Pathophysiology Question

Pathophysiology Question

1. Explain the pathophysiology of gout

Gout is a heterogeneous group of disorders related to the genetic defect of purine metabolism resulting in hyperuricemia. Uric acid is over secreted in the body. Defects in the renal system result in the decreased excretion of uric acid, or both cause hyperuricemia (Hinkle & Cheever, 2018). The disorder occurs most commonly in males than females. Incidences are increased with advanced age and high body mass index. There is primary and secondary hyperuricemia. The elevated urate levels or manifestations of urate depositions are due to faulty uric acid metabolism in the primary hyperuricemia.

It’s caused by severe dieting or starvation, hereditary or increased intake of food that contains purine in large amounts (shellfish, organ meat) (Hinkle & Cheever, 2018). Secondary occurs due to genetic or acquired processes, including conditions that increase cell turnovers, such as leukemia and psoriasis. Also, an increase in cell breakdown is a precipitating factor (Hinkle & Cheever, 2018). Altered renal tubular function due to unintended side effects of certain pharmacological agents (thiazides diuretics and furosemide), low dose salicylates, or ethanol are attributed to the decreased excretion of uric acid.

Hyperuricemia, a serum uric concentration of above 7mg/dl, causes gout syndromes (Manish & Leslie, 2021). The normal concentration of uric acid is between 2-7mg/dl. This leads to the deposition of urate crystals in the synovial fluid, joints, or articular cartilage resulting in an inflammatory response and the beginning of gout attacks. Repeated attacks cause the accumulation of sodium urate crystals known as tophi to be deposited in the peripheral areas of the body, such as the great toe, hands, or ear (Hinkle & Cheever, 2018). The buildup of uric acids crystals in the joints causes pain, increased serum concentration, inflammation, and swelling.

2. Explain why a patient with gout is likely to develop renal calculi

Renal stones are formed when there is an increase in the concentration of uric acid, calcium oxalate, and calcium phosphate(Hinkle & Cheever, 2018). In patients with gout, there is hyperuricemia. The kidneys will increase urinary excretion of uric acid to regulate its composition in blood. Increased composition of uric acids in urine persistently lowers the urinary pH leading to supersaturation dependent on the pH of urine. A decrease in urine pH forms uric acid stones by inducing uric acid dissolution and acid-base status. Uric acid's solubility depends on pH, and a persistent decrease in urine pH, mostly 5.5 or less, enhances crystallization of the acids resulting in renal stones (Manish & Leslie, 2021). Gout patients have periods of immobility due to the severe pain they experience. This slows down renal drainage and alters the metabolism of calcium hence promoting the development of renal calculi.

3. Describe osteoporosis and how it develops pathologically.

Osteoporosis is characterized by reduced bone mass, deteriorations of the bone matrix, and diminished bone architectural strength. The quality and quantity of the bones are reduced due to the alteration of normal homeostatic bone turnover. The rate of bone resorption maintained by osteoclasts becomes greater than the rate of bone formations maintained by the osteoblasts (Hinkle & Cheever, 2018). This causes a reduction in the total bone mass and density. The bones, therefore, become progressively brittle, porous, and fragile resulting in easy fractures under minimal stress, which would not have occurred in normal circumstances. Advanced age causes a decrease in the physiological functions in the body, such as the reduction in the production and secretions of hormones required for normal body functions. Estrogen, calcitonin, and testosterone are some of the hormones that inhibit bone loss. However, its levels are decreased with increased age and menopause in women; hence susceptibility to bone fracture risk is high.

4. The patient had various symptoms. Explain how these factors are associated with RA and what is the difference between RA and OA.

Rheumatoid arthritis is characterized by recurrent inflammation of the joints and surrounding soft tissues. It causes ulnar deviation of the fingers, small muscle wasting, synovial swelling at the carpus, metacarpophalangeal and proximal interphalangeal joints (Hinkle & Cheever, 2018). The symptoms begin with bilateral inflammation of certain joints, often leading to deformities. It commonly affects the small joints of the hands and feet. These are accompanied by swelling, pain, fatigue, and fever. RA occurs due to T cell-mediated immune response, whereby the body attacks the joints' lining and joints (Williams & Hopper, 2015). It can occur at any age. On the other hand, OA is more common later in life (Hinkle & Cheever, 2018). It's caused by mechanical wear and tear of the joints. It affects the cartilage, causing them to soften, crack, fray, and erode. It's also non-inflammatory.

5. Describe what is MS and how did it cause the above patients' symptoms?

Multiple sclerosis is a chronic demyelinating disease of the CNS associated with abnormal immune responses to an environmental factor. Autoimmune responses cause inflammation that destroys the myelin sheath leading to axon dysfunction (Williams & Hopper, 2015). Demyelination refers to the destruction of myelin, the fatty and protein material that surrounds certain nerve fibers in the brain and spinal cord; it results in impaired transmission of nerve impulses (Hinkle & Cheever, 2018). Neurons of the spinal cord, brain stem, cerebrum, cerebellum, and optic nerve are affected. Damage to the optic nerves causes blurred vision, visual field deficits, and optic neuritis, all symptoms experienced by the patient. Involvement in the brain stem causes nystagmus, cognitive dysfunctions, weakness, and bladder and bowel dysfunctions. Manifestations depend on the site affected.

References

Hinkle, J. L., & Cheever, K. H. (2018). Brunner and Suddarth’s textbook of medical-surgical nursing. Wolters kluwer india Pvt Ltd.

Manish, K. C., & Leslie, S. W. (2021). Uric Acid Nephrolithiasis. In StatPearls [Internet]. StatPearls Publishing.

Williams, L. S., & Hopper, P. D. (2015). Understanding medical surgical nursing. FA Davis.