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MSDR > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Describe the factors which play a role in autoimmunity.

A

Genetic susceptibility → development of self-reactive T and B cells → reaction to environmental stimuli (genetic susceptibility is not enough)

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2
Q

Describe the relationship tolerance and autoimmunity.

A
  • Tolerance: ability to discriminate self- versus non-self antigen
  • Autoimmunity: inability to have tolerance
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3
Q

Describe the concept of negative selection and its role in establishing immunological tolerance.

A
  • Used in thymus with T cell maturation
  • Strong binding self-antigens are deleted
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4
Q

Describe the difference between immunogenic antigens and tolerogenic antigens.

A
  • Immunogenic antigens: cause lymphocyte proliferation and differentiation
  • Tolerogenic antigens: cause lymphocyte inactivation
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5
Q

Describe how the establishment of immunological tolerance can be used to prevent unwanted immune reaction.

A
  • Allergic reactions can be treated with desentization
  • Organ transplant rejections can be treated by matching HLA types
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6
Q

List the cell types that are subject to central and peripheral T cell tolerance and where such tolerance occurs.

A
  • Central tolerance: thymus (T cells) and bone marrow (B cells)
  • Peripheral tolerance: secondary lymphoid organs and peripheral tissues
    • Once memory B and T cells, it becomes too late to fully treat
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7
Q

Describe the major mechanism of central T cell tolerance.

A
  • Occurs in the thymus with negative selection of strong binding of self-antigens leads to T cell deletion
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8
Q

What does AIRE do?

A
  • AIRE (autoimmune regulator) protein is required for self-antigen presentation in order for proper negative selection to occur
    • Mutations in AIRE protein can lead to some self-antigens that are not expressed in the thymus → autoimmunity
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9
Q

How do healthy individuals resolve autoimmunity?

A

Even in healthy individuals, there are numerous self-reactive lymphocytes BUT this is solved by peripheral tolerance

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10
Q

Explain the relationship between the lack of B7-CD28 co-stimulation and the induction of peripheral T lymphocyte tolerance.

A
  • Lack of the B7-CD28 (“second signal”) leads to anergy or apoptosis of T cells because IL-2 (proliferation inducing cytokine) is not released
    • APCs presenting self-antigens do not present B7 ligand and do not initiate immune response
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11
Q

Explain how CTLA-4 works?

What is Fas?

A
  • CTLA-4 is an inhibitory receptor that has higher affinity for B7 than CD28 and blocks immune response
    • Anti-CTLA-4 would help induce immune response
    • Fas receptor (death receptor) works via same mechanism
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12
Q

Regulatory T-cells

A
  • Some immature CD4+ T cells that recognize self-antigens with high affinity but do not die enter into peripheral tissues to become regulatory T cells
  • Requires high expression of transcription factor FoxP3
    • Mutation leads to IPEX – systemic autoimmune disease
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13
Q

Regulatory T-cells

Mech. of suppression?

A
  • Mechanisms of suppression
    • Production of inhibitory cytokines (IL-10 and TGF-beta)
    • Expression of CTLA-4
    • Capture IL-2 by expressing high levels of IL-2R
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14
Q

Describe the role receptor editing, deletion, and anergy in central B cell tolerance.

A
  • When immature B cells interact strongly with self-antigens in the bone marrow, B cells undergo receptor editing
    • If receptor editing fails, B cell is deleted
  • When immature B cells interact weakly with self-antigens in the bone marrow, receptor expression is reduced and B cell becomes anergic
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15
Q

Describe the role of anergy, deletion, and regulation by inhibitory receptors in peripheral B cell tolerance.

A

Recognition of self-antigens in the periphery can lead to anergy, deletion, or regulation by inhibitory receptors (aka no immune response)

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16
Q

rheumatoid arthritis (RA)

pathogenesis?

A

Immune dysregulation leading to synovial proliferation and inflammation of affected joints

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17
Q

Compare pain in rheumatoid arthritis (RA) vs. OA?

A
  • nflammatory Pain (RA)
    • Prolonged morning stiffness (>60 minutes)
    • Present at rest and with normal use
    • Associated with fatigue
  • Non-inflammatory pain (OA)
    • Pain during activity, but relieved with rest
    • Short bouts of stiffness (<15 minutes)
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18
Q

rheumatoid arthritis (RA)

clinical manifestations?

A
  • Insidious onset, fatigue
  • Morning stiffness >60 minutes
  • Symmetrical in the affected joint
  • Polyarticular (≥5 joints)
    • Spares lower back and DIPs (OA does not spare DIPs)
  • Gender discrepancy
    • Female:Male = 3:1
  • Extra-articular features – review of systems
    • Rheumatoid nodules
    • Anemia
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19
Q

rheumatoid arthritis (RA)

physcial findings?

A
  • Yellow finger nails (from smoking)
  • Subluxation (dislocation) à ulnar deviation
  • Rheumatoid nodules
  • Synovitis
  • Interosseous muscle atrophy
  • Boutonniere’s Deformity
  • Swan Neck Deformity
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20
Q

Boutonniere’s Deformity vs. Swan Neck Deformity

A
  • Boutonniere’s Deformity – hyperextension of DIP and flexion of PIP
  • Swan Neck Deformity – flexion of DIP and hyperextension of PIP
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21
Q

How to test for inflammation?

A
  • Sedimentation rate (ESR)
  • C-reactive protein (CRP) – acute marker
  • Thrombocytosis (increased platelets)
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22
Q

Important AB test for RA?

A

RF, CCP

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23
Q

Rheumatoid factor (RF)

A
  • Anti-Fc IgG
  • 20% of RA patients will not have positive test
  • Non-specific to RA
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24
Q

Anti-cyclic citrullinated peptide antibodies (CCP)

What does it bind? genetic factor?

A
  • Antibodies against citrullinated residues of type II cartilage (articular cartilage in joints)
  • Associated with MHC class II: HLA-DR4 B101 (beta)
  • Associated with periodontal disease and smoking
  • Think peptidylarginine deiminase (arginine to citrulline conversion)
  • 95% specific when joint swelling is present
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25
Q

Describe the impact of RA on daily activities of patients.

A
  • Increased CAD risk due to increase in inflammation
  • Increased mortality
  • Increased probability of work stoppage
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26
Q

Describe how to approach treatment of RA and autoimmune disease.

A

Decrease pain and inflammation and reduce/prevent joint damage

  • DMARDs
  • Biologics
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27
Q

Name a convetinal Disease Modifying Anti-Rheumatic Drugs (DMARDs)?

A

Methotrexate: in low doses, it only inhibits Dihydrofolate (DHF) Reductase in lymphocytes

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28
Q

MOA for biologics?

A
  • -mab = monoclonal antibody
  • -cept = receptor blocker
  • MOAs
    • Cytokine directed
    • T-cell directed
    • B-cell directed
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29
Q

Why is TB screening necessary before RA treatment?

A
  • Anti-TNF medications can allow for opportunistic pathogens to cause infections
    • Latent TB is major concern during treatment
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30
Q

Natural history and distinguishing radiographic features of OA

4 features

A
  • Localized and asymmetric joint-space narrowing (RA has symmetric)
    • Joints move along superior or medial axes in the hip
  • Subchondral sclerosis (eburnation – wearing away of hyaline cartilage and polishing of bone)
  • Osteophytes (joint enlargement to spread weight bearing = bony spurs)
  • Subchondral cysts (synovial fluid enters into bone from eburnation)
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31
Q
A

OA: asymmetric joint-space narrowing

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32
Q
A

OA: osteophyte

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33
Q
A

RA: Ankylosis

34
Q
A

Erosive OA: seagull wing erosion

35
Q
A

Erosive OA: Interphalangeal ankylosis

36
Q
A

RA: erosion of the joint

37
Q

Common Sites of OA

A
  • Hand
    • DIP joint, PIP joint
    • Most common is 1st CMC joint
  • Wrist, Knee, Hip
  • Foot
    • 1st MTP joint
    • 1st TMT joint
    • Talonavicular joint
38
Q

Erosive OA

3 Feature?

A
  • Also known as osseous ankylosis (fusion of bones)
  • Distinguishing radiographic features
    • Seagull wing erosion
    • Heberden nodes
    • Interphalangeal ankylosis
39
Q

Rheumatoid Arthritis

Location and Presentation?

A
  • Location in decreasing order of frequency
    • Hands > feet > knees > hips > c-spine > shoulder > elbow
      • Feet can occur before hands in 1/5 of people
        • First erosion is lateral aspect of head of the 5th metatarsal
      • Knees occur bilaterally and symmetrically
      • Hips have acetabuli protrusio (tear drops)
      • C-spine findings include pannus formation around the dens, atlantoaxial subluxation, and joint erosions
40
Q

RA

X-ray features

A
  • Symmetrical narrowing of joint space
  • Osteopenia
  • Subluxations
  • Marginal erosions
  • NO BONE FORMATION
  • Synovial cyst formation
  • Ankylosis
41
Q

What do you use MRI and US to detect?

A

marrow edema, synovitis, and tenosynovitis

42
Q

Autoimmunity in normal people?

A

Significant number of healthy individuals still can have significant ANA levels

43
Q

SLE pathogenesis

A

B cells – SLE patients have circulating plasma cells that create high levels of antibodies in all immunoglobulin classes.

44
Q

What AB is sensitive for SLE?

A
  • Sensitive autoantibodies – healthy individuals can still have significant ANA levels
    • Antinuclear antibodies (ANA) – highly sensitive test that screens population with ANA 1:80 titer
45
Q

What AB is are specific for diagnosis of SLE?

A
  • Specific antibodies – appear prior to diagnosis
    • Anti-dsDNA – specific for diagnosis of SLE
    • Anti-Sm – specific for diagnosis of SLE
46
Q

How does Complement change in SLE?

A

Low C3 and C4 may indicate complement deposition which can be cause for concern of tissue damage

47
Q

Mentod for ANA testing?

A
  • Indirect immunofluorescence
    • Method
      • Patient serum is added to plate of nucleated cells
      • Secondary antibodies with fluorochrome are added and bind to components that stuck
      • Different fluorescing patterns correlate with different antigens
48
Q

What are the Daignostic tests for SLE?

A
  • Diagnostic tests
    • ANA 1:80 screens population for SLE – it is highly sensitive
    • ANA 1:640 diagnoses SLE – it is highly specific
49
Q

How is SLE diagnosis made?

A

Requirements: ≥4 criteria (at least 1 clinical and 1 immunologic) OR biopsy-proven lupus nephritis with positive ANA or positive anti-dsDNA

50
Q

Clinical features of SLE?

A
  • Malar Rash – butterfly in shape across face, sparing nasolabial folds
  • Discoid Rash – permanent alopecia (hair loss)
  • Nonerosive arthritis – is not associated with bone damage
  • Serositis – inflammation heart (pericarditis), lung (pleuritis), and abdomen (peritonitis)
  • Lupus glomerulonephritis
  • Central Nervous System – cerebritis or stroke
51
Q

gold standard of diagnosis for SLE

A

Lupus glomerulonephritis – gold standard of diagnosis with kidney biopsy

52
Q

Immunologic features of SLE?

A

ANA, anti-dsDNA, anti-Sm, anti-phospholipid, low complement (C3, C4), and direct Coombs’ test (tests levels of antibodies/complement bound to RBCs)

53
Q

Genetic factors of SLE?

A
  • SLE is highly correlated to genetic contribution, therefore it occurs at younger age
  • 85% of patients are female
54
Q

Treatment for SLE?

A

Meds

  • Hydroxychloroquine
  • Glucocorticoids
  • Immunosuppressives
  • B-cell agents

Non-medical tx

  • Sun protection – UV causes rash for unknown reasons
55
Q

Hydroxchloroquine

A
  • Hydroxchloroquine – downregulates antibodies and cytokines
    • Adverse effect – retina issues
56
Q

Glucocorticoids

A
  • Glucocorticoids – downregulates inflammatory functions and reduces vessel permeability
    • Adverse effects – weight gain, hypertension, infections
57
Q

Immunosuppressives

A
  • Immunosuppressives – used in lupus nephritis
    • Azathioprine
    • Adverse effects – leukopenia, avoid live vaccines, infections
58
Q

B-cell agents

A
  • B-cell agents – attacks B cells
    • Rituximab and belimumab
59
Q

Vasculitis

patho? what are layers of a blood vessel?

where does vasculitis usually occur?

A
  1. Inflammation of the blood vessel wall
    1. Arterial wall is comprised of three layers: endothelial intima, smooth muscle media, and connective tissue adventitia (innermost to outermost layers).
    2. Layers are separated by elastic lamina
60
Q

Vasculitis

Etiology & Clinical features?

A
  1. Etiology is usually unknown
  2. Clinical features include:
    1. Nonspecific symptoms of inflammation (e.g., fever, fatigue, weight loss, and myalgias)
    2. Symptoms of organ ischemia—due to luminal narrowing or thrombosis of the inflamed vessels
    3. Claudication – pain/discomfort due to lack of blood flow
    4. ESR is elevated
61
Q

Temporal (Giant Cell) Arteritis

Type, description, & symptoms?

A
  1. LVV
  2. Granulomatous vasculitis that classically involves branches of the carotid artery
  3. Most common form of vasculitis in older adults (> 50 years); usually affects females

  4. Presents as headache, visual disturbances, and jaw claudication.
  5. Biopsy reveals inflamed vessel wall with giant cells and intima fibrosis

i.Lesions are segmental; diagnosis requires biopsy of a long segment of vessel, and a negative biopsy does not exclude disease.

62
Q

Takayasu Arteritis

Type, description, & symptoms?

A
  1. LVV
  2. Granulomatous vasculitis that classically involves the aortic arch at branch points
  3. Presents in adults < 40 years old (classically, young Asian females) as visual and neurologic symptoms with a weak or absent pulse in the brachial artery (‘pulseless disease’).
63
Q

Polyarteritis Nodosa

Type, description, & symptoms?

A
  1. MVV
  2. Necrotizing vasculitis involving multiple organs; lungs are spared.

  3. Classically presents in young adults as hypertension (renal artery involvement), abdominal pain with melena (mesenteric artery involvement), neurologic disturbances, and skin lesions.
64
Q

Kawasaki Disease

Type, description, treatment, & symptoms?

A
  1. MVV
  2. Classically affects Asian children < 4 years old
  3. Presents with nonspecific signs including fever, conjunctivitis, erythematous rash of palms and soles, and enlarged cervical lymph nodes
  4. Coronary artery involvement is common and leads to risk for thrombosis with myocardial infarction and aneurysm
  5. Treatment with aspirin
65
Q

Buerger Disease


Type, description, & symptoms?

A
  1. MVV
  2. Necrotizing vasculitis involving digits

  3. Auto-amputation of fingers and toes
66
Q

Granulomatosis Polyangiitis (GPA – formerly Wegeners)

Type, description, & symptoms?

A
  1. SSV
  2. Necrotizing granulomatous vasculitis involving nasopharynx, lungs, and kidneys
  3. Classic presentation is a middle-aged male with sinusitis or nasopharyngeal ulceration, hemoptysis with bilateral nodular lung infiltrates, and hematuria
  4. Serum c-ANCA levels correlate with disease activity
67
Q

Eosinophilic Granulomatous Polyangiitis (EGPA – formerly Churg Strauss Syndrome)

Type, description, & symptoms?

A
  1. SSV
  2. Necrotizing granulomatous inflammation with eosinophils involving multiple organs, especially lungs and heart

  3. Asthma and eosinophilia are often present (big difference from GPA)
  4. Serum p-ANCA levels correlate with disease activity
68
Q

LVV

Expression(G/N/A), Location, Symptoms?

*G = granulomatous, N = necrotizing, A = antibody- mediated

A

Expression: G+ N- A-

Location: Aorta and branches (subclavian and carotid), ophthalmic, and temporal

Symptoms: Aneurysm, vision loss, temple pain

69
Q

MVV

Expression(G/N/A), Location, Symptoms?

*G = granulomatous, N = necrotizing, A = antibody- mediated

A

Expression: G- N+ A-

Location: Arteries to nerves, fingers, GI tract, leg

Symptoms: Abdominal pain, wrist drop, foot drop

70
Q

SVV

Expression(G/N/A), Location, Symptoms?

*G = granulomatous, N = necrotizing, A = antibody- mediated

A

Expression: G+ N+ A+

Location: Skin, pulmonary, kidneys

Symptoms: Pupura, hemoptysis, glomerulonephritis

71
Q

How does the aging process cause an increase the likelihood of OA?

A
  • As you age, you are more likely to develop OA
    • For women ages 50-55, menopause causes decrease in estrogen, which is important in cartilage maintenance
    • Peptidoglycan production decreases, which is component of cartilage
72
Q

OA

Symptoms and Complications of Knee

A
  • OA grows bone and RA destroys bone
  • Symptoms
    • Use related pain
    • Stiffness or “gelling” after sitting
    • Crepitation = feeling of grinding
    • Lab results (aka inflammation markers) are normal
  • Knee deformities (places stress on hips and lower back)
    • Varus deformity = bow leg
    • Valgus deformity = knock knee
73
Q

OA

Distribution?

A
  • Men
    • Knee and hip
    • Hand OA distribution: DIP > PIP > 1st CMC
  • Women
    • Hand and knee
    • Hand OA distribution: DIP > 1st CMC > PIP
  • OA spares MCPs
74
Q

Explain the difference between the two images?

A
  • Cartilage features
    • Normal: pairs of chondrocytes spread out
    • OA: clustering of chondrocyte pairs indicates disease
75
Q

What are come secondary casues of OA?

4 categories

A
  • Metabolic: CPPD (pseudogout – calcium pyrophosphate deposition)
  • Anatomic: dislocation, cruciate ligament tear, obesity
    • Obesity
  • Traumatic: fracture, chronic injury
  • Inflammatory: septic arthritis, rheumatoid arthritis
    • IL-1 and TNF-alpha are released from macrophages and chondrocytes
76
Q

Explain the link between obesity and OA?

A
  • Obesity: increase in adipocytes leads to increase in leptin secretion
    • Upregulates IL-1 and MMPs: inflammatory cytokine and damaging enzymes respectively leads to cartilage destruction
77
Q

Treatments for OA?

A
  • Oral medications – NSAIDs
  • Pain management – acetaminophen (not an NSAID), intra-articular corticosteroids, and tramadol
  • Viscosupplementation – hyaluronic acid (HA) injected into joints to provide lube and shock absorption
  • Other – PT and weight loss (aquatic exercise)
  • Surgical – knee replacement
78
Q

Treatment plan for OA with

no symptoms?

A

Exercise

Weight control

79
Q

Treatment plan for OA with

mild symptoms?

A

Pain medications

PT

Steroid injections

Tramadol

80
Q

Treatment plan for OA with

severe symptoms?

A

Viscosupplementation

Steroid injections

81
Q

Treatment plan for OA with

very severe symtoms with night pain?

A

Surgery

Bracing

MSDR (7 decks)

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