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MDCN 360: Course 2 > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

rheumatoid arthritis is the most common systemic rheumatic disease. what is the genetic risk of RA?

A

genetic risk alleles resine in the MHC class 2 locus– HLA-DR4 alleles account for 40% of the genetic risk.

Risk of disease is greater
– in monozygotic twins: 12-15%
– in fraternal twins and first degree relatives: 2-
5%

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2
Q

which sex is more affected by RA?

A

more common in women, but in terms of age, all age groups are affected.

It affects women more commonly than men
– 2 or 3 times
– highest in 50’s – mid-70’s age groups
– But all age groups are affected

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3
Q

general mechanism of autoimmune diseases

A

when the immune system is stimulated it can produce antibodies to self antigens, and inflammatory mediators which cause tissue damage.

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4
Q

In RA, there are ___ antibodies to ____

A

IgM antibodies to self IgG (?)

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5
Q

arthritis refers to inflammation that occurs in a ____, and the inflammatory process occurs in the ____

A

arthritis regers to inflammation that occurs in a JOINT, and the inflammatory process ofccues in teh SYNOVIUM

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6
Q

In RA, the affected joints usually have two articulating surfaces (aka ____)

A

diarthrodial

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7
Q
A
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8
Q

two types of synoviocytes. Where are they located?

A

macrophage and fibroblats– in the INTIMAL layer of the synovium.

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9
Q

role of synoviocyte macrophages

A

they act as an antigen presenting cells.

  • present in the synovial membrane, and ingests and processes antigens.
  • presents them to HLA-DR matched T cells.
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10
Q

3 main functions of dendritic cells in their role in RA

A
  1. potent role in the innate immune repsonse
  2. antigen-presenting capacity
  3. unique ability to activate naive T cells.
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11
Q

T cells are principal regulators of the immune system and is a key player of RA pathophysiology. they interact with APC through MHC class `1 and 2 proteins, and produce___

A

cytokines (interluekins, IFN gamma, TNF alpha and beta)

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12
Q

which lymphocyte is in abundance in the synovium of RA-affected joints?

A

b cells. there is an abundance of B cells in the synobium of RA-affected joints. these lymphocytes can be organized into lymphoid-life structures.

3 critical roles of B cells in RA pathogenesis

  1. antigen presentation and T cella ctivation
  2. autoantibody production
  3. cytokine production.
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13
Q

3 critical roles of B cells in RA pathogenesis

A

3 critical roles of B cells in RA pathogenesis

  1. antigen presentation and T cella ctivation
  2. autoantibody production
  3. cytokine production.
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14
Q

fibroblasts can act in a positive and negative manner in the joint.

normally, they produce ____, an important component of joint fluid.

in the inflammed synovium, they produce ____

A

normally, they produce HYALURONAN, an important component of joint fluid.

in the inflammed synovium, they produce METALLOPROTEINASES

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15
Q

How do complement factors affect RA

A
  • immune complexes in the joint, specifically, RHEUMATOID FACTOR, activate the complement cascade.
  • complement fragments attracts neutrophils, which degranulate and cause enzyme damage to cartilage.
  • new antigens are released to stimulate Ab-AG complexes and the cycle continues.
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16
Q

antigens can come in the form of viruses, bacteria, or mycoplasma, but outline some examples of autoantigens

A
  1. type 2 collagen
  2. proteoglycan
  3. chondrocyte
  4. immunoglobulins (IgG)
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17
Q

Inflammatory cells communicate through cell-to-cell
contact or through the release of soluble mediators
(cytokines).

What is the role of IL-1 and TNF alpha?

What is the role of IL-2?

A

IL-1 (macrophages) and TNFa (T and B cells and macrophages) stimulate production of adhesion molecules, metalloproteinases, and prostaglandins.

IL-2 (T cells) stimulate T cell growth factor and B cell differentiation.

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18
Q

explain the 4 broad cell types that TNFalpha affects, and the outcomes that it leads to.

A
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19
Q

6 general articular effects of IL-6 In RA

A
  1. antibody production (possibly to self antigens)
  2. synoviocyte sitmulation and poliferation
  3. angiogenesis and production of adhesion molecules
  4. synovial inflammation
  5. mediation of chronic inflammation
  6. all of these cause joint destuction and pannus formation.
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20
Q

5 general systemic effects of IL-6 in RA

A
  1. acute phase repsonse
  2. alternations in IRON homeostasis
  3. thrombocytosis
  4. osteoporosis
  5. alterations in lipid metabolism.
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21
Q

how does IL-6 cause anemia of chronic disease/inflmaation?

A

IL-6 causes anemia of chronic inflammation by inducing hepcidin production by hepatocytes

Hepcidin inhibits the release of iron from macrophages (in the reticuloendothelial cells), and also inhibits the absorption of dietary iron (causing iron deficiency)

22
Q
A
23
Q

broadly speaking, what causes joint pain in arthritis?

A

the joint capsule has a rich supply of nerve endings. The lining of the joint, the synovium , has nerve endings.

inflammatory mediatoes are released into the joint in arthritis (cytokines, chemokines and vasoactive proteins)

  • the nerve endings in the capsule and lining are stimulatied.
24
Q
A
25
Q

mechanisms/pharmacological basis of biologic therapies as a treatment for RA

A
  • can be antibodies and cloned receptors that block/modify the activity of TNFa
  • IL1 receptor antagonists are approced for treatment of RA
  • antibodies to B cell surface molecules and T cell co-stimulatory molecules are approved for the treatment of RA
  • antibodies to IL-6 receptors are approved for treatment of RA
  • protein kinase inhibitors are the newest therapy to be approved
  • generally, antibodies against various cytokines or lymphocytes are the current biologic treatments for RA.
26
Q

American College of Rheumatology classification criteria of RA

A
27
Q

T/F Stage 1 pathogenesis of RA involves the arthritis of 2 or less joints

A

false. stage 1 involves the antigen presentation to T and B cells, BUT NO CLINICAL SYMPTOMS

28
Q

Outline the events of Stage 2 pathogenesis of RA

A
  1. T and B cells proliferate, cytokines get released, and angiogenesis occurs
  2. patient may feel unwell, complains of joint pain and swelling.
  3. you’d see joint swelling and tenderness
  4. LAB TEST: CRP IS ELEVATED, C rays of affected joints show soft tissue swelling.
29
Q

outline what is going on in this picture.

A

there is some soft tissue swelling, this is most likely a stage 2 pathogenesis of RA.

30
Q

outline stages 3 and 4 of the pathogenesis of RA

A

3.

  • synovial hypertrophy with cell accumulation in joint space
  • clinically, there is continuous joint pain and swelling, malaise and low energy
  • examination– swollen joints, soft tissue swelling, decreased ROM in the joints, +/- nodules.

4.

  • the pannus invades the joint space, and tehre is enzymatic damage to the cartilage (neutrophils release their granules in the synovial space)
  • clinically, there is an increased loss of function
  • examination is same as stage 3 but early deformities in joints and nodeuls are seen more
  • LAB/XRAY: PERIARTICULAR OSTEOPENIA, PANNUS ON MRI SCAN.

pannus is any abnormal tissue that:

Contains blood vessels

Covers up a normal body structure

In the case of rheumatoid arthritis, pannus tissue invades the space in between a joint’s bones, covering the bones and their protective layer of articular cartilage.

31
Q

stage 5 pathogenesis of RA

A
  • bone erosions, loss of cartilage, ligamentous damage
  • clinically, there is joint pain, swelling, loss of function and deformity
  • examination– swollen joints, deformities with contractures, nodules and extra-articular menifestations
  • lab test and x-rays: joint space narrowing and erosions.
32
Q

T/F: Generally, patients with the greatest load of disease are the ones who will develop extra-articular manifestations of RA.

A

true.

those wiht polyarticular joint involvement, highly elevated RF or anti-CCP antibody levels, and erosive disease at presentation are more likely to have extra-articular manifestations.

33
Q

systemic complains of RA

A

Fatigue – always tired in spite of adequate
rest; decreased energy levels

• Malaise – never feel well

• Fevers – not common but some patients can
present with elevated temperatures

• Weight changes – increased or decreased

34
Q

systemic complains of RA are partly due to the effects of ____ mediators.

  • fever and poor appetite are associated with the central effects of ____.

the fatigue is multifactorial.

A

systemic complains of RA are partly due to the effects of INFLAMMATORY mediators.

  • fever and poor appetite are associated with the central effects of TNF.

the fatigue is multifactorial.

  • decreased cardiovascular fitness
  • extra energy used to function
35
Q

extra-articular features of disease

A

Nodules • Vascular system • Respiratory System • Cardiovascular System • Neurological System

36
Q

where are nodules mainly found?

A
  1. in the skin on extensor and peri-articular surfaces
  2. where there is pressue –achilles tendon, pulp of the digits
  3. on the tendons– associated with triggering of finger
  4. in other organs– lung, heart, brain, eye.

Under what circumstances?

  • In patients with severe disease
  • Strongly RF positive
  • Some patients on methotrexate
37
Q

which medication may predispose someone to forming nodules?

A

methotrexate

38
Q
A

nodule

39
Q
A

nodules

40
Q
A

nodules. this is often mistaken as a bacterial or viral infection

41
Q

chief respiratory system extra-articular manifestation of RA?

A
  1. Pleural disease
    - symptoms of chest pain, dyspnea, and the pain is incresaed by deep breathing or coughing
  2. Interstitial Lung Disease
    - symptoms may be minimal or chronic dyspnea or cough, and may be associated with medications like methotrexate or leflunomide
42
Q

why can arrythmias manifest in RA?

A

because of pericardial disease affecting the cardiac muscle. causes chest pain and a disruption in proper pumping because of the nodules.

43
Q

effects of small vessel disease as an extra-articular manifestation of RA

A
  • vessels involved in the skin, bowel, peripheral nerves and eyes may have an accelerated rate of atherosclerosis.
  • symptoms are dependent on the site of the vasculitis

Skin: can lead to the development of ulcers or gangerene

Bowel: can lead to perforation and gangerene

Nerve: can lead to mononeuritis multiplex

eye: sclritis or episcleritis.

44
Q

which neuropathy causes carpal tunnel syndrome

A

pressure on the MEDIAN NERVE at the wrist causes carpal tunnel syndrome

  • wose with activity or at night
  • loss of muscle bulk in the THENAR EMINENCE
  • decreased grip strength
  • pain may be felt in the forarm.
45
Q

how can neurological symptoms in patients with RA be treated?

A

with TNFi therapies. it’s very important to ask patients about development of new neurological symptoms such as paraesthesiae or muscle weakness.

46
Q

sjogren’s syndrome

A

extra-articular manifestation that involves dry eyes, dry mouth, and other organ dryness like in the lungs and vagina.

47
Q

felty’s syndrome triad

A
  • seropositive chronic RA
  • splenomegaly
  • granulocytopenia

clinical features include joint damage, leg ulcers, and recurrent infections.

48
Q

overall functional classes of RA

A
49
Q

5 factors associated with poor prognosis in RA

A

1 .load of disease- numver of swollen and tender joints at presentation

  1. the presence and titre of rheumatoid factor
  2. the presence of anti-ccp antibodies
  3. HLA- DR4 haplotype (shared epitope)
  4. the prsence of erosions on Xray
50
Q

does the presence of rhematoid factor in the serum make a diagnosis of RA?

A

no. RF is present in a bunch of articular diseases.

also, it can be elevated in infections like endocarditis, hepatitis, acute viral infection, parasitic infection, tuberculosis

as well as lung diseases like interstitial fibrosis, chronic bronchitis, silicosis.

MDCN 360: Course 2 (70 decks)

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