Assignent Solutionnurs

#1. Myasthenia Gravis/ NMJ
The neuromuscular junction (NMJ) location is the connection between the terminal end of a motor nerve and a muscle (Omar et al., 2021). The muscle may be skeletal, smooth, or cardiac (Omar et al., 2021). The transmission of action potential from a nerve to a muscle occurs at NMJ (Omar et al., 2021). NMJ is also a site for the action of many drugs and a potential area for developing many diseases (Omar et al., 2021). Upon depolarization, an action potential voyages down the axon, causing voltage-gated calcium channels to open, resulting in an influx of calcium ions into the nerve terminal. This causes the vesicles to migrate towards the nerve terminal membrane and fuse with the active zones (Omar et al., 2021). The released acetylcholine (ACh) binds with ACh receptors at the postsynaptic part of NMJ (Omar et al., 2021). The binding results in the opening of ACh gated ion channels that allow the influx of sodium ions into the muscle (Omar et al., 2021). The sodium exchange process creates voltage change which generates muscle contraction (Omar et al., 2021). ACh is then metabolized by acetylcholinesterase (Omar et al., 2021).
Breathing, ingestion, skin contact with organophosphate (OP), pesticides, or specific nerve agents used in warfare can cause levels of acetylcholine in the body to elevate (Berry, 2019).
In myasthenia Gravis (MG), auto-antibodies attack ACh receptors, resulting in a decrement in the availability of ACh receptors (Omar et al., 2021). Hence, it prevents endplate potential and muscle contraction (Omar et al., 2021).
Pyridostigmine is a reversible acetylcholinesterase inhibitor and reverses muscle relaxants’ effects (Clinicalinfo, 2021). Pyridostigmine works by inhibiting the acetylcholinesterase (AChE) enzyme from breaking down the neurotransmitter acetylcholine (ACh) and thereby increasing the bioavailability of ACh and enhancing the transmission of nerve impulses at neuromuscular junctions (Clinicalinfo, 2021).
References:
Berry, J. (2019). Acetylcholine: What it is, function, and links with health. Medical and health information. https://www.medicalnewstoday.com/articles/326638#toxins-and-pesticides
Clinicalinfo. (2021). Pyridostigmine – Health professional | NIH. Clinicalinfo | Information on HIV/AIDS Treatment, Prevention and Research | NIH. https://clinicalinfo.hiv.gov/en/drugs/pyridostigmine/health-professional#:~:text=Pyridostigmine%20is%20a%20reversible%20acetylcholinesterase,the%20effects%20of%20muscle%20relaxants.&text=It%20has%20also%20been%20used,the%20chemical%20nerve%20agent%20Soman
Omar, A., Marwaha, K., & Bollu, P. (2021, May 9). Physiology, neuromuscular Junction – StatPearls – NCBI bookshelf. National Center for Biotechnology Information. https://www.ncbi.nlm.nih.gov/books/NBK470413/#:~:text=The%20neuromuscular%20junction%20(NMJ)%20is,action%20for%20many%20pharmacological%20drugs
#2. Osteoarthritis
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Hermenegildo Potestades posted Apr 19, 2022 2:29 PM
Hermenegildo “Jun” Potestades
Eight Week’s Initial Post: Osteoarthritis
Osteoarthritis is “a disease of articular cartilage and subchondral bone in diarthrodial joints” (MSN 570, 2022).
Articular Cartilage and Subchondral Bone
Articular Cartilage
According to Zhu et al. (2021), osteoarthritis is caused by articular cartilage loss and degradation. Damage to articular cartilage, hyaline connective tissue, and its function in diarthrodial joints are all affected (Zhu et al., 2021). For example, articular cartilage cannot “absorb” (Zhu et al., 2021) joint movement shock. In addition, chondrocytes in articular cartilage multiply and manufacture proteoglycan and collagen molecules to maintain the cartilaginous matrix (Johns Hopkins Arthritis Center, 2022). However, as osteoarthritis progresses, cartilage loss thwarts reparative efforts (Johns Hopkins Arthritis Center, 2022). In addition, brittleness, “erosion, and cracking” (Johns Hopkins Arthritis Center, 2022) start at the cartilage’s surface and progress deeper, resulting in clinically evident erosions. When the cartilage matrix in the joints starts to break down, it does not get better very quickly (Johns Hopkins Arthritis Center, 2022).
Subchondral Bone
Because the subchondral bone is weak, it cannot keep the joint tissue homeostasis (Zhu et al, 2021) that it needs to keep. The subchondral bone, which includes the subchondral trabecular bone and the subchondral cortical plate, can no longer provide “mechanical [support]” (Zhu et al, 2021). Articular cartilage lacks low-friction surfaces for “weight-bearing and joint [motion]” (Zhu et al, 2021). Early osteoarthritis reduces the thickness of the subchondral cortical plate even when the articular cartilage is healthy (Zhu et al, 2021). The subchondral trabecular bone also loses bone. Some trabeculae fail badly, while others thicken a little (Zhu et al, 2021). Sclerosis of the subchondral trabecular bone occurs with late osteoarthritis (Zhu et al, 2021).
The Role of Osteophytes in Osteoarthritis
When subchondral bone stiffens and infarcts, subchondral cysts and osteophytes develop at the joint margin (Kontzias, 2020). These osteophytes, such as “fibroblasts, mesenchymal pre-chondrocytes, maturing chondrocytes, hypertrophic chondrocytes, and osteoblasts” (Wong, Chin, & Yan, 2016), aim to support the joint in which they are located (Kontzias, 2020). Breaking off pieces of osteophytes and cartilage into the synovial cavity causes inflammation and enlargement of the synovium (Dlugasch & Story, 2021, p. 612). Inflammatory mediators and proteases are produced by inflammation (Dlugasch & Story, 2021, p. 612). However, they do not induce osteoarthritis (Dlugasch & Story, 2021, p. 612). Localized damage or obstructive repair of the matrix and cells might weaken and loosen surrounding muscles and ligaments (Dlugasch & Story, 2021, p. 612). These modifications induce “joint space narrowing, instability, stiffness, and pain” (Dlugasch & Story, 2021, p. 612). Unbeknownst to the 65-year-old man, these alterations cause a “significantly swollen [and] painful left finger [which he is] unable to bend” (MSN 570, 2022).
NSAIDS
NSAIDS, or nonsteroidal anti-inflammatory drugs, are used to treat a variety of ailments (Gorczyca et al., 2016). If acetaminophen does not work for osteoarthritis pain, these drugs do (Gorczyca et al., 2016). The drug’s blood-borne suppression of COX-1 and COX-2 reduces thromboxane and prostaglandin production (Gorczyca et al., 2016). These include “leukotriene [suppression], lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation” (Gorczyca et al., 2016), and other cell membrane activities.
Inflammation is caused by an enzyme called cyclooxygenase (COX), also known as prostaglandin synthase (PGS) synthase (Batham, 2011). COX transforms arachidonic acid into prostanoids (Batham, 2011). Prostaglandins E, D, and F2a are also prostaglandins (Batham, 2011). The two most important are PGE2 and prostacyclin (Batham, 2011). Thromboxane also helps platelets clot (Batham, 2011). PGD2 helps allergic reactions, and PGF2a helps the uterus contract (Batham, 2011).
Excess Weight and Weight Loss in Osteoarthritis
The cartilage between bones in joints wears off over time, causing osteoarthritis (Griffin, 2017). Osteoarthritis affects the “hands, knees, hips, back, and neck” (Johns Hopkins Arthritis Center, 2022).
Excess Weight
Excess weight or being overweight may affect osteoarthritis. Excess weight may increase stress on joints, such as the knee, leading to cartilage degeneration (Johns Hopkins Arthritis Center, 2022). Walking, for example, applies a force three to six times one’s body weight over the knees (Johns Hopkins Arthritis Center, 2022). Several studies have linked hand osteoarthritis to excess weight, indicating a “circulating systemic” (Johns Hopkins Arthritis Center, 2022) component.
Weight Loss
Weight loss can help treat osteoarthritis. Weight loss, says Summut, relieves knee and hip discomfort (Griffin, 2017). Excess weight causes stress on the body, which causes wear and tear (Griffin, 2017). A “10-pound weight loss can [eliminate] 30-40 pounds of [knee] pressure” (Griffin, 2017) when walking. Losing weight may reduce edema-causing proteins (Griffin, 2017). Fat cells induce edema and joint injury (Griffin, 2017). Weight loss can help reduce edema and fat in non-weight-bearing joints (Griffin, 2017).
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