The thyroid gland is responsible for helping to regulate basal metabolism and calcium levels. The thyroid gland secretes calcitonin, synthesized from C-cells, to reduce free calcium levels in the blood. Calcitonin antagonizes parathyroid hormone (PTH), which serves to increase the free calcium levels in the blood.

Parathyroid hormone is released from the parathyroid gland. Thyroid-stimulating hormone is released from the anterior pituitary. Aldosterone is released from the adrenal cortex.

Parathyroid hormone is secreted by the parathyroid glands, and acts in a few ways to directly and indirectly increase blood calcium levels. Parathyroid hormone increases calcium reabsorption in the collecting tubule of the kidney, increases calcium absorption in the gut, and increases bone resorption to free stored calcium.

Parathyroid hormone and calcitonin act in a negative feedback loop to maintain calcium levels. Calcitonin is released from the thyroid, and serves to decrease blood calcium.

Maintaining blood calcium levels is particularly important because heart attacks can become common in low calcium settings, as calcium is crucial to maintaining cardiac muscle contractions.

Iodine is an element that plays a key role in the function of thyroxine (T4), a thyroid hormone. There are two main types of thyroid hormones: T3 and T4 (or thyroxine). Both hormones contain iodine atoms (T3 contains three and T4 contains four) and both are essential in order to maintain basal metabolic rate. Since the doctor observed a decrease in iodine concentration, the patient must experience a decrease in the production of functional thyroxine. 

Glucose concentration does not depend on iodine; therefore, an increase or decrease in glucose concentration in blood is irrelevant to this question. Thyroid-stimulating hormone (TSH) is a peptide hormone released by the anterior pituitary gland. Its main function is to stimulate the thyroid gland to release T3 and T4. Iodine atoms are not necessary for the proper functioning and production of TSH. Iodine deficiency will cause TSH to stimulate the release of dysfunctional T3 and T4 hormones. 

Of all the hormones listed, antidiuretic hormone (ADH) is the only one that neither acts on, nor is released by, the adrenal cortex. ADH is released from the posterior pituitary and causes the kidneys to retain more water.

Aldosterone (a mineralcorticoid) and cortisol (a glucocorticoid) are both incorrect choices because they are released by the adrenal cortex and would be greatly affected by trauma to that area. ACTH is released by the anterior pituitary and acts to stimulate the adrenal cortex; these hormones act as part of a negative feedback chain, so damage to the target area would temporarily cause more ACTH to be produced. The same goes for CRH, which is released by the hypothalamus and stimulates secretion of ACTH.

Endocrine glands secrete hormones into the blood stream, lined with endothelium, allowing them to travel through the blood and to act at a distant site. Exocrine organs, in contrast, secrete products into lumens that are lined with epithelium.

Mammary glands are used in lactation. Because the milk is not secreted into the blood, the mammary glands are not endocrine glands.

The hypothalamus releases hormones into the blood, such as corticotropin-releasing hormone (CRH). The pituitary releases hormones such as prolactin. The adrenal gland secretes hormones such as cortisol.

The adrenal medulla, derived from neural crest cells, is responsible for making and releasing epinephrine and norepinephrine. Epinephrine and norepinephrine are responsible for increasing heart rate and activating the sympathetic nervous system when released.  

In contrast, the adrenal cortex is derived from mesoderm and releases steroid hormones like aldosterone and cortisol. Corticotropin-releasing hormone is made by the parvocellular neurons of the hypothalamus.

Epinephrine and norepinephrine are released by the neuroendocrine cells of the adrenal medulla. In times of stress and sympathetic nervous system activation, the adrenal medulla will release epinephrine to cause blood vessel constriction. These hormones allow for the "fight-or-flight" response.

In contrast, the adrenal cortex will secrete cortisol and other mineralcorticoids in response to long-term stress. These hormones are not involved in the fight-or-flight response, and rather serve to prepare the body to endure prolonged harsh conditions, such as dehydration, starvation, and extreme temperatures. Adrenocorticotropic hormone is released from the anterior pituitary to stimulate the adrenal cortex.

Growth hormone and thyroid-stimulating hormone do not interact with the adrenal gland.

Hormones cortisol and aldosterone are synthesized in the adrenal glands. Adrenal glands are made up of the adrenal cortex and the adrenal medulla. Adrenal medulla is involved in the synthesize of catecholamines (epinephrine and norepinephrine) whereas adrenal cortex synthesizes mineralocorticoids (aldosterone), glucocorticoids (cortisol), and androgens (testosterone, DHT, and DHEA). 

Aldosterone is released upon stimulation from the renin-angiotensin system and serves to increase reabsorption of sodium in the collecting ducts of the kidney. Cortisol is released due to stress and serves to increase the metabolic rate. 

Luteinizing hormone is produced and secreted by the anterior pituitary gland.

Antidiuretic hormone is produced by the hypothalamus, but secreted by the posterior pituitary gland. Epinephrine is produced by the adrenal medulla; aldosterone is produced by the adrenal cortex. Thyroxine (T4) is produced by the thyroid.

The pancreatic alpha cells produce the hormone glucagon, which is responsible for stimulating gluconeogenesis and glycogenolysis. Gluconeogenesis is de novo formation of glucose, while glycogenolysis is the breakdown of glycogen into glucose. An increase in glucagon production through hyperactive alpha cells will result in increased blood glucose levels, at least temporarily. In a healthy individual, this will be combatted by an increase in insulin production from the pancreatic beta cell.