Discussion

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Etiology

Osteoarthritis (OA) is the most common form of arthritis affecting peripheral and central joints, including the hips, knees, hands, and spine (O’Brien et al., 2019). OA occurs due to the degeneration and loss of cartilage, osteophytes, and changes within the subchondral bone. It is highly associated with aging and the incidence and prevalence of OA increases with age. OA can also occur after joint injury, obesity due to weight-bearing, genetics, and anatomic factors, such as congenital acetabular dysplasia or valgus/varus alignment (O’Brien et al., 2019).

Presentation

Clinical manifestations include joint pain, stiffness, and limited restriction. Narrowing of the joint space due to cartilage loss causes pain and stiffness which is provoked by overuse of the joints or weight-bearing, but can be relieved by rest (O’Brien et al., 2019). Stiffness is worse in the morning but lessens within minutes of movement. Other manifestations include muscle weakness, poor balance, and comorbidities. The clinical marker for generalized OA is the presence of Heberden nodes, which are swellings of the DIP joints, and Bouchard nodes which are swellings of the PIP joints (Cibulka et al., 2017).

Differential Diagnosis

OA is commonly confused with rheumatoid arthritis when it involves the joints of the hands. The stiffness typically worsens after any effort in OA while in RA it worsens after resting. Another DD is psoriatic arthritis as it targets the DIP joints similar to OA. However, psoriatic arthritis may only affect just one finger and there are characteristic changes of the nail (Cibulka et al., 2017).

Diagnostic work-up

Diagnosis is based on the patient’s signs and symptoms. Clinical diagnosis includes persistent usage-related joint pain, age >45 years, and morning stiffness lasting <30 minutes (Cibulka et al., 2017). Imaging modalities can be utilized to assess the presence and severity of OA; however, it is not a routine test to consider. Treatment plan/Preventative measures The goals of OA management include pain management and optimize function. Patients should initially exercise for weight management and use assistive devices if required. Pharmacologic therapy should be initiated if the patient’s symptoms are severe and there is no response to the initial nonpharmacologic measures. The main medication of OA includes oral and topical NSAIDs and duloxetine can be considered with multiple joints and concomitant comorbidities that may contraindicate the use of NSAIDs (Cibulka et al., 2017). Surgical treatment is considered for patients with severe knee and hip OA. Referrals For surgical considerations, a referral should be made to an orthopedic surgeon. Other referrals for management may include a physical therapist, exercise program, and a nutritionist for weight loss. Geriatric considerations OA is more common in older patients ages >50 years. Women present with pain and stiffness in the hands and knees whereas more men will experience pain in the hips (O’Brien et al., 2019). Therefore, due to joint pain, muscle weakness, and poor balance, geriatrics are at risk for falls and functional impairment. Additionally, patients with OA and concomitant comorbidities, such as diabetes and cardiovascular disease, are at the higher right of mortality.

References

Cibulka, M. T., Bloom, N. J., Enseki, K. R., Macdonald, C. W., Woehrle, J., & Mcdonough, C. M. (2017). Hip pain and mobility deficits – Hip osteoarthritis: Revision 2017. Journal of Orthopaedic & Sports Physical Therapy, 47(6), A1–A25. https://doi.org/10.2519/jospt.20170301

O’Brien, D. W., Chapple, C. M., Baldwin, J. N., & Larmer, P. J. (2019). Time to bust common osteoarthritis myths. New Zealand Journal of Physiotherapy, 47(1), 18-24. https://doi.org/10.15619/NZJP/47.1.03

Q-2

Giant cell arteritis is a systemic inflammatory vasculitis involving the medium to larger arteries and occurs most frequently in adults (Hayreh, 2021). This inflammatory process then leads to ischemia of the optic nerve with potential vision loss on the affected side, and a small chance that the contralateral side would be affected as well (Hayreh, 2021). The most common affected artery is the temporal artery, followed by the aorta, subclavian, iliac, ophthalmic, occipital and vertebral arteries (Ameer et al., 2021).

The exact etiology of giant cell arteritis is unknown, but there are hallmarks of the disease process especially in the arteries that are involved (Ameer et al., 2021). One factor that is known is that it is due to the dysregulation of the innate immune system of the body’s response to vascular endothelial injuries (Ameer et al., 2021).

There are some common presentations with Giant Cell arteritis such as vague, non-specific constitutional symptoms such as fatigue, weight loss, anorexia, and malaise (Ameer et al., 2021). Other common presentations include headaches, jaw claudication, temporal artery abnormality like enlargement, swelling, tenderness, or loss of pulses (Ameer et al., 2021). There could also be visual symptoms, polymyalgia rtheumatica, neurological symptoms, respiratory symptoms, and extracranial symptoms (Ameer et al., 2021).

Evaluation begins with lab workup where a marked elevation in the ESR is the hallmark of the acute phase of the disease process (Ameer et al., 2021). Normally a highly elevated ESR of 50mm/hr is found in these patients (Ameer et al., 2021). Other elevated labs include CRP which serves as a sensitive marker of inflammation, and serum IL-6 levels (Ameer et al., 2021). With lab values elevated, and positive history and physical, the next step to confirm would be a histopathological confirmation of the temporal artery which is known as the gold standard diagnostic test (Ameer et al., 2021).

There is a growing number of providers who utilize CTA and MRAs of the vascular system to locate and diagnose giant cell arteritis instead of biopsy (Ameer et al., 2021).

Treatment includes a corticosteroid trial of at least one year, with the addition of one of the following: Tocilizumab (IL-6 inhibitor), Methotrexate, and Asprin, with the overall goal of preventing vision loss or worsening of vision loss (Ameer et al., 2021).

An important note regarding the use of chronic corticosteroid use in the geriatric population is that chronic corticosteroids reduce bone density which increases the risk to the elderly of fractures or breaks when the patient falls (Ameer et al., 2021). It is imperative that the patient’s functionality be considered when preparing to prescribe chronic corticosteroid treatments (Ameer et al., 2021).

References:

Ameer, M.A., Peterfy, R.J., Bansal P, et al (2021). Temporal Arteritis. StatPearls Treasure Island StatPearls Publishing. Retrieved from: https://www.ncbi.nlm.nih.gov/books/NBK459376/

Hayreh, S. S. (2021). Giant cell arteritis: Its ophthalmic manifestations. Indian Journal of Ophthalmology, 69(2), 227–235. https://doi-org.lopes.idm.oclc.org/10.4103/ijo.IJO_1681_20

Q-3

Rheumatoid Arthritis (RA)

Etiology: Rheumatoid arthritis (RA) is a chronic autoimmune disorder that involves multiple joints bilaterally characterized by inflammation of the tendon, resulting in both cartilage destruction and bone erosion. swelling primarily affecting the peripheral joints. The progressive damage of the synovial lined joints and variable extra-articular manifestations with tendon and bursal involvement.

Typical presentation: RA can affect any joint, usually affects metacarpophalangeal, proximal interphalangeal and metatarsophalangeal joints, wrist and knee joints and less affected joints were sacroiliac and the lumbar spine and distal interphalangeal and cricoarytenoid joints. Articular and periarticular manifestations include joint swelling and tenderness to palpation with morning stiffness and severe motion impairment in the involved joints. Insidious onset of pain with symmetric swelling of small joints is the most frequent findings. Monoarticular both slow and acute forms with extra-articular synovitis, polymyalgia-like onset, and general symptoms such as malaise, weight loss, fever. The joint symptoms are more apparent in the morning as joint stiffness lasting for an hour before maximal improvement is the typical sign of RA. Various extra-articular involvement such as rheumatoid nodules, vasculitis, hematologic abnormalities, Felty’s syndrome, and visceral involvement.

Common differential diagnosis: Pigmented villonodular synovitis, osteoarthritis, traumatic joint inflammation, Lupus erythematosus, osteomyelitis, and gout, spondylarthritis, neuropathic arthropathy, tuberculosis, fungal and rare parasitic infections, Crystal arthropathy, and underlying renal diseases (Sarazin, Schiopu, & Namas, 2017).

Diagnosis tests: Physical examination shows diffuse swelling of the joints affected, joint tenderness, and warmth, and loss of anatomical markings. Clinically synovial thickening within finger joints, hand joints soft tissue swelling, and mild juxta-articular osteoporosis. Systemic inflammation is the classic feature of RA which includes ESR, Rheumatoid factor, and CRP and ESR provide the best information on the acute phase (Sarazin, Schiopu, & Namas, 2017). Plain radiography is the standard test to assess the extent of erosive changes in rheumatoid arthritis in patients. US shows effusion with hyperemia supporting underlying synovitis and MRI and CT and scintigraphy and high power doppler ultrasound may reveal extensive distention of the joints with effusion withy blood products (Sarazin, Schiopu, & Namas, 2017). A synovial biopsy may show few plasma cells, lymphocytes and hemosiderin-filled macrophages are diagnostic for RA.

screening tools/diagnostic specific tools: according to Sarazin, Schiopu, & Namas, (2017), the 2010 CR/EULAR criteria for definite RA consist of a point-based system that includes four domains

1. Confirmed synovitis in at least one joint (higher scores are assigned by a higher number of small joints involved (0-5).

2. Presence of RA antibodies (RF and anti-cyclic citrullinated peptide antibody (anti-CCP) (0-3).

3. Elevated acute phase reactants (CRP) and ESR (0-1).

4. Symptom duration of 6 weeks or longer (0-1).

Treatment plan: Disease-modifying anti-rheumatic drugs (DMARDS) which target inflammation and thereby prevent further joint damage and greatly improves disease symptoms and prevent disease progression in RA patients. These DMARDS are 3 types which are 1. conventional synthetic (methotrexate, hydro chloroquine, and sulfasalazine) and 2. targeted synthetic DMARDs (pan-JAK-and JAK1/2-inhibitors) and 3. biologic DMARDs (tumor necrosis factor-alpha inhibitors, TNF receptor inhibitors, IL-6 inhibitors, IL-6 R inhibitors, B cell depleting antibodies, and inhibitors of co-stimulative molecules) (Lin, Anzaghe, & Schülke, 2020).

Prevention: The primary prevention is early identification of disease and starts the therapy on time. Other prevention is by accurately classifying the individual for progression to the next worse stage of disease, understanding the biology of disease in each stage on each individual, and providing optimal interventions. Managing comorbidities will prevent worsening of the rheumatoid arthritis and other complications.

Referrals: Referral to rheumatologist, spinal surgeon and orthopedic specialist, cardiologist, and other specialist depending on the type and nature of problems encountered.

Geriatric presentation and information: In the elderly RA characterized by polymyalgia rheumatica which is clinically indistinguishable, and the symptoms will be atypical leading to misdiagnosis as osteoarthritis instead of RA.

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