Nursing Essay on Arthritis & Non-Steroidal Anti-Inflammatory Drugs

Question

Task: Write a nursing essay on the topic “Arthritis and non-steroidal anti-inflammatory drugs (NSAIDs)”. Your essay must describe the pathophysiology of a specific disease or condition, as well as present the pharmacology that is used to address this.

Answer

Arthritis and Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)
Arthritis is a disease in which one or more synovial joints become inflamed and sore. Its primary symptoms are joint stiffness and discomfort(Aletaha&Smolen, 2018).There are several types of arthritis, but the common ones are osteoarthritis and rheumatoid arthritis (RA). In osteoarthritis, the cartilage deteriorates faster than its regeneration, while in RA, the immune system attacks and destroys the joints and its surroundings. The treatment is primarily aimed at managing the symptoms to improve the quality of the patients' lives. Nonsteroidal Anti-inflammatory Drugs (NSAIDs) are the majorly used drugs for pain management treatment(Bullock et al., 2018).

Normal Physiology and Homeostasis of The Joints
There are several types of joints in the human body, with a synovial joint being the most common. A synovial joint cavity is an essential structural feature that fibrous or cartilage joints lack. The articulating surfaces of the bones meet in this fluid-filled region. The articular surfaces of synovial joints are lined with smooth articular cartilage. This enables the bones of the synovial joint to move in lockstep, leading to greater joint mobility(Mazaleuskaya et al., 2015).Synovium lines all synovial joints and are specialized connective tissue that is essential for maintaining the intra-articular environment by protecting the synovial membrane, lubricating the articular surface, and maintaining synovial fluid. It is necessary to protect the synovial surface in order for it to remain non-adherent to the joint components. The synovium serves as a selective barrier, preserving the composition and volume of synovial fluid, which nourishes chondrocytes inside the extracellular matrix's avascular matrix. Hyaluronate formation increases the viscosity of synovial blood, adding cushioning between articular surfaces(Redondo et al., 2019).

Figure 1: Synovial Joint

Pathophysiology
Pathophysiology of Rheumatoid Arthritis (RA)
Synovitis, stiffness, and joint injury are all symptoms of active rheumatoid arthritis. These symptoms are caused by various autoimmune and inflammatory pathways affecting elements of both the innate and adaptive immune systems. Synovitis is a condition that occurs as a result of leukocyte invasion of the synovium(Aletaha&Smolen, 2018). The synovium's accumulation of leukocytes is not due to local cellular proliferation but due to leukocyte movement from othergrowth sites in reaction to adhesion molecules and chemokines released by activated endothelial cells in synovial micro-vessels. The inflamed synovium's interior is hypoxic, most likely due to synovial cell proliferation and reduced synovial capillary flow due to elevated synovial fluid thickness(Derksen et al., 2017).

Pathophysiology of Osteoarthritis
As the rate of fracturing approaches the rate of healing, bone and cartilage degenerate, impairing the joint's ability to dissipate load efficiently. This results in a biomechanical and biochemical degeneration mechanism. The shock-absorbing cartilage gradually deteriorates, raising the load on the bone and eventually causing bone harm (bone marrow lesions). This results in increased cartilage erosion, shrinking of the joint gap (the space between the bones), and bone overgrowth (osteophyte formation), resulting in painful lumps around the joints. Additionally, the degenerative joint disease results in painful and tender synovial lining inflammation (synovitis) and joint swelling (effusion). Though cartilage, bone, and the synovial lining are all necessary components of the joint, pathogenesis occurs in the joint(Stewart &Kawcak, 2018).

Pharmacological Treatments
NSAIDs are often used in rheumatology due to their anti-inflammatory and analgesic effects. Apart from rheumatoid arthritis (RA) and osteoarthritis (OA), NSAIDs are often used to alleviate the symptoms of other rheumatic disorders characterized by chronic musculoskeletal inflammation and various types of acute pain. Ibuprofen was chosen as the test drug(Vina et al., 2020).

Ibuprofen is (2RS)-1[4-(2-methyl propyl) phenyl] propionic acid (BP. 2004). Ibuprofen was the first propionic acid product to be marketed as a safer option to Aspirin in 1969. Ibuprofen is available in tablet form in doses ranging from 200 to 800 mg. The recommended dosage is 400–800 mg three times daily. The drug is completely removed from the body 24 hours after the last dose via metabolism. The drug is highly protein-bound, heavily metabolized in the liver, and only a small amount is excreted unchanged(Shin et al., 2017).

Pharmacodynamics
Ibuprofen is an over-the-counter nonsteroidal anti-inflammatory medication (NSAID) that is often used for its analgesic, anti-inflammatory, and antipyretic properties. It is used to aid in the relief of arthritis symptoms. Ibuprofen blocks the synthesis of prostaglandins from arachidonic by inhibiting the enzyme cyclooxygenase (COX). COX is needed for the body's conversion of arachidonic acid to prostaglandin H2 (PGH2)(Shin et al., 2017). Prostaglandins are then synthesized using the PGH2. Ibuprofen activates COX, causing the body to produce a small number of prostaglandins. Prostaglandins are needed for the transmission of impulses such as pain and inflammation. Antipyretic signs can be caused by hypothalamic relaxation, which results in vasodilation, increased peripheral blood flow, and heat dissipation. Additionally, COX inhibition regulates anticoagulant effects by converting arachidonic acid to thromboxane A2, a critical component of platelet accumulation that results in the formation of blood clots. COX is synthesized in the body in two ways: COX-1 and COX-2. NSAIDs inhibit COX-2, while COX-1 inhibition blocks thromboxane production (Vina et al., 2020).

Pharmacokinetics
Ibuprofen is quickly and completely absorbed after oral administration (depending on the active drug for 1–2 hours); unbound concentrations adopt a linear pharmacokinetic pattern at widely used doses. At clinical concentrations, it is firmly linked to plasma proteins (>98 percent). While Ibuprofen can displace other medications with a strong affinity for protein binding, agents with a low extraction ratio, such as warfarin and phenytoin, are unlikely to have clinically relevant drug-drug interactions as a result(Shin et al., 2017). While Ibuprofen, with its high affinity to plasma protéins, has a limited apparent amount of distribution (0,1–0,2 l/kg), it can file the central nervous system (CNS) and focus on peripheral locations where its analgesic and anti-inflammatory effects are needed. Ibuprofen is present in normal, unbound quantities in the cerebrospinal fluid and in the synovial fluid of arthritic patients' inflamed joints. Ibuprofen's analgesic, antipyretic, and anti-inflammatory properties are characterized by a broad clinical dose spectrum (10–50 mg/l) and a brief plasma half-life (t1/2, 1–3 h), which necessitates repeated administration to maintain therapeutic plasma concentrations(Jamali & Brocks, 2015).

Though some studies indicate that young children (0.5–5 years old) have higher clearances of Ibuprofen, in the pediatric population (> 0.5 years of age), the pharmacokinetic profile of Ibuprofen is equal in the majority with that of adults(Jamali & Brocks, 2015). However, the half-life of Ibuprofen in premature neonates is 30-45 hours after intravenous administration. It can be ascribed to a wide range of factors, including developed effects on the enzyme function of cytochrome P450 (CYP) and a reduction in glomerular filtration rate in neonates in comparison to adults.

Administration route
To be consumed orally. Ibuprofen can be used with meals for patients with upset stomachs. When administered shortly after eating, the start of action of Ibuprofen may be delayed. To be taken with or without food and, ideally, plenty of fluids.To prevent oral inflammation and throat pain, ingest ibuprofen tablets completely, without chewing, slicing, crushing, or sucking.

Contraindications, precautions, and adverse consequences
Ibuprofen is used to treat rheumatoid arthritis, ankylosing spondylitis, osteoarthritis, and other seronegative arthropathies (non-rheumatoid).Ibuprofen should not be used for patients who are allergic to either the active ingredient or the excipients. Additionally,Ibuprofen is associated with complications in patients with a history of gastrointestinal bleeding or ulceration due to previous NSAID therapy(Aletaha&Smolen, 2018).It is also not prescribed for patients with severe heart failure, liver disease, or renal disease. Additionally, it is contraindicated during pregnancy's final trimester.

Owing to an elevated risk of ulceration or bleeding, Ibuprofen should not be used in conjunction with other nonsteroidal anti-inflammatory medications (NSAIDs), including selective cyclooxygenase-2 antagonists. Additionally, prolonged alcohol use in conjunction with NSAIDs, such as Ibuprofen, can increase the chance of developing an adverse gastrointestinal (GI) bleeding or central nervous system injury.

Gastrointestinal effectsare the most often reported adverse events. Complications such as peptic ulcers, perforation, or abdominal bleeding are likely. These complications may be fatal in the elderly. Ibuprofen administration has been associated with nausea, puking, bloating, indigestion, stomach pain, ulcers, and GIbleeding(Aletaha&Smolen, 2018). Additionally, NSAIDs have been linked to oedema, hypertension, and heart problems. Clinical trials also indicate that taking Ibuprofen at elevated doses of more than 2400 mg/day can raise the risk of arterial thrombotic events such as myocardial infarction or heart attack(Aletaha&Smolen, 2018).

Other Treatments
Adults with rheumatic conditions and musculoskeletal discomfort are often advised to relax and engage in moderate physical exercise on a daily basis. Aerobic fitness and physical therapy are both recommended by the American College of Rheumatology and the American Pain Society(Aletaha&Smolen, 2018). Additionally, flexibility/range of motion exercises can help relieve some of the effects of rheumatic disorders, including fatigue, weakness, and reduced mobility.

Relevance to Clinical Practice
Learning about arthritis and its pharmacological treatments is beneficial to any clinical practice because it will help to distinguish the diseases from other differential diseases. Besides, learning about the various drugs that are used to relieve the symptoms is also crucial. It shows who to give the drugs, the risks associated, the precautions, and the long-term side effects.

Conclusion
Arthritis is a common inflammatory condition that causes swelling and inflammation of the joint's synovium and often results in the deterioration of both the bony and cartilaginous components of the joint if left untreated. Arthritis' pathophysiology varies according to its form. Additionally, the therapy entails the use of NSAIDs, which are primarily used to alleviate discomfort. Additionally, there are nonpharmacological therapies that require exercise. Thus, to obtain the best outcomes, arthritis treatment can include both pharmacological and nonpharmacological components.

References
Aletaha, D., & Smolen, J. S. (2018). Diagnosis and Management of Rheumatoid Arthritis. JAMA, 320(13), 1360. https://doi.org/10.1001/jama.2018.13103

Aletaha, D., & Smolen, J. S. (2018b). Diagnosis and Management of Rheumatoid Arthritis. JAMA, 320(13), 1360. https://doi.org/10.1001/jama.2018.13103

Bullock, J., Rizvi, S., Saleh, A., Ahmed, S., Do, D., Ansari, R., & Ahmed, J. (2018). Rheumatoid Arthritis: A Brief Overview of the Treatment. Medical Principles and Practice, 27(6), 501–507. https://doi.org/10.1159/000493390

Derksen, V. F. A. M., Huizinga, T. W. J., & van der Woude, D. (2017). The role of autoantibodies in the pathophysiology of rheumatoid arthritis. Seminars in Immunopathology, 39(4), 437–446. https://doi.org/10.1007/s00281-017-0627-z

Jamali, F., & Brocks, D. R. (2015). The Pharmacokinetics of Ibuprofen in Humans and Animals. Ibuprofen, 81–131. https://doi.org/10.1002/9781118743614.ch4

Redondo, M. L., Christian, D. R., &Yanke, A. B. (2019). The Role of Synovium and Synovial Fluid in Joint Hemostasis. Joint Preservation of the Knee, 57–67. https://doi.org/10.1007/978-3-030-01491-9_4

Shin, D., Lee, S. J., Ha, Y. M., Choi, Y. S., Kim, J. W., Park, S., & Park, M. K. (2017). Pharmacokinetic and pharmacodynamic evaluation according to absorption differences in three formulations of Ibuprofen. Drug Design, Development and Therapy, Volume11, 135–141. https://doi.org/10.2147/dddt.s121633

Stewart, H. L., &Kawcak, C. E. (2018). The Importance of Subchondral Bone in the Pathophysiology of Osteoarthritis. Frontiers in Veterinary Science, 5, 1. https://doi.org/10.3389/fvets.2018.00178

Vina, E. R., Hannon, M. J., Masood, H. S., Hausmann, L. R., Ibrahim, S. A., Dagnino, J., Arellano, A., &Kwoh, C. K. (2020). Nonsteroidal Anti-Inflammatory Drug Use in Chronic Arthritis Pain: Variations by Ethnicity. The American Journal of Medicine, 133(6), 733–740. https://doi.org/10.1016/j.amjmed.2019.11.016