*
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3
Q

typical labs that would confirm the diagnosis for a presentation typical of RA

A
  • high CRP (over the max 5.0 normal)
  • high platelets = thrombocytosis (over the 450 normal) (is possible in chronic systemic inflammation)
  • high rheumatoid factor (over the max normal 20.0)
  • high anti-CCP (above the max normal 5)
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4
Q

(EXAM) inflammatory joint symptoms charact (as in RA)

A
  • pain is accompanied with SWELLING
  • worse with immobility
  • morning stiffness lasts over 60 minutes
  • associated systemic symptoms (fatigue, anorexia, fever)
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5
Q

(EXAM) non-inflammatory joint symptoms

A
  • pain WITHOUT swelling
  • worse with mobility and use
  • morning stiffness <30 minutes
  • no associated systemic symptoms
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6
Q

important epi things in RA

A
  • more common in females

- small genetic influence

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7
Q

RA classification purposes + main things

A

for research, not clinical

  • joint distribution
  • serology (RF and ACPA + low vs high positive)
  • symptom duration (has to be >6 weeks)
  • acute phase reactants (CRP and ESR)
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8
Q

why is symptom duration important in classification of RA

A

some viruses can give a transient arthritis. but will not last>6 weeks

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9
Q

how to dx RA in the clinic

A
  • 3+ joints + symmetrical
  • positive RF and-or anti-CCP
  • elevated CRP and-or ESR
  • exclude ddx
  • duration sx > 6 wks
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10
Q

important thing about joint distribution in RA in making the dx

A

can start with knee sx and develop into the wrist and hands sx typical of RA

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11
Q

important thing about serology in RA in making the dx

A

seronegative RA exists (RF and anti-CCP negative.) (but this dx may also be discovered to be something else later in life)

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12
Q

early vs interm vs late RA

A
  • early = swelling joints + shiny
  • interm = crooked fingers
  • late = very deformed fingers
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13
Q

RA on XR

A

erosions, space between bones narrowing bc cartilag ebeing eaten out

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14
Q

in early disease, what is a good marker of the level of disability in RA

A

level of inflammation

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15
Q

in not early disease, what is a good marker of the level of disability in RA

A

radiographic severity

want to prevent damage therefore

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16
Q

pathology of RA

A
  • > 1-2 layers of synoviocytes (hypertrophy)
  • inflammatory medium with pannus (tumor of many cells of innate and adaptive immunity. pannus hypertrophied causing destruction of cartilage and bone)
17
Q

branches of immune system involved in RA

A
  1. FIRST, adaptive immunity involved (slow, specific antigen R, memory, T and B cells)
  2. LATER, innate immunity involved (fast, microbial patterns, lacks memory, macrophages, neutrophils, mast cells)
    * so inversed ordered and it’s an AUTOIMMUNE DISEASE*
18
Q

what’s an autoinflammatory disease

A

diseas eof innate immune response, no B and T cells involved

19
Q

most abundant cells in the synovium in RA

A

T cells (especially CD4 helper). they recognize Ags on MHC2 cells

20
Q

alleles associated with RA

A

HLA-DRB1

  • shared sequence of hypervariable region
  • 30% of the genetic effect
21
Q

one of main APCs in RA

A

B cells

  • make cytokines
  • propagate inflam
  • regulate immunity down (IL-10)
  • make Abs
22
Q

rheumatoid factor is what

A
  • Ab that binds the Fc portion of an IgG (so Ab to an Ab) = immune complexes, propagation of immune resp, complement cascade, chronic inflam
  • 20% pts are seronegative
  • 70% sensitivity
  • 60-80% specif
23
Q

important thing about RF

A

if positive, doesn’t mean RA bc many diseases can have + RF

24
Q

(imp) serology better than RF in RA

A

anti-CCP (cuclic citrullinated peptide). during apoptosis, cells downregulate proteins by deiminating arginine of proteins, this is caleld citrullination)

  • better sensitivity**
  • can be found BEFORE the arthritis**
  • indicates a POOR prognosis
25
Q

most important environmental risk factors for RA (for citrullination. bc RA = Abs attack citrullinated proteins)

A 
#1 smoking
#2 periodontal disease
26
Q

immune cascade in RA and most imp thing

A
  1. APC to T cell then cytokines and Abs
  2. synovium has IMMUNE COMPLEXES***
  3. innate recruited (macrophages, mast cells) and make cytokines
  4. this destroys bone and causes synovial hypertrophy
27
Q

some RA tx (biologics)

A
  • rituximab (anti-CD20) for B cells

- anti-TNF, anti-IL1, anti-IL6 (cytokines of mast cells)

28
Q

effect of TNF cytokine in RA

A
  • recruits macrophages
  • makes endothelial cells more permeable in fibrous joint capsule so that more cells recruited
  • synoviocites activation: THEY produce MMP which causes cartilage destruction
29
Q

(imp) what cells cause the cartilage destruction in RA

A

synoviocytes (make MMP in resp to cytokines)

30
Q

bad cytokines produced by synoviocytes (on top of them making MMP) in RA

A
  • TNF, IL-1, IL-6, RANKL: activate osteoclasts

- DKK-1: reduces osteoblast precursors transformation to osteoblasts

31
Q

starting cell in pathogenesis of RA

A

T cell

32
Q

what’s pre-RA

A

anti-CCP positive before clinical disease (but like for RF, there’s a ddx for that)

33
Q

extra-articular manifestations of RA

A
  • rheumatoid nodules on extensor surface of elbow and hands
  • episcleritis (red eye) inflam of superficial lining of sclera
  • ILD (interstitial lung disease on CT)
34
Q

RA non pharma tx

A
  • pt education
  • psychosocial
  • rest, exercise, PT OT
  • nutrition counselling
  • reduce CV risk, smoking, lipid control
  • tx and screen osteoporosis
35
Q

note about risk of infections in RA patients

A

just having RA = higher risk for infections than normal population

36
Q

pharma tx in RA

A
  • NSAIDs, CSs (for sx management but NOT DISEASE MODIFYING)
  • DMARDs (methotrexate, leflunomide, sulfasalazine, hydroxychloroquine)
  • new bio drugs
37
Q

how to monitor RA pts

A

XR for following erosion

Bloc H - Movement (48 decks)

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