NURS 6501 Knowledge Check: Neurological And Musculoskeletal Disorders

Pathophysiology; Urate crystals are formed when the body breaks down purines a naturally occurring substance in the body and found in red meat and mostly raised when high fructose sugar is ingested having hypertension and being obese.  Formation of uric acid occurs and this substance is excreted by the kidney, in this case, the kidney may have failed to eliminate the uric acid and what happens next is that the uric acid dissolves in blood and is transported in the body. When this acid reaches the joints, it forms sharp urate crystals in the joint tissues. this causes pain, swelling, and inflammation of the joint hence the symptoms that are brought in by the patient.

Gout depends on metabolic processes. Purines must first be available and then breaking down leads to the formation of way too much uric acid that the kidneys. Kidneys are then overwhelmed in excreting, and, therefore, leading to retention in the blood that leads to urate crystals forming.

in summary: Gout is caused by a defect in purine metabolism and kidney function. Uric acid is a byproduct of purine nucleotides. People with gout may have an elevated level of purine synthesis accompanied by a rise in uric acid levels.

Gout is an inflammatory response to excessive quantities of uric acid in the blood and other body fluids including synovial fluid. The elevated level of uric acid lea to the formation of monosodium urate crystals in and around joints. When the uric acid levels exceed approximately 6.8 mg/dl, it crystalizes and forms an insoluble precipitate that are deposited into connective tissue through the body. When crystallization occurs in synovial fluid, it triggers Tumor Necrosis Factor (TNF)-α, which causes the release of inflammatory cytokines and interleukins. The result is an acute inflammatory response within the joint.

Gout is caused by a defect in purine metabolism and kidney function. Uric acid is a byproduct of purine nucleotides. People with gout may have an elevated level of purine synthesis accompanied by a rise in uric acid level.

Most uric acid is eliminated from the body through the kidneys. Urate is filtered at the glomerulus and undergoes reabsorption and excretion within the proximal renal tubules. In primary gout, urate excretion by the kidneys is sluggish. This may be caused by a decrease in glomerular filtration of urate or acceleration in urate reabsorption. This allows for urate crystals to be deposited in the renal tubules.

The two types of osteoporosis are primary and secondary. Primary osteoporosis, the most common is hormone mediated where bone loss is accelerated by declining levels of estrogen in women and testosterone in men. Secondary osteoporosis is caused by other conditions including endocrine disorders such as hyperparathyroidism, hyperthyroidism, diabetes mellitus,  also certain medications like heparin, corticosteroids, phenytoin, barbiturates, and lithium, as well as tobacco and alcohol.

There are three major bone cells that are involved in the formation, maintenance, and reabsorption of bone. Osteoblasts are immature bone cells that under ideal circumstances allow the bone to be formed and laid down. Osteocytes are cells that are responsible for the normal maintenance, or the cycle, of bone. Osteocytes removed old bone cells which allow the osteoblasts to form new bone.

Osteoclasts are responsible for the reabsorption of bone. Hormonal influences remain important in maintaining bone health, but new research has demonstrated that genetic factors and the role of oxidative stress also contribute to the development of osteoporosis. Reactive oxygen species (ROS) serve as signaling molecules for osteoblasts, osteocytes, and osteoclasts. An imbalance between osteoblast formation and osteoclast reabsorption is the primary cause of osteoporosis.

Osteoporosis is considered a metabolic bone disease. Osteoporosis, also called porous bone, is the most common bone disease in humans. Its main features include low bone mineral density, impaired structural integrity of bone, decreased bone strength and increased risk of fractures. The two types of osteoporosis are primary and secondary. Primary osteoporosis, the most common is hormone mediated where bone loss is accelerated by declining levels of estrogen in women and testosterone in men. Secondary osteoporosis is caused by other conditions including endocrine disorders (hyperparathyroidism, hyperthyroidism, diabetes mellitus) and certain medications such as heparin, corticosteroids, phenytoin, barbiturates, and lithium) as well as tobacco and alcohol. There are three major bone cells that are involved in the formation, maintenance, and reabsorption of bone. Osteoblasts are immature bone cells that under ideal circumstances allow bone to formed and laid down. Osteocytes are cells that are responsible for the normal maintenance, or the cycle, of bone. Osteocytes removed old bone cells which allows the osteoblasts to form new bone. Osteoclasts are responsible for reabsorption of bone. Hormonal influences remain important in maintaining bone health, but new research has demonstrated that genetic factors and the role of oxidative stress also contributes to the development of osteoporosis. Reactive oxygen species (ROS) serve as signaling molecules for osteoblasts, osteocytes, and osteoclasts. An imbalance between osteoblast formation and osteoclast reabsorption is the primary cause of osteoporosis.

Osteoarthritis (OA) is localized destruction of articular cartilage which can either be idiopathic or secondary. Secondary OA is due to a prior injury or infectious process that may affect the normal cartilage. Primary OA is very common in people >65 years of age and there is a strong correlation between obesity and the development of OA. OA is a non-inflammatory disease process

Rheumatoid arthritis is an inflammatory, systemic disease that is autoimmune in nature. Symptoms are mediated by antibodies against self-antigens and inflammatory cytokines, especially CD4+ T cells that promote inflammation. Multiple inflammatory cells are involved, and TNF and Interleukin-1 stimulate the synovial cells to secrete protease that damages the hyaline cartilage. The inflammatory cytokines convert the synovium into an abnormally thick layer of granulation tissue called pannus. The pannus acts like a locally invasive tumor. Pannus is the tissue responsible for destruction of the articular cartilage. The other inflammatory mediators affect the soft tissue structures like the tendons, ligaments, and even the valves of the heart, especially the aortic valve. Long standing inflammation causes interstitial fibrosis of the lungs which reduces pulmonary function. Osteoarthritis (OA) is localized destruction of articular cartilage which can either be idiopathic or secondary. Secondary OA is due to a prior injury or infectious process that may affect the normal cartilage. Primary OA is very common in people >65 years of age and there is a strong correlation between obesity and the development of OA. OA in a non-inflammatory disease process

One of the earliest steps in lesion formation is the breakdown of the blood-brain barrier. Enhanced expression of adhesion molecules on the surface of lymphocytes and macrophages seems to underlie the ability of these inflammatory cells to penetrate the blood-brain barrier. The elevated immunoglobulin G (IgG) level in the cerebrospinal fluid, which can be shown by an oligoclonal band pattern on electrophoresis, suggests an important humoral (i.e., B-cell activation) component. Variable degrees of antibody-producing plasma cell infiltration have been demonstrated in MS lesions. The patient’s symptoms are directly related to the inflammation and demyelination of the nerve sheath. The short-term memory loss indicates that there may be demyelinating lesions in the brain as well.

MS is a chronic inflammatory disease involving degeneration of CNS myelin, scarring (or sclerosis or plaque formation) and loss of axons. It is caused by an autoimmune response to self or microbial antigens in genetically susceptible people. The usual age of onset is between 20 and 40 years of age and is more common in women. When reviewing the demyelinating lesions in the spinal cord and brain of patients with MS shows myelin loss, destruction of oligodendrocytes, and reactive astrogliosis, often with relative sparing of the axon cylinder. In some MS patients, however, the axon is also aggressively destroyed. One of the earliest steps in lesion formation is the breakdown of the blood-brain barrier. Enhanced expression of adhesion molecules on the surface of lymphocytes and macrophages seems to underlie the ability of these inflammatory cells to penetrate the blood-brain barrier. The elevated immunoglobulin G (IgG) level in the cerebrospinal fluid, which can be shown by an oligoclonal band pattern on electrophoresis, suggests an important humoral (i.e., B-cell activation) component to. Variable degrees of antibody-producing plasma cell infiltration have been demonstrated in MS lesions. The patient’s symptoms are directly related to the inflammation and demyelination of the nerve sheath. The short- term memory loss indicates that there may be demyelinating lesions in the brain as well.

After platelets are activated, procoagulant platelet microparticles are released, and thrombocytopenia occurs. This is followed by the production of thrombin, and activation of inflammatory cells, and injury to the endothelium which produce the arterial and venous thrombus features observed in HIT. The ris of HIT increases with continued use of thrombophylaxis post-operatively. However, it can also develop even with minor exposure to heparin through intravascular flushes especially when trying to maintain patency of an indwelling venous catheter. The platelets usually collect in the micro-circulation to form an emboli or thrombus. In large arteries of lower and upper extremities, the formation of arterial emboli can lead to necrosis if not promptly identified.

The platelets aggregate in the microcirculation, leaving to systemic thrombocytopenia but the platelets clump together and form thrombi and emboli. Arterial emboli usually form in the larger arteries of the upper and lower extremities and if not identified quickly, limb necrosis occurs. Treatment is not warfarin which could lead to skin necrosis but rather withdrawal of the heparin and the use of thrombin inhibitors such as argatroban.