Kembara Xtra - Medicine - Osteoarthritis

Kembara Xtra - Medicine - Osteoarthritis 
​Primary osteoarthritis (OA) - Idiopathic: classified by clinical characteristics (localized, generalized, erosive) Progressive loss of articular cartilage with reactive alterations at joint borders and in subchondral bone


Secondary OA - Posttraumatic (e.g., ACL rupture, fracture of the distal radius, dislocation of the shoulder, etc.)
- Childhood anatomical anomalies (such as slipping capital femoral epiphysis [SCFE] and congenital hip dysplasia)
- Metabolic conditions that run in families, such as Wilson disease, alkaptonuria, and hemochromatosis
- Charcot joints affected by neuropathic arthropathy
- Acromegalic arthropathy, hyperparathyroidism, and hypothyroidism are endocrinopathies.
- Paget syndrome
- Non-infectious inflammatory arthritis, such as spondyloarthropathies and rheumatoid arthritis (RA)
Osteoarthrosis and degenerative joint disease (DJD) are synonyms for gout and calcium pyrophosphate deposition disease (pseudogout).

Epidemiology 
The most prevalent kind of joint disease in the United States, OA is most prevalent in individuals over 40, it is the leading cause of disability in people over 65, and it mostly affects weight-bearing joints.
Incidence
The prevalence of symptoms in the hip and knee is 88 per 100,000 and 240 per 100,000, respectively.
More than 30 million Americans are affected by the disease, and the prevalence rises with age; many people over 65 have radiographic evidence of OA.
 3-6% of white people have moderate-to-severe hip OA; 1% of East Asians, Blacks, Chinese, and Native Americans have.


Pathophysiology and Etiology 

failure of chondrocytes to keep the ratio of extracellular collagen matrix production to breakdown in check.
Proteoglycan matrix is altered as a result of collagen loss, which also increases susceptibility to degenerative change.


Genetics Up to 65% of OA cases may be inherited, while end-stage hip OA has a heritability of up to 27%.


Risk Elements 

 Growing older: >50 years
The main risk factor for hip and knee OA is age.
 Trauma, infection, or inflammatory arthritis Female gender (knee and hand) Obesity (weight-bearing joints); BMI >35

Prevention 
Weight management; frequent physical activity, peri-joint muscle strengthening—"prehabbing"

A rotator cuff tear may be accompanied by one or more of the following conditions: obesity, trauma history, or shoulder arthritis.

Diagnose OA by comparing it to other forms of arthritis based on the following criteria: - Absence of systemic symptoms - Minimal articular inflammation
- Location of the affected joints (such as the distal and proximal interphalangeal joints); OA is characterized by a gradually worsening joint pain. An aching or burning sensation is a common description of pain.
Numerous individuals report anecdotally that their pain changes as the weather does.
 Temporary stiffness that tends to go away 10 to 15 minutes following joint activity, notably after waking up in the morning and after sitting.
The hand's most typical joints are as follows:
- Thumb carpometacarpal > proximal interphalangeal > distal interphalangeal > MCP

clinical assessment 
Joint bony expansion
 Reduction in the range of motion in the afflicted joints
Particularly in knees with progressive meniscal damage, mechanical symptoms (clicking, locking) may be evident.
 Meniscus tear in the presence of advanced or terminal knee disease In the lack of mechanical symptoms, OA is an OA issue and should be treated as such.
Changes in joint alignment (genu varum [bowlegs] and genu valgum [knock-knees]) with OA of the spine; local discomfort and stiffness; radicular pain (if compression of nerve roots)

Differential diagnosis of inflammatory arthritides (RA), spondyloarthropathies (reactive arthritis; psoriatic arthritis), and septic arthritis in cases of crystalline arthropathies (gout; pseudogout).
 Lyme illness; avascular necrosis; and fibromyalgia

Laboratory Results 
Initial examinations (lab, imaging)
Regular chemistries are useless for diagnosis.
X-rays are typically normal in the early stages of an illness.
Plain films reveal the following changes as OA progresses: - Narrowed, asymmetric joint space, osteophyte formation, subchondral bone sclerosis, and subchondral cyst formation.
MRI may show chondral deterioration and related meniscal tears in particular. A 5–10% weight loss is linked to subchondral bone edema, decreased chondral loss, and a slowing of arthritic processes.

Tests in the Future & Special Considerations

 Keep an eye on NSAID therapy (renal insufficiency and GI hemorrhage).
abnormal lab findings connected to an underlying illness in secondary OA, such as hemochromatosis (abnormal iron tests),

Other Joint Aspiration/Diagnostic Procedures (often not required for diagnosis)
OA: typically 500 or less cells per millimeter, mostly mononuclear
 Cell count is often greater than 2,000 cells per millimeter, primarily neutrophils.
Test Interpretation for Birefringent Crystals in Gout () and Pseudogout (+)
Bony hypertrophy and patchy cartilage destruction are histologic stages.
- Subchondral bone trabecular microfractures and sclerosis with osteophyte formation - Extracellular matrix edema and cartilage microfissures - Subchondral fissuring and pitting - Erosion - and creation of osteocartilaginous loose masses

Management 
• Quadriceps strengthening for knee OA • Periscapular strengthening and range of motion for shoulder OA • Weight management together with exercise/physical therapy to preserve or recover joint motion and muscle strength
- Gait mechanics and abductor and core strengthening for hip OA
 Switch to non-weight-bearing workouts (such as the elliptical, stationary cycle, and swimming); Maintain activity; advantages are lost six months after stopping.
 Prevent misuse of joints; ambulatory aids and well-fitting footwear are helpful.
In individuals with biomechanical instability, bracing, joint supports, or insoles are more helpful in those who have unicompartmental illness of the knee. Numerous nonpharmacologic treatments, especially aerobic, aquatic, and/or resistance training, as well as weight loss, are highly advised for treating knee OA.

First Line of Medicine

 Controlling inflammation and discomfort
- Acetaminophen up to 1,000 mg TID: useful for OA of the knee and hip pain alleviation
- Topical NSAID gels and creams offer quick relief (4 weeks). The main treatment for OA of the hands and other joints with little soft tissue covering is topical NSAIDs.
- Consider an oral NSAID/COX-2 inhibitor if acetaminophen or topical NSAIDs are insufficient. Utilize the shortest time at the lowest effective dose.
- Use low-dose ibuprofen (1,600 mg/day) or nonacetylated salicylates (such as salsalate and choline-magnesium salicylate). If daily NSAIDs are required to ensure compliance, think about doing so.
- Although safe alternatives, the effectiveness of glucosamine sulfate and chondroitin sulfate is still up for debate.
 Contraindications to NSAIDs:
- Although the analgesic effects of the PO NSAIDs/COX-2 inhibitors are similar in strength, they differ in terms of their potential GI and cardiorenal damage.
- Patients with renal illness, CHF, HTN, active peptic ulcer disease, and prior hypersensitivity to an NSAID or aspirin should abstain from taking NSAIDs.
NSAIDs and full-strength aspirin (325 mg) should not be taken together.
- Combination of a nonselective NSAID plus low-dose aspirin (81 mg) is advised for people with a high cardiovascular risk.
- Corticosteroids used orally or parenterally are not advised.

Caution 

An increased risk of adverse cardiovascular events is linked to NSAIDS. The patient's age, comorbidities, the specific NSAID used, the dose, and the length of usage all affect the absolute risk.
 Safety measures:
Proton pump inhibitors are advised if PO NSAID/COX-2 inhibitor therapy is required for a patient who is older than 65 or who is younger than 65 and has higher GI-bleeding risk factors.
- Important potential interactions:
NSAIDs impair the efficiency of diuretics and ACE inhibitors.
NSAIDs and aspirin, but not COX-2 inhibitors, may make anticoagulants work more effectively.
Salicylates lessen the effects of uricosurics and spironolactone (Aldactone).
Ascorbic acid and ammonium chloride decrease salicylate excretion and may be hazardous, but corticosteroids and some antacids promote salicylate excretion.

ASA and NSAIDs have been linked to fetal risk throughout the first and third trimesters of pregnancy.
 Suitable for breastfeeding

Next Line
Capsaicin and topical NSAIDs can reduce the gastrointestinal and renal hazards connected to oral NSAID use.
 Bracing: Both lateral and medial unloader braces work well, and long leg alignment x-rays can aid choose the right brace.
TENS pain management techniques may be more effective than hyaluronic acid (HA) injections.


Fourth Line

Intra-auricular corticosteroid injections may be utilized for individuals who are experiencing acute flare-ups and are not responding to first- and second-line therapies. Reduce injections to three per joint annually at most.
While platelet-rich plasma (PRP) is a secure alternative for treating early-stage knee OA, it doesn't seem to have any therapeutic advantages over HA (4).
HA and PRP combination offered long-term alleviation and improved outcomes at 6 months in knee arthritis when compared to HA or PRP alone.
Cryotherapy combined with physical therapy is more effective than physical therapy alone for treating knee arthritis. Bone marrow aspirate concentrate (BMAC) injections show no difference in patient outcome in knee OA when compared to saline injections.


Referral criteria include: OA-related musculoskeletal injury, disease that is resistant to conservative treatment, worry about an infected joint or gout.

Further Therapies 

Discuss psychological variables, such as self-efficacy and coping mechanisms. Check for and treat depression and anxiety as needed. Boost the social network.


Total knee arthroplasty (TKA), total hip arthroplasty (THA), total shoulder arthroplasty (TSA), reverse total shoulder arthroplasty (RTSA), and total ankle arthroplasty (TAA) are all surgical procedures that patients with the aforementioned joint conditions still have as choices if conservative therapy is unsuccessful.
Patients who fail conservative treatment of the carpometacarpal joints have the option of undergoing ligament repair and tendon interposition (LRTI).
For the treatment of OA, knee arthroscopy is not typically advised in the absence of obvious mechanical symptoms (such as locking, clicking, etc.).

Healthcare Alternatives 
Nutritional supplements with low toxicity, such glucosamine and chondroitin sulfate, may help certain individuals.
Standardized outcome evaluations are lacking. There have been conflicting trial outcomes with glucosamine and chondroitin. Use should be stopped after six months if there is no response.
TENS, yoga, and acupuncture have all demonstrated advantages.

Follow-up Follow-up at 3-month intervals to evaluate the conservative management therapy and potential future courses of action.
 Suggest yearly plain films of the affected joint.

Patient observation
Assess functional status and range of motion on a regular basis.
• Periodic CBC, renal function tests, and stool for occult blood in patients on prolonged NSAID medication. • Monitor for GI blood loss and cardiac, renal, and mental state in elderly patients taking NSAIDs or aspirin.
DIET
Continue to make sure patients get enough vitamin D and have enough of it in their bodies to promote bone health.


Prognosis
​Chronic and progressive disease; early on, rest might relieve pain; later, pain may linger during sleep and at rest.
As the disease advances, joint effusions and hypertrophy may happen, particularly in the knees.
 The development of osteophytes (spurs), particularly near joint borders


Complications include impaired renal function on long-term NSAID or aspirin therapy, decompensated CHF, GI bleeding, and the primary source of musculoskeletal pain and disability.

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