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- Historical background of the Hypoparathyroid Disease
- Causes of Hypoparathyroidism
- Symptoms of Hypoparathyroidism
- Diagnosis of Hypoparathyroidism
- Prognosis and Progression of Hypoparathyroidism
- Current Research and Future Trends of Hypoparathyroidism
- Autoimmune Hypoparathyroidism
- Treatment
- References
Historical background of the Hypoparathyroid Disease
Bilezikian, Khan & Potts et al. (2011) indicate that hypoparathyroidism is caused by the reducing levels of parathyroid hormone (PTH) in the body, which is generated by parathyroid glands located around the neck area. The PTH controls the calcium and phosphorus concentrations in the blood. Therefore, if the secretion of PTH reduces, a patient is likely to generate minimal calcium amounts in contrast with the excess phosphorous content (Henderson & Mahony, 2005). Calcium is a vital necessity for human bodies since it is serves three primary functions. First, it supplies electrical energy to the body’s nervous system; thus, acting as a conductor of the electrical impulses of the messages throughout the body system. In addition, it provides energy for the muscles enabling their expansion or contraction. Variations of the calcium can cause muscle cramps (Bilezikian, Khan & Potts et al, 2011). The bones have storage systems to allow for absorption of calcium meaning that damage to parathyroid glands can result from injuries during surgical procedures or the genetic history of a person. Madam A is likely to suffer from similar conditions. Consequently, this paper will compare her symptoms and experiences with hypoparathyroidism.
Laboratory and radiological findings of Patient.
Causes of Hypoparathyroidism
According to Henderson & Mahony (2005), hypoparathyroidism is caused by various factors, which can lead to the destruction of parathyroid glands. Initially, the underdevelopment of the parathyroid glands or possible omission in one’s body may cause the ailment. Underdevelopment means the efficiency of the PTH secretion will not be optimal; therefore, the calcium production will not be sufficient. The incomplete development manifests itself in the branchial arches bringing about varying secretion of parathyroid and thymic hypoplasia (Hendy, Cole & Bastepe, 2011). Secondly, injury from the surgical treatment in the parathyroid gland can affect its functionality; hence, preventing the satisfactory production of PTH. Another cause could be medical conditions, for instance, cancer, neck trauma, which can impair the suitable conditions necessary to allow PTH production. Madame A’s report indicates that she had multiple scars from previous surgeries. This is a causal factor since she might have experienced injuries from these surgeries, which contribute to the suffering. If the previous surgeries were around the neck, the excision could have damaged the parathyroid glands slightly. However, it became grim as time elapses.
Symptoms of Hypoparathyroidism
According to Bilezikian, Khan & Potts et al, (2011), hypoparathyroidism is rare amongst individuals. However, the symptoms are easy to identify since they affect the physical conditions of the patients. A common symptom is dry and coarse skin, dry hair and brittle nails. In addition, an irritating tingling sensation of the fingers, lips and toes are also potential signs that facilitate the diagnosis for hypoparathyroidism. Muscle cramps are another indicator of possible hypoparathyroidic infections, but they affect the whole body (Henderson & Mahony, 2005). If an individual experiences muscle cramps, it becomes difficult to be freely mobile. Since the PTH is responsible for creating electrical impulses along the body muscles to allow movement, it can be difficult to move multiple muscles of the body. Interestingly, it also becomes daunting to move the facial muscles because of the pain associated with muscle cramps.
Furthermore, malformations of the teeth are likely symptoms that result from weakening of the protective enamel in teeth (Hendy, Cole & Bastepe, 2011). These will affect the patient’s ability to eat properly; hence, limiting his/her intake of food. Cataracts cause the eye lens to become opaque and cloudy thereby leading to decrease in vision of the patient. Treatment of cataracts usually involves a surgical process to remove it. Additionally, the patient suffers from memory loss and relentless headaches that become frequent as the disease advances. Increase in neuromuscular irritability is another symptom that signifies the presence of hypocalcemia. The dry skin of Madame A is a likely indication of hypoparathyroidism.
Diagnosis of Hypoparathyroidism
Henderson & Mahony (2005) indicate that the diagnosis of hypoparathyroidism can be done through various methods. This includes determining if the complication arises from inheriting the disease from his/her familial lineage. The surgeries and operations around the neck have to be examined to determine if they were liable for the current symptoms of the patient. Moreover, an individual may diagnose hypoparathyroidism by undertaking blood tests, which will indicate the calcium levels, PTH composition and serum albumin in the blood. Tests on the urine samples are vital in determining the PTH concentrations of the body (Bilezikian, Khan & Potts et al, 2011). Furthermore, physical examinations that will assist in identifying if the individual suffers from muscle cramps are crucial; furthermore, exercising the body to establish other areas that may be painful is useful. Examination of the eyes to check whether cataracts are developing is fundamental. These can ultimately make the individual blind. Subsequently, tapping of the elbow and knee muscle reflexes is critical. X-rays of the hands and legs are necessary to detect the exact formation of the bones, which will identify if the bone structure is changing because of deficiency of calcium within the bones.
Calcium is an essential component in development of the bone structure; variations in its supply will affect the health of the bone (Henderson & Mahony, 2005). The secretion of PTH is inversely proportional to that of serum-ionized calcium. Essentially, “a high serum calcium secretion inhibits the production of PTH by the parathyroid glands whereas low calcium concentration prompts the release of PTH” (Henderson & Mahony, 2005). Vitamin D is a vital component in the construction of bones and increases both “serum calcium and phosphorus” (Petit & Adamec, 2005). The primary function of vitamin D is to advance the inclusion of “calcium, magnesium and phosphorous” into the intestines (Petit & Adamec, 2005). PTH and Phosphorous are crucial in controlling the hydroxylation process, which occurs in the kidneys. High PTH concentration and low phosphorus elevate the formation of 1, 25-dihydroxyvitamin (Henderson & Mahony, 2005). If the concentrations of phosphorus are high and PTH low, this cause decline in the renal hydroxylase activity; therefore, limiting the creation of active vitamin D metabolite (Petit & Adamec, 2005).
Preliminary assessment in the laboratory will be necessary to determine the concentration of ionized serum calcium. Therefore, to ensure an accurate interpretation of total calcium it has to have values of 1 g/dl of albumin below 4 g/dl and a calcium concentration of 0.8 g/dl should be added to the total calcium requirement (Bilezikian, Khan & Potts et al, 2011). If signs of hypocalcaemia are established, it will be essential to undertake tests on the “magnesium, serum and phosphorous levels”. Additionally analysis of the patients’ urine sample is mandatory. Bilezikian, Khan & Potts et al (2011) emphasize in medical standards patients enduring hypoparathyroidism have low PTH of less than15pg/mL, calcium levels below 8 mg/dL and high phosphorous of concentration above 5.0 mg/dL.
According to Madame A’s medical records, she seems to have a PTH level of below 15 pg/mL, clearly signifying her PTH production is less than the normal standards. Having a PTH concentration of 4 pg/mL illustrates that her body is deficient of the PTH, increasing the potential of minimal calcium in her blood. Furthermore, her laboratory tests indicate her calcium is 6.8 mg/dL, which is attributable to the damage of the parathyroid glands. This is because her family history does not indicate evidence of occurrences of hyproparathyroidism. A concentration of 6.8 mg/dL is less than the average of 8 mg/dL, which can undoubtedly show a considerable decline in her calcium content. From a medical perception if the calcium falls further, her condition can worsen and make her experience exceedingly painful muscle cramps followed by memory loss in the late stages (Henderson & Mahony, 2005). Several laboratory tests will be vital in ascertaining the extent of the parathyroid gland damage. First, the doctor has to conduct bloods tests frequently to measure the capacity of “calcium and phosphorous in the blood system” (Petit & Adamec, 2005). If the concentration of calcium continues to decline, the medical team will have to adopt a more drastic method of treatment. Moreover, X-rays of her bone structure can assist in outlining the areas that the calcium absence is affecting most.
Prognosis and Progression of Hypoparathyroidism
Hendy, Cole & Bastepe (2011) identifies categorization of the parathyroid disorders as critical in the treatment and diagnosis of the disease. Usually, this disease is identifiable as hereditary; thus, leading to the abnormalities in the underdevelopment of parathyroid gland and insufficient PTH secretion. However, other complex syndroms are responsible for causing complications in the PTH secretions of the body. Hypocalcaemia is observable in a variety of disorders that involve the lessening of calcium in the body system. Hypoparathyroidism is treated with the introduction of calcium or vitamin D into the body. Currently, the surgical procedures on the parathyroid glands are not reassuring since compromising the condition of the gland is possible (Henderson & Mahony, 2005). Postoperative Hypoparathyroidism are common in patients, and it becomes unlikely for them to recover from the damage on their parathyroid glands (Bilezikian, Khan & Potts et al, 2011). Detection of the symptoms, for instance, dry skin and muscle cramps will be critical in undermining the effects of the low calcium levels to the patient’s body. Understanding of the medical history of the patients and family health history can provide insight of the patient’s disease to the physician (Hendy, Cole & Bastepe, 2011). Identification of the hypoparathyroid disorders will determine the management plan for specific hypoparathyroidism, for example, hypocalcaemia and hypercalcuria. Indeed, hypercalcemia patients require considerable intake of calcium supplements and Vitamin D to counter the increase of phosphorus in the body (Bilezikian, Khan & Potts et al, 2011).
Current Research and Future Trends of Hypoparathyroidism
Current research indicates that Postoperative Hypoparathyroidism is the most widespread cause of hydrparathyroidism in most adults especially if they have a history of operations. The frequency of complete hypoparathyroidism after the surgical procedure is high as 6.6% (Bilezikian, Khan & Potts et al, 2011). Research suggests that postpoperative hypoparathyroidism is likely among persons who have been subjected to several neck operations. A study of patients of neck injuries illustrates PTH levels of low than 15 mg/dL and calcium of less than 7.6 mg/dL after two days of operation. Comparison of risks of Postoperative Hypoparathyroidism and Intraoperative Monitoring did show the latter is less risky.
Autoimmune Hypoparathyroidism
Future research will focus on demystifying Autoimmune Hypoparathyroidism. It entails the alteration of the activities of the polyglandular system, bringing about Autoimmune Polyglandular Syndrome (APS). According to Bilezikian, Khan and Potts et al (2011), the antibodies of the anti-parathyroid gland were observable in 38% of 75 patients with idiopathic hypoparathyroidism. It is apparent that the succeeding investigations would indicate that the “anti parathyroid gland antibodies were reactive with the endomysial antigens” (Bilezikian, Khan & Potts et al, 2011).
Treatment
The treatment of hypoparathyroidism entails the intake of calcium and Vitamin D supplements to enhance the renal tubular re-absorption of calcium (Petit & Adamec, 2005). The PTH activates 1, 25-dihydroxyvitamin that is usually in an inactive mode. Interestingly, transplantation of the parathyroid tissue is uncommon since it seems impractical. Additional research into hypoparathyroidism will improve the treatment of patients. However, the calcium supplements remain the only suitable solution to this disorder.
References
Bilezikian, J., Khan, A. & Potts, J. et al. (2011). Hypoparathyroidism in the Adult: Epidemiology, Diagnosis, Pathophysiology, Target-Organ Involvement, Treatment, and Challenges for Future Research.Journal of Bone and Mineral Research, 26, 10, 2317–2337. Web.
Henderson, A. & Mahony, O. (2005). Hypoparathyroidism: Pathophysiology and Diagnosis. Compedium, 270-279. Web.
Hendy, G., Cole, D, & Bastepe, M. (2011). Hypoparathyroidism and Pseudohypoparathyroidism. Endotext. Web.
Petit, W. & Adamec, C. (2005). The Encyclopedia of Endocrine Diseases and Disorders. New York, NY: Infobase Pub.
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