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Bukovinian State Medical University
Department of Developmental Pediatrics
METHODICAL INSTRUCTIONS
to the practical class for medical students of 3-rd years
Modul 1: Child’s development
Submodul 2:
Topic 4:
Subject: PHYSIOLOGICOANATOMICAL PECULIRIATIES OF
ENDOCRINE SYSTEM. METHODICS OF ENDOCRINE
GLANDS INVESTIGATION. SEMIOTICS OF HYPOAND HYPERFUNCTION OF SOME ENDOCRINE
GLANDS. TAKING CARE OF THE CHILDREN WITH
THE DISEASES OF THE ENDOCRINE SYSTEM
It is completed by:
MD, MSc, PhD Strynadko Maryna
Chernivtsy – 2007
SUBJECT: Developmental Pediatrics.
TOPIC:
OBJECTIVES:
PROFESSIONAL MOTIVATION:
BASIC LEVEL: Basic knowledge of pediatrics.
INTEGRATED SKILL ACTIVITY:
1. Care of the children. 2. Anatomy. 3. Histology. 4. Pysiology.
STUDENT’S PRACTICAL SKILLS:
THE BASIC THEORETICAL ITEMS OF INFORMATION
The major chemical regulators of the body are the internal secretions and their
secreting cells, which are collectively known as the endocrine system.
Ordinarily the endocrine system of the newborn is adequately developed, but
its functions are immature. For example, the posterior lobe of the pituitary gland
produces limited quantities of antidiuretic hormone (ADH), or vasopressin, which
inhibits diuresis. This renders the neonate highly susceptible to dehydration.
The effect of maternal sex hormones is particularly evident in the newborn
because it causes a miniature puberty. The labia are hypertrophied, and the breasts
may be engorged and secrete milk during the first few days of life. Female newborns
sometimes have pseudomenstruation from the sudden drop in the levels of
progesterone and estrogen.
The endocrine system is adequately developed at birth,but its functions are
immature. The interrelatedness of all the endocrine organs has a major effect on the
function of any one gland. The lack of homeostatic control because of various
functional deficiencies renders the infant especially vulnerable to imbalances in fluid
and electrolytes, glucose concentration, and aminoacid metabolism.
For example, corticotropin (ACTH) is produced in limited Quantities during
infancy. ACTH acts on the adrenal cortices to produce their hormones, particularly
the glucocorticoids and aldosterone. Because the feedback mechanism between
ACTH and the adrenal cortex is immature during infancy, there is much less
tolerance for stressful conditions, which affect fluid and electrolytes and the
metabolism of fats, proteins, and carbohydrates. In addition, although the islets of
Langerhans produce insulin and glucagon during fetal life and early infancy, blood
sugar levels tend to remain labile, particularly under conditions of stress.
The function of the endocrine system is:
• to secrete intracellularly synthesized hormones into the circulation,
• to serve as pacemaker substances for metabolic processes,
• together with the closely related but more rapidly reacting nervous system,
• to serve to integrate the various physiologic functions of the organism in
adjusting to external and internal environmental demands.
Endocrine substances even in extremely small concentrations are effective in
modifying metablism, behavior, and development. The endocrine system consists of
three components:
(1) the cell, which sends a chemical message by means of a hormone;
(2) the target cells, or end organs, which receive the chemical message;
(3) the environment through which the chemical is transported (blood, lymph,
extracellular fluids) from the site of synthesis to the sites of cellular action.
Some hormones, such as acetylcholine, have specific local effects; others are
secreted by specific endocrine glands and then transported by the fluids to create
their effects on target tissues at locations distant from the secreting glands. Some of
the general hormones, such as thyroid hormone and growth hormone, affect most
cells of the body, whereas the effect of others, such as the tropic hormones, is chiefly
restricted to some specific tissues.
Fig - 1. Anterior pituitary hormones and their organs. Tropic hormones: ACTH
(adrenocorticotropic hormone); TSH (thyroid-stimulating hormone); FSH (folliclestimulating hormone); LH (luteinizing hormone); ICSH (male analogue of LH);
MSH (melanocyte-stimulating hormone); GH (STH) (growth hormone)
Neuroendocrine interrelationships
Homeostasis is maintained by two regulatory systems: the endocrine and the
autonomic nervous systems (also called collectively the neuroendocrine system).
The endocrine system traditionally consists of seven glands located throughout the
body. Three additional structures are also considered endocrine glands, although for
the following reasons they are not usually included. The functions of the pineal body
(epiphysis cerebri), which is located in the cranial cavity behind the midbrain and
third ventricle, are largely speculative. The thymus, located behind the sternum and
below the thyroid gland, plays an important role in immunity, but only during fetal
life and early childhood. The placenta, which secretes ovarian hormones and
chorionic gonadotropin, is only a temporary endocrine gland. The endocrine glands
secrete chemicals known as hormones directly into the bloodstream. Because the
glands have no ducts, they are sometimes called ductless glands, in contrast to
exocrine, or duct glands.
The autonomic nervous system consists of the sympathetic and
parasympathetic systems. It controls nonvoluntary functions, specifically of smooth
muscle, myocardium, and glands. The parasympathetic system is primarily involved
in regulating digestive processes, whereas the sympathetic system functions to
maintain homeostasis during stress. The higher autonomic centers, located in the
hypothalamus and limbic system, help control both sympathetic and
parasympathetic functioning. The autonomic chemical transmitters are
acetylcholine, released by cholinergic fibers, and nor-epinephrine, released by
adrenergic fibers. Neural release of norpinephrine into the plasma produces the same
effects as secretion of this substance by the adrenal medulla. This similarity in
chemical activity demonstrates the interrelatedness between the two systems.
The neuroendocrine system acts by synthesizing and releasing various chemical
substances that regulate body functions. Information is carried by means of neural
impulses in the autonomic system and by the blood in the endocrine system. In
general, neural responses are more rapid and localized; endocrine responses are more
lasting and widespread. The two systems function synergistically because neural
impulses transmitted to the central nervous system stimulate the hypothalamus to
manufacture and release several releasing or inhibiting factors. These substances are
transferred to the anterior pituitary gland, where they lead to the release of certain
tropic hormones.
Control of the endocrine system
The endocrine system controls or regulates metabolic processes governing
energy production, growth, fluid and electrolyte balance, response to stress, and
sexual reproduction. Hormones (chemical transmitters) are released by the endocrine
gland into the bloodstream, in which they are carried to tissues that are responsive
to them (target cells). The target may be another endocrine gland or an organ or
tissue. Regulation of hormonal control is based on a feedback system. Usually the
feedback control is one of negative function, which means that an increase in one
hormone results in a decrease in another substance.
The main endocrine gland controlling the release of other hormones is the
pituitary gland (hypophysis). For this reason it is often called the "master gland."
The anterior lobe of the pituitary secretes tropic (which literally means "turning")
hormones that regulate the secretion of hormones from various target organs.
Decreased levels of target cell hormones result in increased secretion of tropic
hormones. As blood concentrations of the target hormones reach normal levels, a
negative message is sent to the anterior pituitary to inhibit its production of the tropic
hormone. For example, thyroid-stimulating hormone (TSH) responds to low levels
of circulating thyroid hormone (TH). As blood levels of thyroid hormone reach
normal concentrations, a negative feedback message is sent to the anterior pituitary,
resulting in a diminished release of thyroid-stimulating hormone.
The pituitary gland is under the influence of the hypothalamus. Especially in
times of stress, the hypothalamus receives messages from the central nervous system
that result in the synthesis and secretion of certain hypothalamic chemicals called
neurosecretions or releasing factors. These chemicals are transported by way of the
pituitary portal system to the anterior pituitary, where they stimulate the secretion of
tropic hormones. An example of this is the secretion of corticotropin-releasing factor
(CRF) by the hypothalamus, which stimulates the pituitary to secrete
adrenocorticotropic hormone (ACTH). In this instance the anterior pituitary is the
target of the hypothalamus and secondarily effects a response from another target
gland, the adrenals. The adrenals in turn secrete glucocorticoids, which have
multiple target sites throughout the body.
Not all hormones are dependent on other hormones for their release. For
example, insulin production depends on blood glucose concentrations. Other
hormones not under the control of the pituitary gland are glucagon, parathyroid
hormone (PTH), antidiuretic hormone (ADH), and aldosterone.
Because of the interdependent relationship of these glands, a malfunction in
one gland produces effects elsewhere in the body. Endocrine dysfunction may result
because of an intrinsic defect in the target gland (primary) or because of a diminished
or elevated level of tropic hormones (secondary). Endocrine problems occur from
hypofunction or hyperfunction of the glands. Primary hypofunction is usually
associated with a more profound deficiency of the target gland hormone because
little or no hormone is secreted. In secondary dysfunction the target glands secrete
some of their hormones but in smaller amounts and less rapidly. Hyperfunction may
be the result of an increase in the tropic hormones (primary) with a consequent
increase in the target gland hormones (secondary) or a hypersecretion of the target
glands.
The major hormones that promote physical growth are thyroid hormone,
growth hormone, and sex hormones. Insulin can be said to promote growth by its
effect on carbohydrate metabolism, whereas cortisol inhibits growth. Therefore,
deficiencies of growth-promoting hormones or an excess of cortisol can cause
growth retardation in children. Endocrine deficiencies can be the result of abnormal
secretory function in the glands responsible for their production, the pituitary
hormones that stimulate their secretion; or the releasing factors from the
hypothalamus. In some instances growth retardation may be the result of increased
production of factors that inhibit hormone secretion.
Thyroid hormone deficiency. Thyroid hormone deficiency is always
associated with poor growth and delayed bone maturation. Hypothyroidism that is
present from birth causes severe stunting of linear growth, which is evident early in
life. When the deficiency begins before the skeletal age of 9 or 10 years, the child
maintains infantile proportions with short legs compared to the length of the spine;
he tends to be pale, sluggish, inactive, and obese; and intellectual achievement at
school deteriorates. Acquired hypothyroidism varies with the degree and duration of
the deficiency, but skeletal age is delayed if the condition has been present more
than 12 months.
Growth hormone deficiency. Growth hormone deficiency, associated with
hypopituitarism, inhibits somatic growth in all cells of the body. Although children
with hypopituitarism are normal at birth, they show growth patterns that
progressively deviate from the normal growth rate, often beginning in infancy. The
chief complaint
in most instances is short stature. Of those who seek help, boys outnumber girls
three to one. Skeletal proportions are normal for the age, but these children appear
younger than their chronologic age, tend to be relatively inactive,and are less apt to
participate in aggressive, sporting type activities. Bone age is nearly always retarded
but is closely related to height age; the degree of retardation depends on the duration
and extent of the hormonal deficiency. Diminished function of recent onset may
show little retardation in skeletal age, whereas children with a long-standing
deficiency may evidence a skeletal age only 40% to 50% of their chronologic age.
In children with a partial growth hormone deficiency, the growth retardation is less
marked than in children with a growth hormone deficiency.
Growth hormone deficiency may be attributed to an idipathic or organic
etiology. The extent of idiopathic growth hormone deficiency may be complete or
partial, but the cause is unknown. It is frequently associated with other pituitary
hormone deficiences, such as deficiences of thyroid-stimulating hormone and
ACTH; thus it is theorized that the disorder is probably secondary to hypothalamic
deficiency. It has also been observed that there is a higher than average frequency in
some families,which indicates a possible genetic etiology in a number of instances.
The most common organic causes of growth hormone deficiency are tumors of
the pituitary or hypothalamic region, in which case the child may evidence growth
retardation for quite some time before developing any symptoms or signs of
increased intracranial pressure, local compression, or destructive effects of the
tumor. Other causes sometimes include encephalitis, head trauma (rarely), and
congenital hypoplasia of the hypothalamic area.
Sex hormone deficiency. Sex hormone deficiency that causes delayed puberty
can occur as a result either of pituitary dysfunction or of hypogonadism. A
hypofunctioning pituitary gland, as briefly discussed in the preceding segment on
endocrine dysfunction, can produce a deficiency in either the gonadotropic
hormones, which retards maturation of the gonads, or growth hormone, which will
diminish total growth during childhood. In addition, there are a large variety of
disorders that cause absence or deficiency of sex hormone secretion by their effect
on the gonads directly. These may be genital abnormalities that are related to
defective gonadal differentiation or those that are associated with functional
abnormalities of the already differentiated fetal gonad. The largest group of disorders
in which deficient gonadal development is a prominent feature includes the sex
chromosomal aberrations, e.g. Klinefelter's and Turner's syndromes.
Cortisol excess. Cortisol excess as a result of organic causes or of prolonged
cortisone therapy also has an adverse effect on growth in children. This effect is
produced by direct action on growing cartilage, interference with production of
growth hormone, or interference with the response to or production of somatomedin.
Because of the growth-suppressing effect of cortisone in excess of minimal
requirements, therapy is limited to short-term administration whenever possible.
Syndromes of primary gonadal failure. The most frequently seen disorders
associated with primary gonadal failure are the sex chromosomal defects categorized
collectively as gonadal dysgenesis, principally Turner's syndrome. Chromosomal
impairment of male sexual function is most commonly caused by Klinefelter's
syndrome. Derangements that become apparent at puberty are more common.
Clinical presentation in the female may be masculinization, sexual infantilism or
hypoplasia, primary absence of menstruation (amenorrhea), or abnormally scanty or
infrequent menstruation (oligomenorrhea or hypomenorrhea).
Psychosocial dwarfism. Psychosocial, or deprivation, dwarfism is a term
applied to children who are significantly retarded in growth because of
environmental circumstances. Children from homes in which they receive little, if
any, psychosocial stimulation display markedly delayed skeletal development, and
various tests in these children for growth hormone release are consistent with those
that indicate a pituitary dysfunction. When these children are removed from the
deprived environment, their growth proceeds at a normal or increased rate. This has
been repeatedly demonstrated in infants and very young children. Some
investigations attribute the growth retardation to malnutrition. Although this may be
a factor in infants, it may also be a contributing factor in adolescents with short
stature and delayed puberty secondary to psychosocial factors, particularly in the
loss of appetite related to the disorder anorexia nervosa.
Although the mechanism is not entirely clear, it is hypothesized that deprivation
dwarfism occurs as a response to increased cortisol secretion that results from the
prolonged stress of a disturbed environment or unsettled patterns of sleep. Evidence
indicates that deprivation dwarfism is also associated with sleep abnormalities. Since
growth hormone is secreted in largest amounts during sleep, it follows that anything
interfering with normal sleep patterns will interfere with the hormone secretion.
"For each anterior pituitary hormone there is a corresponding hypothalamic
releasing factor. A deficiency in these factors caused by inhibiting anterior pituitary
hormone synthesis produces the same effects (see text for more detailed
information).
In the male, LH is sometimes known as interstitial cell-stimulating hormone
(ICSH).
Disorders of pituitary function. The pituitary gland (hypophysis) actually
consists of two separate glands: the anterior pituitary (adenohypophysis) and the
posterior pituitary (neurohypophysis). Since each of these lobes secretes different
hormones, they are discussed separately. In general the more common pituitary
disorders during childhood affect one lobe rather than both.
The anterior pituitary secretes seven hormones: growth hormone (GH),
adrenocorticotropic hormone (ACTH), thyrotropin or thyroid-stimulating hormone
(TSH), two gonadotropins - follicle-stimulating hormone (FSH) and luteinizing
hormone (LH) in females or interstitial cell-stimulating hormone (ICSH) in males,
prolactin, and melanocyte-stim-ulating hormone (MSH). With the exception of
melanocyte-stimuiating hormone, each of these hormones controls somatic and
sexual development.
Growth hormone or somatotropin. Growth hormone promotes growth of
bone and soft tissues without affecting sexual development. Its direct effect on
protein anabolism promotes cellular growth. It accelerates fat catabolism and
utilization for energy. Although its exact effect on carbohydrate metabolism is not
known, it tends to increase the blood glucose concentration a hyperglycemic
response.
The secretion of growth hormone is under the influence of somatotropinreleasing factor (SRF) from the hypothalamus. Hyposecretion of growth hormone
during the years of skeletal growth results in a condition called dwarfism. If it occurs
after epiphyseal closure (during late adolescence) it causes a rare condition known
as Simmonds' disease (pituitary cachexia). Hypersecretion during the years of active
bone growth produces gigantism, whereas excess growth hormone during adult life
results in acrotnegaly.
Criteria for diagnosis of GHD
• Height below 3rd percentile
• Prepubertal growth velocity less than 4 cm per year.
• Bone age below the chronological age.
• Abnormal 24-hour GH secretory pattern.
• Peak GH levels less than 10 ng/ml during provocative stimulation tests.
• Low IGF-1 and IGFBP-3 levels for age.
• Resumption of growth following GH administration.
Acromegaly main symptoms
• weakness
• enlargement of the distal parts of the body
• thickening of facial features
• widening of the fingers
• hypogonadism
• narrower field of vision
• increase of the level of somatotropin hormone in the plasma
• excessive hairiness
Adrenocorticotropic hormone. The main function of adreno-corticotropic
hormone is to control the adrenal gland's secretion of the glucocorticoids and, to a
lesser extent, of androgen. The control of adrenocorticotropic hormone secretion is
under the influence of the hypothalamic chemical corticotropin-releasing factor.
Hyposecretion or hypersecretion of adrenocorticotropic hormone results in clinical
manifestations directly attributable to a lack or excess of hormones from the target
gland, the adrenal cortex.
Adison disease
• brown colour of the skin
• progressive fatigue
• loss of weight
• anerexia
• loss of blood pressure
• anemia
Thyrotropin or thyroid-stimulating hormone. As its name implies, thyroidstimulating hormone promotes and maintains growth of the thyroid gland and
stimulates its secretion of thyroid hormone (thyroxine and triiodo-thyronine). The
secretion of thyroid-stimulating hormone is controlled by thyro-tropin-releasing
factor (TRF) from the hypothalamus. Hyposecretion or hypersecretion of thyroidstimulating hormone produces symptoms directly attributable to a lack or excess of
thyroid hormone.
Gonadotropic hormones. The gonadotropic hormones follicle-stimulating
hormone, luteinizing hormone, interstitial cell-stimulating hormone, and prolactin
are responsible for the growth and maturation of the gonads at puberty and for the
ongoing stimulation of germ cell production during adulthood. The function of these
hormones is discussed in relation to puberty and will not be elaborated here.
Disorders of thyroid function
Etiological classification of goiter
1. Physiologic: puberty goiter.
2. Inflammatory: acute suppurative thyroditis, subacute viral thyroditis.
3. Autoimmune: graves disease, chronic lymphocytic thyroditis.
...
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