Drugs and Hormones - Pharmacology

Think of hormones as messengers that can increase or decrease tissue, organ, and cellular activities by the amount of hormones that are carried by the blood. Sometimes, through aging or disease, an inappropriate amount of hormones are produced causing the patient to experience adverse reactions.

Hormonal drug therapy is used to return the patient to hormonal balance by either replacing the missing hormone or by inhibiting the secretion of the hormone. Hormonal drug therapy is used for hormones produced by the pituitary, thyroid, parathyroid, and adrenal glands.


Growth hormone (GH) is secreted by the pituitary gland to influence growth. Gigantism (during childhood) and acromegaly (after puberty) can occur with GH hypersecretion.They are frequently caused by a pituitary tumor. If the tumor cannot be destroyed by radiation, or bromocriptine, a prolactin-release inhibitor can inhibit the release of GH from the pituitary. Octreotide (Sandostatin) is a potent synthetic somatostatin used to suppress growth hormone release. It is very expensive and gastrointestinal side effects are common.

If the pituitary gland produces too little GH, the patient will not reach a normal height. This is referred to as GH deficiency. Patients with this deficiency undergo GH replacement using Somatrem (protropin) and somatropin (Humatrope) to replenish the missing GH and enable normal growth to occur.

The posterior pituitary gland secretes antidiuretic hormone (ADH) and oxytocin. ADH is a vasopressin. Oxytocin is released to start labor contractions. ADH promotes water reabsorption from the renal tubules to maintain water balance in the body’s fluids. A deficiency of ADH, called diabetes insipidus (DI), causes the kidneys to excrete large amounts of water. This leads to severe fluid volume deficit and electrolyte imbalances.

Diabetes insipidus can also be caused by head injury and brain tumors resulting in trauma to the hypothalamus and pituitary gland. You must monitor fluid and electrolyte balance in patients who have diabetes insipidus. ADH replacement may be needed.

Some of the drugs used for pituitary disorders include desmopressin acetate (DDAV), desmopressin (Stimate), lypressin (Diapid), vasopressin (aqueous) (Pitressin), vasopressin tannate/oil (PitressinTannate).


There are two adrenal glands located near the top of each kidney. The adrenal gland is comprised of two parts: the adrenal medulla and the adrenal cortex.

The adrenal cortex produces glucocorticoids (cortisol) and mineralocorticoids (aldosterone). Corticosteroids promote sodium retention and potassium excre-tion. Corticotropin (Acthar) is an ACTH drug that is used to diagnosis adrenal gland disorders.

Corticotropin (Acthar) is also used to treat adrenal gland insufficiency and as an anti-inflammatory drug in the treatment of allergic reactions such as anaphy-laxis shock.

ACTH given intravenously increases the serum cortisol levels in 30 to 60 minutes if the adrenal gland is properly functioning. ACTH will eventually stimulate cortisol production if pituitary insufficiency causes steroid deficiency.

Table(Effects of adrenal hyposecretion and hypersecretion)shows the effects of an adrenal gland that produces too much (hypersecretion) or too little hormone (hyposecretion). Adrenal hyposecretion is called Addison’s disease and hypersecretion is called Cushing’s syndrome.

ACTH is a hormone released by the anterior pituitary gland that influences the glucocorticoids that are secreted by the adrenal gland. Glucocorticoids affect carbohydrate, protein, and fat metabolism in addition to muscle and blood cell activity.

Effects of adrenal hyposecretion and hypersecretion

TABLE : Effects of adrenal hyposecretion and hypersecretion.

Glucocorticoids can cause sodium absorption from the kidney that result in water retention, potassium loss, and increased blood pressure. Cortisol, the primary glucocorticoid, has anti-inflammatory, anti-allergic, and antistress effects.

Glucocorticoid therapy is used in trauma, surgery, infections, emotional upsets, and anxiety. Most glucocorticoid drugs are synthetically produced and are administered orally, IM, IV, topically (see Chapter (Skin Disorders) ), intranasally (see Respiratory Diseases), and as aerosol inhalers (see Respiratory Diseases).

Glucocorticoid drugs include beclomethasonedipropionate (Vanceril), betamethasone (Celestone), cortisone acetate (Cortone Acetate), dexamethasone (Decadron), fludrocortisone acetate (Florinef Acetate), hydrocortisone (Hydrocortone), methylprednisoline (Medrol, Solu-Medrol, Depo-Medrol), prednisolone, and prednisone. The adrenal medulla synthesizes, stores, and releases epinephrine and norepinephrine. Hypersecretion causes prolonged or continual sympathetic nervous system responses. A lack of secretion from the adrenal medulla has no significant effects.


The thyroid gland secretes two hormones that regulate protein synthesis,enzyme activity, and stimulate mitochondrial oxidation. These are thyroxine (T4) and triiodothyronine (T3). The thyroid gland secretes 20% of the circulating T3. The remaining 80% comes from degradation of T4 hormone. Approximately 40% of T4 is degraded and becomes T3.

T3 and T4 are carried in the blood by thyroxin e-binding globulin (TBG) and albumin, which protects the hormones from being degraded. T3 is more potent than T4. Only unbound free T3 and T4 are active and produce a hormonal response.

A decreased amount of T3 and T4 is produced in a condition called hypothyroidism. This is caused by a disorder of the thyroid gland or a secondary lack of TSH secretion. Hyperthyroidism is an increase in circulatory T4 and T3 caused by an overactive thyroid gland or an excessive output of thyroid hormones.


Primary hypothyroidism is characterized by a decrease in T4 and an increase in TSH levels. Primary hypothyroidism is caused by acute or chronic inflammation of the thyroid gland, radio iodine therapy, excess intake of antithyroid drugs, and surgery.

Myexedema is severe hypothyroidism characteristic by lethargy, apathy, memory impairment, emotional changes, slow speech, deep coarse voice, edemaof the eyelids and face, thick dry skin, cold intolerance, slow pulse, constipation, weight gain, and abnormal menses.

In children, hypothyroidism can have a congenital (cretinism) or pre pubertal (juvenile hypothyroidism) onset.

Hypothyroidism is treated by administering levothyroxine sodium (Levothroid, Synthroid), which increases levels of T3 and T4. Levothyroxine sodium (Levothroid, Synthroid) is also used to treat simple goiter and chronic lymphocytic (Hashimoto’s) thyroiditis.

Lyothyronine (Cytomel) is a synthetic T3 that is used for short-term treatment of hypothyroidism. It isn’t used for maintenance therapy because lyothyronine has a short half-life and duration.

Liotric (Euthroid, Thyrolar) is a mixture of levothyroxine sodium and liothy-ronine sodium with no significant advantage over levothyroxine sodium. Thyroid and thyroglubin (Proloid) are seldom used.


Hyperthyroidism is an increase in circulating T4 and T3 levels resulting from an overactive thyroid gland or excessive output of thyroid hormones. Hyperthyroidism may be mild with few symptoms or severe leading to vascular collapse and death.

Graves’ disease or thyrotoxicosis is the most common type of hyperthy-roidism and is caused by a hyper functioning thyroid gland. Graves’ disease is characterized by a rapid pulse (tachycardia), palpitations, excessive perspiration, heat intolerance, nervousness, irritability, exopthalmos (bulging eyes), and weight loss. Treatment involves surgical removal of a portion of the thyroid gland (subtotal thyroidectomy), radioactive iodine therapy, or antithyroid drugs that inhibit either the synthesis or the release of thyroid hormones.

Antithyroid drugs reduce the excessive secretion of T4 and T3 by inhibiting thyroid secretion. Thiourea derivatives (thioamides) are the drugs of choice used to decrease thyroid production.

Propylthiouracid (PTU) and methylthiouracil (Tapazole) are effective thioamideantithyroid drugs used for treating thyrotoxic crisis and in preparation for subtotal thyroidectomy. Methimazole does not inhibit peripheral conversion of T4 to T3 as does PTU, but it is 10 times more potent and has a longer half-life than PTU. Prolonged use of thioamides may cause a goiter because of theincreased TSH secretion that inhibits T4 and T3 synthesis. Minimal doses should be given when indicated to avoid goiter formation.

Strong iodide preparations such as Lugol’s solution are used to suppress thyroid function in patients having a subtotal thyroidectomy for Graves’s disease. Sodium iodide administered intravenously is useful for the management of thyrotoxic crisis.


The parathyroid glands secrete parathyroid hormone (PTH) that regulate calcium levels in the blood. A decrease in serum calcium stimulates the release of PTH. A decrease of PTH is called hypoparathyroidism and an increase in PTH is hyperparathyroidism.

Hypoparathyroidism is treated with PTH drugs and hyperparathyroidism is treated with calcitonin. Calcitonin decreases serum calcium levels by promoting renal excretion of calcium.

PTH deficiency can cause hypocalcemia, which is a deficit of serum calcium. Hypocalcemia can also be caused by vitamin D deficiency, renal impairment, or diuretic therapy.

Hypocalcemia is treated with PTH replacement that corrects the calcium deficit by promoting calcium absorption from the GI tract, promotes calcium reabsorp-tion from the renal tubules, and activates Vitamin D. Calcitriol is a vitamin D analogue that promotes calcium absorption from the GI tract and secretion of calcium of bone to the bloodstream.

Hyperparathyroidism is caused by malignancies of the parathyroid glands or ectopic PTH hormone secretion from lung cancer, hyperthyroidism, or prolonged immobility during which calcium is lost from bone.


The pancreas secretes insulin that is used to metabolize glucose. The patient contracts diabetes mellitus if insufficient insulin is produced. Diabetes mellitus is a chronic disease resulting from deficient glucose metabolism caused by insufficient insulin secretion from the beta cells of the pancreas. Table(Hypoglycemic reactions and diabetic ketoacidosis)illustrates hypoglycemic and hyperglycemic reactions caused by a deficient glucose metabolism. There are two types of diabetes mellitus: Type I and Type II.

Type 1 diabetes mellitus

Type 1 diabetes mellitus is referred to as insulin-dependent diabetes mellitus (IDDM) or juvenile-onset diabetes because Type 1 diabetes mellitus usually begins in childhood or adolescence. In Type 1 diabetes mellitus, the pancreas produces little or no insulin.

Type 1 diabetes mellitus is characterized by a sudden onset that occurs more frequently in populations descended from Northern European countries (Finland, Scotland, Scandinavia) than in those from Southern European countries, the Middle East, or Asia.

Approximately 3 in 1000 people in the United States develop Type 1 diabetes and are dependent on regular insulin injections.

Type 2 diabetes mellitus

Type 2 diabetes mellitus, sometimes called age-onset or adult-onset diabetes, is the common form of diabetes mellitus that effects approximately 5% of Americans under the age of 50 and 15% of those 50 and older. More than 90% of the diabetics in the United States have Type 2 diabetes mellitus.

Patients with Type 2 diabetes mellitus are often overweight and don’t exercise. They can produce insulin but are unable to use it effectively. Type 2

Hypoglycemic reactions and diabetic ketoacidosis

TABLE : Hypoglycemic reactions and diabetic ketoacidosis.

diabetes mellitus is more common in people of Aboriginal, Hispanic, and African-American descent. People who have emigrated to the West from India, Japan, and Australian, more likely to develop Type 2 diabetes mellitus than those who remain in their original countries.

Type 2 diabetes mellitus is considered a milder form of diabetes mellitus because of its slow onset (sometimes developing over the course of several years) and because it can usually be controlled with diet and oral medication. Type 2 diabetes mellitus is also called noninsulin-dependent diabetes (NIDDM), a term that is somewhat misleading. Many people with Type II diabetes mellitus can control the condition with diet and oral medications. However, insulin injections are sometimes necessary if treatment with diet and oral medication is not adequate.

Uncontrolled and untreated Type 2 diabetes mellitus is as serious as Type 1 diabetes mellitus.

Gestational diabetes mellitus

Gestational diabetes mellitus develops during pregnancy and resolves after delivery. Gestational diabetes mellitus develops during the second or third trimester of pregnancy in about 2% of pregnancies and is treated by diet. However, insulin injections may be required. Women who have gestational diabetes mellitus are at higher risk for developing Type 2 diabetes mellitus within 5-10 years.


The signs and symptoms of diabetes are polyuria (increased urine output), polydipsia (increased thirst), and polyphagia (increased hunger). Certain drugs increase blood sugar and can cause hyperglycemia in pre diabetic persons. These include glucocorticoids (cortisone, prednisone), thiazide diuretics (hydrochlorothiazide [HydroDIURIL]), and epinephrine. Usually the blood sugar returns to normal after the drug is discontinued.


Insulin is a protein that cannot be administered orally because GI secretions destroy the insulin structure. Insulin is therefore administered subcutaneously in a special insulin syringe (see Chapter (Route of Administration) ). The site and depth of the injection affects the absorption and is greater when given in the deltoid and abdominalareas than when given in the thighs and buttocks. Heat and massage can increase subcutaneous absorption. Cooling the area can decrease absorption.

Insulin can also be delivered via insulin pump. An insulin pump is surgically implanted in the abdomen and delivers an insulin infusion and bolus doses with meals either intraperitoneally or intravenously.

Insulin can also be administered intranasally to provide a rapid-onset effect for a short duration although this method is expensive and rarely used.

Insulin injectors deliver insulin under high pressure through the skin into fatty tissue without a needle. Insulin injectors can cause bruising, pain, and burning and are not indicated for children or the elderly. Insulin injectors are expensive.

Insulin types

There are three standard types of insulin:

  • Rapid-acting (regular or Lispro [Humalog] insulin), onset 1/2 to 1 hour, peak 2 to 4 hours, and a duration of 6 to 8 hours
  • Intermediate-acting (NPH, Humulin N, Lente, and Humulin L insulin), onset 1-2 hours, peak 6-12 hours, duration 18-24 hours
  • Long-acting (Ultralente insulin), onset 5-8 hours, peak 14-20 hours, duration 30-36 hours

There are also combinations that include Humulin 70/30 (NPH 70%, regular 30%) and Humulin 50/50 (NPH 50%, regular 50%).

Unopened insulin vials are refrigerated until needed. Once an insulin vial has been opened it may be kept at room temperature for 1 month or in the refrigerator for 3 months. An open insulin vial should not be put in the freezer, placed in direct sunlight, or in a high-temperature area.


Oral antidiabetic drugs such as sulfonylureas are administered to patients who have Type 2 diabetes mellitus to stimulate beta cells to secrete insulin. This results in an increase in insulin cell receptors, enabling cells to bind to insulinduring glucose metabolism. Sulfonylureas are chemically related to sulfonamides but lack antibacterial activity.

Sulfonylureas are classified as first- and second-generation drugs and each generation is divided into short-acting, intermediate-acting, and long-acting antidiabetics.

First-generation sulfonylureas are:

  • Tolbutamide (Orinase)
  • Acetohexamide (Dymelor)
  • Tolazamide (Tolinase)
  • Chlorpropamide (Diabinese)

Second-generation sulfonylureas include

  • Glipizide (Glucotrol)
  • Glyburide non micronized (DiaBeta, Micronase)
  • Glimepiride (Amryl)

Second-generation sulfonylureas increase tissue response to insulin and decrease glucose production by the liver. This results in greater hypoglycemic potency at smaller doses. Second-generation sulfonylureas have a longer duration of action and cause few side effects, but should not be used if the patient has liver or kidney dysfunction.

Non sulfonylureas are new drugs that affect the hepatic and GI production of glucose. For example, metformin (Glucophage) is a nonsulfonylureabiguanide compound that acts by decreasing hepatic production of glucose from stored glycogen. The result is a reduced increase in serum glucose following a meal and limits the degree of post-prandial (after a meal) hyperglycemia.

Metformin (Glucophage) also decreases the absorption of glucose from the small intestine and may increase insulin receptor sensitivity as well as peripheral glucose uptake at the cellular level. Metformin does not produce hypoglycemia or hyperglycemia and can cause GI disturbances. Metformin can be used alone. When combined with a sulfonylurea, however, it is useful in cases resistant to oral antidiabetics.

Alpha-glucosidase inhibitors (acarbose [Precose]) inhibit alpha glucosidase, the digestive enzyme in the small intestine that is responsible for the release of glucose from the complex carbohydrates in the diet. By inhibiting alpha glucosidase, carbohydrates cannot be absorbed and instead, pass into the large intestine. Acarbose has no systemic effects, is not absorbed into the body in significant amounts, and does not cause a hypoglycemic reaction.

Thiazolidinediones such as Pioglitazone (Actos), decrease insulin resistance and help muscle cells to respond to insulin and use glucose more effectively. Thiazolidinediones may be used in addition to sulfonylurea, metformin, or insulin for insulin-resistant patients. Pioglitazone (Actos) has no significant side effects or adverse effects.

Rapaglinide (Prandin) is used alone or in combination with metformin as a short-acting similar to sulfonylureas, however Rapaglinide does not cause a hypoglycemic reaction.


Glucagon is a hyperglycemic hormone secreted by the alpha cells of the islets of Langerhans in the pancreas and increases blood sugar by stimulating glycogenolysis (glycogen breakdown) in the liver.

Glucagon protects the body cells, especially those in the brain and retina, by providing the nutrients and energy needed to maintain body function. Glucagon, available for parenteral use, treats insulin-induced hypoglycemia when other methods of providing glucose are not available. Glucagon can increase blood glucose level in patients who are semiconscious or unconscious and unable to ingest carbohydrates.

Oral diazoxide (Proglycem) increases blood sugar by inhibiting insulin release from the beta cells and stimulating release of epinephrine (Adrenalin) from the adrenal medulla. Oral diazoxide (Proglycem) is used to treat chronic hypoglycemia caused by hyperinsulinism due to islet cell cancer or hyperplasia, but not for hypoglycemic reactions. Patients don't experience hypotension when taking oral diazoxide (Proglycem).

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