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MSS > Introduction to Joint Disease; Mono and polyarthritis > Flashcards

Introduction to Joint Disease; Mono and polyarthritis Flashcards

1
Q

What do synovial joints do?

A

They allow for gliding movement facilitated by lubricated cartilaginous surfaces

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2
Q

What is the function of hyaline cartilage on articular surfaces?

A

Elastic shock absorber that spreads weight across surface of joint; friction free surface

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3
Q

What is hyaline cartilage composed of?

A

Type 2 collagen Water Proteoglycans Chondrocytes Avascular

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4
Q

What makes up the synovial cavity?

A

Synovial cells – cuboidal cells, 1-4 layers thick

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5
Q

What happens in the synovial cavity?

A
  1. Synovial fluid is produces 2. Debris is removed (phagocytic function) 3. Movement of solutes, electrolytes and proteins from capillaries to synovial fluid is regulated
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6
Q

What is synovial fluid made of?

A

Viscous filtrate of plasma containing hyaluronic acid Lubricant Provides nutrients to articular cartilage

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7
Q

What types of crystals are involved in inflammatory mono arthritis?

A

Monosodium urate (gout) Calcium pyrophosphate (pseudogout)

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8
Q

What types of things may cause inflammatory mono arthritis?

A

Trauma Crystals Septic joint

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9
Q

Clinical assessment of inflammation

A

Morning stiffness > 1 hour Erythema and warmth (usually with crystal arthritis and septic arthritis) Synovitis– thickening of synovium around joints; tender upon firm palpation

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10
Q

What lab tests can help diagnose inflammation?

A

Inflammatory markers – erythrocyte sedimentation (ESR), C reactive protein (CRP) Peripheral blood leukocytosis (septic arthritis) Joint fluid analysis

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11
Q

What radiographic changes point to inflammation?

A

X-rays that show erosions of bone at joint margins

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12
Q

What levels of WBC correspond to non-inflammatory, inflammatory or septic fluid analysis?

A

Non-inflammatory: <2000

Inflammatory: >2000

Septic: >50000

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13
Q

What percentage of PMNs correspond to non-inflammatory, inflammatory or septic fluid analysis?

A

Non-inflammatory: <10%
Inflammatory: 50-90%

Septic: >90%

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14
Q

What causes gout?

A

Metabolic disorder resulting in elevation of uric acid (hyperuricemia) beyond the level of saturation Overproduction – 10% Underexcretion – 90%

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15
Q

Does gout affect males of females more?

A

Males 1.3 : Females 0.5 Increase in females after menopause because estrogen promotes urate renal excretion

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16
Q

What other factors contribute to the likelihood of developing gout?

A

Higher in some non-Caucasian groups BMI

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17
Q

About how many milligrams of irate do we excrete per day?

A

600 mgms/day

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18
Q

What are the two types of hyperuricemia that you can get?

A

Overproduction (10%) Underexcretion (90%)

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19
Q

What types of things can cause an overproduction of uric acid?

A

Enzymatic abnormalities Increased cell turnover Diet EtOH

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20
Q

What types of things can cause an under excretion of uric acid?

A

Metabolic syndrome Renal disease Drugs: diuretics, cyclosporine EtOH

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21
Q

How do they diagnoses MSU crystals?

A

With bifringence – crystals that are yellow when parallel = gout Should have negative bifringence.

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22
Q

What is polyarticular gout?

A

Gout affecting multiple joints

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23
Q

What is tophaceous gout?

A

Chronic form of gout where crystals are deposited in soft tissue areas of the body – especially in areas of decreased temperatures (ears).

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24
Q

How does elevated MSU lead to inflammation?

A

Monosodium urate is recognized by pattern recognition proteins, phagocytosed and the inflammasome is activated. Caspase-1 activates IL-1B which is an inflammatory cytokine that sets up the inflammation process (released pro-inflammatory mediators and recruits neutrophils).

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25
Q

How common is calcium pyrophosphate deposition disease?

A

It affects approximately 12% of the elderly – increasing incidence with age

26
Q

What causes calcium pyrophosphate deposition disease?

A

Unknown but in most cases there is a related overproduction of PPi – PPi binds Ca well and precipitates to CPPD (calcium pyrophosphate dihydrate) May be found as “mixed crystals” with urate crystals

27
Q

What is pseudogout?

A

Attacks of acute arthritis similar to gout, but usually in larger joints (knee, wrist, shoulder)

28
Q

How is psuedogout diagnosed?

A

Rhombodial shaped, positively birefringent crystals in joint fluid X-ray: diagnosis may be suggested by “chondrocalcinosis” but not seen in all cases.

29
Q

How can CPPD arthritis present?

A
  1. Asymptomatic – most common
  2. Pseudogout
  3. Osteoarthritis (OA)
  4. RA-like (MCP joint enlargement) – may produce chronic low grade inflammation
30
Q

CPPD is also called….

A

Chondrocalcinosis

31
Q

What is rheumatoid arthritis?

A

Inflammatory polyarthritis that may cause crippling disease in about 1% of population.

Immunological (T cell) disease), but with significant B cell contribution – Invasion by immune lineage cells, but with recruitment of local cells (synovial fibroblasts). Proliferation of synovium (synovitis) with characteristiscs of benign, locally invasive tumor.

32
Q

What are some things that contribute to RA?

A

Genetic predisposition (HLA-DR shared epitope)

Hormonal contribution (F>M)

Environmental factors (smoking)

33
Q

Pathology of Rheumatoid Arthritis

A

Chronic inflammation of the synovium: CD4+ T cells, plasma cells and macrophages, giant cells – frequently forming lymphoid follicles

Accompanied by synovial cell hyperplasia– papillary pattern on surface of the synovium

Neutrophils and fibrin on joint surfaces in acute phase

Hyperplastic inflammed synovium extends over the articular surface forming a pannus which fills the joint space

34
Q

What are rheumatoid nodules?

A

Develop most common on skin in areas exposed to pressure

35
Q

What do rheumatoid nodules look like microscopically?

A

Grossly: non-tender, firm, round/oval

Microscopically: central zone of fibrinoid necrosis surrounded by rim of epithelioid histiocytes, and then lymphocytes and plasma cells

36
Q

What causes rheumatoid nodules?

A

Necrosis secondary to vascular damage possibly secondary to vasculitis associated with RA

37
Q

What is the classical presentation of Rheumatoid Arthritis?

A
  • Gradual onset of joint pain, swelling and inflammatino present for greater than 6 weeks in 3 or more joints
  • Symmetrical in nature
  • Morning stiffness lasting greater than 1 hours present for more than 6 weeks
  • Difficulty turning door knobs, opening jars, buttoning shirts, pain in the ball of the foot (metatarsalgia) upon arising from be d
38
Q

What are the specific HLA genes that increase the risk of developing RA?

A

HLA-DR4 and HLA-DR1

39
Q

Are males or females more likely to develop RA? Why?

A

Females 2.5 times more than males

Estrogen decreases apoptosis of B cells, potentially permitting selection of autoreactive clones

75% of pregnant women with RA experience spontaneous remission

40
Q

Does the presence of rhematoid factor mean RA?

A

No - not present in all patients with RA

Rheumatoid factor is an IgM antibody for the Fc portion of IgG

41
Q

What is a better indicator of RA and might be present in early RA?

A

Anti-cyclic citrullinated peptide (CCP)
Postitive in some cases of RF negative RA

Same sensitivity as RF but more specific

Correlates with overall disease activity

42
Q

What causes swan neck deformity in fingers of patients wtih RA?

A

D/t tightness of intrinsic muscles

43
Q

What are the criteria for classification of RA?

A
  1. AM stiffness > 1 hr
  2. Symmetrical arthritis
  3. At least 3 swollen joints
  4. Wrist, MCP, PIP involvement
  5. Rheumatoid nodules
  6. Positive rheumatoid factor
  7. X-ray change typical of RA in hand/wrist

Dx: 4/7 > 6 wks

44
Q

Does RA diagnosis usually come with a family history of the diease?

A

Uncommon, but some families have multiple affected members

45
Q

What are some systemic features of RA?

A

Sjogren’s in about 20%

CV: RA is risk fact for CVD

Pulm: RA lung involvement

GI: NSAIDs or other medication side effects

Neuro: hand numbness, neuropathy

46
Q

How can RA pulmonary involvement present?

A
  • Rheumatoid pleuritis with effusion (exudate, low glucose)
  • Interstisial fibrosis
  • Nodules
  • Caplan’s syndrome: rheumatoid pneumoconiosis
  • Medication related: MTX, leflunomide, anti-TNS (usually chronic infections)
47
Q

How is CVD different in patients with RA?

A

More likely to have CV events between 25-65 yo

Inflammation-mediated atherosclerosis

48
Q

Pathogenesis of rheumatoid arthritis

A
  1. Dendritic cells phagocytose antigens and present them to T cells
  2. Activated T cells stimulate the production of B and T cells
  3. B cells produce plasma cells that form rheumatoid antibodies
  4. Helper T cells activate macrophages and cytotoxic T cells
  5. T cells, macrophages and cytotoxic T cells produce cytotoxic cytokines (TNF-a, IL-1, IL-6 and others) and prostaglandins that cause joint inflammation, synovial proliferation, and bone and cartilage destruction
49
Q

Progressive disorder of the joints caused by gradual loss of cartilage

A

Osteoarthritis

(Non-inflammatory polyarthritis)

50
Q

What are some risk factors for osteoarthritis?

A

Female gener

Increasing age

Race/ethnicity

Genetic predisposition

Obesity

Trauma

51
Q

What are some of the earlier changes that occur in the pathology of osteoarthritis?

A

Superficial layers of cartilage are destroyed

Fibrillation and cracking of cartilage matrix

Limited chondrocyte proliferation and new matrix formation

52
Q

What is subchondral sclerosis?

A

When more dense bone develops underneath areas where cartilage is gone

53
Q

What is a subchondral cyst?

A

Formed by a break in cartilage; this allows synovial fluid to be forced into subchondral space, forming a fibrous walled cyst

54
Q

What are osteophytes?

A

Bony outgrowths that develop at margins of articular surface in characteristic locations for specific joints; result in increased joint size

55
Q

How does osteoarthritis occur?

A

Imbalance of cytokine and growth factor activity resulting in matrix loss and degradation (breakdown of normal physiologic processes)

56
Q

How does RA differ from Osteoarthritis anatomically?

A

RA creates a pannus, can lead to akylosis

Osteoarthritis creates subchondral sclerosis, and thinned and fibrillated carilage

57
Q

What are some secondary causes of osteoarthritis?

A
  • Post-traumatic
  • Other joint/bone disease
  • Calcium deposition disease
  • Gout
  • Congenital/devo diseases
  • Metabolic
  • Neuropathic arthropathy
58
Q

What joints are commonly affected by osteoarthritis?

A

Small joints in hand (except MCPs – more RA)

Bunions, hips, knees

59
Q

Are blood tests used to diagnose OA?

A

Blood tests are typically not helpful to diagnosis OA but may be helpful to determine what treatments to use

60
Q

What does synovial fluid look like in OA?

A

Imaging

Synovial fluid aspiration – typically viscous and translucent, non-inflammatory WBC (<2000/mm^3)

61
Q

What can be seen on radiography in OA?

A

Narrowing of joint space (d/t loss of articular cartilage)

Osteophytes

Changes in subchondral bone including cysts, sclerosis, shape changes, loss of bone volume

MSS (24 decks)

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