Significant amount of blood loss results in a sudden and large drop in blood pressure due to the decreased fluid volume in the body. To compensate for this change, the body will attempt to increase fluid retention. This is directly accomplished by increasing the level of ADH (anti-diuretic hormone) that allows reabsorption of water in the kidneys. Therefore, increased ADH level is the best response.

The function of antidiuretic hormone, or vasopressin, is to reabsorb water in the kidney tubules, thereby retaining water in the body. After dehydration, the camper's antidiuretic hormone levels would be high in order to preserve the water in his or her body.

Glucocorticoids, such as cortisol, have various functions; they reduce inflammation and prepare the body for long-term stress. Dehydration signals the body to prepare for long-term stress, increasing glucocorticoid levels.

Aldosterone increases sodium retention, drawing water out of filtrate and acting to counter dehydration. We would expect aldosterone to be elevated.

Insulin lowers blood glucose, but the camper would need to use glucose as energy causing this hormone to be decreased.

Addison's disease is a disorder in which the adrenal cortex is unable to be stimulated by adrenocorticotropic hormone (ACTH). The adrenal cortex is responsible for the secretion of aldosterone and cortisol. Aldosterone is responsible for the increased reabsorption of sodium and increased excretion of potassium, leading to water retention. This process helps raise the blood pressure. Since aldosterone is not being adequately produced in a patient with Addison's disease, the patient's blood pressure will be lower than normal.

Calcitonin generally antagonizes the effect of parathyroid hormone (PTH). When the c-cells of the thyroid sense a high calcium level, they will secrete calcitonin. Calcitonin then serves to inhibit osteoclasts and stimulate osteoblasts, promoting osteogenesis and sequestration of blood calcium into the bone matrix.

In contrast, parathyroid hormone stimulated osteoclasts and inhibits osteoblasts, causing degeneration of the bone matrix and increase in blood calcium levels.

Aldosterone is a mineralcorticoid, meaning that it is released by the adrenal cortex, not the anterior pituitary.

Mineralcorticoids are also steroids, and are able to cross the cell membrane due to their lipophilic nature. Both aldosterone and antidiuretic hormone (ADH) increase blood volume by acting on different regions of the nephrons in the kidney. Finally, angiotensin-converting enzyme (ACE) inhibitors do decrease the secretion of aldosterone, since aldosterone is activated by the renin-angiotensin system and the inhibitors block a vital conversion step in this chain.

Growth hormone is secreted by the anterior pituitary and is responsible for increased metabolism and cell growth. Growth hormone increases glucose and free fatty acid levels in the blood, increasing substrates for metabolism for other cells in the body.

All of the following are examples of the effects that elevated blood cortisol levels have on the body's metabolism. Cortisol is glucocorticoid that is released in response to stress. One main function of cortisol is also to elevate blood glucose levels after long periods of fasting. Glycogenesis is incompatible with this effector response, and thus is the correct answer.

When blood glucose is high, beta cells of the islets of Langerhans in the pancreas sense the high glucose and release insulin. Insulin binds to cells throughout the body and encourages production of additional glucose transporters on the cell surface in order to take up more glucose from the blood.

Glucagon, in contrast, is secreted when glucose levels are low and acts to prevent glucose uptake from the blood. It also stimulates gluconeogenesis and glycogenolysis.

Calcitonin, produced by the thyroid, decreases (or "tones down") the blood calcium level. Calcitonin decreases the amount of calcium in the blood by inhibiting the activity of osteoclasts, which break down bone and release calcium in the bloodstream. By inhibiting osteoclasts, calcitonin directly reduces the blood calcium level.

Parathyroid hormone, released by the parathyroid gland, increases the blood calcium level. Parathyroid hormone stimulates osteoclasts to break down bone and release calcium into the bloodstream. Insulin and glucagon are produced by the pancreas and are responsible for the regulation of blood glucose levels. Insulin lowers blood glucose and increases glycogen stores, while glucagon increases blood glucose by stimulating the conversion of glycogen to glucose in the liver.

There are three main classes of hormones: peptide hormones, steroid hormones, and tyrosine-derivatives. Peptide hormones act by binding to plasma membrane receptors. They are large and polar, preventing them from crossing the plasma membrane. Steroid hormones and tyrosine-derivatives, on the other hand, are lipid soluble and are able to cross through the plasma membrane and bind to receptors in the cytosol.

We know from the base of the question that this drug has similar chemical properties to testosterone. Testosterone is a steroid hormone; thus, our drug likely acts in a similar manner to steroid hormones by crossing the membrane and entering the cell to elicit its effects.