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EXAM 1 > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

What type of autoimmune disease is RA?

A

Systemic autoimmune diseases

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2
Q

What is Rheumatoid Arthritis?

A

A chronic autoimmune , progressive, systemic, inflammatory disorder affecting synovial joints

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3
Q

What other organs can RA affect?

A

The inflammation may also affect eyes, lungs, heart

RA can affect any joint but commonly hand, feet, knee, hip

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4
Q

What percentage of the population are affected by RA and which gender is it most common in?

A
  • Affects between 0.3 and 1.5% of population
  • It affects 600,000 (1%) of the UK
  • Most sufferers develop RA between the ages of 25 and 50

The ratio of women to men in the RA patients is 2-3 to 1. ( contraceptive pill)

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5
Q

What genes are involved in RA?

A

RA - 70% of RA = Human leukocyte antigen (HLA)-DR4

STAT4 (signal transducer and activator of transcription 4)

TRAF1/C5 (tumour necrosis factor-receptor associated factor 1/complement component 5)

PTPN22 (protein tyrosine phosphatase, non-receptor type 22)

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6
Q

What are the environmental factors that are involved in RA?

A

Tobacco smoke, Air pollution,

Mineral oil and silica

Infectious agents,

Female hormones

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7
Q

What factors (Cellular) are involved in RA regards to autoimmunity?

A

Autoimmunity, including antibodies such as anti-citrullinated peptide antibodies (ACPAs) and rheumatoid factors (RFs), is associated with RA.

Immune dysregulation, antibody responses to modified peptides and increased production of cytokines and chemokines may contribute to pathophysiology of RA

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8
Q

What infections are associated with RA?

A

Infections – definite associations lacking, but Mycobacterium, Streptococcus, Mycoplasma, Epstein-Barr virus and Parvovirus have all been suggested

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9
Q

What are the 4 phases of RA?

A
  1. Initiator phase
  2. Inflammation phase
  3. Self perpetuating phase
  4. Destruction phase
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10
Q

What is the Initiator phase of RA?

A
  1. Initiator phase - Initiating event unknown and reason for joint specific localisation is unknown.

Injury, infection, exposure to toxic substances.
APCs and citrullination of
proteins  now seen as non-self

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11
Q

What is the Inflammation phase of RA?

A
  1. Inflammation phase – self antigens (citrullinated proteins) presented

 Clonal expansion of T and B
cells

 Insufficiently controlled by
Tregs

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12
Q

What is the self perpetuating phase of RA?

A
  1. Self perpetuating phase – inflammatory damage in synovium causes self antigens previously ‘unseen’ by immune system to be exposed

 Immune response against cartilage
 Infiltration of immune cells

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13
Q

What is the Destruction phase of RA?

A
  1. Destruction phase – synovial fibroblasts and osteoclasts activated by cytokines (TNF, IL-6)

 Destruction of bone and cartilage

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14
Q

What do B-Cells do in RA?

A

Produce autoantibodies which can activate
complement and also bind to activated macrophages in
synovium. Activated macrophages perpetuate
inflammation.

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15
Q

What do Autoantibodies do in RA?

A

Rheumatoid factor (RF) (directed against
Fc fragment of IgG) and anti-citrullinated peptides(anti- CCP) are directed against antigens commonly present
outside of the joint. Other autoantibodies too.

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16
Q

What do T-Cells do in RA?

A

Potentially activate monocytes, macrophages and
synovial fibroblasts

 produce TNFα, IL-1 and IL-6

  • These cytokines induce the production of matrix
    metalloproteinases (MMPs) – which degrade the cartilage

Joint destruction might be caused by CD4 T-cell cytokine: RANK ligand (belongs to TNF-family), this promotes osteoclasts (resorb bone)

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17
Q

What are some of the Co-Morbidities linked to RA?

A
  1. IL-6 acute-phase response, hepcidin in liver
  2. TNF-a and IL-6 Free fatty acid and + CS= Stroke, MI
  3. TNF-a and IL-1 MUSCLE insulin resistance
  4. TNF-a, RANKL BONE low bone mineral density, fractures
18
Q

What are the current therapies used in RA?

A

Focus on anti-inflammatory and immunosuppressive drugs

  1. NSAIDs
    * (COX-2 inhibitors)
  2. DMARDs
  3. Biologics
19
Q

What are the signs and symptoms of RA?

A

Insidious onset
* Fever, malaise, weakness

Symmetrical – inflammation - pain, tenderness, swelling, stiffness, redness and joint warmth

Progressive articular deterioration – loss of function
* Inflammation, destruction of bone and cartilage
* Deformity, limited motion, pain on motion

General symptoms – weight loss, fatigue, mental health changes

  • Extra-articular manifestations – including: lungs, heart, eyes, skin
  • RA nodules
20
Q

Symptoms of RA in joints?

A

Dislocation of toes
Bone erosion
Bone displacement

( Increased risk of morbidity and mortality)

21
Q

What are some of the Co-Morbidities associated with RA?

A

Comorbidities increase patients - cardiovascular risk, risk of infection, risk of respiratory disease, risk of osteoporosis, risk of malignancy and risk of depression

22
Q

What happens when treatment for RA is delayed?

A

Patient outcomes are compromised when treatment is delayed

Appropriate treatments can alter the course of the disease

23
Q

What tests are carried out in RA?

A

BLOOD TESTS?
INFLAMMATORY MARKERS:
*Erythrocyte sedimentation rate (ESR)
*C-reactive protein (CRP)

IMMUNILOGICAL PARAMETERS:
* Rheumatoid factor (RF)
* Antinuclear antibody (ANA)
* Anti-cyclic citrullinated peptide (anti-CCP)

RADIOLOGY?

24
Q

What happens during OE in RA?

A

Limitation of motion

Tenderness on palpation

SQUEEZE TEST: Identifying subtle inflammation in the absence of obvious swelling or tenderness of individual MCP or MTP joints. If the squeeze causes undue pain it raises the possibility of underlying joint inflammation.

25
Q

What are the different parts that make up the diagnosis of RA?

A

Complete history taking:
*Morning stiffness for greater than 30 minutes
*Stiffness after quiescence
*Family history
*Lifestyle

Complete history taking:
*Symmetrical effects on synovial joints – symptoms as discussed

Investigations:
*Inflammatory markers
*Haematological parameters
*Immunological parameters
*Radiological investigations

26
Q

NICE Guidelines on Diagnosis?

A

Referral - Primary care to specialist– refer those with suspected persistent synovitis.

Urgently if : affecting small joints of hands and feet, more than 1 joint, delay of >3 months before seeking medical advice

Diagnosis - If found to have synovitis on clinical examination – Determine Rheumatoid Factor, consider Anti-CCP antibodies (if negative for RF), x-ray hands and feet.

Additional investigations – any of the above not done during diagnosis, plus Health Assessment Questionnaire (HAQ).

27
Q

What is used to monitor RA disease?

A

DAS28
A measure of disease activity – 4 different measures
* Number of swollen joints (out of 28)
* Number of tender joints (out of 28)
* Measure ESR or CRP
* ‘Global assessment of health’
* Giving overall disease activity score

  • Scores:
  • DAS 28 = >5.1 = active disease
  • DAS 28 = <3.2 = low disease activity
  • DAS 28 = <2.6 = remission
  • Allows disease/treatment monitoring, criteria for eligibility for biologic treatment
28
Q

According to NICE Guidelines what are the appropriate management of early therapy?

A
  • Improves symptoms
  • Improves function
  • Reduces mortality
  • May reduce comorbidities
29
Q

What are the appropriate treatment guideline aims of treatment in RA?

A
  • Minimising joint pain and swelling
  • Preventing deformity and radiological damage (i.e. erosion)
  • Maintaining QoL
  • Controlling extra-articular manifestations
30
Q

What classes of drugs are used to treatments of RA according to guideline?

A

FIRST LINE: Monotherapy cDMARD e.g. M,S,L (HQ if mild or palindromic disease)

SECOND LINE: step-up stategy 2 cDMARDs or HQ

THIRD LINE: TNFa, bDMARD, tDMARD

Consider short term bridging with glucocorticoid therapy when starting a new DMARD.

31
Q

What are the examples of bDMARDS?

A

Anti-TNF - (Adalimumab, Etanercept, certolizumab, golimumab, infliximab)

Other biologics – IL-6 receptor inhibitor= Tocilizumab / sarilumab

– Anti-B cell (anti-CD20 antibody) = Rituximab

– Antibody blocking T-cell (lymphocyte) activation ( Co-stimulation modulator CD80/86)= Abatacept

– IL-1 receptor inhibitor = Anakinra

32
Q

What are examples of tDMARD?

A

JAK inhibitors – tofacitinib / baricitinib /upadacitinib / filgotinib

33
Q

What is “treat to target”?

A

A strategy which should include frequent review, formal
assessment of joints and escalation of therapy if inflammation is still present
until good control is reached.

Patients have an individual target (remission DAS 28 < 2.6 or low activity DAS 28 <3.2)

34
Q

What are the improvements of DAS score in moderate disease?

A

For those with moderate disease – they must have a moderate response
(DAS 28 improvement of  0.6 and  1.2) at 6 months to continue.

35
Q

What are the improvements of DAS score in severe disease?

A

For those with severe disease – they must have a moderate response (DAS
28 improvement of  1.2) at 6 months to continue.

36
Q

When should step-down strategy be considered?

A

If maintained for at least 1 year (without corticosteroids (used for a flare)

  • Consider cautiously reducing drug doses or stopping drugs
  • Return to previous DMARD regime if target no longer me
37
Q

What drug should be used for symptom control and should it managed?

A

Consider NSAID (traditional and COXII inhibitors) when control of pain and
stiffness is inadequate.

  • Consider drug toxicities and patients risk factors
  • Use the lowest affective dose for shortest time
  • Offer a PPI
  • Review risk factors regularly
38
Q

What drug should be used for flare management?

A
  • For patients with recent onset or established RA - short term glucocorticoids can rapidly reduce inflammation.
  • These should be – STOPPED
  • The only reason these may continue is – when ALL other treatment
    options have been offered.
39
Q

How should patients be monitored when on Anti-rheumatic drugs?

A

They should be provided with how/when to seek specialist care by having rapid access during a flare and ongoing drug monitoring.

REVIEW 6 months after target is achieved = Maintenance

ANNUAL REVIEW: Disease activity, development of co-morbidities, effect on personal life.

40
Q

What do the drug choices depend on for initial therapy?

A
  • Patient preference
  • Patient characteristics
  • Co-morbidities, risk factors
  • Treatment characteristics
  • cautions / contraindications / side effects / dosing / interactions /
    monitoring requirements etc
41
Q
A

EXAM 1 (14 decks)

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