Transcript Diseases of the Endocrine System

Human Diseases
A Systemic Approach
Sixth Edition
Mary Lou Mulvihill
Mark Zelman
Paul Holdaway
Elaine Tompary
Jill Raymond
Chapter 13
Diseases of the Endocrine System
Mulvihill, Zelman, Holdaway, Tompary, and Raymond
Human Diseases: A Systemic Approach, 6e
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Chapter 13
Diseases of the Endocrine System
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The Endocrine System
Diabetes
Diabetes (continued)
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Functions of the Endocrine Glands
 Secrete hormones
 Major organs
– Hypothalamus
– Pituitary gland
– Thyroid gland
– Parathyroid glands
– Pancreatic islets
– Adrenal glands
– Testes and ovaries
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Anatomy and Physiology of the
Endocrine System
 The endocrine system is a collection of
glands that secrete hormones into the
bloodstream.
 Hormones are chemicals that act on target
organs to increase or decrease the
target’s activity level.
 The endocrine system is instrumental in
maintaining homeostasis.
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Click on the screenshot to view an animation showing the
endocrine system.
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Figure 13-1: The endocrine glands.
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Types of Glands
 Two types of glands in
 Endocrine glands, on the
the body: exocrine glands
and endocrine glands.
 Exocrine glands release
their secretions into a
duct that carries them to
the outside of the body.
 Example: sweat glands
other hand, release
hormones directly into the
bloodstream. Since they
have no ducts, they are
referred to as ductless
glands.
 Example: thyroid gland
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Glands of the Endocrine System
 2 adrenal glands
 4 parathyroid glands
 Pancreas
 Pineal gland
 Pituitary gland
 2 ovaries in the female
 2 testes in the male
 Thymus gland
 Thyroid gland
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Figure 13-2: The pituitary gland and its relation to the brain.
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Figure 13-3: Anterior pituitary gland and its target organs.
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Physiology of the Endocrine Glands
 Hormones are released from endocrine glands
into the bloodstream, where they affect activity in
cells at distant sites.
– Some hormones affect the whole body whereas
others act only on target organs. Most hormones are
composed of proteins or chains of amino acids;
others are steroids or fatty substances derived from
cholesterol.
 The pituitary gland, which is sometimes called
the master gland, is controlled by the
hypothalamus.
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Physiology of the Endocrine Glands
(continued)
 The body is conservative and secretes
hormones only as needed.
– Control via negative feedback
 Overactivity = hyperactive gland
– Gland secretes an excessive amount of its hormone
– May be caused by a hypertrophied gland or by a
glandular tumor.
 Underactivity = hypoactive
– A gland that fails to secrete its hormone or secretes
an inadequate amount
– May be caused by disease or tumor, or it may be
caused by trauma, surgery, or radiation
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The Pituitary Gland
 Located on the underneath side of the
brain.
 Small pea-sized gland is divided into an
anterior lobe and a posterior lobe.
 Both lobes are controlled by the
hypothalamus in the brain.
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The Anterior Pituitary
 Secretes seven
hormones:
 Growth hormone (GH), also
 Follicle-stimulating hormone
called somatotropin, promotes
growth of the body by
stimulating cells to rapidly
increase in size and divide.
 Thyroid-stimulating hormone
(TSH) regulates the function 
of the thyroid gland.
 Adrenocorticotropin hormone
(ACTH) regulates the function
of the adrenal cortex.

 Prolactin (PRL) stimulates
milk production in the breast
following pregnancy and birth.
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(FSH) responsible for the
development of ova in ovaries
and sperm in testes; also
stimulates the ovary to secrete
estrogen.
Luteinizing hormone (LH)
stimulates secretion of sex
hormones in both males and
females and plays a role in
releasing ova in females.
Melanocyte-stimulating
hormone (MSH) stimulates
melanocytes to produce more
melanin, darkening the skin.
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The Posterior Pituitary
 Secretes two hormones:
 Antidiuretic hormone (ADH), also called
vasopressin, promotes water reabsorption
by the kidney tubules.
 Oxytocin stimulates uterine contractions
during labor and delivery, and after birth
the release of milk from the mammary
glands.
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The Structure and Function of
the Pituitary Gland
 Hypophysis: has two parts
Anterior = adenohypophysis
– Activity directed by the hypothalamus
– Secretes six tropic hormones
– Regulates the adrenal gland
Posterior = neurohypophysis
– Receives hormones secreted by the hypothalamus
and then stores them for subsequent release
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Diseases of the Anterior Pituitary
 Hyperpituitarism
– Giantism
– Acromegaly
 Hypopituitarism
– Absence of tropic hormones
– Pituitary dwarf
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Hyperpituitarism – Anterior
Pituitary
 Giantism: hypersecretion of growth
hormone prior to puberty
– Retards normal closure of bone seal
– Decreased sexual development
– Mental development normal or retarded
 Etiology: adenoma
 Treatment: removal of adenoma or
radiation to reduce the size of the tumor
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Hyperpituitarism – Anterior Pituitary
 Acromegaly
– Hypersecretion of growth hormone after puberty
– Long bones no longer grow
– Excessive growth of soft tissue
– Enlargement of the face with coarse facial features
– Protrusion of the tongue
– Curvature of the spine
 Etiology: adenoma
 Treatment: surgical removal, radiation,
supportive treatments
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Hypopituitarism – Pituitary
 Etiology
– Damage to the anterior lobe of the pituitary gland
– Fracture at the base of the skull, tumor, ischemia
– Inadequate secretion of hormones
 Mild or severe
 Panhypopituitarism: entire anterior lobe is
destroyed
– No pituitary hormones are secreted
 Pituitary dwarf
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Figure 13-4: Effects of pituitary failure.
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Abnormalities – Absence of
Tropic Hormones
 Lack of thyroid hormone: lethargy
 Lack of ACTH: salt imbalance, improper
metabolism of nutrients
– ACTH essential for life
 Absence of gonadotropic hormones
– Depresses sexual function
– Before puberty – impaired sexual development
– After puberty
– Cessation of menstruation
– Aspermia in males
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Pituitary Dwarf
 May occur in children
– Inadequate growth hormone
– Mentally bright but small and underdeveloped
sexually
– All growth processes are retarded; teeth are
late in erupting.
– Replacement therapy with injections of growth
hormone is currently used to treat children
with pituitary dwarfism.
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Hypopituitarism – Treatment
 Hormonal supplements
– Thyroxine, cortisone, growth hormone, and
sex hormones can compensate for the
dysfunctional glands.
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Function of the Posterior
Pituitary Gland
 Posterior pituitary, or neurohypophysis
– Secretes oxytocin, and vasopressin (ADH)
 Oxytocin: causes smooth muscle
contraction of the uterine muscles
 ADH: prevents excessive water loss
through the kidneys
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Hyposecretion of the
Posterior Pituitary Gland
 Diabetes insipidus
– Deficiency of ADH
– In the absence of ADH, water is not reabsorbed by
the kidney and is lost in the urine. Extreme thirst or
polydipsia and excessive production of diluted urine
or polyuria results.
 A central diabetes insipidus can result from
inadequate production of ADH by the
hypothalamus or failure of the pituitary gland to
release ADH into the bloodstream.
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Hyposecretion of the
Posterior Pituitary Gland (continued)
 Nephrogenic diabetes insipidus: ADH levels are
normal
– Involves a defect in the kidney; the kidney fails to
concentrate urine in response to the instructions of
ADH.
 Excessive water loss can quickly lead to
dehydration.
 Treatment: the underlying cause of diabetes
insipidus must be corrected. Modified forms of
ADH may be taken orally, by injection, or by
nasal spray to maintain normal urine output.
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Figure 13-6: Normal action of antidiuretic hormone (ADH).
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Figure 13-7: Effect of antidiuretic hormone (ADH)
deficiency.
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The Thyroid Gland
 Resembles a butterfly
 Produces the
in shape; has right and
left lobes
 Located on either side
of the trachea and
larynx
 Thyroid cartilage, or
Adam’s apple, is
located just below the
thyroid gland
hormones thyroxine,
also known as T4,
and triiodothyronine,
which is called T3
 These are produced
in the thyroid gland
from the mineral
iodine.
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Structure and Function of the
Thyroid Gland
 Regulates metabolic rate
 Secretes thyroxine, governs cellular oxygen
consumption, and thus, energy and heat
production; the more oxygen that is used, the
more calories are metabolized (“burned up”).
Thyroxine assures that enough body heat is
produced to maintain normal temperature even
in a cold environment.
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Structure and Function of the
Thyroid Gland (continued)
 Structure of the thyroid gland
– Located in the neck region, one lobe on either side of
the trachea; a connecting strip, or isthmus, anterior to
the trachea, connects the two lobes
– Just below the Adam’s apple, the protrusion formed
by part of the larynx
– The thyroid gland consists of follicles, microscopic
sacs. Within these protein-containing follicles, the
thyroid hormones, thyroxine and triiodothyronine, are
made. Thin-walled capillaries run between the follicles
in a position ideal to receive the thyroid hormones.
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The Thyroid Gland
 Also secretes calcitonin in response to
hypercalcemia (too high blood calcium
level).
 Its action is the opposite of parathyroid
hormone and stimulates the increased
deposition of calcium into bone, thereby
lowering blood levels of calcium.
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Figure 13-8: The thyroid gland.
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Function of the Thyroid Gland
 The thyroid gland synthesizes, stores, and
releases thyroid hormones, which contain
iodine.
– Most of the iodide ions of the body are taken into the
thyroid gland by a mechanism called the iodide trap.
– Iodine combines with an amino acid; two of these
groups join, and the thyroid hormones are formed.
 The hormones are stored until needed and then
released into the blood capillaries. In the blood,
the thyroid hormones combine with plasma
proteins.
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Effects of Thyroid Hormones
 Thyroxine: secreted in the largest quantity.
– Thyroxine stimulates cellular metabolism by
increasing the rate of oxygen use with subsequent
energy and heat production.
– Nutrients are converted to energy in the presence of
oxygen and the waste products of metabolism,
including carbon dioxide, are formed.
– As cellular metabolism increases, respiration and
cardiac output increases.
– Heat is produced through cellular metabolism
– Increases secretion of digestive enzymes and
movement through the digestive system.
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Figure 13-9: Effects of thyroxine.
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Control of Circulating
Thyroxine Level
 Anterior pituitary gland stimulates the thyroid by
releasing thyroid-stimulating hormone, TSH.
 The thyroid, in turn, releases thyroxine, which
circulates in the blood to all cells and tissues.
When the level of circulating thyroxine is high,
the anterior pituitary is inhibited and stops
releasing TSH (negative feedback mechanism).
– An adequate level of thyroxine prevents further
synthesis of the hormone. When the level of thyroxine
falls, the anterior pituitary is released from the
inhibition, and once again sends out TSH. This
feedback mechanism is shown in Figure 13.10.
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Figure 13-10: Control of thyroxine secretion through
negative feedback.
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Histology of normal thyroid gland showing follicles
containing thyroglobin.
(© M. Peres / Custom Medical Stock Photo.)
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Nodular goiter. Note the distorted follicles.
(© O.J. Staats / Custom Medical Stock Photo.)
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Negative Feedback Failure
 Constitutes one basis for a thyroid disease
 The thyroid gland may be perfectly healthy, but if
the body’s iodine supply is inadequate, the gland
cannot produce thyroxine.
 It is possible for the thyroid gland to be overstimulated or understimulated by the anterior
pituitary.
 The thyroid gland itself may be diseased, with a
resultant hyperactivity or hypoactivity. These are
some of the conditions that will be discussed.
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Goiter
 An enlargement of the thyroid gland.
 May be caused by hypoactivity or hyperactivity
of the thyroid or a deficiency in iodine needed to
synthesize thyroid hormones
 Types: diffuse colloidal goiter or nontoxic goiter
 Endemic goiter because it is common in a
particular geographic region
– The usual cause of an endemic goiter is insufficient
iodine in the diet.
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Goiter (continued)
 Etiology of goiter
– Continuous secretion of thyroid-stimulating hormone
causes the thyroid gland to enlarge as a
compensatory mechanism.
– An enlargement of the neck is generally the only
symptom. Usually enough thyroxine is produced to
prevent the symptoms of hypothyroidism.
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Goiter (continued)
 Treatment: iodides: the use of iodized salt prevents
endemic goiter formation. If the goiter is very advanced,
surgery may be necessary. A very large goiter puts
pressure on the esophagus, causing difficulty in
swallowing, or presses on the trachea, causing a cough
or choking sensation.
 Other factors can cause a simple diffuse colloidal goiter;
for example, a defect in the thyroxine-synthesizing
mechanism. A young girl entering adolescence may
develop this type of goiter because of an increased need
for thyroxine at this time.
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Adenomatous or Nodular Goiter
 Secrete an excessive amount of thyroxine, a
condition of hyperthyroidism
 Symptoms: nervousness and tremors, a
shakiness, particularly in the hands: metabolism
increases, causing sweating and a rapid pulse; a
nodule or adenoma may put pressure on the
trachea or esophagus.
 Treatment: Surgery is sometimes necessary to
remove part of the thyroid gland, but medication
is often effective in preventing further
enlargement.
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Graves’ Disease
 Goiter develops; the entire gland hypertrophies, and
there are no nodules
 Severe hyperthyroidism
 More common in women than in men and usually affects
young women
 Characteristic facial expression is strained and tense,
and there is a stare in the eyes. The eyeballs protrude
outward, a condition called exophthalmos. This is
caused by edema in the tissue behind the eyes. The
bulging of the eyes can be so severe that the eyelids do
not close, and the swelling sometimes damages the
optic nerve. This symptom generally persists even when
the hyperthyroidism is corrected.
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Graves’ Disease (continued)
 The person has a tremendous appetite but loses weight
to the point of appearing emaciated, as calories are
burned up at a rapid rate. Thyroxine speeds the passage
of food through the digestive tract. There is no time for
the normal reabsorption of water from the large intestine,
so diarrhea frequently accompanies the disease.
 Tachycardia, rapid pulse rate, and palpitation are also
among the symptoms. The person is extremely nervous,
excitable, and is always tired but has difficulty sleeping
because of the hyperactivity of the body. The high
metabolic rate causes excessive heat production, which
results in profuse perspiration. The skin is always moist,
and an insatiable thirst follows the loss of water.
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Signs and Symptoms of
Graves’ Disease












Exophthalmos
Profuse perspiration
Hand tremors
Goiter
Weight loss
Nervousness/excitability
Rapid pulse
Polydipsia
Diarrhea
Tachypnea
Insomnia
Graves’ disease is an autoimmune condition in which antibodies to a thyroid antigen
stimulate hyperactivity of the thyroid gland. This causes the thyroid to produce too
much thyroxine.
 Graves’ disease can sometimes be treated with medication that inhibits the synthesis
of thyroxine, or by administration of radioactive iodine, which destroys the thyroid
gland. Removal of the thyroid gland, however, may be necessary. If the gland is
removed, hormonal supplements must be given. Partial removal of the thyroid gland
allows the remaining portion to secrete hormones.
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Hypothyroidism
 Myxedema severe hypothyroidism, an inadequate level
of thyroxine
 Symptoms: bloated appearance, thick tongue, puffy
eyelids, dry scaly skin, little perspiration, muscular
weakness and somnolence, excessive sleepiness,
sluggish mental and physical processes, slurred speech,
slow reflexes, decreased heart rate, slowed circulation,
edema to develop.
 Lack of thyroxine increases the amount of circulating
lipids, which leads to the development of atherosclerosis.
 The digestive system works sluggishly, so the patient
suffers from constipation. Weight gain also accompanies
the disease.
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Myxedema
 Affects women more than men, and usually affects
women of middle age.
 Etiology: Radiation damage to the thyroid gland or
develops after thyroid surgery if thyroxine is not
administered
 Primary disease of the thyroid gland or secondary to
pituitary disease.
– If the pituitary gland does not secrete thyroid-stimulating
hormones, the thyroid gland ceases to function.
 Myxedema is treated by administering thyroxine. The
condition generally responds well to treatment, and the
symptoms disappear.
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Cretinism
 Congenital thyroid deficiency in which thyroxine is not synthesized;




thyroxine is essential to both physical and mental development.
Mental retardation and an abnormal, dwarfed stature
Etiology: error in fetal development if the thyroid gland fails to form
or is nonfunctional, or may be endemic where the mother suffers
from an inadequate iodine supply
The cretin is a dwarf with a stocky stature and a characteristically
protruding abdomen. The sexual organs do not develop, and the
face of the cretin is typically misshapen: a broad, sunken nose,
small eyes set far apart, puffy eyelids, and a short forehead. A thick
tongue protrudes from a wide-open mouth, and the face is
expressionless.
The earlier this condition is diagnosed and treated with thyroxine,
the more optimistic is the prognosis. Lifelong hormonal therapy will
be required.
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Diagnostic Test
Activity of the Thyroid Gland
 Tests to determine the activity of the thyroid gland are
based on this combination of triiodothyronine (T3) and
thyroxine (T4) with plasma proteins.
 Serum is incubated with radioactive thyroid hormones
and resin.
– The resin absorbs the hormones that are not bound to the blood
proteins.
– Radioactivity counts of the serum and resin are made, and the
percentage of thyroid hormones absorbed by the resin is
calculated.
– A low percentage of absorption indicates a poorly functioning
thyroid gland.
– A high percentage of absorption indicates hyperactivity.
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Two Adrenal Glands
 Located above each of the kidneys
 Each gland is composed of two sections:
– Adrenal cortex
– Adrenal medulla
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Figure 13-11: The adrenal glands.
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Outer Adrenal Cortex Manufactures
Several Different Families of Hormones
 They are all produced by
 The adrenal cortex of
the cortex; they are
collectively referred to as
corticosteroids.
 The mineralocorticoid
hormone, aldosterone,
regulates sodium (Na+)
and potassium (K+)
levels in the body.
 The glucocorticoid
hormone, cortisol,
regulates carbohydrates
in the body.
both men and women
secretes steroid sex
hormones: androgens,
estrogen, and
progesterone. They
regulate secondary
sexual characteristics.
 The inner portion of the
adrenal medulla secretes
epinephrine and
norepinephrine.
 Epinephrine is also called
adrenaline.
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Structure and Function of the
Adrenal Glands
 The adrenal glands are located on top of
each kidney. Each of the glands consists
of two distinct parts: an outer part (the
adrenal cortex) and an inner section (the
adrenal medulla). The cortex and medulla
secrete different hormones. The adrenal
cortex is stimulated by ACTH,
adrenocorticotropic hormone, from the
anterior pituitary gland.
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Disease of the Adrenal Cortex
 Hyperactivity of the adrenal cortex is usually
caused by hyperplasia (enlargement of the
glands), a tumor. Hyperactivity may also result
from over-stimulation by the anterior pituitary
gland.
 Hypoactivity of the adrenal cortex sometimes
results from a destructive disease, such as
tuberculosis. Some steroid hormones can cause
the adrenal glands to atrophy by interfering with
the normal control mechanism for corticosteroid
release.
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Hyperadrenalism
 Overactivity of the adrenal cortex
(hyperadrenalism) can take different forms
depending on which group of hormones
are secreted in excess.
– Cushing’s syndrome
– Conn’s syndrome
– Adrenogenital syndrome
– Pheochromocytoma
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Table 13-1: Signs and symptoms of Graves’ disease.
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Cushing’s Syndrome
 Excess of glucocorticoid hormones
 Signs and symptoms: result from decreased
protein synthesis
– Hyperglycemia (adrenal diabetes)
– Mobilization of lipids (trunk obesity, buffalo hump, but
the arms and legs remain normal, moon shaped face)
– Sodium and water, retention resulting in hypertension
– Atherosclerosis develops as a result of excess
circulating lipid.
– Muscular weakness and fatigue accompany the
disease, and the person finds it difficult even to climb
stairs.
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Cushing’s Syndrome
(continued)
 Signs and symptoms: result from decreased
protein synthesis (continued)
– Easy bruisability, striae (stretch marks) develop on
the abdomen, buttocks, and breasts
– Poor wound healing
– Increased susceptibility to infection
– Bones, particularly the vertebrae and ribs, are likely to
fracture.
 Treatment: surgical removal of the enlarged
glands or tumor can correct the condition.
Hormonal therapy is then required to replace the
hormones normally secreted by the adrenal
cortex.
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Conn’s Syndrome
 Aldosterone is secreted in excess
– Retention of sodium and water, and abnormal loss of
potassium in the urine
– Hypertension develops as a result of the salt
imbalance and water retention.
– Muscles become weak to the point of paralysis.
– Excessive thirst (polydipsia) caused by the salt
retention
– Polyuria follows the great intake of water.
 Conn’s syndrome is usually caused by a tumor
that can be removed surgically, and the
prognosis is usually good.
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Adrenogenital Syndrome
 Adrenal virilism
– Androgens, male hormones, are secreted in excess. If this
occurs in children, it stimulates premature sexual development.
Sex organs of a male child greatly enlarge. In a girl, the clitoris
enlarges, a male distribution of hair develops, and the voice
deepens.
 Etiology: a block in the synthesis of cortisol from
cholesterol or from other corticosteroids.
– Cortisone is generally inactive until it is converted to cortisol.
Cortisone is prepared synthetically from animal and plant tissue.
Inasmuch as steroids cannot be converted to cortisol, because of
the blockage in the pathway, they are converted to androgens.
Cortisol treatment can prevent this overproduction.
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Adrenogenital Syndrome
(continued)
 Excessive androgen secretion in a woman
causes masculinization (adrenal virilism). Hair
develops on the face, a condition called
hirsutism, and the hairline recedes. The breasts
diminish in size, the clitoris enlarges, and
ovulation and menstruation cease. In an adult,
the cause is usually an androgen-secreting
tumor of the glands.
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Pheochromocytoma
 A rare tumor of the adrenal medulla that causes
overproduction of epinephrine and norepinephrine
 Occurs equally in men and women, most commonly
between the ages of 30 and 60
 Symptoms of palpitations, increased blood pressure,
rapid heart rate, chest pain, and weight loss may appear
suddenly and sporadically.
 Treatment: surgical removal the tumor; medications are
also used before surgery to control symptoms caused by
excessive epinephrine and norepinephrine
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Hypoadrenalism
 Addison’s disease—adrenal glands fail to
produce corticosteroids, aldosterone, and
cortisol
 Etiology: destruction or damage to the adrenal
glands by cancer, infections, or inhibited by
chronic use of steroid hormones, such as
prednisone; many cases are called idiopathic
 Aldosterone deficiency renders the patient
unable to retain salt and water. Kidneys are
unable to concentrate urine and, eventually,
dehydration ensues. Severe dehydration can
ultimately lead to shock.
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Hypoadrenalism (continued)
 Cortisol deficiency leads to low blood sugar, impaired
protein and carbohydrate metabolism, and generalized
weakness.
 Pituitary gland produces more corticotropin in response
to a deficiency of corticosteroids. Corticotropin normally
stimulates the adrenal gland and production of a skindarkening pigment called melanin. Persons with
Addison’s disease develop a peculiar yellow-brown
discoloration.
 Addison’s disease can be life-threatening and must be
treated with corticosteroid replacement. Injectable
cortisol treatment is used initially to treat severe cases.
Oral cortisol treatment is required for life. Medication to
restore normal excretion of salt and water is also
administered.
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Parathyroid Glands
 Four tiny glands
located on the dorsal
surface of the thyroid
gland
 The parathyroid
hormone (PTH)
secreted by these
glands regulates the
amount of calcium in
the blood.
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 If calcium levels in the
blood fall too low,
parathyroid hormone
levels in the blood are
increased and will
stimulate bone
breakdown to release
more calcium into the
blood.
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Figure 13-12: Parathyroid glands.
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Function of the Parathyroids
 Regulate the level of circulating calcium and
phosphate, and osteoclastic and osteoblastic
activity
 When the blood calcium level falls,
parathormone is secreted.
– Parathormone increases the amount of calcium that is
absorbed out of the digestive tract by interaction with
ingested vitamin D.
– It prevents a loss of calcium through the kidneys and
releases calcium from bones by stimulating
osteoclastic activity.
– When the proper level of circulating calcium is
restored, parathormone is no longer released.
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Hyperparathyroidism
 Excessive parathormone raises the level of
circulating calcium above normal, the condition
called hypercalcemia.
– Much of the calcium comes from bone resorption
mediated by parathormone. As the calcium level
rises, the phosphate level falls.
 With the loss of calcium, the bones tend to
weaken, bend, become deformed, and fracture
spontaneously. Giant cell tumors and cysts of
the bone sometimes develop.
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Hyperparathyroidism
(continued)
 Excessive calcium causes formation of kidney
stones because calcium forms insoluble
compounds.
 Calcium deposited within the walls of the blood
vessels makes them hard. It may also be found
in the stomach and lungs.
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Figure 13-13: Tetany of the hand in hypoparathyroidism.
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Complications of Hyperparathyroidism
– Hypercalcemia
 See Table 13-3
 Kidney stone formation
 Calcification of blood vessel walls
 Calcification of organ walls
 Spontaneous fractures
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Hyperparathyroidism
 With its concurrent excess of calcium, causes
generalized symptoms
 Bone pain, depression of the nervous system
and muscle weakness; heart muscle is affected
and the pulse slows
 Gastrointestinal disturbances, abdominal pain,
vomiting, and constipation develop.
 Deposits of calcium sometimes form in the eye,
causing irritation and excessive tearing.
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Hyperparathyroidism
(continued)
 Hyperparathyroidism usually results from a
tumor. If the tumor is removed, parathormone
secretion returns to normal, and the level of
circulating calcium is again properly controlled.
 Hyperparathyroidism can develop from other
conditions that reduce the level of circulating
calcium. Any decrease in calcium stimulates the
parathyroid glands to hypertrophy and to
increase their rate of secretion.
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Table 13-3: Complications of hyperparathyroidism hypercalcemia
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Hypoparathyroidism
 The principal manifestation of
hypoparathyroidism is tetany, a sustained
muscular contraction.
 The muscles of the hands and feet contract in a
characteristic fashion.
 Laryngeal muscles are very susceptible to these
spasms, which can obstruct the respiratory tract,
and death may follow.
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Hypoparathyroidism (continued)
 The low level of calcium in the blood,
hypocalcemia, makes the nervous system
hyper-excitable.
 As the nerves discharge spontaneously, the
skeletal muscles are over-stimulated.
 Administration of calcium and vitamin D, which
assists in the absorption of calcium from the
gastrointestinal tract, will correct the condition.
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Pancreas
 Located along the lower
 Insulin, produced by islet cells,
curvature of the stomach.
 The only organ in the body that
has both endocrine and
exocrine functions.
 The exocrine portion of the
pancreas releases digestive
enzymes through a duct into
the duodenum of the small
intestines.
 The endocrine sections of the
pancreas, islets of
Langerhans, produce insulin
and glucagon.
stimulates the cells of the body
to take in glucose from the
bloodstream.
 Loss of insulin results in
diabetes mellitus (DM) and
hyperglycemia, which is a high
blood sugar level.
 Overproduction of insulin will
result in hypoglycemia, or a
low blood sugar level.
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Figure 13-14: Islet of Langerhans.
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Figure 13-15: Control of blood glucose level.
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Endocrine Function of the
Pancreas
 Control of glucose level in the blood; accomplished
through the secretion of two hormones, insulin and
glucagon
– Insulin is secreted by certain cells of the pancreas called beta
cells, located in patches of tissue named the islets of
Langerhans or pancreatic islets.
– Lowers serum glucose, insulin facilitates the entry of glucose into
the cells where it is primarily stored as glycogen and metabolized
for energy. Glucose enters primarily skeletal muscle cells and fat
cells.
 Glucagon is secreted by the alpha cells of the islets.
– When the level of blood glucose falls below normal, glucagon is
released. Glucagon circulates to the liver and stimulates the
release of glucose from its stored form, glycogen
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Diabetes Mellitus
 Type 1
 Type 2
 Destruction of the islet
 The person makes a
cells; the person fails to
produce an adequate
amount of insulin
 Must take insulin
injections to replace the
insulin the pancreas is
unable to produce
 Called insulin-dependent
diabetes mellitus (IDDM)
sufficient amount of
insulin, but it has lost its
ability to influence the
cells of the body.
 Do not take insulin
 Called non-insulindependent diabetes
mellitus (NIDDM)
 Treated by diet, exercise,
and oral medications
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Table 13-2: Hyperadrenalism Signs and Symptoms.
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Symptoms of Diabetes Mellitus
 Polyuria, caused by excessive filtration of
glucose into the kidney tubule and the volume of
water required to carry it away, or the diuretic
effect of glucose
 Excess glucose is excreted in the urine, a
condition called glycosuria
 Polydipsia: an unusual excessive thirst
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Symptoms of Diabetes Mellitus
(continued)
 Cells prefer to metabolize glucose, but in its
absence, cells metabolize fats first and proteins
last.
– Because glucose cannot enter the cells without the action of
insulin, the diabetic metabolizes a large amount of fat. Fat
metabolism produces a large number of fatty acids, ketone
bodies, acetone, and related substances.
 The production of acids lowers the body’s pH,
resulting in the condition of acidosis
– Normal pH range is 7.35 to 7.45.
– Coma and death results with a pH below 6.9 to 7.0.
– Weight loss and fatigue due to mobilization of fat and protein for
energy
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Complications of Diabetes Mellitus
 Atherosclerosis: increased lipid mobilization, serum






cholesterol, poor wound healing
Blockage of a coronary artery causes myocardial infarction
Thromboembolic strokes
Occlusion of a leg artery can result in gangrene;
atherosclerosis generally causes poor circulation
Diabetic retinopathy, a vascular disorder of the retina that can
result in blindness; the minute retinal blood vessels become
sclerotic and rupture
The nervous system is affected by poor circulation, as
manifested by pain, tingling sensations, loss of feeling, and
paralysis.
Kidney failure
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Figure 13-16: Complications of diabetes mellitus.
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Treatment of Diabetes Mellitus
 Regulation of diet, exercise, insulin, and hypoglycemic
medications
 Regulation of the proper insulin dosage may vary
– Illness or emotional stress can temporarily alter a patient’s
needs.
– Monitoring blood sugar levels is an essential part of diabetes
care. Self-monitoring of blood glucose enables the diabetic to
determine his or her blood glucose and adjust insulin dosage
according to a measured reading.
 Oral medications mostly used for type 2 diabetes
– These are oral hypoglycemic agents, which stimulate secretion
of insulin from beta cells that still have some capacity or make
cells more responsive to insulin.
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Diabetic Coma
 Develops from failure to take enough insulin or
deviation from a prescribed diet. Acidosis and
dehydration can follow if proper treatment is not
given immediately.
– Symptoms: deep, labored breathing, acidosis, fruity
acetone breath, dry mouth, flushed and dry skin
– Treatment of diabetic coma (diabetic ketoacidosis)
requires urgent replacement of fluids to correct the
dehydration. Insulin, usually given intravenously, is
given as well. Because diabetic coma adversely
affects sodium and potassium, the serum electrolytes
must be checked frequently as therapy proceeds.
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Insulin Shock
 Too much insulin, not enough food, or excessive





exercise
Symptoms: light-headedness, faintness, trembles, and
perspiration
Taking sugar in some form, candy or orange juice for
example, may be adequate treatment at this stage.
If the glucose level is not raised, speech becomes thick
and walking becomes unsteady. Double vision may be
experienced, a loss of consciousness may follow.
Without treatment coma may result. Shallow breathing
Intravenous injections of glucose must be given
immediately for insulin shock. The administration of
epinephrine raises the blood sugar level.
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Table 13-3: Complications of Hyperparathyroidism:
Hypercalcemia.
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Insulin Shock
 See Figure 13-7
 Difference between insulin shock and
diabetic coma
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Tests for Diabetes Mellitus
 Urine test for ketones
 Fasting blood glucose levels, glucose tolerance testing,
and glycosylated hemoglobin testing are used to monitor
and diagnose diabetes.
– For the fasting blood glucose level test, a sample of blood is
taken after the person has fasted for eight hours.
– The glucose tolerance test challenges the body’s ability to
secrete and use insulin. The test is performed after a 10-hour
fast. The patient drinks a standard glucose solution, and blood
and urine sample are taken and analyzed for the next three
hours. No glucose should appear in the urine, and the blood
glucose levels should not exceed 170 mg/dl of blood if insulin is
being produced and utilized.
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Tests for Diabetes Mellitus
(continued)
 Fasting blood glucose levels, glucose tolerance
testing, and glycosylated hemoglobin testing are
used to monitor and diagnose diabetes
(continued).
– Glycosylated hemoglobin determination is a simple
blood test that is used to monitor long-term control of
diabetes. It generally indicates the average blood
glucose levels over the past 90 days. Normal values
should be below 6, and levels for diabetics should be
less than 7.
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Abnormalities in Secretion
of Sex Hormones
 The gonads (ovaries and testes) are
endocrine glands as well as the source of
the ova and sperm.
 They secrete the hormones estrogen and
testosterone directly into the blood.
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Human Diseases: A Systemic Approach, 6e
Copyright ©2006 by Prentice-Hall, Inc.
Upper Saddle River, New Jersey 07458
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Hypergonadism (Hypersecretion)
 Abnormally increased functional activity of the gonads
before puberty produces precocious sexual development
in both sexes.
 In a male child, excessive production of testosterone
may be caused by a tumor in the testes.
– This causes rapid growth of musculature and bones but
premature uniting of the epiphyses and shaft of long bones.
– Normal height, therefore, is not attained.
 Hypersecretion of ovarian hormones in the female is rare
because of the negative feedback mechanism with
gonadotropic hormones.
Mulvihill, Zelman, Holdaway, Tompary, and Raymond
Human Diseases: A Systemic Approach, 6e
Copyright ©2006 by Prentice-Hall, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Hypogonadism in the Male
 Several factors can cause hypogonadism
– Congenital: born without functional testes
– The testes may fail to descend and thus atrophy
– Castration: the testes may be lost through castration
 Testes fail to develop because of lack of gonadotropic hormone.
 Loss of the male gonads before puberty causes the condition of
eunichism, in which sexual characteristics do not develop.
Development of male traits depends on testosterone secreted by the
testes.
 Castration after puberty causes some regression of secondary
sexual characteristics, but masculinity is retained.
 Hormonal therapy, the administration of testosterone, can be
effective.
Mulvihill, Zelman, Holdaway, Tompary, and Raymond
Human Diseases: A Systemic Approach, 6e
Copyright ©2006 by Prentice-Hall, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Hypogonadism in the Female
 Hyposecretion of hormones by the ovaries may
be caused by poorly formed or missing ovaries.
 When ovaries are absent or fail to develop,
female eunichism results.
 Secondary sexual characteristics do not
develop.
 A characteristic of this condition is excessive
growth of long bones because the epiphyses do
not seal with the shaft of the bone as normally
occurs at adolescence.
Mulvihill, Zelman, Holdaway, Tompary, and Raymond
Human Diseases: A Systemic Approach, 6e
Copyright ©2006 by Prentice-Hall, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Changes in Endocrine Function
with Age
 Decrease in growth hormone
– In men after age 30 a decrease in lean body mass
and decreases in thickness and strength of bone
matrix.
– Increased body fat is correlated with greater risk of
diabetes, heart disease, and cancer. Decreased bone
density makes bones more susceptible to fracture.
 A slight decrease in T3/T4 ratio, resulting in
decreased metabolic rate.
Mulvihill, Zelman, Holdaway, Tompary, and Raymond
Human Diseases: A Systemic Approach, 6e
Copyright ©2006 by Prentice-Hall, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Changes in Endocrine Function
with Age (continued)
 Aldosterone levels remain relatively steady: age-related
decline in the kidney’s sensitivity to aldosterone,
diminished capacity of the kidney to secrete renin when
needed.
 The body is less able to deal with the stress of changes
in blood pressure, dehydration, and disease in general.
There is an increased incidence of abnormalities in blood
pressure, sodium and potassium levels, acid/base
balances, and osmotic pressure.
 The pancreas retains the ability to secrete insulin at
normal levels with age, but tissue responsiveness to
insulin decreases. Insulin resistance leads to a greater
incidence of NIDDM.
 Androgen and estrogen levels drop with age.
Mulvihill, Zelman, Holdaway, Tompary, and Raymond
Human Diseases: A Systemic Approach, 6e
Copyright ©2006 by Prentice-Hall, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Diagnostic Procedures
 Serum Assay
– Growth hormone levels (pituitary disorders)
– TSH, T3, T4 (thyroid disorders)
– Parathyroid hormone, calcium (parathyroid disorder)
– Cortisol (adrenal disorder)
– Glucose levels, tolerance test, hemoglobin A1c
 Urine specimen and vasopressin test
 CT scan
 Ultrasound
Mulvihill, Zelman, Holdaway, Tompary, and Raymond
Human Diseases: A Systemic Approach, 6e
Copyright ©2006 by Prentice-Hall, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.