Diabetes; Hyper- and Hypothyroidism; Adrenal Disorders Essay

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

SIADH describes symptoms which    occur   following the excretion of antidiuretic hormone (ADH) in the absence of either physiologic or osmotic stimuli. Perfect examples of such stimuli include: an increase in the osmolality of serum, hypotension, and a decrease in the volume of plasma. When the osmolality of plasma reduces, there is inhibition in the production and secretion of ADH.  In SIADH, patients    experience the following symptoms, dilutional hyponatremia, concentrated urine, hypochloremia, fluid retention, and lack of depletion of intravascular volume. Therefore, the primary characteristics of SIADH include; normal to increased blood volume in hyponatremic, nonedematous, and normoproteinemia in patients with normal endocrine and renal function.   The primary function of ADH is to regulate   the balance of water in the body. The synthesis of ADH occurs in the hypothalamus and storage is in the posterior pituitary gland. When ADH is secreted, it increases the permeability of the collecting and distal tubules to water. This increases the reabsorption of water   to the circulation and reduces the volume of water. Besides, it results in the production of more concentrated urine.Diabetes; Hyper- and Hypothyroidism; Adrenal Disorders Essay

 Question 2: Explain why the patient exhibited these symptoms? 

For patients to experience adrenal insufficiency, there must be a potential stressor or trigger such as trauma, surgery, an acute withdrawal of glucocorticoids or an acute infection. The patient’s current situation was influenced by several   factors.  First, the patient had   a 20 year RA   which   she was being managed with oral prednisolone.  For the body to effectively adapt to   Corticotropin-releasing hormone (CRH) released by the hypothalamus, there must be an increase in the levels of both aldosterone and cortisol which eventually influence the anterior pituitary gland to release ACTH with subsequent  secretion and synthesis of  cortisol by the adrenal cortex. Cortisol has an effect on the skeletal muscle. It mobilizes amino acids stored in skeletal muscles, augments the capacity of the liver   to perform gluconeogenesis, maintaining the integrity of the cardiovascular system, and normal activity of the immune system. Catecholamines cause blood vessels to vasoconstrict. In the kidneys, vasoconstriction influences the release of renin thus stimulating the rennin-angiotensionaldosterone-system (RAAS). During periods of stress, the posterior pituitary and hypothalamus release ADH. However, to help sustain a sufficient vascular volume, both ADH and aldosterone conserve water.

Question 3: What is the role of parathyroid hormone in the development of primary hyperparathyroidism? 

In primary hyperparathyroidism, there is excessive and unregulated production of parathyroid hormone (PTH) which causes an abnormal   balance of calcium. As a result, the   secretion of PTH   increases   but not under the usual   mechanisms of feedback controls.  Due to an abnormal   calcium balance, there is an increase in the absorption of calcium in the GI tract which influences a subsequent increase in   the levels of calcium in blood. However, there is no inhibition in the secretion of PTH at normal calcium levels since the calcium feedback threshold is higher as compared to the abnormal parathyroid tissues.  Therefore, the clinical hallmark symptoms of hyperparathyroidism are hypophosphatemia and hypercalcemia. Diabetes; Hyper- and Hypothyroidism; Adrenal Disorders Essay

Question 4: Explain the processes involved in the formation of renal stones in patients with hyperparathyroidism

Hypercalciuria occurs when there is an increase in the calcium load being filtered in the renal system. This also affects   the   functions of the proximal renal tubule, leading to an abnormal production of highly alkaline urine and metabolic acidosis. The hypersecretion of PTH also influences the excretion of phosphates leading to hyperphosphatemia and hypophosphatemia. When combined; alkaline urine, hypercalciuria, and hyperphosphaturia result in the formation of renal stones.

Question 5: Explain how a patient with hyperparathyroidism is at risk for bone fractures.  

When there is excess osteocytic and osteoclastic activity, reabsorption in the bone increases, which weakens the bone. It is for this reason that patients with hyperparathyroidism exhibit kyphosis of the dorsal spine and compression fractures of the vertebral bodies.

Question 6: What serious consequences of hypoparathyroidism occur and why? 

Continuous destruction of the parathyroid glands either from surgery or autoimmune-mediated, impaired action of PTH, altered production and regulation of PTH, and abnormal development of the parathyroid gland cause hypoparathyroidism. In patients who have undergone surgery, the acute manifestations of hypoparathyroidism are   caused by acute hypocalcemia whose hallmark is tetany.  Patients with   tetany may exhibit mild or severe symptoms. However, the classic clinical signs    that can be found in patients who have neuromuscular irritability   with latent tetany are the Chvostek’s and Trousseau’s signs.Diabetes; Hyper- and Hypothyroidism; Adrenal Disorders Essay

Question 7: The patient exhibited classic signs of Type 1 diabetes. Explain the pathophysiology of “polydipsia.”

An increase in the levels of glucose in blood   influences osmosis where water is attracted to cells in the body leading to intracellular dehydration and thirst stimulation by the hypothalamus

Question 8: The patient exhibited classic signs of Type 1 diabetes. Explain the pathophysiology of “polyuria

Hyperglycemia is an osmotic diuretic which influences an increase in the amount of glucose filtered by the kidney glomeruli and exceeds   the amount that the renal tubules reabsorb.  This leads to excretion of large amounts of water in urine and glycosuria.

Question 9: The patient exhibited classic signs of Type 1 diabetes. Explain the pathophysiology of “polyphagia.”

When the stores of   fats, carbohydrates and proteins are depleted,   the cells become starved with a corresponding increase in hunger.Diabetes; Hyper- and Hypothyroidism; Adrenal Disorders Essay

Question 10: The patient exhibited classic signs of Type 1 diabetes. Explain the pathophysiology of “weight loss.”

In osmotic diuresis,   patients lose water. Patients also lose fat which corresponds to body tissue. The effects of insulin deficiency cause proteins to be used for energy.

Question 11: The patient exhibited classic signs of Type 1 diabetes. Explain the pathophysiology of “fatigue.”

When there are metabolic changes in the body,   food products are used poorly and this often leads to fatigue and lethargy. Severe nocturia also causes sleep deprivation which is another contributing factor to fatigue.

Question 12: How do genetics and environmental factors contribute to the development of Type 1 diabetes?

ORDER A PLAGIARISM -FREE PAPER NOW

Patients with autoimmune polyendocrine deficiency   have Islet cell autoantibodies (ICAs) in serum. The same autoantibodies have   been noted to occur in patients with type 1 diabetes who are newly diagnosed and prediabetics. The autoantigens form on beta cells that produce insulin and continue to circulate in the lymphatics and blood. The antigen presenting cells process and present the autoantigens with subsequent activation of macrophages that release TNFα and IL-,  T helper 1 and 2 lymphocytes, and particular T cytotoxic CD8 cells. B lymphocytes are also activated with the resultant production of ntiGAD65 and islet cell antibodies leading to beta cells destruction with a decrease in the production of insulin.Diabetes; Hyper- and Hypothyroidism; Adrenal Disorders Essay

Question 13: The hormones involved in intermediary metabolism, exclusive of insulin, that can participate in the development of diabetic ketoacidosis (DKA) are epinephrine, glucagon, cortisol, growth hormone. Describe how they participate in the development of DKA. 

DKA is primarily caused by   a deficiency in insulin and an increase in cortisol, glucagon, catecholamines, and growth hormone commonly referred to as   counter regulatory hormones since they antagonize insulin by influencing an increase in the production of glucose and reducing the utilization of glucose by tissues. Insulin deficiency causes an increase in the mobilization of fat and a decrease in the uptake of glucose with continuous glycogenesis, gluconeogenesis, and ketogenesis. When insulin is absent,   adipocytes produce free fatty acids which increase ketone bodies production in the liver which surpasses peripheral use.  When ketone bodies accumulate, the pH drops triggering   metabolic acidosis. When there is impaired use of ketones by peripheral tissues, hyperketonemia sets in, permitting    the free circulation of strong organic acids. As a result, bicarbonate buffering fails to occur and a person gradually develops metabolic acidosis.

Question 14: Explain the underlying processes that lead to HHNKS or HHS.Diabetes; Hyper- and Hypothyroidism; Adrenal Disorders Essay

DKA is different from HHNKS in terms of the degree of insulin deficiency, increase in the levels of glucose in blood and extent of deficiency of fluids. The primary mechanism in HHS   is the decrease in the   levels of insulin circulating   and the levels of counter regulatory hormones. Patients do not also develop marked ketoacidosis as it occurs in DKA but the amounts of insulin remain sufficient to inhibit ketogenesis and lipolysis yet insufficient   to prevent hyperglycemia. Lipolysis can also be decreased by hyperosmolarity. When this occurs, the amount of free fatty acids that is available for ketogenesis is limited. The concentration of serum glucose in patients with HHS is very high with near normal pH and serum bicarbonate. In most cases, the osmolality of serum is usually more than 320 mOsm/L but the levels of ketones in serum and urine can either be present or low.

Question 15: How would you differentiate Cushing’s disease from Cushing’s syndrome? 

Cushing syndrome occurs when the adrenal glands produce excess cortisol triggered by factors such as a tumor. However, if the source of excess production of cortisol is the pituitary, it is referred to Cushing disease, which is more common in women compared to men between 20-40 years of age. In ACTH dependent hypercortisolism, there is excess ACTH which stimulates excessive cortisol production with the loss of control of the secretion of negative feedback of ACTH. As a result, most people with Cushing syndrome lack circadian patterns of production of ACTH and when triggered by a stressor, do not increase the secretion of cortisol and ACTH.

Question 16: What is the pathogenesis of primary hyper-aldosteronism? 

Bilateral or unilateral adrenal gland hyperactivity can   trigger primary hyperaldosteronism. The latter is usually caused by benign tumors and rarely hyperplasia or an adrenal cancer. When aldosterone is autonomously secreted in excess without regulation by angiotensin II, hypokalemia sets in and triggers cardiovascular remodeling, insulin resistance, dysfunction of the endothelium, and inflammation. The differentiation and functioning of the adipose tissue is also affected. This implies that, primary hyperaldosteronism can result in features of metabolic syndrome, such as obesity, hyperglycemia, obesity, insulin resistance, and  dyslipidemia.Diabetes; Hyper- and Hypothyroidism; Adrenal Disorders Essay

Question 17: What is the basic underlying pathophysiology of Type II DM? 

The development of type II diabetes is influenced by peripheral resistance to insulin, a decline in the functioning of β-cells, hepatic production of glucose and subsequent failure of β –cells. Type 2 DM comprises of   dysfunctional hyperglycemia which   results from resistance to the action of insulin, excess secretion of glucagon, and inadequate secretion of insulin.

Question 18: What causes diabetes insipidus (DI)? 

In diabetes insipidus, patients pass   huge volumes of highly diluted urine. It can occur in the form of either nephrogenic or central DI. In the latter, there is a decrease in the secretion of ADH while in the former; there is a decrease in the ability to concentrate urine that is caused by   resistance to the action of ADH in the kidneys. The major determinant of the excretion of free water in the body is AVP. It does this by targeting the kidneys where it acts by changing the permeability of water in the collecting tubules found in the medullar and cortical. The water is then reabsorbed to the systemic circulation by osmotic equilibration   in the hypertonic interstitium.

Question 19: Explain how the negative feedback loop controls thyroid levels.

In hypothyroidism, there is excess   production and synthesis of T3 and T4. The excess production triggers a hypermetabolic state which can easily result in   thyrotoxicosis. Normally, the thyroid gland is regulated by TSH secreted in the pituitary gland which is regulated by the hypothalamus in a negative-feedback loop. Calcitonin is a hormone which affects the levels of calcium in blood produced by   the thyroid gland. Under normal circumstances,   thyroid hormone production is controlled by a mechanism involving  inhibitory and stimulatory factors. Besides, the pituitary is stimulated by TRH to release TSH continuously by long-acting thyroid stimulator (LATS).Diabetes; Hyper- and Hypothyroidism; Adrenal Disorders Essay

Question 20: How did the patient develop thyroid storm? What were the patient factors that lead to the development of thyroid storm? 

A thyroid storm refers to a hypermetabolic state which is   triggered by an excess release of thyroid hormones in people   with thyrotoxicosis. The symptoms are primarily influenced by a sudden   production and action of T3 and T4 which exceed the metabolic demands. To prevent   life threatening complication such as delirium, high-output heart failure, hypovolemia due to excess vomiting and hyperthermia symptoms must be managed rapidly.

Question 21: What causes hypothyroidism? 

In primary hypothyroidism, patients have increased levels of TSH and a decrease in the levels of free hormone. Patients with increased levels of TSH   and normal free levels of hormone ae categorized as having subclinical or mild hypothyroidism. Hypothyroidism is commonly caused by Hashimoto’s disease, a form of autoimmune thyroiditis. In primary hypothyroidism, patients have progressively high levels of TSH with increased conversion of T4 to T3 but the levels of T3 remain constant. In the early phase of the disease, the levels of TSH are increased, levels of T4 range from normal to low and levels of T3 are normal.

Question 22: What causes myxedema coma? 

The critical factors that trigger myxedema coma in a patient with underlying hypothyroidism are trauma, drugs, infection, and exposure to cold. Although most patients are not comatose, they remain at a high risk of suffering from pulmonary and cardiovascular complications. They might also exhibit hypotension, lactic acidosis, hypoventilation, and hypoglycemia and coma.

Question 23: What is a pheochromocytoma and how does it cause the classic symptoms the patient presented with? 

A pheochromocytoma refers to an adrenal gland tumor which progressively and uncontrollably secretes   catecholamines. Patients might experience hypertension due to an increase in peripheral vascular resistance which might be life-threatening. Patients also experience sweating and hypermetabolism which is associated with chronic activation   of the sympathetic receptors in hepatocytes and adipocytes. When the catecholamines trigger the inhibition of insulin released the pancreas, patients may   experience glucose intolerance. The catecholamines released   are metabolized    in chromaffin cells, epinephrine is metabolized to metanephrine, and Norepinephrine is metabolized to normetanephrine. Since all these processed occur within a tumor, clinicians can best diagnose pheochromocytomas by measuring  the associated metabolites.Diabetes; Hyper- and Hypothyroidism; Adrenal Disorders Essay

Question 24: What are the treatment goals for managing pheochromocytoma? 

The primary recommendation is a preoperative blockade of hormonally functional paraganglioma and pheochromocytoma besides medical treatment to normalize the heart rate and blood pressure, with a high-sodium diet and increased intake of fluids to prevent severe hypotension the tumor is removed. Post-surgery, the providers should closely monitor a patients; heart rate, levels of glucose and blood pressure. Diabetes; Hyper- and Hypothyroidism; Adrenal Disorders Essay