Types of Endocrine Disorders

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Most endocrine disorders fall into one of four categories: (1) too little hormone (hyposecretion); (2) too much hormone (hypersecretion); (3) reduced response of the target cells (hyporesponsiveness); and (4) increased response of the target cells (hyperresponsive-ness). In the first two categories, the phrases "too little hormone" and "too much hormone" here mean too little or too much for any given physiological situation. For example, as we shall see, insulin secretion decreases during fasting, and this decrease is an adaptive physiological response, not too little insulin. In contrast, insulin secretion should increase after eating, and if its increase is less than normal, this is too little hormone secretion.


An endocrine gland may be secreting too little hormone because the gland is not able to function normally. This is termed primary hyposecretion. Examples of primary hyposecretion include (1) genetic absence of a steroid-forming enzyme in the adrenal cortex, leading to decreased cortisol secretion, and (2) dietary deficiency of iodine leading to decreased secretion of thyroid hormones. There are many other causes—infections, toxic chemicals, and so on—all having the common denominator of damaging the endocrine gland.

In contrast to primary hyposecretion, a gland may be secreting too little hormone not because the gland is abnormal but because there is not enough of its tropic hormone. This is termed secondary hyposecre-tion. For example, there may be nothing wrong with the thyroid gland, but it may be secreting too little thyroid hormone because the secretion of TSH by the anterior pituitary is abnormally low. Thus, the hypose-cretion by the thyroid gland in this case is secondary to inadequate secretion by the anterior pituitary.

This example raises the next question applicable to any of the other anterior pituitary hormones as well: Is the hyposecretion of TSH primary (that is, due to a defect in the anterior pituitary), or is it secondary to a hypothalamic defect causing too little secretion of TRH? If the latter were true, then we would have the following sequence: hypothalamic defect n primary hyposecretion of TRH n secondary hyposecretion of TSH n tertiary hyposecretion of TH.

In diagnosing the presence of hyposecretion, a basic measurement to be made is the concentration of the hormone in either plasma or, for some hormones, urine. The finding of a low concentration will not distinguish between primary and secondary hyposecre-tion, however. To do this, the concentration of the relevant tropic hormone must also be measured. Thus, in our example, if the hyposecretion of TH is secondary to hyposecretion of TSH, then the plasma concentrations of both will be decreased. If the hyposecretion of TH is primary, then TH concentration will be decreased and TSH concentration will be increased because of less negative-feedback inhibition by TH over TSH secretion.

Another diagnostic approach is to attempt to stimulate the gland in question by administering either its tropic hormone or some other substance known to elicit increased secretion. The increase in hormone secretion elicited by the stimulus will be normal if the original hyposecretion is secondary, but less than normal if primary hyposecretion is the problem.

The most common means of treating hormone hy-posecretion is to administer the hormone that is missing or present in too small amounts. In cases of secondary hyposecretion, there is a choice since at least two hormones are involved. In our example, the TH deficiency resulting from primary hyposecretion of TSH could theoretically be eliminated by administering either TH or TSH.


A hormone can also undergo either primary hypersecretion (the gland is secreting too much of the hormone on its own) or secondary hypersecretion (there is excessive stimulation of the gland by its tropic hormone). One of the most common causes of primary hypersecretion is the presence of a hormone-secreting endocrine-cell tumor.

The diagnosis of primary versus secondary hypersecretion of a particular hormone is analogous to that of hyposecretion. The concentrations of the hormone and, if relevant, its tropic hormone are measured in plasma or urine. If both concentrations are elevated, then the hormone in question is being secondarily hy-persecreted. For example, if both TSH and TH are increased in plasma, then the increased TH must be secondary to increased TSH. If the hypersecretion is primary, there will be a decreased concentration of the tropic hormone because of negative feedback by the high concentration of the hormone being hyper-secreted. Again as with hyposecretion, one can get hypersecretion of a hypophysiotropic hormone, leading to secondary hypersecretion of an anterior pituitary hormone, leading to tertiary hypersecretion of the peripheral endocrine gland.

PART TWO Biological Control Systems

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

PART TWO Biological Control Systems

When an endocrine tumor is the cause of hypersecretion, it can often be removed surgically or destroyed with radiation. In many cases, hypersecretion can also be blocked by drugs that inhibit the hormone's synthesis. Alternatively, the situation can be treated with drugs that do not alter the hormone's secretion but instead block the hormone's actions on its target cells.

Hyporesponsiveness and Hyperresponsiveness

In some cases, the endocrine system may be dysfunc-tioning even though there is nothing wrong with hormone secretion. The problem is that the target cells do not respond normally to the hormone. This condition is termed hyporesponsiveness (Table 10-3). An important example of a disease resulting from hypore-sponsiveness is the major form of diabetes mellitus ("sugar diabetes"), in which the target cells of the hormone insulin are hyporesponsive to this hormone.

One cause of hyporesponsiveness is deficiency of receptors for the hormone. For example, certain men have a genetic defect manifested by the absence of receptors for dihydrotestosterone, the form of testosterone active in many target cells. In such men, these cells are unable to bind dihydrotestosterone, and the result is lack of development of certain male characteristics, just as though the hormone were not being produced.

In a second type of hyporesponsiveness, the receptors for a hormone may be normal, but some event occurring after the hormone binds to receptors may be defective. For example, the activated receptor might be unable to stimulate formation of cyclic AMP or open a plasma-membrane channel.

A third cause of hyporesponsiveness applies to hormones that require metabolic activation by some other tissue after secretion. There may be a lack or deficiency of the enzymes that catalyze the activation. For example, some men secrete testosterone normally and have normal receptors for dihydrotestosterone but are missing the enzyme that converts testosterone to di-hydrotestosterone.

In situations characterized by hyporesponsiveness to a hormone, the plasma concentration of the hormone in question is normal or elevated, but the response of target cells to administered hormone is diminished.

Finally, hyperresponsiveness to a hormone can also occur and cause problems. For example, the thyroid hormone causes an up-regulation of certain receptors for epinephrine; therefore, hypersecretion of the thyroid hormones (hyperthyroidism) causes, in turn, a hyperresponsiveness to epinephrine. One result of this is the increased heart rate typical of persons with hyperthyroidism.

TABLE 10-3 Use of Plasma Hormone

Measurements to Diagnose the Problem in a Person with Symptoms of Hyperthyroidism

TABLE 10-3 Use of Plasma Hormone

Measurements to Diagnose the Problem in a Person with Symptoms of Hyperthyroidism

Plasma Concentrations



Primary hypersecretion of TH (primary problem is in thyroid gland)


Secondary hypersecretion of TH (primary problem is in hypothalamus or anterior pituitary)

Normal TH

Hyperresponsiveness to TH (problem is in target cells for TH)



I. The endocrine system is one of the body's two major communications systems. It consists of all the glands that secrete hormones, which are chemical messengers carried by the blood from the endocrine glands to target cells elsewhere in the body.

Hormone Structures and Synthesis

I. The amine hormones are the iodine-containing thyroid hormones—thyroxine and triiodothyronine—and the catecholamines secreted by the adrenal medulla and the hypothalamus. The majority of hormones are peptides, many of which are synthesized as larger molecules, which are then cleaved.

Steroid hormones are produced from cholesterol by the adrenal cortex and the gonads, and by the placenta during pregnancy.

a. The most important steroid hormones produced by the adrenal cortex are the mineralocorticoid aldosterone, the glucocorticoid cortisol, and two androgens.

b. The ovaries produce mainly estradiol and progesterone, and the testes mainly testosterone.

Hormone Transport in the Blood

I. Peptide hormones and catecholamines circulate dissolved in the plasma water, but steroid and thyroid hormones circulate mainly bound to plasma proteins.

Hormone Metabolism and Excretion

I. The liver and kidneys are the major organs that remove hormones from the plasma by metabolizing or excreting them.

The peptide hormones and catecholamines are rapidly removed from the blood, whereas the steroid and thyroid hormones are removed more slowly. After their secretion, some hormones are metabolized to more active molecules in their target cells or other organs.


Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

Principles of Hormonal Control Systems CHAPTER TEN

Principles of Hormonal Control Systems CHAPTER TEN

Mechanisms of Hormone Action

I. The great majority of receptors for steroid and thyroid hormones are inside the target cells; those for the peptide hormones and catecholamines are on the plasma membrane.

II. Hormones can cause up-regulation and down-

regulation of their own receptors and those of other hormones. The induction of one hormone's receptors by another hormone increases the first hormone's effectiveness and may be essential to permit the first hormone to exert its effects.

III. Receptors activated by peptide hormones and catecholamines utilize one or more of the signal transduction pathways available to plasmamembrane receptors; the result is altered membrane potential or activity of proteins in the cell.

IV. Intracellular receptors activated by steroid and thyroid hormones function as transcription factors, combining with DNA in the nucleus and inducing the transcription of DNA into mRNA; the result is increased synthesis of particular proteins.

V. In pharmacological doses, hormones can have effects not seen under ordinary circumstances.

Inputs That Control Hormone Secretion

I. The secretion of a hormone may be controlled by the plasma concentration of an ion or nutrient that the hormone regulates, by neural input to the endocrine cells, and by one or more hormones.

II. The autonomic nervous system is the neural input controlling many hormones, but the hypothalamic and posterior pituitary hormones are controlled by neurons in the brain.

Control Systems Involving the Hypothalamus and Pituitary

I. The pituitary gland, comprising the anterior pituitary and the posterior pituitary, is connected to the hypothalamus by a stalk containing nerve axons and blood vessels.

II. Specific axons, whose cell bodies are in the hypothalamus, terminate in the posterior pituitary and release oxytocin and vasopressin.

III. The anterior pituitary secretes growth hormone (GH), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), prolactin, and two gonadotropic hormones—follicle-stimulating hormone (FSH) and luteinizing hormone (LH). The functions of these hormones are summarized in Figure 10-14.

IV. Secretion of the anterior pituitary hormones is controlled mainly by hypophysiotropic hormones secreted into capillaries in the median eminence of the hypothalamus and reaching the anterior pituitary via the portal vessels connecting the hypothalamus and anterior pituitary. The actions of the hypophysiotropic hormones on the anterior pituitary are summarized in Figure 10-16.

V. The secretion of each hypophysiotropic hormone is controlled by neuronal and hormonal input to the hypothalamic neurons producing it.

a. In each of the three-hormone sequences beginning with a hypophysiotropic hormone, the third hormone exerts a long-loop negative-feedback effect on the secretion of the hypothalamic and/or anterior pituitary hormone.

b. The anterior pituitary hormone may exert a short-loop negative-feedback inhibition of the hypothalamic releasing hormone(s) controlling it.

c. Hormones not in a particular sequence can also influence secretion of the hypothalamic and/or anterior pituitary hormones in that sequence.

Candidate Hormones

I. Substances that are suspected of functioning as hormones but have not yet been proven to do so are called candidate hormones.

II. Melatonin is a candidate hormone secreted with a 24-h rhythm by the pineal gland; it probably exerts effects on the body's circadian rhythms.

Types of Endocrine Disorders

I. Endocrine disorders may be classified as hyposecretion, hypersecretion, and target-cell hyporesponsiveness or hyperresponsiveness.

a. Primary disorders are those in which the defect is in the cells that secrete the hormone.

b. Secondary disorders are those in which there is too much or too little tropic hormone.

c. Hyporesponsiveness is due to an alteration in the receptors for the hormone, to disordered postreceptor events, or to failure of normal metabolic activation of the hormone in those cases requiring such activation.

II. These disorders can be distinguished by measurements of the hormone and any tropic hormones under both basal conditions and during experimental stimulation of the hormone's secretion.


endocrine system

steroid hormone

endocrine gland




target cell


amine hormone


thyroid gland




thyroxine (T4)


triiodothyronine (T3)


thyroid hormones (TH)




adrenal gland


adrenal medulla


adrenal cortex

tropic hormone

epinephrine (E)

pituitary gland

norepinephrine (NE)



anterior pituitary

peptide hormone

posterior pituitary


median eminence

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

PART TWO Biological Control Systems

PART TWO Biological Control Systems hypothalamo-pituitary portal vessels oxytocin vasopressin antidiuretic hormone (ADH)

hypophysiotropic hormones follicle-stimulating hormone (FSH)

luteinizing hormone (LH) growth hormone (GH) thyroid-stimulating hormone

(TSH) prolactin adrenocorticotropic hormone

(ACTH) gonadotropic hormones insulin-like growth factor I (IGF-I)

corticotropin releasing hormone (CRH) growth hormone releasing hormone (GHRH) thyrotropin releasing hormone (TRH) gonadotropin releasing hormone (GnRH) somatostatin (SS) dopamine (prolactin-

inhibiting hormone, PIH) long-loop negative feedback short-loop negative feedback candidate hormones melatonin pineal gland


1. What are the three general chemical classes of hormones?

2. What essential nutrient is needed for synthesis of the thyroid hormones?

3. Which catecholamine is secreted in the largest amount by the adrenal medulla?

4. What are the major hormones produced by the adrenal cortex? By the testes? By the ovaries?

5. Which classes of hormones are carried in the blood mainly as unbound, dissolved hormone? Mainly bound to plasma proteins?

6. Do protein-bound hormones cross capillary walls?

7. Which organs are the major sites of hormone excretion and metabolic transformation?

8. How do the rates of metabolism and excretion differ for the various classes of hormones?

9. What must some hormones undergo after their secretion to become activated?

10. Contrast the locations of receptors for the various classes of hormones.

11. How do hormones influence the concentrations of their own receptors and those of other hormones? How does this explain permissiveness in hormone action?

12. Describe the sequence of events when peptide or catecholamine hormones bind to their receptors.

13. Describe the sequence of events when steroid or thyroid hormones bind to their receptors.

14. What are the direct inputs to endocrine glands controlling hormone secretion?

15. How does control of hormone secretion by plasma mineral ions and nutrients achieve negative-feedback control of these substances?

What roles does the autonomic nervous system play in controlling hormone secretion? What groups of hormones receive input from neurons located in the brain rather than in the autonomic nervous system?

Describe the anatomical relationships between the hypothalamus and the pituitary.

Name the two posterior pituitary hormones and describe their site of synthesis and mechanism of release.

List all six well-established anterior pituitary hormones and their functions.

List the major hypophysiotropic hormones and the hormone whose release each controls.

What kinds of inputs control secretion of the hypophysiotropic hormones?

Diagram the CRH-ACTH-cortisol system.

What is the difference between long-loop and short-

loop negative feedback in the hypothalamo-anterior pituitary system?

How would you distinguish between primary and secondary hyposecretion of a hormone? Between hyposecretion and hyporesponsiveness?


masculinization of a female pharmacological effect iodine-deficient goiter jet lag seasonal affective disorder hyposecretion hypersecretion hyporesponsiveness hyperresponsiveness primary hyposecretion secondary hyposecretion tertiary hyposecretion primary hypersecretion secondary hypersecretion tertiary hypersecretion diabetes mellitus absence of receptors for dihydrotestosterone


(Answers are given in Appendix A.)

1. In an experimental animal, the sympathetic preganglionic fibers to the adrenal medulla are cut. What happens to the plasma concentration of epinephrine at rest and during stress?

2. During pregnancy there is an increase in the production (by the liver) and, hence, the plasma concentration of the major plasma binding protein for the thyroid hormones (TH). This causes a sequence of events involving feedback that results in an increase in the plasma concentration of TH, but no evidence of hyperthyroidism. Describe the sequence of events.

3. A child shows the following symptoms: deficient growth; failure to show sexual development;

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

Principles of Hormonal Control Systems CHAPTER TEN

Principles of Hormonal Control Systems CHAPTER TEN

decreased ability to respond to stress. What is the most likely cause of all these symptoms?

4. If all the neural connections between the hypothalamus and pituitary were severed, the secretion of which pituitary hormones would be affected? Which pituitary hormones would not be affected?

5. An antibody to a peptide combines with the peptide and renders it nonfunctional. If an animal were given an antibody to somatostatin, the secretion of which anterior pituitary hormone would change and in what direction?

6. A drug that blocks the action of norepinephrine is injected directly into the hypothalamus of an experimental animal, and the secretion rates of several anterior pituitary hormones are observed to change. How is this possible, since norepinephrine is not a hypophysiotropic hormone?

7. A person is receiving very large doses of a cortisol-like drug to treat her arthritis. What happens to her secretion of cortisol?

8. A person with symptoms of hypothyroidism (for example, sluggishness and intolerance to cold) is found to have abnormally low plasma concentrations of T4, T3, and TSH. After an injection of TRH, the plasma concentrations of all three hormones increase. Where is the site of the defect leading to the hypothyroidism?

Vander et al.: Human I II. Biological Control I 11. Muscle I I © The McGraw-Hill

Physiology: The Systems Companies, 2001

Mechanism of Body

Vander et al.: Human I II. Biological Control I 11. Muscle I I © The McGraw-Hill

Physiology: The Systems Companies, 2001

Mechanism of Body

Defects And Hormone

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