PATHOPHYSIOLOGY

PATHOPHYSIOLOGY

1. Define SIADH and identify any patient characteristics that may have contributed to the development of SIADH.

Syndrome of inappropriate antidiuretic hormone ADH release (SIADH) is a condition whereby there is inappropriate and excessive release of the antidiuretic hormone. Antidiuretic hormone aids the body in the regulation of the amount of water. It ensures that excess water is lost through urine (Yasir & Mechanic, 2021). It occurs due to the impaired functioning of the pituitary gland, malignancy, pulmonary disorders, central nervous system disorders, substance abuse, and some medications which increase the secretion of ADH. The most common occurrence noted of SIADH occurs as a secondary to another disease process in the body. Signs of SIADH are hypernatremia, hypo-osmolality, and urine osmolality over 100 mmol/kg. Excessive amounts of water in the body cause hyponatremia.

Low blood pressure, increased serum osmolality, and decreased plasma volume all boost normal ADH synthesis. The generation of ADH by tumors arising in various regions of the body is a prevalent cause of SIADH. Fluid retention, dilution hyponatremia, hypochloremia, concentrated urine with abnormally low urine production, and normal fluid volume or edema are all symptoms of SIADH. Dilution occurs as a result of fluid retention, resulting in lower plasma sodium concentrations (Yasir & Mechanic, 2021). Extracellular fluid volume stimulates sodium excretion in the urine, restoring normal extracellular volume and reducing plasma sodium concentration even more. Patients with normal renal and endocrine function have normal to increased blood volume and blood protein levels, with no edema.

The patient smokes 40packs/year of tobacco, which contains nicotine and leads to hyponatremia. The patient's advanced age (77 years old) predisposes her to SIADH because the increase in age leads to the degeneration of several physiological functions in the body. Empyema leads to the ectopic release of ADH by unknown mechanisms. The medications such as selective serotonin reuptake inhibitors, including escitalopram that the patient is taking to treat her situational depression, predispose her to SIADH because they increase ADH secretion (Yasir & Mechanic, 2021). Type II Diabetes with peripheral neuropathy affects the central nervous system, which enhances ADH release from the pituitary gland. Hyponatremia is also a complication of diabetes.

2. Explain the pathophysiology of the three P’s (polyuria, polydipsia, polyphagia) with the given diagnosis of type I diabetes.

Beta cells of the islets of Langerhans in the pancreas secrete the insulin (Corbin et al., 2018).Eating increases the secretion of insulin. The functions of the insulin include stimulating the liver to store insulin in the form of glycogen, promoting the storage of dietary fats in the adipose tissues, accelerating the transport of amino acids into the cells, and signaling the liver to stop the release of glucose(Hinkle & Cheever, 2014).stored glucose, fats and proteins breakdown are inhibited by insulin. Insulin and glucagon maintain the glucose levels at the normal ranges in the body.

The onset of type I diabetes is usually young, less than 30 years of age. The destruction of the beta cells causes a decrease in insulin production, excessive secretion of glucose by the liver and fasting hyperglycemia (Corbin et al., 2018). Also, the glucose derived from food cannot be stored in the body, causing weight loss. The glucose remains in the bloodstream rather than being utilized to provide the energy to perform physiological functions(Hinkle & Cheever, 2014). The kidneys cannot reabsorb all the filtered glucose if the blood glucose concentration exceeds a concentration of 180-200mg/dl.

Polyuria is excessive urination. The inability of the kidneys to reabsorb excessive glucose in the body leads to the overproduction of urine for the body to restore homeostatic imbalances (Corbin et al., 2018). The increased osmotic pressure in the urine causes excessive urination. Polydipsia refers to extreme thirst that is characterized by excessive consumption of water. The endocrine system is activated to release ADH to help the body retain the osmotically lost water. Sodium is also lost in the urine; hence there will be a constant need to replenish the water. Polyphagia is excessive hunger. Lack of insulin in the body leads to a lack of energy in the vital organs because the glucose remains in the bloodstream rather than being absorbed(Hinkle & Cheever, 2014). The 3 P’s are considered the cardinal signs of diabetes.

3. Explain the genetic relationship and how this and the environment contribute to type 1 diabetes.

The prevalence of developing type 1 diabetes in patients with first-degree relatives with a positive history of the condition is high. The disease itself is not inherited but rather the genetic predisposition or the tendency to develop it. Human leukocyte antigen (HLA) found in the genes can be passed down to generations (Hinkle & Cheever, 2014). Also, the autoimmune destruction of the beta cells in the pancreas increases susceptibility. The body's antibodies mediated by the T cells attack pancreatic cells. Interactions of this genetic predisposition and environmental triggers such as a sedentary lifestyle and poor dietary habits lead to the development of diabetes.  

4. How would you describe the pathophysiology of type 2 diabetes?

It occurs in people over 30 years of age and obesity. It is characterized by impaired insulin secretion, insulin resistance, excessive hepatic glucose production, and the abnormal metabolism of fats. Glucose tolerance is near normal in the early stages of the disease despite insulin resistance because the pancreatic beta cells try to compensate by increasing the insulin output (Hinkle & Cheever, 2014). Continuous insulin resistance and compensatory hyperinsulinemia progression cause the pancreatic islets in specific individuals to be unable to sustain the hyperinsulinemic state. This, therefore, leads to an impaired glucose tolerance state that causes postprandial hyperglycemia. Further decline in insulin secretion and increase in hepatic glucose secretion lead to overt diabetes with fasting hyperglycemia. The pancreatic islet's failure can eventually ensue.

5. What causes hypothyroidism?

Hypothyroidism is a condition whereby the thyroid does not produce and release adequate amounts of thyroid hormone into the bloodstream. There is a generalized decrease in the metabolic processes (Hinkle & Cheever, 2014). Causes of hypothyroidism can be classified as either primary, secondary or tertiary. Primary causes are thyroid failure and Hashimoto's Thyroiditis, an autoimmune disorder that causes the immune system to attack the thyroid. The secondary cause is pituitary tumors such as adenoma due to the hypothalamus failure to secrete thyroid-stimulating hormone. Tertiary causes, although they are rare, include hypothalamic deficiency of the thyroid releasing hormone. 

References

Corbin, K. D., Driscoll, K. A., Pratley, R. E., Smith, S. R., Maahs, D. M., Mayer-Davis, E. J., & Advancing Care for Type 1 Diabetes and Obesity Network (ACT1ON). (2018). Obesity in type 1 diabetes: pathophysiology, clinical impact, and mechanisms. Endocrine Reviews, 39(5), 629-663.

Hinkle, J. L., & Cheever, K. H. (2014). Brunner & Suddarth's textbook of medical-surgical nursing (Edition 13.).

Yasir, M., & Mechanic, O. J. (2021). Syndrome of inappropriate antidiuretic hormone secretion. StatPearls [Internet].