Endocrine and Metabolic Pathophysiology Essay

Endocrine and Metabolic Pathophysiology Essay

The endocrine system plays an important role in the body’s metabolism. The thyroid, pituitary, parathyroid, pancreas, adrenal, and glands in the ovary and testes are some of the critical components of the endocrine system. These glands produce hormones that have distant and systemic effects from their site of production. The regulation of the production and effects of these hormones is mainly through negative and positive feedback. The purpose of this paper is to explain the pathophysiologic processes of some diseases and disease processes of the endocrine system.

Diabetes

The description of the term diabetes was in relation to the taste or sweetness in the urine (Kuzina et al., 2022). There are two types of diabetes, diabetes mellitus and diabetes insipidus, which impact the concentration of urine differently. The term diabetes in the current practice is almost synonymous with diabetes mellitus because diabetes mellitus is commoner and has devastating outcomes in the short and long term. Diabetes mellitus arises from disease processes leading to persistently high blood sugar levels. These conditions include gestational diabetes, type 1 diabetes, type 2 diabetes mellitus, mature onset diabetes of the young (MODY), and diabetes secondary to medications and endocrinopathies (McCance & Huether, 2022). The underproduction of insulin or reduced tissue sensitivity to insulin is the two pathophysiologic processes in diabetes mellitus. Persistently high blood glucose can glycate various proteins in the blood, including hemoglobin. High blood sugar and glycated products can cause damage to blood vessels and end organs such as the eyes, kidneys, and nerves.

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Hyperthyroidism

Hypothyroidism refers to high levels of thyroid hormones in circulation. This results when the normal regulatory process secretion of thyroid hormones is lost (Kumar et al., 2021). The thyroid hormone in the body is responsible for stimulatory and hyper-metabolic states. Usually, this hormone stimulates the cardiac and sympathetic branches of the autonomic nervous systems. Therefore, hyperthyroidism causes hypertension because it increases cardiac output and also leads to tachycardia. Patients will report heart racing as a common complaint. Stimulation of the sympathetic system also leads to tremors and diaphoresis. These activities require energy; thus, hyperthyroid states are characterized by the breakdown of energy stores, such as fat stores in the adipose. Patients with hyperthyroidism are always thinner.

Hypothyroidism

Hyperthyroidism refers to lower levels of thyroid hormones in the blood. When the disease starts, the body responds through compensatory mechanisms to raise the levels of active thyroid hormones. Therefore, levels of thyroid-stimulating hormones rise (McCance & Huether, 2022). However, as the disease advances, the compensatory mechanisms are overwhelmed and the thyroid hormone remains persistently lower. Low thyroid hormones cause hypo-metabolic states characterized by a buildup of energy stores and lower adrenergic stimulation. Patients will present with cold, clammy extremities. Hypothyroidism causes a reduction in basal metabolic rates (BMR) and disturbances in energy metabolisms. An increase in cholesterol increases the risk of atherosclerosis and coronary artery disease. Decreased cardiac contractility due to decreased sympathetic stimulations can cause cardiomyopathies and sometimes reduced cerebral blood flow.

Adrenal Disorders

The adrenal glands are located on the upper surface of both kidneys and are responsible for various endocrine and metabolic functions. Apart from producing catecholamines such as adrenaline and noradrenaline, the adrenal glands also produce glucocorticoids such as cortisol and mineralocorticoids such as aldosterone. Common disorders of the adrenal glands arise from alterations in the production of these hormones. Adrenal insufficiency and Cushing’s syndrome are the two most common adrenal disorders. Adrenal insufficiency, sometimes called Addison’s disease, arises when the adrenal glands do not produce sufficient steroid hormones (McCance & Huether, 2022). This can result from autoimmunity, structural adrenal destruction, iatrogenic removal, infections, metastatic invasion of the gland, and insufficient production of adrenocorticotropic hormone from the pituitary glands.

Decreased cortisol production leads to reduced function of the lower and digestive enzymes that reduce blood glucose. Decreased aldosterone leads to an increase in water and sodium loss in the kidneys leading to hyperkalemia and hyponatremia. Decreased blood pressure, acute kidney injury, and dehydration are common complications of Addison’s disease. In the acute presentation, the Addisonian crisis results from this insufficiency. The patient develops sudden abdominal, back, and leg pains, cyanosis, hypotension, rapid, weak pulse, rapid breathing, and pallor.

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Cushing’s syndrome is caused by hypercortisolism. Increased function of the adrenal glands leads to an increase in the secretion of hormones seen in Cushing’s syndrome, especially cortisol. Most of the time, this hyperfunction results from increased corticotrophin production that causes hyperplasia of the adrenal glands (Kumar et al., 2021). Increased cortisol production increases glucose production and the function of the digestive enzymes. Hyperglycemia and peptic ulcers are possible outcomes of this pathophysiological process. Increased aldosterone reduction increases sodium and water retention in the kidneys, thus leading to hypernatremia and hypokalemia. Fluid retention can lead to edema. Increased glucose production leads to fat deposition due to the conversion of excess energy into stores. Buffalo hump, truncal obesity, abdominal striae, muscle wasting, skin ulcers, amenorrhea, moon-faced appearance, and cardiomyopathies are some of the presentations of Cushing’s syndrome.

Hyperparathyroidism

Hyperparathyroidism results from excess parathyroid hormone in the blood. Increased parathyroid hormone (PTH) leads to hypercalcemia and hypophosphatemia. Low calcium and vitamin D cause an increase in PTH to increase calcium in the blood. However, this increase can also be caused by adenomas, hyperplasia, and malignancies of the gland. Chronic kidney disease causes the inadequate conversion of inactive to active vitamin D, resulting in low calcium absorption from the gut (Gould & Dyer, 2019). Therefore, the pituitary gland becomes overworked and can produce excess PTH. Chronic kidney disease is the most common cause of hyperparathyroidism. Excess production of PTH results in increased bone osteoclastic activity that increases available calcium, thus, hypercalcemia. Bone fractures can result from osteoporosis due to increased osteoclastic activity. In the gastrointestinal system, hypercalcemia leads to constipation, pain, and nausea. Urinary calculi and high urine output can result from this hypercalcemia because the kidney will try to work extra to eliminate excess calcium, which, if fails, results in stone formation.

Hypoparathyroidism

Hypoparathyroidism results from low PTH levels. Decreased gland function can result from the destruction of the gland. For example, surgical removal during thyroidectomy and radiotherapy for neck malignancies can cause gland destruction. Inadequate PTH production leads to decreased calcium reabsorption in the gut (Gould & Dyer, 2019). The final outcome is hypocalcemia. Hypocalcemia causes muscle tetany due to muscular irritability. Other outcomes of hypocalcemia are muscle cramps, facial tingling or numbness, dry hair, and cold intolerance. Cardiac arrhythmia and convulsions are serious complications from hypocalcemia.

Feedback Mechanisms

The endocrine system has checks and balances that attempt to keep the hormone levels within normal limits to prevent outcomes of derangements (McCance & Huether, 2022). Negative and positive feedback mechanisms regulate hormonal homeostasis in the body. Various hormones have axes through the stimulus-sensor-control-effector mechanisms that interact to keep hormonal checks and balances. In the negative feedback mechanism, the sensors of the hormone levels in the blood check the levels and report back to the hypothalamus, which reduces stimulus for the production of releasing hormones when the effector hormone levels are high (Story et al., 2020). When the levels are low, the hypothalamus is stimulated to increase the production of releasing hormones. Releasing hormones from the hypothalamus causes the pituitary gland to produce more stimulating hormones, which travel through the blood to reach effector organs such as the thyroid and adrenal glands. In positive feedback, high hormone levels cause a stimulus that will increase the production of the hormone as opposed negative feedback mechanism. An example is uterine contractions during labor, where oxytocin production increases with more contractions.

Syndrome of Inappropriate Antidiuretic Hormone

Syndrome of Inappropriate Antidiuretic Hormone (SIADH) results from excess secretion of antidiuretic hormone. SIADH results from malignancies, brain injury, and medication such as vincristine, cyclophosphamide, and antidepressants. In this disease, the secretion of ADH is inappropriate and cannot be controlled by feedback mechanisms (Peate, 2021). Therefore, excess production from the aforementioned causes leads to water retention from the renal tubules and collecting ducts. This anti-diuresis leads to increases in blood volume that cause movement of excess fluid into the third space. Excess water retention dilutes sodium levels in the blood, thus hyponatremia. Hyponatremia can cause inappropriate neuron firing due to the alteration of the action potential of various nerves and brain neurons. Cerebral edema from hyponatremia can cause headaches and vomiting. In severe cases, neurocognitive changes such as confusion, hallucinations, convulsions, mood swings, and coma can occur.

Pheochromocytoma

Pheochromocytoma is a rare benign tumor of the adrenal gland and most commonly affects individuals in their third to sixth decades of life (Kumar et al., 2021). Failure of oncogenes and tumor suppressor genes to control the proliferation of chromaffin cells in the adrenal medulla is the initial pathogenetic process of this neoplasia change. Adenomas from this neoplastic change become functional and start producing excess adrenaline and noradrenaline (McCance & Huether, 2022). These metanephrines cause hyperactivity of the sympathetic nervous system and catabolic metabolic processes. Uncontrollable catabolism leads to lipolysis and glycogenolysis, which cause hyperglycemia, weight loss, and fatigue. Episodic sympathetic stimulation leads to panic, tremors, anxiety, diaphoresis, and tachycardia. Hypertension also results from pheochromocytoma due to sympatric nervous system stimulation.

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Diabetes Insipidus

Diabetes insipidus results from decreased production of ADH from the pituitary gland. Reduction in ADH levels reduces the permeability of the renal collecting ducts to water. Therefore, water reabsorption is reduced, which means that water loss would increase (McCance & Huether, 2022). Therefore, polyuria results from this diuresis. However, this polyuria has low concentrations of electrolytes, thus reduction of osmolality and specific gravity. This diuresis also depletes the blood fluid volume due to decreased reabsorption leading to dehydration. High plasma osmolality results from dehydration from loss of plain water, thus stimulating the thirst center and leading to polydipsia. It is also notable that the collecting tubules can be less sensitive to ADH, resulting in nephrogenic diabetes insipidus. A pituitary tumor is one of the common causes of diabetes insipidus.

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a diabetic emergency usually seen in type I diabetes mellitus. Inadequate or absolute lack of insulin to prevent lipolysis is a crucial pathophysiologic step in understanding DKA (McCance & Huether, 2022). As the only easily available source of energy, the liver metabolizes free fatty acids through ketogenesis to produce ketoacidosis due to excess ketones in the blood. In the meantime, the glucose levels in the blood remain high, thus causing persistent hyperglycemia. The hypothalamus is stimulated to send hunger signals because this glucose cannot enter cells due to a lack of insulin (Kuzina et al., 2022). The excess glucose and ketones are excreted in the urine, leading to ketonuria and glycosuria. The osmolality of the plasma arises from the electrolytes in urine and excess hydrogen from ketoacidosis. A Triad of diabetes (hyperglycemia), ketosis, and acidosis form the essential outcomes of DKA. Disruption of the gastric enteric system by metabolic acidosis leads to abdominal pain. Respiratory compensation of metabolic acidosis to remove excess carbon dioxide leads to deep and fast breathing, also described as Kussmaul breathing. Fruity odor breath results from ketone breath result from the removal of ketones from the lungs.

Conclusion

An endocrine system is a group of glands that produce hormones that regulate various body processes, including metabolism. Diabetes is a disease that affects the body’s ability to regulate blood sugar levels. There are several types of diabetes, including gestational diabetes, which occurs during pregnancy, and type 1 and type 2 diabetes. Hyperthyroidism is a condition in which the thyroid gland produces too much thyroid hormone, leading to symptoms such as weight loss and rapid heart rate. Hypothyroidism is a condition in which the thyroid gland does not produce enough thyroid hormone, leading to symptoms such as weight gain and fatigue. Adrenal disorders, such as adrenal insufficiency and Cushing’s syndrome, can occur when the adrenal gland does not produce enough or too much of certain hormones. Pituitary disorders can occur when the pituitary gland does not produce enough or too much of certain hormones.

References

Gould, B. E., & Dyer, R. (2019). Pathophysiology for the health professions (4th ed.). Mosby.

Kumar, V., Abbas, A. K., & Aster, J. C. (2021). Robbins Basic Pathology (V. Kumar, A. K. Abbas, & J. C. Aster, Eds.; 10th ed.). Elsevier – Health Sciences Division.

Kuzina, I. A., Goncharova, E. V., Martirosian, N. S., Telnova, M. E., Nedosugova, L. V., Tulsky, A. A., & Petunina, N. A. (2022). Historical aspects of diagnosis and control of diabetes mellitus. Terapevticheskii arkhiv94(10), 1216–1220. https://doi.org/10.26442/00403660.2022.10.201890

McCance, K. L., & Huether, S. E. (2022). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Mosby.

Peate, I. (Ed.). (2021). Fundamentals of applied pathophysiology: An essential guide for nursing and healthcare students (4th ed.). Standards Information Network.

Story, L., Costello, A., & McCuistion, L. (2020). Pathophysiology: A practical approach (4th ed.). Jones and Bartlett.

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Please discuss a brief pathophysiology of the following with references:Diabetes
Hyper- and hypothyroidism
Adrenal disorders
Parathyroidism (hyper and hypo)
Checks & balances / negative feedback
Syndrome of Inappropriate Antidiuretic Hormone
Pheochromocytosis
Diabetes insipidus
Diabetic ketoacidosis

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