Rheumatoid Arthritis 2b Flashcards

1
Q

Which molecule is most sensitive for diagnosing RA? [1]

A

ACPAs - Anti-citrullinated peptide antibodies

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2
Q

Describe role of ACPAs in RA [3]

A

ACPAs bind directly into osteoclast
* Causes osteoclast to make IL-8
* IL-8 drives osteoclast and neutrophil recruitment (which causes NETosis)

ACPA can also bind to macrophages in SF and synovial membrane: produce pro-inflammatory cytokines and drive disease progression

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3
Q

90% of people that have no symptoms who are positive for ACPAs develop RA within [] years

A

3 years!

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4
Q

Describe the prognosis of RA if found to have PAD4 autoantibodies [2]

A

PAD4 autoantibodies are associated with more severe, erosive RA that persists despite treatment with TNF inhibitors

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5
Q

Describe what the process of carbamylation is [1]

What process causes this to occur more? [1]

Whic autoantibodies are associated with carbamylation [1]

A

Carbamylation converts lysine into homocitrullines by chemical reaction with cyanate

Smoking

Anti-carbamylated protein antibodies (anti-CarP antibodies): go to range of self-proteins and can bind to osteoclasts (and make IL-8 etc) but also cause further inflamation.

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6
Q

Which three molecules, if found, are a very good indicator have RA? [3]

A

Triple positivity (RF, ACPA and A-CarP) almost exclusive in RA not in other forms of early arthritis

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7
Q

Treatment of RA

What information is important (with regards to pathophysiology of RA) is key for treatment for patients? [1]

A

Diversity of AMPAs (anti-modified protein antibodies)

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8
Q

What is the anchor drug for RA? [1]

What is difference in dose for seropositive / seronegative? [1]

A

Methotexate

Seropositive: need higher dose to start and go on dose for longer

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9
Q

Which types of drugs are better for seropostive patients? [1]

Which types of drugs are better for seronegative patients? [1]

A

Seropositive RA patients:
* biologicals that target B-cells or inhibit T-cell co-stimulation are particularly effective (compared to TNF-a inhibitors)

seronegative RA patients
* Biologicals that target cytokines less difference

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10
Q

How quickly should methotrexate be started within RA symptom onset? [1]

A

3 months

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11
Q

Which molecule is required for NET formation and bacterial clearance? [1]

A

PAD4

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12
Q

Which drug targets autoantibodies in RA? [1]

A

Rituximab

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13
Q

IL-1, Il-6 and and TNF-a leak out into the blood stream in RA and cause systemic inflammation. State 4 diseases this can cause [4]

A

Anaemia
Thombocytosis
Osteoporosis
Fatigue
Muscle waisting

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14
Q

Name an extra-occular disease caused by RA [1]

A

Scleritis

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15
Q

State the type of anaemia initially seen in RA [1]

State the type of anaemia seen in progressive RA [1]

A

Initially:
* Normocytc, normochromic anaemia

Progession:
* Hypochromoic, normocytic anaemia

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16
Q

Explain the pathophysiology of anaemia with RA [4]

A
  • Dysregulation of iron homeostasis
  • Decreased iron availability for RBC production
  • Blunted EPO response
  • Impaired proliferation of erythroid progenitor cells
  • Shortened lifespan of RBC
17
Q

What are rheumatoid nodules [1]

A

Firm subcutaneous lumps that form in around 20% of RA patients

Usually form around joints that are subject to trauma (pressure)

Finger joints and elbows are common but also back of the heel

18
Q

Which of these joints would you least likely see swollen & painful joints in RA?

A