inflammatory joint conditions

Question 1

rheumatoid arthritis

Answer 1

aetiology–> overractive immune system
clinical features–> inflammation, swelling, bulge at joint lining, cartilage and bone destruction, bursitis, nerve compression, decreased ROM
xray findings–> fusiform soft tissue swelling and juxtaarticular osteoporosis, malalignment, uniform cartilage space narrowing, and bone erosions. MRI- synovitis, tendon damage, and bone erosion
pathophysiology–> initiation of disease seems to result from an interaction among genetic susceptibility, environmental triggers, and chance. RA is characterized by dysregulated inflammatory processes in the synovium of the joint that eventually leads to the destruction of both cartilaginous and bony elements of the joint, with resulting pain and disability
management–> medication (NSAIDs), corticosteroids, disease modifying anti-rheumatic drugs, biologics, cold/ hot therapies, physical therapies, splints

Question 2

reactive arthritis

Answer 2

=Reactive arthritis develops in reaction to an infection in your body, often in your intestines, genitals or urinary tract
aetiology–> bacteria, sexually transmitted infections, foodborne infections
clinical features–> pain/ stiffness, eye inflammation, urinary problems, inflammation of tendons and ligaments, swollen toes/ fingers, rashes, lower back pain
xray findings–> Soft tissue swelling, Bilateral asymmetrical distribution, Juxta-articular osteoporosis, Uniform joint space loss, Bone proliferation
pathophysiology–> an immune-mediated syndrome triggered by a recent infection. It is hypothesized that T lymphocytes are induced by bacterial fragments when invasive bacteria reach the systemic circulation. These activated cytotoxic-T cells then attack the synovium and other self-antigens through molecular mimicry. It is believed thatanti-bacterial cytokine response is also impaired in reactive arthritis, resulting in the decreased elimination of the bacteria
management–> medication (NSAIDs, steroids, rheumatoid arthritis drugs), physical therapy

Question 3

gout

Answer 3

=form of arthritis
aetiology–> urate crystals accumulate in joint- form when there’s high levels of uric acid in blood (produced when body breaks down purines)
clinical features–> sudden attacks of pain/ swelling, redness, tenderness in joints (most common in hallux), feeling of big toe being on fire, limited ROM
findings–> can only be done in active flare up. lab tests look for uric acid crystals in joint. xray- ASYMMETRICAL POLYARTICULAR DISTRIBUTION, TOPHI, PUNCHED-OUT EROSIONS, PRESERVED JOINT SPACE
pathophysiology–> occurs in response to the presence of monosodium urate (MSU) crystals in joints, bones, and soft tissues. It may result in one or a combination of acute arthritis (a gout flare), chronic arthritis (chronic gouty arthritis), and tophi (tophaceous gout)
management–> NSAIDs, change to lifestyle and diet, prevent tophi and kidney stones

Question 4

pseudo gout

Answer 4

=a form of arthritis
aetiology–> calcium pyrophosphate crystals
clinical presentation–> swollen, warm, severely painful
findings–> blood tests- check for thyroid and parathyroid glands and mineral imbalances linked to pseudogout. fluid sample. xrays- joint damage and crystal deposits in joint cartilage
pathophysiology–> Calcium pyrophosphate crystal formation and deposition
management–> medications (NSAIDs, Colchicine, Corticosteroids), joint drainage, rest, ice

Question 5

polymyalgia rheumatica

Answer 5

= an inflammatory disorder that causes muscle pain and stiffness, especially in the shoulders and hips
aetiology–> genetics, environmental exposure (possibly viral)
clinical presentation–> aches/ pains in shoulder/ neck/ upper arms/ buttocks/ hips/ thighs, stiffness in affected areas, limited ROM, stiffness in am especially
findings–> blood tests- erythrocyte sedimentation rate (sed rate) and C-reactive protein will be high. imaging tests- distinguish polymyalgia rheumatica from other conditions
pathophysiology–> an immune-mediated disorder, and elevated inflammatory markers are one of the mostcommon features. IL-6 appears to have a central role in mediating inflammation
management–>medications (corticosteroids, calcium and vitamin D, Methotrexate), physical therapy, lifestyle change

Question 6

ankylosing spondylitis

Answer 6

=chronic inflammation of the spine
aetiology–> gene HLA-B27 forming reactive arthritis due to klebsiella infection
clinical presentation–> back pain/ stiffness, pain/ swelling in other parts of the body, extreme fatigue
findings–> xray- check for changes in joints and bones. MRI- more-detailed images of bones and soft tissues. lab tests- Blood can be tested for the HLA-B27 gene
pathophysiology–> The primary pathology of spondyloarthropathies is enthesitis with chronic inflammation, including CD4and CD8T lymphocytes and macrophages. Cytokines, particularly tumor necrosis factor-α (TNF-α) and transforming growth factor-β (TGF-β), are also important in the inflammatory process by leading to inflammation, fibrosis, and ossification at sites of enthesitis
management–> medications (NSAIDs, TNF blockers), physical therapy