Hypoactivity, Hyperactivity and Related Endocrine Disorders

Every endocrine gland described earlier in this chapter secretes its hormone within a fairly narrow, appropriate physiological range under normal conditions, held there chiefly by the feedback mechanisms described in the preceding section. Disease affecting any of these glands, however, can disturb this balance in either of two directions: hypoactivity (or hyposecretion), in which the gland secretes too little of its hormone, or hyperactivity (or hypersecretion), in which it secretes too much. Because each hormone has its own specific physiological role, a hypo- or hyperactivity disorder of a particular gland produces its own characteristic and often clearly distinguishable pattern of symptoms, several of which are named explicitly in the WBCHSE syllabus.

Growth hormone disorders illustrate this hypo/hyper contrast especially clearly, and also show how the timing of the disorder relative to a person's skeletal development changes its outcome. If growth hormone secretion is deficient during childhood, before the epiphyseal growth plates of the long bones have fused, the result is dwarfism: severely stunted overall stature, though — unlike some other growth disorders — with body proportions that generally remain close to normal, since growth is reduced roughly uniformly across the skeleton. If growth hormone is instead secreted in excess during childhood, again before epiphyseal fusion, the long bones continue to lengthen for an abnormally extended period, producing gigantism, in which final adult height is abnormally increased, sometimes very substantially so. If growth hormone excess instead develops (or persists) in an adult, after the epiphyseal plates have already fused and the long bones can therefore no longer increase in length, the excess growth hormone instead causes disproportionate thickening and enlargement of the bones and soft tissues that can still grow — chiefly the hands, feet, jaw and facial features — together with coarsening of the skin, a condition called acromegaly, distinguished from gigantism precisely by this difference in the timing of onset relative to bone maturity.

Thyroid hormone disorders show a similarly informative range of hypo- and hyperactivity conditions. Cretinism results from a deficiency of thyroid hormone specifically during infancy and early childhood, a period when adequate thyroid hormone is essential for normal development of the nervous system as well as of the skeleton; the result is a combination of severely stunted physical growth together with impaired mental development, underlining why thyroid hormone's role in growth is not confined to bone alone, unlike growth hormone's more purely skeletal effect. Simple (iodine-deficiency) goitre arises when insufficient dietary iodine limits the thyroid gland's ability to synthesise T3 and T4; falling thyroid hormone level removes the normal negative feedback restraint on TSH secretion from the pituitary, so TSH rises and continuously over-stimulates the iodine-starved thyroid tissue, causing it to enlarge visibly in the neck even though its hormone output remains low — a goitre is therefore, somewhat counterintuitively, a sign of thyroid hormone deficiency (hypoactivity) rather than excess, brought about indirectly through this feedback mechanism. Exophthalmic goitre (Graves' disease), by contrast, is a hyperactivity disorder: an autoimmune condition in which antibodies mimic the action of TSH, chronically overstimulating the thyroid gland to secrete excess T3/T4 (hyperthyroidism), producing an enlarged thyroid together with a raised metabolic rate, weight loss despite normal or increased appetite, and, characteristically, protrusion of the eyeballs (exophthalmos) caused by swelling of the tissue behind the eyes. …