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MSK Summative > Pathology of Joint Pain > Flashcards

Pathology of Joint Pain Flashcards

1
Q
  • What is a joint?
    • What are two types of joints and what is their function?
A
  • Joint is a connection between two bones
    • Solid joints:
      • tightly connected to provide structal strength (e.g. cranial structures)
    • Synovial joints
      • have joint space to allow for motion
      • Synovium lining the joint capsule scretes fluid rich in hyaluronic acid
      • lubricate joint and facilitate smooth motion
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2
Q
  • Articular surface of adjoining bones is made of?
  • What is it surrounded by?
A
  • Made of hyaline cartilage (type II collagen)
  • Surrounded by joint capsule
    • lined by synovium
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3
Q
  • Osteoarthritis / Degenerative Joint Disease is?
  • Due to?
  • What are major risk factors?
A
  • Progressive degeneration of articular cartilage (layer on top of bone at joint to help with movement)
    • most common type of arthritis
  • Most often due to wear and tear
  • Major risk factor= age
    • Others: obesity and trauma
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4
Q
  • Which joints does osteoarthritis affect?
A
  • Affects limited number of joints (oligoarticular):
    • hips
    • lower lumbar spine
    • knees
    • distal interphalangeal joints (DIP) of fingers
    • proximal interphalangeal joints (PIP) of finger
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5
Q

What is classic presentation of osteoarthritis?

A

Joint stiffness in the morning that worsens during the day

  • when you use the joints you begin to feel the pain
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6
Q

What are 3 pathological findings of osteoarthritis?

A
  1. Disruption of cartilage that lines the articular surface
    • fragments of cartilage floating around in joints pace are called “joint mice”
  2. Eburnation (polishing) of subchondral bone
    • bone rubbing against bone
  3. Eburnation leads to osteophyte formation (reactive bony outgrowths)
    • arise in DIP (Herberden nodes) of joints of fingers
    • PIP (Bouchard nodes) of joints of fingers
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7
Q
  • Rheumatoid Arthritis is what kind of a disease?
    • classically affects?
    • associated with?
A
  • Chronic, systemic autoimmune disease
    • classically arise in women of late childbearing age
  • Associated with:
    • HLA-DR4
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8
Q
  • Although rhematoid arthritis is a systemic autoimmune disease is is characterized by involvement of?
  • What is the hallmark feature?
    • what does it lead to?
A
  • Characterized by:
    • involvement of joints
  • Hallmark feature:
    • Synovitis (inflmmation of joint capsule) that leads to formation of pannus (inflammed granulation tissue)
      • granulation tissue has fibroblast, blood vessels and myofibroblasts
  • Leads to:
    • myofibroblasts cause contraction which lead to:
      • movement of joint in different directions (deformities)
      • destruction of cartilage
      • ankylosis (fusion of joint)
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9
Q
  • Describe the change in pain and stiffness over the day with rheumatoid arthritis?
A
  • Morning stiffness that improves with activity
    • inflammation builds up a night (leads to stiffness in morning)
    • as use the joint it squeezes the joints free of the granulation debris
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10
Q
  • What joints are involved in rheumatoid arthritis?
    • how does it differ from osteoarthritis?
A
  • Symmetric involvement of:
    • PIP joints of the fingers (swan neck deformity)
    • wrist (ulnar deviation)
    • elbows, ankles and knees
  • DIP is usually spared, unlike osteoarthritis
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11
Q

What is seen on X-ray of rheumatoid arthritis?

A
  • Joint space narrowing
    • synovial inflammation
  • Loss of cartilage
    • replaced by granulation tissue
  • Osteopenia
    • wearing away of bone underneath cartilage
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12
Q

What are 5 systemic symptoms of rheumatoid arthritis?

A
  1. Fever, malaise, weight loss, myalgias (muscle pain) (bc autoimmune)
  2. Rheumatoid nodules
    • central zone of necrosis surrounded by epitheliod histiocytes (skin)
  3. Vasculitis
    • multiple organs can be involved
  4. Baker cyst
    • swelling of bursa behind knee
  5. Pleural effusions, lymphadenopathy, interstitial lung fibrosis
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13
Q
  • What are the classic lab findings of rheumatoid arthritis?
    • What are complication of RA?
A
  • Labs:
    • IgM autoantibody against Fc portion of IgG (rheumatoid marker)
      • maker of tissue damage and disease activity
    • neutrophils and high protein in synovial fluid
  • Complications:
    • Anemia of chronic disease
      • chronic inflammation release acute phase proteins, hepcidin—> prevent release of Fe from macrophage
    • Secondary amyloidosis
      • acute phase reactants produce protein SAA in liver—-> converted to AA—> deposits in tissues
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14
Q

Seronegative Spondyloarthropathies are group of joint disorders characterized by what 3 things?

A
  1. Lack of rheumatoid factor (seronegative)
  2. Axial skeleton involvement (spondylo)
  3. HLA-B27 association
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15
Q
  • Ankylosing spondyloarthritis (seronegative)causes?
    • invovle which joints?
  • Who does it most common affect?
  • What does it present as?
A
  • Inflammatory disease that leads to fusion of vertebrae
    • Involves sacroiliac joint and spine
  • Arise in young adults often males
  • Presents with:
    • low back pain
    • invovlement of vertebral spine eventually arise
      • lead to fusion of vertebrae (“bamboo spine”)
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16
Q

Reactive Arthritis (Reiter Syndrome) is a type of seronegative spondyloarthropathy.

  • Characterized by?
  • Who does it arise in?
  • skin findings?
A
  • Characterized by:
    • triad of arthritis, urethritis and conjunctivis
      • “can’t see, can’t pee, can’t climb a tree”
        • inflammation in multiple DIP and PIP
        • sausage fingers/toes
  • Arise in young adults, usually male
    • weeks after a GI or Chlamydia trachomatis infection
  • Skin findings:
    • keratoderma blenorrhagicum
    • Circinate balanitis
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17
Q
  • Psoriatic arthritis is seen in 10% of cases of?
    • what joints are most commonly affected?
A
  • Associated with psoriasis
  • Joints affected:
    • DIP joints of hands and feet
      • “sausage” fingers or toes
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18
Q
  • Infectious arthritis is due to?
  • What are two common causes and who do they affect?
  • What joint does it affect?
    • What does it present as?
A
  • Arthritis due to infectious agent; usually bacterial
    1. N. gonorrhoeae: young adults, sexually active
    2. S. aureus: older children and adults
  • Involve one joint; usually knee
  • Presents as:
    • warm joint, erythematous
    • limited range of motion
    • fever
    • increased white count
    • elevated ESR
      • measure of inflammation
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19
Q

What are risk factors for acute infectous arthritis?

A
  • Advanced age
  • Co-morbid conditions
    • rheumatoid arthritis
    • Diabetes mellitus
  • Prosthetic joints
  • IV drug abuse
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20
Q
  • What is pathogenesis/how do bacteria cause infectious arthritis?
A
  • Bacteria invade joint
  • Release bacterial products
    • formation of immune complex
    • activate complement
    • inflammation
  • Degredation of cartilage
    • local activation of coagulation
    • Fibrin deposited in joint
  • Nidus (place for bacterial growth) and microvascular obstruction in synovium
    • continued joint damage
    • formation of pannus
      • granulation tissue composed of macrophage and fibroblasts
  • Continued release of MMP and activation of osteoclast
    • continued degredation of cartilage and erosion of subchondral bone (just below cartilage)
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21
Q

HLA-B27 is associated with which 4 diseases?

A

PAIR (also known as seronegative arthritis)

  1. Psoritic arthritis
  2. Ankylosing spondylitis
  3. IBD-associated arthritis
  4. Reactive arthritis (Reiter syndrome)
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22
Q
  • What inflammatory cytokines are big players in rheumatoid arthritis?
    • What do they cause formation of?
A
  • Autoantibodies and CK mediated inflammation
  • Important CK’s:
    • INF gamma and IL-17
    • TNF and IL-1
    • RANKL: activated T cells
  • Infammatory cytokines induce pannus formation
    • erodes articular cartilage and bone
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23
Q

What are 6 predisposing factors of rheumatoid arthritis?

A
  1. Female
  2. HLA-DR4
  3. Smoking
  4. Silica exposure
  5. (+) rheumatoid factor
  6. anti-cyclic citrullinated peptide antibody (more specific)
24
Q

Treatment of Osteoarthritis?

A
  • NSAIDs
  • glucocorticoids
  • disease modifying agents
    • MTX
    • Sulfasalazine
    • hydroxychloroquine
    • leflunomide
  • Biological agents
    • TNF- alpha inhibitor
25
Q

Compare pathogenesis of osteoarthritis and rheumatoid arthritis?

A
  • Osteoarthritis:
    • mechanical wear and tear destroys articular cartilage
    • chondrocytes mediate degradation and inadequate reapir
  • Rheumatoid arthritis
    • Autoimmune
    • inflammatory cytokines and cells (CD 4+) induce pannus (proliferative tissue granulation) formation
    • erodes articular cartilatge and bone
26
Q

What are some common causes of viral arthritis?

A
  • Alpha virus
  • parvo B19
  • rubella
  • EBV
  • Hep B and C

Damage to direct infection or secondary reaction

27
Q
  • Who tends to be more affected by gout?
  • What are 3 significant risk factors?
A
  • Men more affected
  • Significant risk factors
    • Obesity
    • Metabolic syndrome
    • Excess EtOH
28
Q
  • Avascular (Aseptic) necrosis is due to?
  • Causes include?
  • Complications?
A
  • Ischemic necrosis (lack of blood) of bone and bone marrow
    • NOT due to bacteria
  • Causes include:
    • trauma or fracture (most common)
    • steroids
    • sickle cell anemia
    • Cassion disease
  • Major complications:
    • osteoarthritis
    • fracture
29
Q

Treatment for Ankylosing Sponylitis?

A
  • First line:
    • NSAID
  • Second line:
    • Anti-TNF alpha therapy
      • can have serious side effects such as infection (TB)
30
Q
  • What is the general features of ankylosing spondylitis?
A
  • Destruction of articular cartilage, primarily axial skeleton
    • Ankylosis: stiffening of a joint secondary to bone fusion
    • Spondylitis: inflammation of the spine
31
Q

What HLA subtype is associated with rheumatoid arthritis?

A

HLA-DR4

“There are 4 walls in a rheum (room)”

32
Q
  • What are the three main functions of the complement system?
  • Activation of complement system is inhibited by?
A
  1. Inflammation
    • stimulation of histamine release by C3a, C5a, C4a
  2. Opsonization of microbes—> phagocytosis
  3. Cell lysis
    • by membrane attack complex

Inhibited by:

  • C1 INH, DAF, and CD59 on cell membranes
33
Q

Antibody Dependent cellular Cytotoxicity is mechanism by which?

A
  • Natural killer cells destroy virally infected or neoplastic cells
    • express TLR on surface
    • nonspecific recognition of bacterial antigens, expressed proteins on virally infected cells
    • activates NFkB pathway
34
Q
  • What is lupus erythematosus?
    • What kind of antibodies are generated?
  • Who does it commonly present in?
A
  • Chronic inflammatory disease
    • flare up and alternating remissions
    • possible environmental tirgger
  • Generate autoantibodies (antinuclear antibody; ANA)
  • Commonly seen in:
    • females of reproductive age
    • African American descent
35
Q

Findings of SLE? (RASH OR PAIN)

A
  • Rash (malar or discoid)
  • Arthritis (nonerosive)
  • Serositis
  • Hematologic disorder (cytopenias)
  • Oral/nasopharyngeal ulcers
  • Renal disease
  • Photosensitivity
  • Antinuclear antibodies
  • Immunologic Disorder
    • (anti-dsDNA, anti-Smith antiphospholipid)
  • Neurological disorders (seizures, psychosis)
36
Q

What is the HLA subtype associated with Goodpasture syndrome?

37
Q
  • In Goodpasture’s syndrome there are autoantibodies against?
  • Causes injury where in the body?
  • Lab findings show?
A
  • Collagen IV
    • component of the glomular basement membrane
  • Causes damage to:
    • lung
    • kidney (renal)
  • ​​Lab findings:
    • linear appearance of IgG depsition on glomular and alveolar basement membrane
38
Q

What type of hypersensitivity is Goodpasture syndrome?

A
  • Type II (antibody mediated)
    • antibodies to glomerular basement membrane and alveolar basement membrane
    • linear IF
39
Q
  • What is type II hypersensitivity reaction?
  • 3 mechanisms of destruction?
A
  • Cytotoxic (antibody mediated)
    • IgM, IgG bind to fixed antigen on enemy cells—> cellular destruction
    • Antibody and complement lead to MAC
  • 3 mechanisms:
    1. Opsonization and phagocytosis
    2. Complement and Fc receptor mediated inflammation
    3. Antibody mediated cell dysfunction
40
Q
  • What is compartment syndrome?
  • Due to?
    • What parts of the body does it usually invovle?
A
  • Compartment syndrome is:
    • After an injury, blood or edema (fluid resulting from inflammation or injury) may accumulate in the compartment.
    • The tough walls of fascia cannot easily expand, and compartment pressure rises
      • preventing adequate blood flow to tissues inside the compartment
        • Severe tissue damage can result
  • Commonly invovles:
    • anterior tibial compartment of leg
    • volar compartment of forearm
    • interosseous compartment of hand
41
Q
  • What injury most commonly leads to compartment syndrome?
    • What is the result?
A
  • Common cause:
    • supracondylar fracture of the humerus
  • Results in:
    • obstruction of brachial artery
      • ischemia and necrosis of flexor group of muscles of the forearm
42
Q
  • Tennis elbow is due to?
    • Where is pain most common?
A
  • Repetitive extension (overuse)
    • pain near lateral epicondyle
43
Q
  • What is golfer’s elbow due to?
  • Pain is common where?
A
  • Repetitive flexion (forehard shots); overuse of elbow
    • pain in epicondyle
44
Q
  • What is De Quervain tenosynovitis due to?
    • What does it cause?
  • Where is the pain?
    • How is this tested for?
A
  • Due to:
    • overuse of hand and wrist
  • Causes:
    • a chronic overuse tendon problem resulting consistent overloading of the tendons.
    • There is friction between the tendon and surrounding synovial sheath, causing intense irritation.
      • In order to function properly, a tendon must be able to glide freely within its synovial sheath.
    • stenosis (narrowing) of fibro-osseous tunnel
  • Pain:
    • on radial aspect of the wrist
  • Test:
    • Finkelstein test
45
Q
  • Carpal tunnel syndrome is the most common ___ syndrome?
    • Due to compression of which nerve?
  • Who are more affected?
  • Bilateral or unilateral?
A

Most common entrapment neuropathy

  • Compression of median n.
  • Women more affected than men
  • Frequently bilateral
46
Q

2 tests for carpal tunnel syndrome?

A
  1. Phalen maneuver:
    • gently flex wrist together as far as possible; hold for 1 min.
  2. Tinel sign:
    • light tapp over transverse carpal ligament
    • produce numbness/tingling in median n.
47
Q
  • What is hypoxia?
  • What does it cause?
A

Deficiency of O2; reduce aerobic oxidative respiration

  • Causes:
    • Ischemia: reduced blood flow
      • reduced O2 (no aerobic metabolism)
      • reduced nutrients (no aerobic glycolysis)
    • Inadequate blood oxygenation
    • deceased oxygen carrying capacity of blood

NOTE:

  • ischemia causes more rapid and severe cell and tissue death than hypoxia alone
48
Q
  • avascular necrosis (osteonecrosis) is?
  • common causes?
A
  • Avascular necrosis:
    • necrosis of bone and marrow or infarction from ischemia
  • Common causes:
    • alcohol abuse
    • infection
    • trauma
    • radiation therapy
    • tumors
49
Q
  • Raynaud phenomenon is due to?
    • Most often occurs where?
A
  • Due to:
    • decreased blood flow to the skin due to arteriolar (small vessel) vasospasm (sudden constriction) in response to cold or stress
      • color change from white (ischemia) to blue (cyanosis; hypoxia) to red (reperfusion)
  • Most often in:
    • fingers and toes
50
Q

Primary vs. Secondary Raynaud?

A
  • Primary (Raynaud’s disease)
    • idiopathic
    • symmetric
  • Seondary (Raynaud’s syndrome)
    • vascular insufficiency due to arterial disease caused by other entities like:
      • SLE, sclerodema, Buerger disease
    • assymmetric
51
Q
  • Scleroderma is a triad of?
  • Results in?
    • commonly presents where?
A
  • Triad of:
    • autoimmune (mostly females) (of connective tissue)
    • noninflammatory vasculopathy
    • collagen deposition with fibrosis
  • Results in:
    • hardening of the skin
  • Commonly:
    • slcerosis of skin, manifesting as puffy taut skin without wrinkles
    • fingertip pitting
      • also sclerosis of renal, pulmonary, cardiovascular and GI
52
Q
  • Diffuse vs. Limited scleroderma?
    • associated with which autoanitbodies?
A
  • Diffuse scleroderma:
    • widespread skin involvement
    • rapid progression with early visceral involvement
    • associated with anti-Scl-70 antibody
  • Limited scleroderma:
    • limited skin involvement confined to fingers and face
    • CREST syndrome
      • Calcinosis*
      • Raynaud phenomenon
      • Esophageal dysmobility
      • Sclerodactyly
      • Telangiectasia
    • Associated with anti-centromere antibody
53
Q

This is image is comparing a normal patients skin to a patient with?

A
  • Systemic sclerosis
    • note extensive deposition of collagen in the dermis
    • virtual absence of appendages (hair follicles) and foci of inflammation
54
Q
  • What is fibrosis?
  • How does it develop in chronic inflammation?
A
  • Fibrosis= excessive deposition of collagen
    • deposition of collagen is normal in wound healing
  • Fibrosis in chronic inflammation:
    • chronic inflammation activates macrophages and lymphocytes
    • lead to production of GF, cytokines which increase synthesis of collagen
    • deposition of collagen is enhanced by decreased activity of metalloproteinases
55
Q

What are extra-articular symptoms of ankylosing spondylitis?

A

Extra articular manifestation include:

  • uveitis (redness of eye, blindness)
  • aortitis (inflammation of aorta)
    • weak walls pull of valvle—> aortic regurgitation

MSK Summative (8 decks)

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