Module 4 Knowledge Check Test
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Question 1. SIADH
SIADH is the syndrome of inappropriate secretion of the antidiuretic hormone that develops when there is excessive secretion of ADH in the pituitary gland. When there is increased ADH secretion, there is resultant increase in water channels in the distal convoluted tubule and the collecting duct of the kidneys (Yasir & Mechanic, 2018). These factors cause retention of water and increased concentration of urine. The increased water retention causes decrease in serum osmolality and corresponding hormonal changes (Yasir & Mechanic, 2018). The hormonal changes that occur include increased production of atrial natriuretic peptide, increased brain natriuretic peptide and decreased production of aldosterone. These hormonal changes cause increased secretion of sodium and water in urine, a process referred to as euvolemic hyponatremia (Yasir & Mechanic, 2018). Other sequelae are the osmotic fluid shifts that may result in cerebral edema and increased intracranial pressure.
Several factors cause the development of SIADH. Infections and drugs may cause the increase in pituitary ADH secretion. CNS conditions such as stroke, head trauma and surgery involving the pituitary are also etiological agents (Yasir & Mechanic, 2018). Chronic diseases such as pneumonia and COPD are also implicated in the development of the condition, as are drugs such as anticonvulsants, analgesics and antidepressants. Other paraneoplastic conditions such as small cell lung carcinoma also cause the condition. In this patient, the obvious etiological factors include emphysema, which is one of the two conditions that form COPD (Yasir & Mechanic, 2018). She is also a chronic smoker and therefore predisposed to the pulmonary condition. She is also on various medications, with the risk posed by ASA and the antidepressant escitalopram. Furthermore, she presents with symptoms of stroke such as stumbling and falling and therefore stroke may have been a risk factor for the condition.
Question 2. Type 1 Diabetes Mellitus
Type I Diabetes Mellitus develops as a result of destruction of the cells that produce insulin in the pancreas. Insulin is responsible for various metabolic processes and in glycemic control. In the case of diabetes mellitus type 1, there is poor glycemic control and therefore the patient has high blood glucose levels (DiMeglio, Evans-Molina, & Oram, 2018). The classic symptoms of the disease include polyuria, polydipsia and polyphagia. The pathophysiology of these characteristic features is based on glycosuria and high blood glucose levels. Polyuria is the production of a higher amount of urine than normal. The development of this characteristic is due to the high levels of glucose in blood passing the renal threshold of 10mmol/L (DiMeglio, Evans-Molina, & Oram, 2018). Above this level, reabsorption is poor and therefore there is glucose in urine. Glycosuria causes osmotic diuresis and therefore increases the excretion of water and therefore polyuria.
Polydipsia is excessive thirst in diabetes mellitus type 1 due to raised plasma osmolality. The increased plasma osmolality is a consequence of polyuria that results in water loss thereby stimulating the thirst center causing increased intake of water (DiMeglio, Evans-Molina, & Oram, 2018). Polyphagia is the excessive hunger in patients with DM type 1 that results from the increased loss of glucose in urine. At the same time, high glucose levels in blood accompanied with low insulin levels hinders entry of the glucose into cells. Therefore, carbohydrate metabolism is affected resulting in increased craving of glucose and therefore polyphagia.
Question 3. Pathophysiology of DM Type 1
One of the risk factors in the development of DM type 1 is genetic predisposition. Therefore, people with a family history of diabetes have a higher risk of development of the condition as compared to the rest of the population. The disease itself is not inherited, but the predisposition is the inherited factor. The susceptible individual usually has human leukocyte antigen genes association, especially HLA-DR3 and HLA-DR4 genes which increase the susceptibility by a factor of 4-6 (Paschou et al., 2018). The HLA genes have various combinations, and the variation between these combinations is the determining factor of the susceptibility. The different variations are referred to as haplotype and the combinations such as HLA-DR3 and HLA-DR4 provide the highest risk (Paschou et al., 2018). However, these genes on their own are not enough to trigger the development of the disease. The trigger in susceptible individuals is the environment.
The environmental factors that are implicated in the development of the condition include hygiene, pollutants, weather variation and infections. Cold weather is one of the environmental factors that has led to the triggering of this condition (Paschou et al., 2018). Research has indicated that DM type 1 development is more common during the winter than it is during the summer and it is more common in colder places (Paschou et al., 2018). Infection with various viruses has also caused the triggering of diabetes in some people. The combination of genetic susceptibility and environmental factors therefore leads to the development of DM type 1.
Question 4. Type 2 DM
Type 2 DM develops as a result of insulin insensitivity rather than lack of insulin as seen in type 1 DM. The development of this insulin insensitivity is multifactorial and therefore the pathophysiology depends on a myriad of factors (Chatterjee, Khunti, & Davies, 2017). The factors include peripheral insulin insensitivity, poor regulation of glucose production in the liver, and poor function of the beta cell. Insulin resistance is seen in DM type 2 coupled with hyperinsulinemia (Chatterjee, Khunti, & Davies, 2017). The resistance is indicative of development of type DM, as prospective research has indicated the presence of insensitivity to insulin prior to development of DM type 2.
In the liver, there is poor regulation of glucose production due to decreased sensitivity to insulin. In normal cases, insulin is able to suppress the production of glucose in the liver in the fasting period and after eating (Chatterjee, Khunti, & Davies, 2017). However, as hepatic insulin resistance progresses, there is increased production of glucose from the liver in the postprandial period. Therefore, in this condition, there is increased production of glucose and poor uptake causing hyperglycemia.
B-cell dysfunction is characterized by poor production of insulin in the early periods after the ingestion of carbohydrates. In this period, there is change in the control point of glucose levels and therefore predating the development of the disease (Chatterjee, Khunti, & Davies, 2017). After the progression of the disease, there is poor release of newly synthesized insulin, and it is paradoxically caused by increased glycose levels. These factors contribute to beta cell dysfunction in type 2 DM.
Question 5. Hypothyroidism
Hypothyroidism is characterized by deficiency of thyroid hormones T3 and T4. It can also describe a situation in which the thyroid hormones are sufficient by there is no peripheral effects of the hormones (Biondi & Cooper, 2019). The hypothyroidism can classified into congenital or acquired classes. The acquired hypothyroidism can be primary, secondary or tertiary. Congenital hypothyroidism in most cases is idiopathic, usually resulting from factors such as thyroid hypoplasia or aplasia (Biondi & Cooper, 2019). In other cases, it can be hereditary result from thyroid hyperplasia or peripheral resistance to the thyroid hormones.
Acquired causes in primary hypothyroidism result from insufficient hormone production. This insufficiency is seen in cases of Hashimoto thyroiditis and other autoimmune conditions, nutritional insufficiency of iodine or granulomatous thyroiditis (Biondi & Cooper, 2019). Other rare causes of primary hypothyroidism include postpartum thyroiditis, increased iodine ingestion above the required levels. Iatrogenic causes also play a role, and the include thyroid surgery resulting in removal of the thyroid gland, radioiodine treatment and anti-thyroid drugs. In secondary disease, the disorder is at the level of the pituitary, caused by various conditions such as trauma or tumours (Biondi & Cooper, 2019). As a result, there is decreased TSH secretion and thereby hypothyroidism. Tertiary causes involve the hypothalamus causing poor TRH release and thereby causing hypothyroidism.
References
Biondi, B., & Cooper, D. S. (2019). Thyroid hormone therapy for hypothyroidism. Endocrine, 66(1), 18-26.
Chatterjee, S., Khunti, K., & Davies, M. J. (2017). Type 2 diabetes. The lancet, 389(10085), 2239-2251.
DiMeglio, L. A., Evans-Molina, C., & Oram, R. A. (2018). Type 1 diabetes. The Lancet, 391(10138), 2449-2462.
Paschou, S. A., Papadopoulou-Marketou, N., Chrousos, G. P., & Kanaka-Gantenbein, C. (2018). On type 1 diabetes mellitus pathogenesis. Endocrine connections, 7(1), R38-R46.
Yasir, M., & Mechanic, O. J. (2018). Syndrome of inappropriate antidiuretic hormone secretion (SIADH).