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Musculoskeleton > Pathology Of Mono/polyarthropathies > Flashcards

Pathology Of Mono/polyarthropathies Flashcards

1
Q

Joint classifications

A

Solid (nonsynovial)

Cavitation (synovial)

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2
Q

Synovial membrane contents

A

Lined with type A synoviocytes at surface of joint
(Specialized macrophages

Lined with type B synoviocytes underneath A synovicoytes
(Synthesize hyaluronic acid and proteins)

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3
Q

Chondrocytes

A

Synthesis ECM and enzymatically digest it based on signals.

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4
Q

Osteoarthritis (OA)

A

Also called degenerative joint disease

Charcterized by degeneration of cartilage in synovial joints

MOST common disease of joints

Prevalence increases exponentially once age 50. Usually 40% if 70+

Usually has no underlying initiating cause other than gaining
- primary OA

Can be secondary OA when due to trauma or joint deformity.

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5
Q

Pathogenesis of OA

A

Lesions of OA stem from degeneration of the cartilage and its disordered repair.

ECM disorder Caused by REPEATED biochemical stressors and genetic factors

  • collagen/cartilage degradation exceeds synthesis in chondrocytes.

Late stage = chondrocytes number loss and severely degraded ECM

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6
Q

Matrix mealloprotienases

A

Produced by chondrocytes to degrade collagen type 2 cartilage

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7
Q

Commonly involved joints in OA in decreasing order

A

Hips

Knees

Lower lumbar and cervical vertebrae

Distal IP joints

Metacarpal and metatarsal joints

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8
Q

Heberden nodes

A

Osteophyte growth at the distal interphalangeal joints

Found in OA

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9
Q

Symptoms and characteristics of OA clinically

A

Joint pain that worsens with use, morning stiffness. Not bilateral and usually asymmetrical

Can impinge on spinal foramina by osteophytes results in cervical and lumbar nerve root compression.

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10
Q

Rheumatoid arthritis general characteristics

A

Chronic inflammatory joint pain that is autoimmune origin.

Causes proliferative inflammatory synovitis

Often progresses to destruction of articular cartilage and can cause ankylosis (adhesion/fusion of joints)

More common in women than men
- also more common in 30s-50s

Almost purely genetic and environmental based

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11
Q

Pathogenesis of RA

A 
50% of risk is inheriting genetics 
- specifically the HLA class 2 locus

Infection (specifically periodontitis) and smoking can cause new epitopes forming which promotes autoimmune action via citrullination of self-proteins.

CD4 Tcells initiate the autoimmune response

Synovium of RA joints include plasma cells that produce antibodies in the synovium to the citrulinated proteins

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12
Q

Specific cytokines that play in RA

A

IFN-y = activates macrophages in the in the type A synoviocytes degrade cartilage

IL-17 = recruiters neutrophils and monocytes to the area

RANKL = stimulates osteoclasts and bone resorption

TNF and IL-1: overstimulate macrophages to secretary’s proteases that destroy hyaline cartilage

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13
Q

Auto antibodies and citrullinated protiens

A

Antibodies in the synovium react to citrullinated proteins produced in the beginning stages of RA.

Produces complexes of autoantibodies and proteins in the joints which causes inflammation

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14
Q

Rheumatoid factor

A

Most common pathogenesis of RA.

80% of RA patients have serum antibodies that bind to self IgG Fc regions.

DOESNOT necessarily indicate RA, but RA patients do have high rheumatoid factor

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15
Q

Symptoms and clinical charcterisitcs of RA

A

Symmetric arthritis

Pain bouts last for long time (1 hour+)

Usually affects small joints

Can cause fibrous ankylosis and bony ankylosis via pannus bridging of the bones of the joint if left untreated.

  • anticitrullinated protein antibodies ALWAYS mark RA
  • symptoms include malaise, fatigue and pain that grows progressively worse

Radiographic findings show joint effusions and osteopenia with erosions/ loss of cartilage

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16
Q

Rheumatoid nodules

A

Infrequent manifestations of RA but occur in subcutaneous tissues in forearm elbow and occiput

Resemble necrotizing granulomas

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17
Q

Seronegative spondyloarthropathies

A

Heterogenous group of disorders

All share the following characteristics:

  • Absence of rheumatoid factor
  • ligamentous attachments pathogical changes, not synovium.
  • associated with HLA-B27 gene impairments
  • leads to ankylosis
  • usually involves in sacroiliac joints if joint issues
  • are immmune mediated and triggered by T-cells that cross-react with self-antigens on bones and ligaments.
18
Q

Ankylosis spondylitis

A

Prototypical spondyloarthropathy

Directly affects peripheral joints and spine and appears bamboo like in the spine.

90% of all patients are HLA-B27 positive

Anti IL-17 antibody can treat it

19
Q

Reactive arthritis

A

“Triad of arthitis”

  • nongonococcal urethritis
  • cervicitis
  • conjunctivitis
  • HLA-B27 positive and tends to affect men in their 20-30s
  • Hypothesized to be autoimmune related, initially caused by a GI or GU infection
  • Ankles, feet and knees are most commonly affected and show an asymmetric pattern
  • can be indistinguishable from ankylosis spondylitis if severe.
20
Q

Psoriatic arthritis

A

Chronic inflammatory arthropathy marked with psoriasis affecting peripheral and axial joints ligaments and tendons.

Affects both sexes equally at ages 30-50

Can be a secondary disease to psoriasis but usually isn’t

HLA-B27 and HLA-Cw6 genes affected

Most common site is distal interphalngeal joints producing a “pencil in the cup” appearance radiographically

21
Q

Calcium pyrophosphate crystal deposition disease (Pseudogout)

A

Also known as CPPD

Has 3 types, sporadic, hereditary and secondary

  • autosomal dominant variant is hereditary through germline

Caused by degradation of articular cartilage proteoglycans, allowing crystals to form around chondrocytes

  • usually found in 50 years plus
  • associated with hyper parathyroidism
22
Q

Gout

A

1st crystal induced arthritis introduced

  • crystals are monosodium urate crystals in joints and surrounding soft tissues during acute arthritis attacks

Can be primary or secondary (cause unknown)

23
Q

Joint mice, fibrous-walled cysts and bone eburnation

A

Found in OA especially late stages

Joint mice = dislodged pieces of cartilage or bone that break off and tumble around in the joint

Bone eburnation: polished ivory appearance of bone caused by direct subchondral bone rubbing together

Fibrous walled-cysts: small fractures that have forced synovial fluid within them

24
Q

Usual treatment of OA

A

NSAIDs

Intra articular corticosteroids (if permitted)

Arthroplasty if severe

Educate the patient for good health habits

25
Q

Citrullination of proteins

A

AA arginine is converted into citrulline. (Turns polar into non polar so less functional protein)

  • immune system does not recognize this as self and attacks it.
  • catalyzed by arginine deiminases.
26
Q

Pannus

A

A mass of edematous synovium, inflammatory cells, granulation tissue and fibroblasts that grow over the articular cartilage and causes erosion of the cartilage

If untreated, can cause ankylosis by “bridging” the bones in the joint.

Found in RA

27
Q

Treatment of RA

A

Corticosteroids

Methotrexate

TNF antagonists
TNF is most effective cytokine to treatment against for RA

28
Q

Gout pathogenesis

A

Hyperuricemia (above 6.8mg/dL plasma urate) is necessary, but does not definitively prove gout.

Hypothesized to include abnormal purine production since purine catabolism produces Uric acid

  • repeated acute arthritis attacks leads to TOPHI formation (aggregates of urate crystals and inflamed tissue)
  • can form pannus as well if not treated.
29
Q

Primary vs secondary gout

A

Primary gout: elevated uric acid levels caused by decreased excretion which is unknown as to why.

Secondary gout: increased production of purine or decreased excretion.
- increased production is caused by rapid cell lysis and tumor lysis syndrome

30
Q

Factors that lead to gout

A

Genetic predisposition

Alcohol consumption

High BMI

High fructose levels

Being male

Possessing metabolic syndrome or having renal failure past/present.

31
Q

4 clinical stages of Gout

A

Asymptomatic hyperuricemia: usually around puberty and after menopause

Acute arthritis: several years after asymptomatic
- marked by sudden excruciating joint pain, localized hyperemia and warmth

Asymptomatic intercritical period: after resolution of acute arthritis
- marked by symptom free interval w/ occasional mild flare ups that are polyarticular

Chronic tophaceous Gout: 12 years after acute arthritis
- forms tophi

32
Q

Most common place for acute gout

A

1st metatarsal forms podagra

33
Q

Gout treatment

A

Lifestyle modifications

Xanthine oxidase inhibitors are 1st line in chronic only

NSAIDs are first line in acute only

34
Q

CCPD pathogenesis

A

Unknown

  • however is suggested that articular cartilage proteoglycans are degraded which always for pyrophosphate crystals to form.
  • usually appears 1st in IVDs and meniscus (articular cartilage)
  • usually less inflammation than gout
  • likely in patients with chondrocalcinosis appearance
35
Q

CCPD morphology

A

Oval blue-purple aggregates

  • individual crystals appear rhomboid shaped and are blue due to positive birefringent properties
36
Q

Clinical course of CCPD

A

Usually asymptomatic at first

  • can produce acute or chronic arthritis if left untreated
  • can be mono or polyarticular
  • 50% of all infected will experience significant joint damage at some point
  • no treatment to slow disease progression
37
Q

Etiology of septic arthritis

A

Hematogenous spread

Extension of localized ST infections

Direct introduction to pathogen via trauma

38
Q

Most common agents for septic arthritis

A

Staph Aureus is the most common agent for non-Gonoccal

Strep pneumoniae and B-hemolytic step are next

*gonorrhoeae is the most common in sexually active patients and Gonoccal form

39
Q

Risk factors for developing septic joints

A

Prosthetics

Unprotected sex

RA

+ 80 yrs of age

Have diabetes

IV drug abuse

40
Q

Levels of white blood cells with respect to synovialjoint issues

A

Non inflammatory = 0-2000 mg/dL
- OA, traumatic arthritis, CCPD

Inflammatory = 2000mg/dL
- RA, seronegative polyarthropathies

Septic = 20,000 mg/dL
- septic arthritis

Musculoskeleton (36 decks)

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