Osteoarthritis & Rheumatoid Arthritis Flashcards by Jordan Cyr

What is osteomalacia?

softening of bones as a result of inadequate mineralization of the organic matrix (osteoid)

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What causes osteomalacia?

deficiency of vitamin D (dietary or lack of sun)
inadequate metabolic processing and activation of vit D
disturbances of phosphate metabolism

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What is osteomalacia called in children?

Rickets

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What is the etiology of vitamin D deficiency?

inadequate intake (malnutrition, dietary restrictions)
inadequate exposure to sunlight
abnormal intestinal absorption
hypophosphatemia
-renal disease (kidney unable to retain P)
-excessive losses or failure to add P to bone leads to
osteomalacia

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What is the pathology of osteomalacia?

excess nonmineralized osteoid
bone deformities and fractures
serum calcium and phosphorus low

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What are the consequences of rickets?

bowlegs
widened costochondral junction (rachitic rosary)
craniotabes (bulging forehead)
delayed dentition

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What are the symptoms of osteomalacia?

bone fractures with very little injury
muscle weakness
widespread bone pain, especially in the hips
symptoms due to low calcium:
-abnormal heart rhythms
-numbness around mouth
-numbness of arms and legs
-spasms of hands or feet

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What is the most common joint disease, especially with old age?

osteoarthritis

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What part of the body does osteoarthritis affect?

weight-bearing joints but also small joints of hands and feet

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True or false: those of smaller stature are more commonly impacted by osteoarthritis and prior injury has no impact on a patients pre-disposition

false
more commonly larger persons
prior injury may pre-dispose

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What are the classifications of osteoarthritis?

primary: cause unknown or multifactorial
secondary: related to another disease

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What is the pathology of osteoarthritis?

irregular joint space
fragmented cartilage
loss of cartilage
sclerotic bone
cystic change
advanced stage:
-osteophytes
-periarticular fibrosis
-calcified cartilage

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What are the symptoms of osteoarthritis?

pain
crepitus (joint noises)
swelling and warmth
joint deformation
loss of normal mobility

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What is the management of osteoarthritis?

exercise: for ROM, muscle strength, weight loss
PT/OT, assistive devices
analgesics, NSAIDs, corticosteroids, hyaluronic acid
surgery: joint replacement

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What is rheumatoid arthritis?

chronic multisystem disease primarily involving the joints

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How do we characterize rheumatoid arthritis?

chronic, symmetrical inflammatory synovitis
joint destruction
muscle atrophy
bone destruction

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Aside from joints, what are other areas of the body that may be affected by rheumatoid arthritis?

lungs (fibrosis/nodules)
eyes (dry)
blood vessels (vasculitis)
skin (ulcers)

What is the pathogenesis of rheumatoid arthritis?

earliest pathology is microvascular injury and increase in the number of synovial cells
rheumatoid synovium is characterized by presence of a number of secreted products of activated lymphocytes, macrophages, and altered fibroblasts
local production of cytokines and chemokines accounts for many of the pathological and clinical manifestations of RA

What is the management of rheumatoid arthritis focused on?

reducing inflammation and suppressing the immune response

What is a pannus?

abnormal, hypertrophied synovium, an abnormal tissue that develops in the rheumatic joint
causes tissue destruction because it releases damaging enzymes, proteins, and acids that break down bone and cartilage leading to joint destruction

What are the stages of rheumatoid arthritis?

synovitis
pannus
fibrous ankylosis
bony alkylosis

What is the MOA of hydroxychloroquine for RA?

raises lysosomal pH in APCs, thereby reducing antigen processing efficacy
less self-proteins being presented as antigens to be attacked
older DMARD, works slowly

What is the MOA of sulfasalazine for RA?

older DMARD, works slowly
prodrug–>5-ASA + sulphapiridine (5-ASA is not absorbed)
multiple mechanisms:
-effects on bacterial flora in gut
-inflammatory cell function, cytokine and Ab production
-inhibition of folate-dependent enzymes
-inhibition of synovial neovascularization
-increase in free radical scavenging activity

What is the MOA of minocycline for RA?

complex mechanisms:
-reduces IL-10, suppresses B and T cells
-reduces NO synthase (enzyme that breaks down cartilage)
-synergistic with NSAIDs

What is the MOA of methotrexate for RA?

inhibits purine and pyrimidine synthesis adenosine receptor agonist reduces IL-6, IL-1, and TNF-alpha complex effects on immune cell proliferation and activity

True or false: methotrexate works slowly

false works quickly

Differentiate rheumatoid arthritis vs osteoarthritis.

rheumatoid: -typically very stiff and lasts >1hr after waking -pain and stiffness gets better through the day -fatigue -soft tissue swelling osteoarthritis: -tend to transiently stiff for seconds-minutes after waking -problems worsen through the day on activity -post rest stiffness (gelling) is typical and lasting secs-mins

What is ankylosing spondylitis?

form of chronic inflammation of the spine and sacroiliac joints -chronic inflammation in these areas=pain and stiffness in and around the spine -over time can lead to complete fusion of the affected vertebrae -fatigue is common during active inflammation

What are other organs that can be affected by ankylosing spondylitis?

eyes heart lungs kidneys

Who is typically affected by ankylosing spondylitis?

young men but also children *HL-B27 gene is present (90%)*

What is the pathogenesis of ankylosing spondylitis?

initial inflammation may be a result of an activation of the body's immune system, perhaps by a preceding bacterial infection (Yersinia, Salmonella) or a combination of infectious microbes once activated, the body's immune system becomes unable to turn itself off, even though the initial bacterial infection may have long subsided

True or false: bones are the primary structure affected in ankylosing spondylitis

false ligaments more than bones

What is psoriatic arthritis?

chronic joint inflammation associated with psoriasis -30% of psoriasis patients

What are the DMARDs for arthritis?

conventional: -methotrexate -sulfasalazine -hydroxychloroquine -leflunomide biologics: -TNF inhibitors -B cell depleting agents -T cell modulators -IL6 inhibitors -Il17 inhibitors targeted synthetic: -JAK inhibitors

What are the treatments for joint pain in psoriatic arthritis?

NSAIDs (ibuprofen, naproxen, Rx NSAIDs) DMARD: reduce tissue damage and disease progression -methotrexate, leflunomide, sulfasalazine immunosuppressants: reduce autoimmune inflammation -azathioprine, cyclosporine TNF-a inhibitors: reduce joint swelling, pain and stiffness -etanercept, infliximab, adalicumab, golimumab, certolizumab

What are the risks associated with TNF-a inhibitors?

serious infections and malignancy allergic reactions development of inactivating antibodies liver toxicity

What is septic arthritis?

join infections joints may be infected with pyogenic bacteria or TB

How is septic arthritis usually derived?

hematogenous route of spread -gonorrhea (F>M, young adults), bacterial endocarditis -staphylococci, streptococci, pneumococci, gram - rods -in children usually due to H. influenzae

How many joints are usually affected by septic arthritis?

usually one large joint (monoarticular) TB: spine wrist, knee, hip, ankle, elbow or shoulder synovial membranes become edematous and congested, joint fills with pus could ulcerate and affect the articular cartilage, leading to joint destuction

What puts someone at greater risk of septic arthritis?

aging population resistance to antibiotics orthopedic procedures immunosuppressive agents diabetes, leukemia, cancer, etc

What is the pathogenesis of osteomyelitis?

pathogens are seeded into the bone inflammatory response, with pus formation, tissue destruction and systemic symptoms of acute inflammation local edema puts pressure on vascular supply, compromising blood flow local necrosis can result