NUR 425 Week 10 Osteoarthritis & Rheumatoid Arthritis PDF

**[Week 10 -- Osteoarthritis & Rheumatoid Arthritis ]** [ ] **[Osteoarthritis]** - Progressive, degenerative disease of the joints - Most commonly affects hips, knees, spine, hands - Most people over the age of 40 have radiologic evidence of osteoarthritis - May be secondary to a c...

**[Week 10 -- Osteoarthritis & Rheumatoid Arthritis ]** [ ] **[Osteoarthritis]** - Progressive, degenerative disease of the joints - Most commonly affects hips, knees, spine, hands - Most people over the age of 40 have radiologic evidence of osteoarthritis - May be secondary to a condition or trauma, but many cases have no single cause **Risk factors (osteoporosis)** - Increased Age - Obesity more weight on the bearing joints - Traumatic injuries or overuse of joints in athletes - Assigned female at birth biomechanical load, estrogen levels - Genetic traits **Structure of synovial joint (ask phuc for notes)** - Synovial joint accounts for ½ of the joints in the body - Cartilage provides cushioning - Degrades over time until none left aka. Wear and tear - Synovial membranes -- produce fluid, nourishing the joint and cartilage - Often see inflammation (synovitis) in OA - Responsible for some of the clinical manifestations - Synovial fluids -- reduce friction - See changes in the composition of the fluid and quantity in OA - Joint capsule -- provide stability in the joint - Can become stiff and less flexible in OA - Subchondral bone - Supporting the cartilage - Absorbing the impact of movement - OA lead to increased bone density less able to absorb shock - Often sees bone spurs (osteocytes) - See cartilage degradation, mechanical load transfer to underlying bone bone remodelling denser and less structurally sound - Microcracks and less ability to absorb shock - Remodelling cause osteocytes at the edge causing pain upon movement **Cartilage & osteoarthritis** - Cartilage is created by cells called chondrocytes - Articular cartilage cushions the joints - With osteoarthritis, there is the degeneration of this cartilage - Healthy cartilage is smooth, white & translucent with degeneration, cartilage becomes yellow, dull & granular **Clinical manifestations of OA** - Joints - Pain -- impact QoL, ability to do things - Stiffness -- most noticeable in the morning OA resoles in 30 mins in the morning; RA lasts for longer bc of inflammatory response - Crepitation -- grading sensation and indicating those cartilage surfaces are not smooth anymore - Unilateral -- inflammatory joint conditions are often bilateral, but OA can be unilateral  - Early changes in OA - Gradual destruction of the articular cartilage - See joint space that are now narrow - Synovium (lining of the joint) becomes inflamed - Contribute to pain, swelling, stiffness - Joint capsule can be inflamed and filled with fluids - Cartilage splitting and eroded - Later changes in OA - Formation of osteophytes (bony outgrowths) due to increased mechanical stress and frictions - Subarticular bone cysts occur bc of the degeneration and inflammatory system with OA weaken bone over time - Further loss of cartilage until bone grinding on bone Reduces mobility OA: Commonly affected joints Carpometacarpal (CMC) joint (Lewis, 2023, p. 1667) Hip proximal interphalangeal (PIP) Cervical vertebrae Lower lumbar vertebrae (MCP) Distal interphalangeal (DIP) Metatarsophalangeal (MTP) - Hips are supporting body weight - Upper body C spine - Lumbar, shoulders, ankles depend on previous injury and usage on a daily basis **Clinical manifestations of Heberden's node and Bouchard's node** - H nodes inflammation on distal - B nodes proximal, less common - Both results from degradation of the cartilage - Significantly impact hand function - Pan management, PT, surgery, etc. **Evaluation** - History and physical exam - Joint pain, stiffness, functional limitations - Previous injury - Family hx genetics - MSK: look at the joint, swelling, crepitations, ROM, stiffness, pain - Expect to see stiffness and crepitation on movement - ROM: functionally reduced if progressive OA, and PAIN - X-ray - Subchondral sclerosis: thickening of the bone beneath cartilage in joints, often as result of OA. - Radiological sign of the disease and is commonly found in the knees, hips, spine, and ankles - Synovial fluid analysis (not done commonly) - Not necessary to confirm diagnosis but to eliminate other conditions **Management (conservative)** - Nonpharmacologic interventions should be tried first - Need to balance rest & activity - Nutritional therapy and exercise - Exercise has similar function and activity as NSAIDs - Eating healthy diet - Weight management - Possible use of splint or brace with certain movement - Heat or cold application - Complementary & alternative therapies (e.g. acupuncture, massage, supplements) **Management (pharmacologic & surgical)** - Based on symptom severity - Mild to moderate pain: acetaminophen - Moderate to severe pain: NSAIDs - Topical (few joints, especially hand/knee) - Oral (multiple joints, hip OA) - Surgery (with advanced knee and hip OA when conservative therapies have failed to provide adequate relief); associated with risks, and about 20% reported moderate/severe long-term post-op pain **[Cyclooxygenase inhibitors ]** **Prostaglandins** - Prostaglandins are inflammatory mediators - They are pro-inflammatory, chemical messengers - Help promote inflammatory processes - Includes pain, inflammation, increased body temperature, plt aggregation A blue and black text Description automatically generated - Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase (COX), which inhibits production of prostaglandins **Two forms of cyclooxygenase (COX)** +-----------------------------------+-----------------------------------+ | **COX-1** | **COX-2** | +===================================+===================================+ | - Found in almost all tissues, | - Found mostly at sites of | | including tissue that | tissue injury, where it plays | | | a role in mediating | | - Protects gastric mucosa | inflammation | | | | | - Supports renal function | - Adverse effects of inhibiting | | | COX-2 are renal impairment, | | - Promotes plt aggregation | promotion of myocardial | | | infarction and stroke | | - Adverse effects of inhibiting | | | COX-1 are gastric erosion & | | | ulceration, renal impairment, | | | and bleeding | | +-----------------------------------+-----------------------------------+ **Non-steroidal anti-inflammatory drugs (NSAIDs)** - The first generation of NSAIDs are the most widely used - Inhibit COX-1 and COX-2 - NSAIDs inhibit prostaglandins help with inflammation and pain - Examples: - Aspirin (ASA) - Ibuprofen (Motrin, Advil) - Naproxen (Aleve) - Analgesic, antipyretic & anti-inflammatory - Take with food or large glass of water - Contraindicated in pregnancy (affects fetal heart and lungs development) - Avoid in children due to link with Reye's syndrome (ASA) -- swelling in the brain - Caution with asthma as allergic reactions are more common **NSAIDs: Adverse Effects** - Adverse effects are related to inhibiting cyclooxygenase - Platelet dysfunction - Impaired renal function - Renal insufficiency is a relative contraindication to NSAID use - GI effects: dyspepsia, ulceration, bleeding, perforation **NSAIDs: Risk of GI side effects** - Risk is influenced by dose of NSAID, length of time on medication, and patient characteristics - Risk factors: - History of an NSAID-induced ulcer - Prior ulcer disease - Older adults - Steroid use - Anticoagulant therapy **COX-2 Inhibitors** - Second generation of NSAIDs - COX-2 inhibitors do not inhibit COX-1 (fewer GI side effects) - Associated with increased risk for MI and stroke - COX-2 inhibitors are also associated with renal impairment - Only COX-2 inhibitor in Canada is Celecoxib (aka celebrex) - NSAIDs like Meloxicam and Diclofenac found to be more selective for COX-2 (but also inhibit COX-1) **Acetaminophen (Tylenol)** - Acetaminophen is a weak inhibitor of cyclooxygenase - Able to decrease prostaglandin synthesis in the central nervous system, and in this way, is thought to reduce fever and pain - Mechanism of action is not well understood - Max daily dose = 4 grams/day in healthy individuals - Use caution and lower doses with: - Regular heavy drinking - Older adults - Malnourishment - Active liver impairment - Coumadin use - Lower doses: 2.6 grams/day **[Rheumatoid Arthritis ]** - Systemic, autoimmune disease -- may be genetic & environmental triggers - Inflammation of connective tissue in the synovial joints - Pain and swelling degrading the joints - Considered the most disabling form of arthritis - Incidence peaks between ages 30-50 - More often affects individuals who are assigned female at birth **Autoimmune theory of rheumatoid arthritis** 1. Presence of antigen triggers formation of an abnormal IgG 2. Autoantibodies form against this abnormal IgG 3. Autoantibodies & the abnormal IgG create an immune complex (in synovial membrane) 4. Inflammatory response - Autoantibodies: rheumatoid factor (RF), Anticitrullinated protein antibody (ACPA)  +-----------------------------------+-----------------------------------+ | **Early stage of RA** | Early stage of (Lewis, 2023, p. | | | 1674) Thick synovium Fibrin | | - Synovium thickened, inflamed | Lymphocyte infiltrate Inflamed | | leads to pannus formation | synovium Soft tissue swelling | | later in progression | | | | | | - Lymphocytes infiltrate joint | | | space immune response | | | | | | - The infiltration is the body | | | response trying to fight | | | against what it perceives as | | | threats autoimmune type of | | | condition | | | | | | - Perpetuates the cycle of | | | inflammatory system and bone | | | degradation | | | | | | - Reduces ROM | | | | | | - Joint pain | | +===================================+===================================+ | **Moderate stage of RA** |  | | protein | | | | | | - Granulation develops new type | | | of connective tissue | | | | | | - Inflamed synovial tissue | | | produce pannus destroying | | | joint periphery | | | | | | - Causing pain, difficult with | | | movement | | | | | | - Pannus can degrade or destroy | | | bone below | | +-----------------------------------+-----------------------------------+ | **Severe stage of RA** | stage of (Lewis, 2023, p. 1674) | | | Loss of bone density Joint | | - Affecting joint, significant | deformity c Destruction of | | impairment | cartilage Erosion of edges of | | | bone Increased soft tissue | | - Loss of bone density | swelling due to inflammation and | | overactivity of osteoclast | thickening of synovium and | | (for bone resorption) joint | capsule | | deformity | | | | | | - Continued destruction of | | | cartilage causing increasing | | | pain and stiffness | | | | | | - Erosion of bone edges as it | | | progresses | | | | | | - Further joint stability and | | | deformity | | | | | | - Seeing things like soft | | | tissue swelling and | | | thickening of synovial | | | membrane and joint capsule | | | pain and reduced ROM | | +-----------------------------------+-----------------------------------+ **Clinical manifestations of RA** - Onset of disease is usually subtle - Joint pain - Any joint can be affected but early in the course of RA, the joints most commonly involved include: - Small joints of the hands and feet, wrists, elbows, shoulders, knees, ankles - Stiffness (Joint stiffness lasts longer than OA) - Loss of motion of affected joints - Low-grade fever - Deformity and disability with severe disease **Rheumatoid arthritis deformities/disabilities** +-----------------------------------+-----------------------------------+ | **Ulnar Drift** | **Boutonniere deformity** | | | | |  | generated | | | | | | - Splinting | | | | | | - Surgical intervention to help | | | improve functionality of | | | hands | +===================================+===================================+ | **Swan neck deformity** | **Foot issues & deformities** | | | | |  | A diagram of a foot with | | | rheumatoid problems Description | | - Hyperextension of proximal | automatically generated | | and flexion of distal because | | | of inflammation | - Makes walking/standing still | | | challenging | | | | | | - Characteristic skin rashes | | | from vasculitis | | | | | | - Lumps under the skin pressure | | | points or causing pain, if | | | rubbed against shoes | +-----------------------------------+-----------------------------------+ | **Rheumatoid Nodules** | - In areas that are subject to | | | pressure (heel or forearms) | |  | | | | - Inflammatory cells or | | | dead cells | | | | | | - Seen on CXR, not a major cell | | | concern unless affecting ADL | | | or gets infected | +-----------------------------------+-----------------------------------+ **Evaluation of RA** - - History and physical exam - Low grade fever, fatigue, tenderness etc. - Laboratory tests to confirm diagnosis and monitor disease - Rheumatoid factor (RF) -- specific marker 80% - Erythrocyte sedimentation rate (ESR) - C-reactive protein (CRP) - ACPA (anti-cyclic citrullinated peptide antibodies) - Antinuclear antibody (ANA) - To identify signs of inflammation - Synovial fluid analysis -- most specific - Imaging - X-ray - Bone scan **Management of RA** - Pain management - Rest and exercise - Address quality of life - Pharmacologic management - NSAIDs - Corticosteroids -- rapid relief, short course only - DMARDs -- targeted treatment early and aggressive use of DMARDs +-----------------------------------+-----------------------------------+ | **DMARDs** | **Conventional DMARDs** | | | | | - Disease modifying | - **Methotrexate** | | anti-rheumatic drugs | *(chemotherapy)* is typically | | | the first DMARD prescribed | | - Used in RA to suppress the | | | immune system | - MOA is not clear | | | | | - Conventional | - Folate antagonist -- inhibit | | | enzymes that metabolize | | - Biologic | folate | | | | | | - Target DNA synthesis, | | | cell replication improves | | | immune system activity | | | | | | - AEs: skin reaction, bone | | | marrow suppression, fibrosis | | | of the liver ulcerations of | | | the GI tract, pneumonitis | | | | | | - Recommended that pts take | | | folic acid as a supplement | | | | | | - Teratogenic | | | | | | - Be careful if pregnant | +-----------------------------------+-----------------------------------+ **OA vs RA** **OA** **RA** --------------------- --------------------------------------------------------------------------------------------------- --------------------------------------------------------------------------------------------------------- **Disease** Degenerative Autoimmune **Manifestations** Morning stiffness lasting less than 30 min; joint pain, muscle weakness, reduced motion, creaking Morning stiffness lasting more than 30 min; joint pain, inflammation, nodules, fatigue, fever, anorexia **Age** Generally affects older adults Can affect people of any age, peak age b/w 30-50 **Onset** Develops gradually over years Can develop and worsen over weeks or months **Patho** Cartilage loss Inflamed synovium **Joints involved** Hip, knee, lower back, feet and fingers Can appear in any joint, most common targets are hands, wrists and feet **Symmetry** Asymmetrical Symmetrical